WB SAUNDERS

An imprint of Elsevier Science Limited

© Harcourt Publishers Limited 2002

© Elsevier Science Limited 2002. All rights reserved.

� is a registered trademark of Elsevier Science Limited

The right of Tim Mair, Tom Divers and Norman Ducharme to be identified as editors of this work has been asserted
by them in accordance with the Copyright, Designs and Patents Act 1988

All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any
form or by any means, electronic, mechanical, photocopying, recording or otherwise, without either the prior per­
mission of the publishers (Permissions Manager, Elsevier Science Limited, Robert Stevenson House, 1-3 Baxter's
Place, Leith Walk, Edinburgh EHI 3AF), or a licence permitting restricted copying in the United Kingdom issued by
the Copyright Licensing Agency, 90 Tottenham Court Road, London WIT 4LP.

First published 2002

Reprinted 2002

ISBN 0 7020 2486 4

BRITISH LIBRARY CATALOGUING IN PUBLICATION DATA

A catalogue record for this book is available from the British Library

LIBRARY OF CONGRESS CATALOGING IN PUBLICATION DATA

A catalog record for this book is available from the Library of Congress

NOTE
Medical knowledge is constantly changing. As new information becomes available, changes in treatment, proce­
dures, equipment and the use of drugs become necessary. The editors/authors/contributors and the publishers
have taken care to ensure that the information given in this text is accurate and up to date. However, readers are
strongly advised to confirm that the information, especially with regard to drug usage, complies with the latest legis­
lation and standards of practice.

Existing UK nomenclature is changing to the system of Recommended International Nonproprietary Names

(rINNs). Until the UK names are no longer in use, these more familiar names are used in this book in preference to
rINNs, details of which may be obtained from the British National Formulary.

Typeset by Phoenix Photosetting, Chatham, Kent

Printed in the UK by Bath Press Limited
The
publisher's
policy is to use
paper manufactured
from sustainable forests

I
Contributors
Jennifer E Adolf
Internist Private Practitioner
Ledgewood Equine Medical Center
Ontario, New York, USA
Dorothy Ainsworth
Associate Professor of Medicine
Department of Clinical Sciences
College of Veterinary Medicine
Cornell University
Ithaca, New York, USA
Fairfield T Bain
Internal Medicine Practitioner
Haygard-Davidson-McGee Associates
Lexington, Kentucky, USA
Michael A Ball
Private Practitioner
Early Winter Equine Medicine and Surgery
Lansing, New York, USA
Jacqueline Bartol
Private Practitioner
Rochester Equine Veterinary Clinic
Rochester, New Hampshire, USA
William V Bernard
Private Practitioner
Rood & Riddle Equine Hospital
Lexington, Kentucky, USA
Mark Bowen
HBLB Resident in Equine Thoracic Medicine
Sefton Equine Referral Hospital
Royal Veterinary College
University of London
Hatfield, Herts, UK
T Douglas Byars
Director of Internal Medicine
Haygard-Davidson-McGee Associates
Lexington, Kentucky, USA
Christina 5 Cable
Private Practitioner
Early Winter Equine Medicine and Surgery
Lansing, New York, USA
Gary Carlson
Professor of Equine Medicine
Department of Medicine
School of Veterinary Medicine
University of California, Davis
Davis, California, USA
Noah D Cohen
Associate Professor of Medicine
LA Medicine and Surgery, CVM
Texas A and M University
College Station, Texas, USA
Thomas J Divers
Professor of Medicine
Department of Clinical Sciences
College of Veterinary Medicine
Cornell University
Ithaca, New York, USA
Richard Drolet
Professor of Pathology
Universite de Montreal
Departement de Pathologie et Microbiologie
Saint Hyacinthe, Quebec, Canada
Normand G Ducharme
Professor of Surgery
Department of Clinical Sciences
College of Veterinary Medicine
Cornell University
Ithaca, New York, USA
G Barrie Edwards
Professor of Equine Studies
University of Liverpool
Leahurst
Neston, South Wirral, UK
xi
CONTRIBUTORS

Ryland B Edwards III Laurie R Goodrich

Clinical Assistant Professor of Large Animal Surgery PhD candidate for cellular and molecular biology
University of Wisconsin Department of Clinical Sciences
Madison, Wisconsin, USA Cornell University
Ithaca, New York, USA
Andrew T Fischer Jr
Private Practitioner Richard Hackett
Chino Valley Equine Hospital Professor of Large Animal Surgery
Chino, California, USA
Department of Clinical Sciences
Cornell University
Lisa A Fortier
Ithaca, New York, USA
Assistant Professor of Surgery and Molecular Medicine
Department of Clinical Sciences
Reid Hanson Jr
College of Veterinary Medicine
Associate Professor of Surgery
Cornell University
Department of Large Anrmal Surgery and Medicine
Ithaca, New York, USA
Auburn University
David E Freeman Auburn, Alabama, USA
Associate Professor of Equine Surgery
Head of Equine Surgery and Medicine Philip D Van Harreveld
University of Illinois Associate
College of Veterinary Medicine Vermont Large Animal Clinic
Urbana, Illinois, USA Milton
Vermont, USA
Sarah L Freeman
Lecturer in Equine Surgery
Mark H Hillyer
Department of Farm Animal and Equine Medicine and
Lecturer in Equine Soft Tissue Surgery
Surgery Studies
Department of Veterinary Medicine
Royal Veterinary College
University of Bristol
University of London
Langford House, Bristol, UK
Hatfield, Herts, UK

John Freestone J Geoff Lane

Resident Veterinarian Senior Lecturer in Veterinary Surgery

Coolmore Australia School of Veterinary Science

Jerry's Plains University of Bristol

New South Wales, Australia Langford House, Bristol, UK

Susan L Fubini Jean-Pierre Lavoie

Professor of Surgery Professor of Equine Medicine
College of Veterinary Medicine Departement de Science Cliniques
Cornell University Universite de Montreal
Ithaca, New York, USA Saint Hyacinth, Quebec, Canada

Earl Gaughan
Sandy Love
Professor of Large Animal Surgery
Head of Division of Equine Clinical Studies
Department of Clinical Sciences
Kansas State University Department of Veterinary Medicine
University of Glasgow
Veterinary Medical Teaching Hospital
Bearsden, Glasgow, UK
Manhattan, Kansas, USA

Robin D Gleed J Lyons

Associate Professor of Anesthesiology Veterinary Student
Department of Clinical Sciences Faculty of Veterinary Medicine
Cornell University University College Dublin
Ithaca, New York, USA Dublin, Republic of Ireland

xii
 CONTRIBUTORS

Tim S Mair Claude A Ragle

Private Practitioner Associate Professor of Equine Surgery
Bell Equine Veterinary Clinic College of Veterinary Medicine,
Mereworth, Maidstone Washington State University
Kent, UK Pullman, Washington, USA

Celia Marr Peter Rakestraw

Head of Equine Division Assistant Professor of Large Animal Surgery
Department of Farm Animal and Equine Medicine and Texas A and M University
Surgery Large Animal Medicine and Surgery
Royal Veterinary College College Station, Texas, USA
University of London
Hatfield, Herts, UK Sarah Ralston
Associate Professor of Animal Sciences
PO Eric Mueller Department of Animal Science
Associate Professor of Surgery Rutgers University
Department of Large Animal Medicine New Brunswick, New Jersey, USA
College of Veterinary Medicine
University of Georgia Johanna M Reimer
Georgia, USA Private Practitioner
Rood and Riddle Equine Hospital
Michael J Murray Lexington, Kentucky, USA
Professor in Equine Medicine
Marion Dupont Scott Equine Medical Centre BA Rucker
Leesburg, Virginia, USA Private Practitioner
SW Virginia Vet Services
James A Orsini
Lebanon, Virginia, USA
Associate Professor of Surgery
University of Pennsylvania School of Veterinary
Elizabeth Santschi
Medicine
Clinical Associate Professor of Large Animal Surgery
Philadelphia, Pennsylvania, USA
University of Wisconsin-Madison
Madison Wisconsin, USA
Simon F Peek
Clinical Assistant Professor of Medicine
Jim Schumacher
Department of Medical Sciences
Professor of Equine Surgery
The University of Wisconsin-Madison
Department of Clinical Sciences
Madison, Wisconsin, USA
Auburn University
Auburn, Alabama, USA
Gillian Perkins
Instructor in Large Animal Medicine
Chris M Schweizer
Department of Clinical Sciences
Lecturer in Therogeniology
Cornell University
Cornell University
Ithaca, New York, USA
Ithaca, New York, USA

Scott Pirie
Lecturer in Veterinary Medicine Stacey A Semevolos

Easterbush Veterinary Centre Lecturer in Large Animal Surgery

University of Edinburgh LA Medicine and Surgery, CVM

Rosylin, Midlothian, UK Texas A and M University

College Station, Texas, USA
Chris J Proudman
Lecturer in Equine Surgery Kim Sprayberry
University of Liverpool Practitioner of Internal Medicine
Leahurst, Neston Haygard-Davidson-McGee Associates
South Wirral, UK Lexington, Kentucky, USA

xiii
CONTRIBUTORS

Frank GR Taylor R Weller

Senior Lecturer in Equine Medicine Student in Equine Surgery
Division of Companion Animals Department of Farm Animal and Equine Medicine
University of Bristol and Surgery Studies
Langford, Bristol, UK Royal Veterinary College
University of London
Beth Valentine Hatfield, Herts, UK
Assistant Professor
Department of Biomedical Sciences Jamie Whiting
College of Veterinary Sciences Internist
Oregon State University Dubai Equine Hospital
Corvallis, Oregon, USA Dubai, UAE

Catherine Walsh Alison A Worster

Resident in Anaesthesiology Resident in Animal Surgery
Department of Clinical Veterinary Medicine Department of Clinical Sciences
University of Cambridge Cornell University
Cambridge, UK Ithaca, New York, USA
 -

Plate 2.1 Normal peritoneal fluid sample showing neu­ Plate 2.4 Yellow-green discoloration of peritoneal fluid
trophils and large mononuclear cells (macrophages and caused by leakage of bile into the abdomen
mesothelial cells). A small number of red blood cells are
present caused by iatrogenic bleeding during collection of
the sample

Plate 2.2 Peritoneal fluid from a horse with early bowel

rupture showing the presence of plant material in the
fluid in the absence of an increase in neutrophils

Plate 2.5 Normal endoscopic view of the stomach of a 2-

week-old foal. The stomach is seen along the right side
and greater curvature. The squamous mucosa (top) is nor­
mally pale, and because the stomach wall of foals is rela­
tively thin, submucosal vessels can be seen. Often the
spleen can be observed through the relatively translucent
stomach wall of foals. The glandular mucosa (bottom) is
normally red

Plate 2.3 Peritoneal fluid from a horse with hemoperi­

toneum showing free red blood cells and erythrocyto­
phagia by a macrophage
 Plate 4.1 Transillumination of large colon wall showing
mucosal stages of cyathostome larvae

Plate 2.6 Normal endoscopic view of the stomach of an

adult horse. The stomach is seen along the greater curva­
ture. The squamous mucosa (top) is normally pale and the
glandular mucosa (bottom) is normally red

Plate 4.2 Tapeworms (Anoplocephala perfoliata)

Plate 4.3 Strongylus vulgaris arteritis. Section through

mesenteric artery showing S. vulgaris larvae and
associated arteritis (courtesy JL Duncan)
Plate 2.7 Normal endoscopic view of the stomach of an
adult horse, seen along the lesser curvature of the stom­
ach. Gastric secretions can be seen at the bottom of the
plate and the antrum and pylorus lie underneath the shelf
of squamous mucosa along the lesser curvature. The
cardia, through which the endoscope has entered the
stomach, is just out of view at the top of the photograph
(arrow)
Plate 4.4 Ascarid impaction. Post-mortem appearance
showing numerous ascarids causing obstruction of the
small intestine (courtesy MJ Martinelli)

Plate 12.1 A large area of ulceration of the gastric squa­

mous mucosa adjacent to the margo plicatus along the
right side of the stomach in a 3-year-old Standardbred
racehorse that had poor appetite, weight loss, and inter­
mittent abdominal discomfort

Plate 11.1 In the early stage of distributive shock mucous

membranes become brick red and can form a dark red line
bordering the teeth

Plate 12.2 Generalized erosion and ulceration of the

gastric squamous mucosa along the lesser curvature in a
Plate 11.2 During the late stages of distributive shock
4-year-old Thoroughbred race horse with a poor appetite
mucous. membranes become cyanotic
and low-grade intermittent abdominal discomfort. The
endoscope can be seen entering the cardia at the top left
of the photograph
( Plate 12.5 Squamous cell carcinoma in a 15-year-old
Plate 12.3 The antrum of a 6-year-old Thoroughbred
horse that presented because of tachypnea and recent
steeplechase horse that presented because of poor perfor­
poor appetite. Multiple neoplastic masses can be seen in
mance and poor appetite. There is thickening with ulcera­
the gastric squamous mucosa. The neoplasia had extended
tion of a ruga
into adjacent abdominal viscera

Plate 12.4 Ulceration and inflammation with fibrosis of

the pylorus of the horse in Plate 12.1. There is pyloric
.
stenosis because of chronic ulceration and fibrosis. This
resulted in delayed gastric emptying and the ulceration
seen In Piate 1 L.l (among other sites of ulceration). The
tissue surrounding the pylorus felt very stiff when
manipulated with a biopsy forceps

Plate 13.1 Adhesions of jejunum causing kinking of

intestine and partial obstruction
Plate 13.2 Pedunculated lipoma originating closed to the Plate 13.5 Mid-jejunal intussusception. Surgeon's finger
mesenteric attachment to jejunum. This horse suffered present at the point of invagination of intussusceptum
recurrent colic as a result of partial obstruction caused by into intussuscipiens
this lipoma

Plate 13.3 Short loop of ileum and distal jejunum

entrapped and strangulated through the epiploic foramen

Plate 16.1 Type 4 rectal prolapse

Plate 13.4 Edema and sub-serosal hemorrhage of small

intestine. These changes are characteristic of anterior
enteritis
Plate 17.1 Post-mortem appearance of extensive fibrin Plate 17.4 Omental and mesenteric adhesions to a mesen­
deposition in diffuse septic peritonitis teric abscess caused by foreign body penetration of the
jejunum

Plate 17.2 Thick, turbid, orange peritoneal fluid typical of Plate 17.5 Hemangiosarcoma of the spleen causing hemo­
acute septic peritonitis (left) compared with peritoneal peritoneum in a pony
fluid sample from a normal horse (right)

Plate 17.3 Large mesenteric abscess due to Streptococcus Plate 17.6 Focal annular lymphosarcoma lesion of the
equi subsp. equi ('bastard strangles'), post-mortem small intestine causing partial bowel obstruction and
appearance recurrent colic
 Plate 18.2 Preputial edema in a gelding, caused by
Plate 17.7 Large mesenteric abscess which caused chronic hypoproteinemia secondary to small intestinal
and recurrent colic (post-mortem appearance) malabsorption (alimentary lymphosarcoma)

Plate 17.8 Gross post-mortem appearance of the large Plate 18.3 Severe alopecic skin lesions secondary to
colon of a case of sub-acute grass sickness, note the black small intestinal malabsorption (chronic inflammatory
coating over the firm fecal impaction exposed following bowel disease)
reflection of the colonic wall

Plate 18.1 Post-mortem appearance of granulomatous

enteritis showing enlargement of the mesenteric lymph
nodes
 Plate 19.2 Gross lipemia in a plasma sample (left) com­
pared with a normal plasma sample (right)

Plate 18.4 Severe coronitis as part of the skin lesions

associated with multisystemic eosinophilic epitheliotropic Plate 19.3 Fatty infiltration of the liver
disease

Plate 19.1 Large calcium bilirubinate choledocholith Plate 21.1 Large colon of a horse with phenylbutazone
(arrow) obstructing the common bile duct at the junction toxicosis. Note the line of demarcation between the
of left and right hepatic ducts affected right dorsal colon and the remainder of the large
colon
 Plate 23.3 Linear erosions and ulcers in the antrum,
Plate 23.1 Multifocal erosions and ulcer in the gastric
extending to the pylorus in a 5-month-old foal with inter­
squamous mucosa in a 4-week-old foal with no clinical
mittent, mild to moderate abdominal discomfort
signs of gastric ulcers. The ulcer at the top of the photo­
graph has contracting margins and is healing

Plate 23.4 Severe duodenitis in a 4-month-old foal that

presented with fever for 5 days, diarrhea, and acute
abdominal discomfort. There was severe, hemorrhagic
ulceration of the gastric squamous and glandular mucosal
Plate 23.2 Bleeding ulcer in the gastric glandular mucosa
surfaces. The duodenal mucosa was replaced by a fibrino­
of a 4-month-old foal that had been treated for pneumo­
necrotic exudate. A large blood clot is at the lower right of
nia but had a poor appetite that persisted after a favor­
the photograph
able clinical response to the pneumonia
 Plate 27.1 Post-mortem appearance of the small intestine
of a foal affected by Clostridium perfringens type C show­
ing hemorrhagic enteritis

Plate 23.5 Contracture of the stomach of a 3-month-old

foal, as a sequel to severe ulceration of the squamous
mucosa along the lesser curvature. The foal reportedly
had not had ulcer signs and was presented to the hospital
for fever of unknown origin.

Plate 27.2 Photomicrograph of cryptosporidial oocysts

(pink structures) in feces from a foal with cryptosporidial
diarrhea (100 x)

Plate 25.1 Overo mare and lethal white foal

Plate 28.1 Tyzzer's disease. Filamentous bacterium,

Clostridium pi/iformis, from the liver section of an affected
foal
Preface
Gastrointestinal diseases constitute a large and diverse
group of diseases. Many of them are common and seri­
ous, and they are encountered in horses of all ages,
breeds and types. The Manual of Equine Gastroenterology
is a comprehensive guide to the diagnosis and treat­
ment of gastrointestinal disorders in horses and foals.
The last 30 years have seen a dramatic advancement
in our knowledge about gastrointestinal diseases of the
horse, and this, coupled with advances in surgical
techniques and therapeutics, has led to considerable
improvements in the success rates for treatment of the
conditions. In some cases, successful treatment of an
individual horse involves the input of expertise in the
fields of surgery, internal medicine and critical care. As
these disciplines become more and more specialised, so
it becomes increasingly difficult for individual veterin­
arians to keep abreast of developments in all of these
areas. One of the main objectives of this manual is to
condense information from these separate fields into
one, readily accessible source.
We feel this text is unique in at least 2 ways: first and
foremost are the many wonderful contributions from
experts in the field of equine gastroenterology; second,
there is an almost equal blend of contributions from
European and American clinicians in private practice
or from university hospital clinicians. We would like to
dedicate this manual to all of our contributing authors,
who have in this text, as in their many other publica­
tions, contributed greatly to our understanding of the
diagnosis and treatment of equine gastrointestinal dis­
orders. We would like to thank Anne Littlejohn and
Debbie Lent for their assistance in maintaining
communications with the many authors, forwarding
materials from North America to Europe and preparing
several chapters. We trust you will find the book a useful
source of information for the management of equine
gastrointestinal disorders.
Tim Mair
Tom Divers
Norm Ducharme
2001
xv
 1
Physical examination
General physical examination
and auscultation
F Taylor
HISTORY AND GENERAL
OBSERVATIONS
When exploring the history of a patient with suspected
gastroenteric disease the following topics should be
included.
• has there been an associated change in the dietary
management?
• were there any medications or other treatments
prior to the onset?
• is the grazing safe (e.g. check for sandy topsoil,
agrochemicals, poisonous plan ts)?
• is the animal's food intake reduced; if so is this
associated with inappetance or evidence of
dysphagia?
• is the animal's demeanor normal, depressed,
excitable?
• in cases of abdominal pain, was the onset acute and
severe or insidious and low grade; is the pain
continuous or intermittent?
• are feces being passed; if so in what volume and
consistency, and with what regularity?
• is the worming history suited to the animal's
environment?
• has this animal suffered previous episodes; are
other animals in the group affected?
In addition, the age and sex of the patient may help to
narrow the differential diagnoses. For example, neona­
tal foals are prone to meconium retention (day 1) and
systemic infections which may involve the alimentary
tract (days 1-4). Older foals become susceptible to
gastrointestinal parasites and/or gastroduodenal ulcer­
ation, and horses below 3 years of age are more likely to
succumb to intussusception than adults. In stallions, the
possibility of inguinal herniation of the small intestine
should be considered in all cases of colic. In the mare,
uterine torsion in late gestation can produce colic-like
signs, whereas postpartum colic may be associated with
hemorrhage into the broad ligament, or rupture of the
cecum or colon during fetal expulsion.
PHYSICAL EXAMINATION AND
AUSCULTATION
The initial physical examination of a patient with
suspected gastroenteric disease should pay particular
attention to the head and trunk. Additional aids to
physical examination will be required and are outlined
in the latter part of this section.
The head
The rate, regularity, and quality of the pulse are most
easily appreciated at the facial artery as it crosses the
horizontal ramus of the mandible. The rate and
regularity are dictated by the heart (see below), but the
quality will also be influenced by peripheral events. An
increasing pulse rate of deteriorating quality suggests
circulatory compromise and impending shock.
The color of the mucous membranes and the capil­
lary refill time (CRT) reflect the horse's circulatory
3
1 PHYSICAL EXAMINATION
status. The normal appearance is moist and pink and
the normal CRT is less than 2 seconds. The CRT indi­
cates whether perfusion, hydration, and vascular tone
are impaired. Increasing refill times indicate progres­
sively inadequate perfusion and are usually accompa­
nied by dryness and discoloration of the membranes.
The mouth should be examined to detect abnormal­
ities of tooth wear, sharp edges on the cheek teeth, or
other dental or mucosal diseases which may interfere
with feeding.
The thorax and abdomen
Abnormal swellings, particularly of the ventral
thorax and abdomen, may reflect edema associated
with venous and/or lymphatic congestion, or hypo­
proteinemia. Abdominal distention in cases of colic is
frequently a result of tympany.
The heart is auscultated to assess rate and regularity.
Increases in the heart and pulse rate are influenced to
some extent by pain, but most particularly by dehydra­
tion, decreased venous return, and toxemia.
Rapid, shallow respiration can be a feature of pain
and/or metabolic acidosis. Severe gastric distention or
hindgut tympany will exert pressure on the diaphragm
resulting in dyspnea. On rare occasions dyspnea
accompanies rupture of the diaphragm, especially if
the hindgut is prolapsed.
Slight increases in rectal temperature can be associ­
ated with pain, but significant increases suggest infec­
tion. In cases of colic, temperatures in excess of 38.6°C
(101°F) suggest a differential diagnosis of a systemic
disease for which colic is an early incidental sign, for
example salmonellosis or acute peritonitis. A decreasing
temperature, coupled with a rapid weak pulse, indicates
the development of shock and carries a grave prognosis.
Abdominal auscultation
Abdominal auscultation enables appreCIation of gut
activity and its greatest value is in the assessment of
colic. At least four sites should be auscultated: these are
both paralumbar fossae and both sides of the lower
abdomen behind the costal arch.
Two types of sound can be appreciated: weak sounds
associated with localized bowel contractions (mixing
the ingesta), and louder fluid sounds or borborygmi
associated with propulsion of ingesta. Sounds heard in
the right paralumbar fossa reflect ileocecal (and possi­
bly cecocolic) valve activity and differ from sounds
heard at the other sites. Here, a period of silence is
broken once or twice a minute by a sudden rush of fluid
rumbling as secretions from one compartment pass
through the valve and hit the gas-fluid interface of the
next.
4
Increased movement (hyperperistalsis) can be pro­
voked by a simple obstruction in an otherwise healthy
gut. The best example is spasmodic colic in which con­
tinuous sounds, of greater than usual intensity, are
heard at all sites. In contrast, reflex movement is
reduced by inflammation and ischemia. An absence of
sound, or infrequent sounds of reduced intensity, may
therefore be associated with peritonitis or the develop­
ment of gut hypoperfusion during colic. An absence of
sound is also associated with alimentary paralysis as in
postoperative ileus and grass sickness.
The presence of entrapped gas (tympany) is
denoted by low-pitched tinkling sounds which may be
superimposed on other alimentary sounds - as, for
example, in tympany associated with spasmodic colic.
The localization of entrapped gas in a segment of the
large bowel may be appreciated by simultaneous
percussion and auscultation over the abdominal wall. A
resonant 'hollow' sound is audible where a volume of
gas is trapped against the body wall.
Nasogastric intubation
F Taylor
Apart from therapeutic applications, a nasogastric tube
may be used to deliver sugar solutions for absorption
tests, to assess fluid reflux, and to permit decompres­
sion in cases of gastrointestinal obstruction, or (with
care) to indicate the site of esophageal obstruction.
Nasogastric tubes are manufactured in foal, pony, or
horse sizes. Tubes with an additional hole set in the side
of the leading end are recommended and transparent
tubes are preferable since they allow the passage of
fluid to be seen. Because proprietary tubes are not grad­
uated along their length, it is useful to make an indeli­
ble mark around the circumference at a point that will
indicate that the leading end is approaching the
entrance to the larynx or esophagus. This distance is
approximately 30 cm for pony tubes and 35 cm for
horse tubes.
RESTRAINT
The horse is positioned diagonally in a corner with its
quarters against the wall to restrict backward and lateral
movements. The handler should stand to the left of the
horse's head with his/her back to the horse to minimize
injury if the horse rears. A secure headcollar is essential
but additional restraints will depend upon the horse's
temperament. A horse that struggles during intubation

is more likely to suffer a nosebleed and it is best to apply
a twitch to such patients. Sedation is possible where
clinical circumstances permit, but this will diminish the
swallow reflex as the tube is passed and could affect the
results of an absorption test if intubation is used for this
purpose.
PROCEDURE
The uncoiled tube is draped around the clinician's
neck to prevent it from trailing on the floor; this also
leaves the clinician's hands free to control the tube's
passage. In cold weather a rigid tube should be softened
by passing warm tap water through it. The first 10-
12 em of the leading end is then coated liberally with a
water-soluble lubricant and the tube is grasped just
behind this point for controlled insertion.
The right-handed clinician will be most comfortable
standing to the right of the horse's head with his/her
back to the horse. The handler should attempt to keep
Figure 1.1 Insertion of a nasogastric tube. The thumb of
the left hand is used to elevate the alar cartilage of the
right nostril and the tube is inserted along the floor of the
open nostril
PHYSICAL EXAMINATION 1
the head in a flexed position and the clinician rests
his/her left hand on the bridge of the nose above the
muzzle. Care should be taken not to occlude the oppo­
site nostril inadvertently. The thumb is then used to ele­
vate the alar cartilage of the right nostril, opening wide
the entrance to the nasal cavity.
The lubricated end of the tube is then placed on the
floor of the open nostril, slightly inclined toward the
nasal septum with its curvature directed downward
(Figure l.1), and advanced gently so that it follows the
floor of the ventral meatus. The tube's advance is
stopped once its preset mark arrives at the nostril, indi­
cating that the leading end is approaching the larynx or
esophagus. In most cases, onward passage will result in
entry into the larynx and trachea. To avoid this, the
tube should be turned through 90 degrees before being
advanced further. This has the effect of raising the level
of the leading end with respect to the larynx, thereby
bringing it closer to the opening of the esophagus lying
above the larynx.
Gentle pressure by the leading end against the
esophageal opening will then cause the tube to be
admitted by a swallow. If the tube is accidentally passed
into the larynx, it should be withdrawn to the nostril
mark, given an additional 90 degree turn to raise the
leading end higher, and advanced again. Alternatively,
if gentle pressure meets total resistance the tube is with­
drawn 2-3 cm and gently readvanced in the hope of
provoking a swallow.
If this maneuver fails on 3-4 occasions, the operator
should suspect that the end is pushing against the
pharyngeal recess above both the larynx and the
esophagus. In this instance the leading end is lowered
by turning the tube back through approximately
90 degrees before being advanced again.
CHECKING THE POSITION OF THE TUBE
The commonest error is to pass the tube into the larynx.
In this instance air can be blown or sucked through the
tube without resistance and shaking the larynx will pro­
duce a palpable 'rattle'. If the tube is clean, then unto­
ward effects are unlikely - it is simply withdrawn and
repositioned. When entering the esophagus, there is
often an accompanying swallow which may be repeated
on the downward passage of the tube. Successful intu­
bation is indicated by an increase in the resistance to
passage (esophageal tone) and the appearance of a
swelling in the upper third of the left jugular groove
which moves down the neck following the line of the
esophagus. In addition, there is resistance to air being
sucked through the tube due to esophageal collapse at
the leading end. Alternatively, a short, sharp blow of air
5
1 PHYSICAL EXAMINATION
down the tube produces a momentary inflation of the
esophagus which is seen in the left jugular groove; this
is a useful test if a distinct swelling has not been seen to
travel down the jugular groove.
Once satisfied that the tube is correctly placed the
clinician can advance it to the stomach. There is usually
an audible release of gas as the tube enters the stomach
and gaseous 'bubbling' sounds can be heard when
listening at the open end of the tube.
TUBE WITHDRAWAL
Any fluid medication which has been given by tube and
which is occupying its dead space should be blown
through to the stomach before removal. Failure to do so
may result in inhalation of spilt fluid as the tube is with­
drawn over the larynx. Thereafter, the tube should be
withdrawn slowly and carefully. Particular care should
be taken not to rush out the last 50 cm, otherwise
trauma to the highly vascular nasal mucosa may result
in a nosebleed.
Rectal examination
POE Mueller
INTRODUCTION
The rectal examination is one of the most important
and helpful diagnostic techniques for evaluating adult
horses with abdominal disease. It is frequently essential
in evaluating the need for surgery in horses with acute
abdominal pain (see Chapter 9). Rectal examination
may be used to identifY
• position of intestinal segments
• distention of bowel
• abnormalities of bowel wall thickness
• mesenteric lymphadenopathy
• mesenteric pain
• abnormal masses such as tumors, abscesses,
intussusceptions, foreign bodies
• excessive abdominal fluid
• pneumoperitoneum
• bowel rupture
• cranial mesenteric arteritis/aneurysm
• rectal perforation.
In addition, palpation of other intra-abdominal organs
is possible, including the urinary bladder, uterus and
ovaries, left kidney, and spleen.
6
TECHNIQUE
,,"" ,,, ,''11'' ,,�' \"1"""10' %Jlr'iMF'ot�' ,
When performing a rectal examination, proper
restraint is of the utmost importance to insure the
safety of the horse and the examiner. Inadequate
restraint may result in iatrogenic rectal perforation, a
potentially fatal complication of rectal examination, or
serious injury to the examiner. Horses with signs of
unrelenting abdominal pain should be sedated with an
alpha2 agonist agent such as xylazine (0.3-0.5 mg/kg
i.v.), detomidine (7-10 !lg/kg i.v.) or romifidine
(40-120 !lg/kg i.v.). For more profound sedation, and
to reduce the chance of the horse kicking, the alpha2
agonist may be combined with butorphanol (20 !lg/kg
i.v.). A nose twitch should always be used to control the
patient and promote relaxation of the rectum.
Adequate lubrication of the examiner's hand and arm
is necessary to minimize irritation to the rectal mucosa.
Hydrated methylcellulose and mineral oil are the most
commonly used lubricants. Initial introduction of the
examiner's hand through the anal sphincter is often met
with great resistance. This should therefore be per­
formed with a slow and steady motion. The fingers and
thumb of the hand should be kept together, in an
extended position throughout the entire examination.
Once the hand is through the anal sphincter the feces
within the rectum are evacuated. The amount and con­
sistency of fecal material in the rectum should be noted.
Absence of fecal material, or the presence of dry, fibrin
and mucus-covered feces is abnormal and is consistent
with delayed intestinal transit. Fetid, watery fecal mater­
ial is often present in horses with colitis. Large amounts
of sand within the feces may be indicative of a sand
impaction or sand-induced colitis. After evacuation of
feces from the rectum, intrarectal administration of
50-60 ml of 2% lidocaine via a 60 cc catheter tip syringe
(alternatively a soft tube such as an intravenous exten­
sion set connected to a regular syringe can be used) may
help promote further rectal relaxation and reduce strain­
ing. The syringe may also be used to administer addi­
tional lubrication into the rectum at this time.
The examiner's arm is then re-introduced into the
rectum and advanced slowly and steadily as far as com­
fortably possible. The arm is left in this position without
excessive movement for 20-30 seconds. In most cases
this initial delay in internal palpation will allow the rec­
tum to relax around the examiner's arm, facilitating a
more thorough palpation of the more cranial aspects of
the abdomen. Initial examination of the caudal aspects
of the abdomen with a half-inserted arm is not recom­
mended because it usually results in straining and
excessive peristaltic contraction of the rectum. This pre­
cludes a safe and thorough examination of the more
cranial abdominal contents.
 PHYSICAL EXAMINATION 1

The most severe complication associated with rectal • mesenteric stalk

palpation is iatrogenic perforation of the rectum (see • ventral cecal tenia (no tension)
Chapter 16). Although rare, tears usually occur dorsally • cecal base (empty)
between the 10 o'clock and 12 o'clock positions. Most • pelvic flexure (Figure 1.2).
rectal tears can be avoided by proper restraint, ade­
Normally, the duodenum and remaining small intes­
quate lubrication, and a steady and careful palpation
tine are too soft and relaxed to be identified unless an
technique. If a peristaltic contraction or increased resis­
underlying abnormality exists.
tance is felt during examination, the hand should
The spleen is located in the left dorsal abdomen.
immediately be withdrawn from the rectum to avoid
The caudal edge of the spleen is palpable against the
potential rectal injury as the descending colon can tear
body wall. The nephrosplenic ligament can be palpated
as it contracts on the examiner's hand.
coursing from the head of the spleen, to the right, to
The exact sequence of abdominal structures pal­
the caudal pole of the left kidney. Immediately dorsal to
pated during rectal examination may vary from practi­
the ligament is the renosplenic space. Three to four fin­
tioner to practitioner. Regardless of the sequence, the
gers may be placed in the renosplenic space. The cau­
examination should be performed in a consistent, sys­
dal pole of the left kidney is palpable just to the right of
tematic manner to assure a complete and thorough
the spleen; it may not be possible to reach the kidney in
examination and minimize the chance of missing a
some large horses. Moving the arm to the right and cra­
lesion. The author prefers a clockwise approach, start­
nially along the dorsal midline, the aorta, duodenum,
ing with the spleen in the left dorsal abdominal quad­
and mesenteric stalk may be palpated. The pulse in the
rant. This is followed by examination of the right dorsal,
aorta is easily palpable; the duodenum is identified as a
right ventral, and left ventral quadrants. The pelvic
small intestinal structure perpendicular and attached to
canal and more caudal structures are then examined
just before removal of the hand from the rectum.
In general, palpable characteristics of the abdominal
contents and viscera are often helpful in identifYing the
particular segment of the intestine involved in horses
with colic. Severe gas or ingesta-distended intestine,
tight mesentery or tenia (bands), or thickened or turgid
intestine are indicative of intestinal obstruction or
strangulation. Free peritoneal gas or crepitus within the
intestinal wall is usually indicative of intestinal rupture.
A gritty or granular texture of the peritoneal cavity is
indicative of intestinal rupture with contamination of
the serosal and peritoneal surfaces with ingesta. It
should be emphasized that rectal examination findings
should always be interpreted in conjunction with the
physical examination and laboratory findings.

RECTAL PALPATION OF THE NORMAL

HORSE

In the normal horse, moist, soft fecal balls should be

present in the rectal ampulla. The descending colon is
easily identifiable in the caudal abdomen. It contains
multiple, distinct fecal balls and is freely movable within
the abdomen. Other intra-abdominal structures palpa­
ble in the normal horse starting in the left dorsal
abdominal quadrant, and progressing in a clockwise
direction include
• caudal border of the spleen
• nephrosplenic (renosplenic) ligament
• caudal pole of the left kidney
Figure 1.2 Caudal view of a standing horse demonstrating
abdominal structures that are palpable in the normal
horse during rectal examination. Starting in the left dorsal
abdominal quadrant, and progressing in a clockwise
direction, palpable structures include: caudal border of
the spleen, renosplenic ligament, caudal pole of the left
kidney, ventral cecal tenia, cecal base, and the pelvic
flexure

7
1 PHYSICAL EXAMINATION
the mesenteric stalk. The mesenteric stalk is usually pal­
pable as a sheet of tissue, with a pulse that is only occa­
sionally palpable. In large horses it may not be possible
to reach far enough to palpate the root of mesentery.
Continuing to move in a clockwise direction, the
base of the cecum is palpable in the right dorsal abdom­
inal quadrant. Depending on the amount of ingesta in
the cecum, it may or may not be palpable. The ventral
and sometimes medial cecal tenia are usually palpable
by moving the hand laterally and caudally, hooking the
tenia with the tips of the examiner's forefingers. These
bands usually course in a dorsocaudal to ventrocranial
direction, just to the right of the midline. Because the
majority of the body and apex of the cecum are beyond
the examiner's reach, the tautness of the ventral and
medial cecal tenia is used as an indicator of the amount
of ingesta within the cecum. Normally the cecal tenia
should be loose and easily movable. With increased
amounts of ingesta in the cecum, the tenia become
more taut. Pain elicited upon palpation of the ventral
or medial cecal tenia may be associated with tension of
the ileum or its mesentery. This has been associated
with pain originating from the ileum and its vascula­
ture, such as occurs with entrapment of the ileum in the
epiploic foramen. The duodenum is attached dorsal to
the base of the cecum, but is normally too soft and
relaxed to be palpable. It may, however, sometimes be
palpable as it distends during a peristaltic contraction.
As the hand is moved ventral and caudal to the
pelvic brim, fecal balls in the small colon are usually eas­
ily identified. Small intestine is not usually felt unless it
contracts, when it may be palpable as a tight tubular
structure.
Moving caudally and to the left side, the pelvic flex-
8
ure may or may not be palpable in the caudal left
abdomen, depending on the amount of ingesta within
the large colon. If the pelvic flexure and left dorsal
large colon are palpable, they may be identified by soft
ingesta, and the absence of the tenia and haustra (sac­
culations). The adjacent left ventral colon contains sim­
ilar contents and has two free tenia and haustra. The
tenia should course in a cranial-to-caudal direction,
from the left caudal abdomen to the left cranial
abdomen (Figure 1.2). The left dorsal colon does not
have haustra and contains only one mesenteric tenia.
Additional structures in the caudal abdomen
included in a complete rectal examination include:
bladder, uterus and ovaries in the mare, the aortic
bifurcation, and the internal inguinal rings in the
stallion. The inguinal rings are identified just cranial,
lateral, and slightly ventral to the iliopectineal emi­
nence of the anterior brim of the pelvis. In stallions, the
inguinal rings are large enough for insertion of a finger.
If the testis or epididymis has descended, the ductus
deferens is palpable in the caudomedial aspect of the
ring. In geldings, the inguinal ring is palpable as only a
slight depression and decreases in size with age.
BIBLIOGRAPHY
Rectal examination
KopfN (1997) Rectal examination of the colic patient. In
Current Therapy in Equine Medicine 4th edn, N E Robinson
(ed.). W B Saunders, Philadelphia, pp. 170-4.
White N A (1998) Rectal examination for the acute abdomen.
In Current Techniques in Equine Surgery and Lameness 2nd
edn, N A White and] N Moore (eds). W B Saunders,
Philadelphia, pp. 262-70.
 2
Additional diagnostic procedures

Rectal biopsy PROCEDURE

The horse is restrained as for rectal palpation. The pro­

F Taylor
cedure is usually without discomfort to the patient,
apart from the clinician's hand passing into the rectum,
Diffuse lesions within the mucosa and submucosa of the
and the necessary restraints are minimal.
hindgut are often associated with chronic diarrhea and
A lightly lubricated gloved hand is introduced
can be characterized with surprising frequency in the
through the anal sphincter to wrist depth and the
histopathology of a rectal mucosal biopsy. Rectal biopsy
closed end of the sterilized instrument is passed into
is easily undertaken in the standing horse and therefore
the cupped palm using the other hand (Figure 2.2). A
offers a clear advantage over more proximal intestinal
mucosal fold in the roof of the rectum is palpated and
biopsies which must be obtained either under general
held between finger and thumb and the instrument
anesthesia or via a standing flank laparotomy.
advanced with the jaws open to 'snag' the fold in an
A variety of human rectal and cervical biopsy instru­
adjacent dorsolateral position. Taking biopsies from a
ments are suitable for this purpose. The most suitable dorsolateral position (at 1 o'clock or 1 1 o'clock) avoids
have a folding upper jaw that cuts the specimen against damage to the dorsal vasculature.
a rigid lower jaw (Figure 2.1).

Figure2.2 Rectal biopsy i n the horse. A f o l d of rectal

Figure2.1 Rectal biopsy instrument with a folding upper mucosa is held between a finger and the thumb of one
jaw and rigid lower jaw hand and the i nstrument advanced to obtain a biopsy

9
2 ADDITIONAL DIAGNOSTIC PROCEDURES
The jaws are closed and the sample is removed and
transferred to fixative. If required, a second biopsy for
homogenization and culture may be attempted in the
opposite dorsolateral position. This specimen should
be transferred to sterile saline.
It should be noted that while rectal biopsies can
reflect pathology in the more cranial large bowel, nor­
mal (negative) specimens do not rule out the presence
of colonic lesions.
Liver biopsy
F Taylor
Most of the equine hepatopathies are associated with
diffuse lesions so that biopsy usually provides a repre­
sentative sample for histopathology. Contraindications
for biopsy are
• clinical evidence of concurrent coagulopathy
• suspicion of liver abscessation.
Several medical biopsy instruments are suitable for
the purpose. The 14-gauge disposable Tru-cut needle
(Baxter Healthcare Corporation, CA) retrieves good
specimens with practice. A 1 53-mm (6-in) length is suit­
able for most horses. A spring-loaded automatic biopsy
needle is also available.
BIOPSY SITE
The optimal site for biopsy on the right side can be
ascertained by ultrasonography. If the liver cannot be
visualized by ultrasound on the right, it can almost
always be seen in the left ventral rostral abdomen just
caudal to the diaphragm in front of the spleen. In the
absence of ultrasound the approach is the same for all
instruments. A site is selected in the 1 3th intercostal
space on the right hand side, just in front of the 14th
rib, midway between a 'wedge', the upper and lower
limits of which are delineated respectively by imaginary
lines drawn from the point of the hip to the point of the
shoulder, and from the point of the hip to the point of
the elbow. The 1 4th rib is located by counting back
from the 1 8th rib, ignoring 'floating ribs' (Figure 2.3 ) .
PROCEDURE
Depending upon temperament, the horse may need to
be sedated. An area 100 cm square is clipped and surgi­
cally prepared at the chosen site. Using sterile precau-
10
Figure 2.3 The site for liver biopsy in the horse. A site is
sel ected in the 1 3th intercostal space on the right side
between a n imaginary line from the point of h i p to the
point of shoulder, and another line from the point of hip
to the point of el bow
tions the skin and intercostal muscle beneath are infil­
trated down to the parietal pleura with 4-5 ml of 2%
lignocaine using a 39 x 0.8 mm needle.
A 5 mm skin incision is then created just in front of
the 1 4th rib, taking care to avoid the intercostal vessels
and nerves that run along the caudal border of the
acljacent rib. The biopsy needle is introduced through
the incision, into intercostal muscle and then directed
some 1 0 degrees backwards to pass through the
diaphragm. If insertion is made at the point of fuJI expi­
ration, the risk of damage to the lung is minimized.
When released from the operator's grip, the needle
should be seen to move with the respiratory excursions
of the diaphragm.
The needle is then advanced 5 cm or so into the
liver, which has a 'solid' feel, at this point the instru­
ment is operated. On withdrawal the core of tissue
should be dark in color and sink in fixative. If the first
attempt yields nothing (or a pale tissue that does not
readily sink) , two further attempts may be made
through the same incision, redirecting the needle
slightly and maintaining sterile precautions. If there is
prior clinical evidence of liver infection, a sample
should also be submitted for culture in a sterile con­
tainer.
If the procedure is unsuccessful, it is possible to
repeat it at a different site, preferably after a lapse of 24
hours. Using a 'blind' procedure it is advisable to try
one intercostal space further back, but in older horses
atrophy may cause the liver to be drawn further
forward.
A single interrupted suture may be placed in the
wound . The horse is rested for at least 1 hour to permit
clotting within the biopsy tract.

Complications are rare. Tissues other than liver (e.g.
diaphragm, lung, colon) may be inadvertently sampled
without untoward effect. However, if the core of tissue
obtained does not have the 'feel', color, or texture of
liver it is advisable to give a short course of antibiotics in
case of bowel penetration. Serious hemorrhage is a rare
complication of liver biopsy in the horse, even in
advanced disease.
Clinical pathology
F Taylor
Clinical pathology is complementary to a thorough clin­
ical examination rather than a substitute. It should be
used to confirm a diagnosis or to assist in the systematic
deduction of a diagnosis. Routine clinical pathology
includes hematology, serum or plasma biochemistry,
fluid, electrolyte, and acid-base balance, and fecal
analysis.
HEMATOLOGY
Useful parameters of hematology in the evaluation of
gastroenteric disease are the packed cell volume (PCV) ,
indicators of anemia, and the white cell count (WBC) .
In sub-acute (> 36 hours in duration) or chronic condi­
tions, the plasma fibrinogen concentration should also
be requested; in some laboratories this assay is under­
taken by the hematologist.
Erythrocyte parameters
The PCV is a useful monitor of dehydration and hypo­
volemia if used on a sequential basis. In general terms,
a pev greater than 45 per cent indicates a reduction in
extracellular fluid volume and a loss of sodium. Patients
with a PCV greater than 60 per cent usually have a poor
prognosis, but this is not invariably so.
Anemia is indicated by a significant reduction in
PCV, red cell count (RBC) and hemoglobin concentra­
tion (Hb) . However, acute hemorrhage is only reflected
in the hematology profile after 1 2-24 hours, by which
time there is a compensatory influx of tissue fluid. This
reduces the PCV, RBC, and Hb, and dilutes plasma
protein concentrations. Chronic anemia in the horse is
often non-regenerative and is usually associated with
chronic inflammatory processes. However, a chronic
regenerative anemia could reflect chronic hemorrhage
into the gut or abdomen.
ADDITIONAL D IAGNOSTIC PROCEDU RES 2
Leukocyte parameters
Leukopenia (WBe < 6.0 x 1 0"/1 ) , predominantly due to
neutropenia, is a feature of peracute/acute diseases of
the gastrointestinal tract, for example gut ischemia (as
in surgical colics) , peritonitis , or salmonellosis. In these
situations the count may fall to 2-3 x 1 0"/1, and
neutropenia is especially pronounced in the presence
of endotoxin.
Leukocytosis may accompany acute, progressive, or
more chronic inflammation of the gastrointestinal
tract. This 'reactive leukocytosis' usually features neu­
trophilia and may be accompanied by immature band
forms (,left shift') in acute conditions and a monocyto­
sis in chronic conditions.
Eosinophilia is popularly associated with parasitism,
but high burdens of mature worms do not seem to
affect the circulating eosinophil count. In many
instances eosinophilia probably reflects some form of
hypersensitivity response.
Plasma fibrinogen concentration
The fibrinogen concentration is raised by inflammation,
most particularly septic inflammation, and its level indi­
cates the severity of disease. Concentrations increase
within 1-2 days of an infection, but peaks are not
attained until 3-4 days. A modest increase may therefore
reflect early disease, or alternatively, a chronic low grade
inflammation. High concentrations indicate advanced
and serious disease with a guarded prognosis.
PLASMA OR SERUM BIOCHEMISTRY
Total plasma protein (TPP)
Sequential TPP estimations can be used to monitor dehy­
dration in cases of colic or diarrhea. However, in the
severely compromised gut there may be a concurrent
and progressive loss of protein into the peritoneal cavity
or bowel lumen, thus rendering the technique inferior
to sequential determinations of PCV in whole blood.
Albumin
In horses, hypoalbuminemia is almost invariably associ­
ated with a protein-losing enteropathy as a result of
some lesion within the intestinal mucosa. Much rarer
causes are glomerulonephropathy, liver failure, or
massive exudative effusion.
Globulins
Apart from dehydration, total globulin concentrations
may also be increased by
11
2 ADDITIONAL DIAGNOSTIC PROCEDURES

• acute and chronic inflammatory processes - Electrolyte balance

increases in acute phase protein and
The interpretation of serum or plasma electrolytes in
immunoglobulin concentrations respectively
gastroenteric disease should be undertaken with
• strongyle parasitism - increases in IgG(T)
caution. Increases in sodium, potassium, and chloride
• liver failure - decreased catabolism of globulins.
concentrations are consistent with water deprivation
and dehydration, but there is usually a concurrent
Albumin:globulin (A:G) ratios loss of electrolytes to the gastrointestinal tract. High
obstructive colic is associated with a loss of water,
In health, the A:G ratio approximates to 1 .0. Shifts in
sodium, and chloride from the plasma, but in cases of
the ratio may occur in a number of pathological states.
lower bowel pathology relatively more potassium and
However, the information is seldom useful since it lacks
bicarbonate ions are lost. A meaningful interpretation
specificity. It follows from the preceding paragraphs
of electrolyte shifts can only be undertaken with a
that a fall in this ratio, because of a decrease in albumin
knowledge of the concurrent acid-base status.
and/or an increase in globulin, may be a feature of
either inflammatory intestinal disease, strongyle para­
sitism, liver failure, or any inflammatory process. Acid-base balance

Metabolic acidosis is the most common acid-base disor­

Serum alkaline phosphatase (SAP or ALP)
The brush border of the intestinal epithelium is richly
endowed with ALP and cellular damage increases its cir­
culating concentration. However, ALP is not organ spe­
cific and damage to bone or the biliary tract of the liver
will also increase the circulating ALP concentration.
Many laboratories will assay the isoenzyme intestinal
alkaline phosphatase (lAP) which may help to identity
the origin of a raised ALP.
FLUID, ELECTROLYTE, AND ACID-BASE
BALANCE
Fluid, electrolyte, and acid-base disturbances are asso­
ciated with severe diarrhea and those acute colics in
which fluid is sequestered in the gut lumen and/or
there is associated strangulation. In diarrhea, the extent
of' fluid and electrolyte losses and the development of
acidosis depends upon the severity of the enteric lesion
and whether or not the patient continues to drink
during the illness.
Fluid balance
Simple blood parameters such as PCV and TPP can be
used to indicate the severity of dehydration (see
above) . However, where facilities exist they are best
used in a serial manner to follow the course of dehy­
dration over a critical period. Most serum or plasma
biochemistry parameters, including urea, are also
raised by acute dehydration. However, increases in
both urea and creatinine beyond their normal ranges
indicate prerenal failure associated with deteriorating
perfusion.
der in horses and occurs most frequently in association
with obstructive gastrointestinal disease and diarrhea.
The underlying causes of acidosis in these situations are
either increased base loss and/or reduced peripheral
perfusion (most commonly) causing a switch to
predominantly anaerobic metabolism in tissues with a
consequent build up of lactate.
Although blood gas and pH measurements provide
the only accurate guide to acid-base status, plasma
bicarbonate estimations are acceptable for most clini­
cal situations. However, this requires venous blood
samples to be collected anaerobically for immediate
processing using equipment that may not be readily
available. In practical terms however, the need to
correct a metabolic acidosis by specific bicarbonate
therapy is rare if fluid and electrolyte requirements
are met.
FECAL ANALYSIS
Fecal worm egg count (FWEC) (see Chapter 4 )
Strongyle eggs are readily identified i n the laboratory
using a flotation technique, but it is difficult to distin­
guish between large and small species. However, small
strongyle (cyathostome) eggs usually comprise the vast
m<tiority of the count (> 90% ) .
Presence of fecal larvae ( see Chapter 4)
Unlike worm eggs, larvae are separated from a fecal
sample by sedimentation using the Baermann appara­
tus. Alternatively, a wet fecal smear may be examined
under the microscope. Fresh samples should be
analyzed rapidly and not refrigerated.

12

Bacterial culture of feces
Fecal samples inevitably contain a great many organ­
isms with differing requirements for culture in vitro.
When submitting samples it is therefore necessary to
define the organism (s) of interest to enable selective
culture in the laboratory. In suspected salmonellosis the
num bers of Salmonella organisms shed may be very low,
even during the acute stage of disease. In consequence,
a minimum of three and preferably five fecal samples
should be collected from the rectum at 24-hour inter­
vals to increase the possibility of detection. An adequate
sample should occupy half a universal tube, approxi­
mately 10 ml; swabs are usually unsatisfactory.
Clostridiosis (usually Clostridia perfringens or diJficile) is
another differential diagnosis in cases of
peracute/ acute toxemic colitis. A half universal tube of
feces taken from the rectum is submitted for anaerobic
culture as soon after collection as possible, again swabs
are unsatisfactory. Specific toxin analysis may also be
performed for C. perfringens and difficile.
Fecal leukocytes
The presence of leukocytes and occasionally epithelial
cells in a fecal sample suggests inflammatory injury to
the distal intestinal mucosa; they are a feature of severe
diarrhea (fluid feces), particularly in the acute stage.
High numbers suggest the presence of an intestinal
pathogen such as Salmonella spp.
Fecal blood
If blood is clearly visible in the feces a red discoloration
suggests a recent, distal source such as the small colon
or rectum, while a dark to black discoloration (melena)
suggests a source in the proximal gastrointestinal tract
or large colon. Chronic gastrointestinal loss is usually
occult and may be associated with a state of chronic
regenerative anemia. In the laboratory, fecal occult
blood may be detected qualitatively by demonstrating
the presence of hemoglobin. Fecal occult blood tests in
the horse are not as sensitive or specific as they are in
most other species.
Fecal sand
Sand ingestion from topsoil or water courses may be
associated with colonic impaction and severe diarrhea.
If this is suspected then feces should be tested for the
presence of sand. One volume of feces is mixed vigor­
ously with two volumes of water in a clear container and
allowed to settle. Sand sediments to the base of the mix­
ture; the feces of a healthy individual from an adjacent
location should be tested for comparison.
ADDITIONAL DIAG N OSTIC PROCE D U RES 2
Abdominocentesis
(abdominal paracentesis)
T Mair
INTRODUCTION
Abdominocentesis can be one of the most useful diag­
nostic techniques in horses affected by abdominal
disease. Analysis of the peritoneal fluid reflects the
changes that occur in the tissues and organs within the
abdomen and on the peritoneal surface. The technique
can be useful in the determination of the need to per­
form surgery in acute abdominal pain, as well as in the
diagnosis of peritonitis, hemoperitoneum, and some
forms of abdominal neoplasia (see Chapter 1 7) .
ABDOMINOCENTESIS IN THE ADULT
HORSE
A rectal examination should always be performed
before abdominocentesis in order to recognize an
extremely gas-distended or ingesta-filled cecum or large
intestine. If these abnormalities are identified, extreme
care must be taken when performing abdominocentesis
to avoid accidental enterocentesis.
Abdominocentesis can be performed using either a
needle or a blunt-ending cannula such as a teat cannula
or metal bitch urinary catheter. A blunt-ended cannula
is recommended in horses with intestinal distention or
when a heavy viscus is known to be lying on the ventral
abdominal floor. In other horses, the simplest method
is to use an 1 8- or 1 9-9auge, 3.8 cm (l.5 inch) hypoder­
mic needle. Longer needles may be necessary in obese
horses because of the thickness of the layer of retroperi­
toneal fat. The most dependent site of the ventral
abdomen is prepared and the needle is inserted directly
through the linea alba (Figure 2.4) . Alternatively the
needle can be placed just to the right of the midline to
reduce the risk of splenic puncture. A 3.8 cm needle
may be too short in large and fat horses, since it may not
be long enough to penetrate through the layer of sub­
peritoneal fat (Figure 2.5 ) . Entry of the needle into the
peritoneal cavity is indicated by the flow of varying
amounts of fluid which is collected into a sterile tube
containing edetic acid (EDTA) for cytological analysis,
and a second plain sterile tube (not containing addi­
tives) for culture and sensitivity if required. Normal
peritoneal fluid is pale yellow and clear. If the needle
penetrates bowel (usually cecum or colon) (Figure 2.6)
intestinal contents may drip from the needle; this fluid
13
2 ADDITIONAL DIAGNOSTIC PROCEDURES
----------------� I'"
6
6 the sample will be suitable for cytology. An accidental
Figure 2.4 Abdominocentesis showing the position of
needle placement at the most dependent part of the
abdomen. The needle is i nserted through the l i nea alba
and sub-peritoneal fat to enter the peritoneal cavity
Figure 2.5 Abdominocentesis showing fa i l ure to penetrate
the sub-peritoneal fat l ayer because the needle is too
short
14
Figure 2.6 Abd o m inocentesis showing accidental pu ncture
of the intestine
will appear dark brown or yellow and turbid and will
have a characteristic malodor. If this happens the
needle should be either completely withdrawn, or with­
drawn until it exits the bowel and its tip lies in the
peritoneal cavity. As peritoneal fluid drains through
the needle, it will clear it of contaminated material, and
enterocentesis such as this is very unlikely to cause any
problems in adult horses. Although a mild inflamma­
tory peritoneal reaction will result antibiotic therapy is
unlikely to be necessary.
Peritoneal fluid usually flows from the needle spon­
taneously, although repeated relocation and reposition­
ing of the needle tip may be required until it enters a
pocket of peritoneal fluid. Aspiration rarely helps, and
may simply suck omentum, peritoneum, or bowel wall
into the needle. If fluid is not obtained, insertion of a
second or third needle a few inches away will often be
successful. Air may be blown into one of these needles
using a sterile syringe to break the vacuum in the
abdomen and permit drainage of peritoneal fluid
through the most ventrally placed needle.
Accidental puncture of the spleen will result in
drainage of dark red blood. If this happens, the needle
should be withdrawn and a new needle inserted at
a different site. If hemoperitoneum is suspected,
comparison of the PCV of the sample obtained by
abdominocentesis with the PCV of peripheral blood
may help determine whether the blood was obtained
from a splenic puncture or a true hemoperitoneum.
Blood obtained from the spleen will have an elevated
 ADDITIONAL DIAG NOSTIC PROCEDU RES 2

PCV compared to the pev of peripheral blood; com­

monly the pev of splenic blood will be 65 per cent or
greater than the peripheral blood pev. The PCV of
true peritoneal fluid obtained from horses with hemo­
peritoneum is likely to be lower than the peripheral
blood pev. Blood contamination of the peritoneal
fluid sample may also arise from accidental puncturing
of a vessel in the body wall or the bowel. In such cases,
blood will often be seen to swirl in the peritoneal fluid
as it drains from the needle. This blood contamination
frequently stops spontaneously, but if it doesn't the
needle should be repositioned, or withdrawn and a
fresh needle inserted at a separate site.
In horses where no peritoneal fluid can be obtained
despite several attempts, insertion of a blunt cannula Figure 2.8 Ultrasonogram of the ventral abdomen of a
may prove more successful. In this technique, a small normal horse showing a pocket of anechoic peritoneal
fluid. This scan was obtained usi ng a 7.5 MHz li near array
probe

stab incision is made through the skin and up to the

linea alba. The teat cannula is then forced through
the incision into the peritoneal cavity (Figure 2.7) . This
procedure should be performed using aseptic tech­
nique and sterile gloves should be worn because there is
a greater risk of contamination from handling the can­
nula. Blood from the skin incision can drip down the
cannula and contaminate the sample. This can be pre­
vented by placing sterile gauze around the teat cannula.
A teat cannula should also be used in horses with intesti­
nal distention since it incurs a lower risk of puncturing
and damaging the bowel wall than a needle. However,
bowel distended by sand is easily penetrated using
either a needle or a cannula, and extreme care must be
taken when performing abdominocentesis in horses
with suspected sand impaction. Sand may be seen in the
peritoneal fluid sample in cases where inadvertent
enterocentesis has occurred.
If repeated attempts at paracentesis are unsuccess­
ful, diagnostic ultrasonography using a 7.5 MHz
transducer may be employed to identity pockets of peri­
toneal fluid in the ventral abdomen (Figure 2.8 ) . This
can be used to guide placement of a needle or cannula
to an appropriate area. It can be difficult to obtain peri­
toneal fluid samples from mares in late pregnancy
because of the position of the gravid uterus, and ultra­
sonography should also be used in such cases to locate
peritoneal fluid.

6
Figure 2.7 Abdominocentesis showing use of a teat can­
ABDOMINOCENTESIS IN THE FOAL
nula. A stab i ncision is first made using a no. 1 5 scalpel
blade. The teat can nula is then forced through the linea Abdominocentesis is often not performed in the foal
alba and advanced into the peritoneal cavity because of fears of puncture or laceration of the bowel

15
2 ADDITIONAL DIAGNOSTIC PROCEDURES

wall. Abdominocentesis however, can yield significant CHARACTERISTICS OF NORMAL

information in determining the cause of colic or PERITONEAL FLUID
abdominal distention in foals (see Chapter 22) . If possi­
ble, abdominocentesis in the foal should not be per­ The characteristics of normal peritoneal fluid from
formed before a complete transabdominal ultrasound adult horses are summarized in Table 2 . 1 .
examination is carried out. This examination can deter­ Normal peritoneal fluid i s odorless, non-turbid, and
mine the quantity and location of peritoneal fluid in clear to pale yellow in color. The total nucleated cell
the abdomen. Foals with excessive abdominal fluid are count is normally less than 3-5 x 1 0911 ( 3000-5000
good candidates for abdominocentesis as they can be cells/�I) , with a total protein concentration of less than
heavily sedated, placed in lateral recumbency and 25 gi l (2.5 gl dl) .
restrained well for the procedure. To prevent inadver­ Peritoneal fluid from foals has a lower total nucle­
tent laceration of the bowel in a foal, a teat cannula can ated cell count (less than 1 .5 x 1 09/1 or 1500 cells/�l)
be used rather than hypodermic needles. A small local but similar total protein values to adult horses. Foal
block can be performed with 2% mepivacaine on the peritoneal fluid urea nitrogen levels (mean 1 .96
ventral abdomen to the right of midline, or where fluid mmol/I) are similar to plasma urea nitrogen (mean
is located (being sure to avoid the spleen and the umbil­ 2.0S mmol/I); peritoneal urea levels are elevated in
ical remnants) . A small stab incision is made with a no.
15 blade to penetrate skin and the abdominal muscula­
ture. The sterile teat cannula is then gently introduced
into the abdomen and fluid is collected for evaluation.
Omental herniation may occasionally follow teat can­
nula abdominocentesis in foals. This is generally not a Gross appearance Clear or slightly turbid
serious problem as the omentum can be cut off flush Straw colored or colorless
with the skin and an abdominal wrap applied. If the
abdominocentesis is performed caudal to the umbilical Specific gravity < 1.016
area, this problem is less likely to occur. In older foals
Total protein < 25 gil (usually < 15 gil)
abdominocentesis can be performed safely in the same
(mainly albumin)
way as in adult horses using an I S-gauge needle or teat
cannula, provided the foal is adequately sedated and Total nucleated < 5.0 x 109/1 « 10000 cells/Ill)
restrained. cell count (usually < 2.0 x 10911)

Differential cell 20-90% neutrophils

count 5-60% mononuclearl
mesothelial cells

Analysis of peritoneal fluid 0-35% lymphocytes

0-5% eosinophils
0-1% basophils
T Mair
Total red cell count Negligible
INTRODUCTION Fibrinogen Negligible « 0.1 gil) (does not
clot on standing)
Analysis of peritoneal fluid obtained by abdominocen­
tesis can be an important component of the evaluation Glucose 5.0-6.4 mmo"l (90-115 mgldl)
of horses with abdominal diseases. It may aid in the
decision to undertake exploratory surgery in the
Creatinine 161-237 j.l.moVI (1.8-2.7 mgldl)
horse with acute colic (see Chapter 9 ) , and it may be Urea nitrogen 3.9-8.2 m mo l/! (11-23 mgldl)
diagnostic in horses affected by peritonitis, abdominal
abscesses, and hemoperitoneum (see Chapter 1 7) , or lactate 0.4-1.2 mmol" (3.8-10.9 mgldl)
by some forms of abdominal neoplasia (see Chapter
Total bilirubin 5 1 3 j.l.molll (0.3-0.8 mgldl)
-

1 7 ) . It is also helpful in the evaluation of adult horses

and foals with uroperitoneum (see Chapters 1 7 and Amylase 0-14 lUll
22) .
Samples of peritoneal fluid should be assessed by lipase 0-361UIJ
gross visual examination, total protein determination,
GGT 0-6 lUll
and cytological examination.

16

foals with uroperitoneum. The ratio of peritoneal to
plasma creatinine is the preferred method of confirm­
ing uroperitoneum in foals (see Chapter 2 2 ) . The iden­
tification of calcium carbonate crystals in peritoneal
fluid can also be helpful in the diagnosis of uroperi­
toneum in adult horses.
Peritoneal fluid collected into tubes containing
dipotassium EDTA is suitable for performing both cell
counts and cytological examinations. Alternatively,
fluid may be collected into a plain tube and mixed with
an equal volume of 50% ethanol for cytological exami­
nation. Smears can be made directly from the fluid or
by cytocentrifugation. Wright, Leishman, Giemsa, or
trichrome stains are suitable for cytological examina­
tion. A gram stain should be performed in cases of sus­
pected peritonitis. There is some variation in the total
nucleated cell count of peritoneal fluid in normal
horses, although counts greater than 5 x 1 09/1 are gen­
erally considered abnormal. Most horses have total
nucleated cell counts less than 2 x 1 09/1. These cells
consist of mainly neutrophils and large mononuclear
cells (macrophages and mesothelial cells) in an approx­
imate ratio of 2:1 (neutrophils:mononuclear cells)
(Plate 2 . 1 ) . Small numbers of lymphocytes and
eosinophils are sometimes present. There are no red
blood cells in normal peritoneal fluid, although it is not
unusual to see small numbers of red cells as a conse­
quence of iatrogenic bleeding from the sampling pro­
cedure. Phagocytized material (cellular debris and
neutrophils) is commonly observed in macrophages as
a normal finding. Bi- and tri-nucleate mononuclear
cells, and mitotic figures can sometimes be seen in
normal horses.
INTERPRETATION OF CONTAMINATED
PERITONEAL FLUID SAMPLES
The sample of peritoneal fluid obtained by abdomino­
centesis may become contaminated by blood or intesti­
nal contents. While in some cases it may be evident
during abdominocentesis that iatrogenic blood conta­
mination of the sample has occurred (red streaking of
the yellow fluid ) , in other cases it may be diffic ult to dis­
tinguish this from internal hemorrhage. Blood contam­
ination due to iatrogenic vessel or splenic damage is
likely to contain platelets that may be identified on
microscopy, and splenic blood will contain large
numbers of small lymphocytes, whereas a true
serosanguinous peritoneal fluid due to red blood cell
diapedesis will probably contain very few platelets.
Heavily blood-contaminated samples due to inadver­
tent splenic tap are likely to clot on standing, whereas
true hemoperitoneum samples should not.
ADDITIONAL DIAGNOSTIC PROCEDURES 2
It should be remembered that some blood contami­
nation of the peritoneal fluid sample does not necessar­
ily negate the value of the tap. Blood contamination of
up to 1 7 per cent of the volume of the peritoneal tap
does not significantly alter the interpretation of the
nucleated cell count and protein concentration,
although the red cell countwill be increased significantly.
EFFECTS OF ENTEROCENTESIS
Inadvertent enterocentesis rarely causes significant
complications to adult horses, but it may result in peri­
tonitis and abdominal wall cellulitis in foals or adult
horses with distended bowel.
Experimental enterocentesis in normal horses has
been shown to cause an increase in nucleated cells in
the peritoneal fluid within 4 hours. The peritoneal fluid
total nucleated cell counts peak at 2 days (mean 1 1 .3 x
1 09/1 or 1 1 333 cellS/ill) and then decline rapidly to day
4. Toxic changes can be identified in the neutrophils,
but bacteria are not generally evident. The specific
gravity of peritoneal fluid is also increased following
enterocentesis, but red blood cell counts in the fluid do
not change.
EFFECTS OF PRIOR ABDOMINAL
SURGERY
Exploratory abdominal surgery without any bowel
resection or anastomosis causes an increase in total
nucleated cell counts, percentage of neutrophils, total
protein, and fibrinogen in peritoneal fluid. These
changes are evident within 1 day and remain elevated
for at least 6 days. The total nucleated cell count in the
fluid can exceed 13.7 x 1 09/1 ( 1 3 700 cell/Ill) on the
first day after surgery, and can increase to levels as high
as 400 x 1 09/1 (400 000 cells/ Ill) over the next few days.
Healthy horses that have had small colon resection have
been shown to have similar changes in nucleated cell
counts in peritoneal fluid, but they also show increases
in red blood cell counts.
Laparoscopy also alters the characteristics of the
peritoneal fluid. Insufflation of the abdominal cavity
increases the total nucleated cell count and total pro­
tein concentration in the fluid. These changes have
been attributed to the formation of carbonic acid by the
insufflating gas ( carbon dioxide) .
Open castration has also been shown to induce a
non-septic peritoneal inflammatory reaction, with total
nucleated cell counts rising to approximately 30 x 1 09/1
5 days after the surgery. The cell counts are expected to
return toward normal within 7 days of castration.
17
2 ADDITIONAL DIAGNOSTIC PROCEDURES
Peritoneal fluid can change after parturition, depend­
ing on the nature of the delivery. Normal unassisted
parturition has no effects on peritoneal fluid color, clar­
ity, specific gravity, fibrinogen concentration, or total
protein concentration. The total nucleated cell count
was shown to increase in one study, but it stayed within
the normal range. All peritoneal fluid parameters
remain normal over the week following parturition.
Uncomplicated dystocias cause an increase in
nucleated cell count and percentage of neutrophils, but
values usually remain within the normal range.
Complicated dystocias can result in elevated total pro­
tein concentration and percentage neutrophils, but the
total nucleated cell count remains within the normal
range. If the total protein concentration, total nucle­
ated cell count, and percentage of neutrophils are ele­
vated following parturition, further medical or surgical
therapy may be indicated.
EFFECTS OF DISEASE
As the peritoneal fluid changes with specific diseases,
the fluid can become more turbid because of increases
in protein, red blood cells, and/or white blood cells.
Increased turbidity may be caused by the presence of
low numbers of red blood cells (which may not cause
red discoloration of the fluid) . Changes in the color of
the peritoneal fluid ranging from golden to orange to
red indicate leakage of red cells (usually from capillar­
ies in ischemic bowel wall) . With very early (within 1-2
hours) strangulating obstructions and most simple
obstructions of the small or large intestine, peritoneal
fluid is usually normal. With persistent simple obstruc­
tions, the nucleated cell count and differential cell
count remain normal, but the total protein concentra­
tion may rise. After a few hours of strangulating intesti­
nal lesions, red cells appear in the fluid which becomes
serosanguinous. However, prior to the appearance of
gross sanguinous coloration of the fluid, the presence
of red cells may need to be confirmed by centrifugation
of a sample of the fluid and/ or cytological examination.
With longer-standing strangulating obstructions or
severe intestinal inflammation, the peritoneal fluid may
become grossly serosanguinous, with increases in
nucleated cell count and total protein concentration.
Neutrophils in the peritoneal fluid increase in number
as ischemic bowel undergoes degeneration and
mucosal sloughing. Stimulation of the neutrophils by
the bacteria and toxins leaking into the abdomen
causes toxic changes to the cells (vacuolation, karyoly­
sis, and karyorrhexis ) . The degree of this change as well
18
as the numbers of neutrophils entering the fluid is a
reflection of the degree of intestinal degeneration and
the amount of intestine involved. In most strangulating
intestinal lesions, cytological examination of peritoneal
fluid reveals increased total nucleated cell counts (5-
30 X 1 09/1) with 90 per cent to 95 per cent neutrophils.
Dark brown turbid fluid with the smell of ingesta.
increased nucleated cell count, and increased protein
concentration is suggestive of bowel necrosis and leak­
age. In such cases, the total nucleated cell count may
exceed 1 00 x 109/1. The identification of plant material,
intra- or extra-cellular bacteria, and protozoa is indica­
tive of bowel rupture (Plate 2.2 ) .
Horses affected b y non-strangulating intestinal
infarction usually show changes in the peritoneal fluid
that are similar to those seen in strangulating intestinal
infarction. This includes an increase in protein, red
blood cells, and white blood cells. Nucleated cell
counts may exceed 1 00 x 1 09/1 and may be as high as
400 x 1 09/1.
Although the identification of changes in peritoneal
fluid can be extremely helpful in evaluating horses with
intestinal ischemia, it must be remembered that
changes may not always be identified even in the pres­
ence of severe bowel wall compromise. In some cases,
compartmentalization of fluid occurs, and samples of
peritoneal fluid can be normal because the diseased
segment of bowel is separated from the rest of the
abdomen by an anatomical barrier. Thus,
abdominocentesis of horses with small intestinal, ileo­
cecal, or cecocolic intussusceptions, small intestinal
incarceration in the epiploic foramen, and strangula­
tions in a diaphragmatic hernia can yield normal fluid.
Blood-tinged fluid is indicative of splenic puncture.
intra-abdominal or iatrogenic hemorrhage, or severe
intestinal necrosis. In the case of splenic puncture, the
PCV of the fluid is greater than the peripheral blood
PCV, and contains large numbers of small lymphocytes.
Fluid from horses with hemoperitoneum is expected to
have a lower PCV than peripheral blood, and has
erythrocytophagia (Plate 2.3) and very few platelets.
Bacteria may be identified in peritoneal fluid
because of leakage through ischemic bowel wall or
bowel rupture. They may also be seen in the peritoneal
fluid of horses with abdominal abscesses. Bacteria may
be present free in the fluid or phagocytized within
neutrophils. They are rarely present in large numbers
(other than in cases of bowel rupture) and careful
examination of a gram-stained smear is necessary to
identity them.
Fat may occasionally be observed in peritoneal fluid
samples. This is most likely to have come from the
retroperitoneal fat, but if the horse has been previously
treated with mineral oil, leakage of the oil from a
 ADDITIONAL DIAGNOSTIC PROCEDURES 2

ruptured bowel into the peritoneal cavity should also be
considered as a possibility. Ether placed in the sample
will dissolve fat but not mineral oil. Grossly lipemic peri­
toneal fluid is occasionally observed in nursing foals.
Most of these foals have mild intestinal discomfort (e.g.
ilells) and recover with supportive medical treatments.
True and persistent chylous effusions have been rarely
identified in young foals ( 1 2-36 hours of age) associ­
ated with congenital segmental aplasia of the lymphatic
system of the small intestine. Affected foals present with
colic and chyloperitoneum, at surgery affected small
intestinal segments appear thickened, discolored, and
distended. If the affected segment of bowel is not too
long, resection and anastomosis can be successful.
Chyloperitoneum has also been described in a small
number of adult horses, usually as a secondary feature
to other intra-abdominal diseases (such as intra-abdom­
inal abscess, large colon torsion, tearing of mesenteric
adhesions) .
Grey or black discoloration of peritoneal fluid has
been identified in a small number of horses affected by
melanomas of the peritoneal cavity. Yellow-green discol­
oration of peritoneal fluid may be seen when there has
been leakage of bile into the peritoneal cavity (Plate 2.4) .

T..- t.���.Qf.i:J�fl��;iJ,�t"lhoi's.. ."dJn ...u,�.�_. a.......lft.ldi..

, ' "
, , " , i , " " ,
"
" c "" ,

Gross appearance Total protein (gil) Nucleated cell Cytology

count (x 10911)

Normal Odorless, clear to < 2.5 < 5.0 2: 1 ratio of non-

pale yellow degenerative neutrophils
to macrophages,
no RBCs.

Simple Odorless, clear to Normal to mild Normal to mild Predominantly non-

obstrudlon turbid, pale yellow increase (2.S-3.0) i ncrease (3.0-8.0) degenerative neutrophils.

Very early Odorless, clear to Normal to mild Normal to mild Predominantly non-
strangulating turbid, pale yellow increase (2.5-3.0) i ncrease (3.0-B.0) degenerate neutrophils,
obstrudlon few RBCs.

Strangulating Serosanguinous, Moderate to Moderate to marked Degenerate neutroph ils

obstrudion turbid marked i ncrease increase (> 10.0) ± intra- or extracel lular
(3. 5-6.0) bacteria, RBCs.

Intestinal Malodorous, turbid, Moderate to marked Decreased (< 2 .0) Degenerative neutrophil s,
rupture dark red to brown increase (3. 5-6.0) i ntra- or extracel l ular
bacteria, plant material,
protozoa, RBCs.

Enterocentesis Malodorous, turbid, < 2.5 Few or no Plant material, protozoa.

green to brown nucleated cells

Hemoperitoneum Dark red Similar to peripheral Similar to peripheral PCV less than PCV of
blood blood peripheral blood,
erythrocytophagia, few or
n o platelets.

Splenic pundure Dark red Similar to peripheral Similar to peripheral PCV greater than PCV of
blood blood peripheral blood. High
n umbers of small
lymphocytes.

Peritonitis Thick turbid, dark > 2.5 > 10.0 High numbers of
yellow to orange degenerate and non-
degenerate neutrophi ls,
intra- and extra-cellular
bacteria.

19
2 ADDITIONAL DIAG N OSTIC PROCEDURES
The absence of gross or cytological abnormalities in
the peritoneal fluid does not rule out compromised
intestine. Some strangulating lesions, such as intussus­
ceptions, external hernias, and epiploic foramen
incarcerations may not demonstrate abnormalities in
the peritoneal fluid because of sequestration of the
fluid in the omentum, intussuscipiens, or hernial sac.
Ultrasound examination of the entire abdomen is of
great importance in these cases.
Late in the course of strangulation obstructions,
when distended loops of intestine can be palpated
per rectum, and when gastric reflux may be present,
abdominal paracentesis is unlikely to provide any useful
diagnostic information, and there is a higher risk of
intestinal damage from the procedure. In these cases,
therefore, referral for exploratory surgery is carried out
without performing abdominocentesis in the field,
because of the risk to the patient and the examiner.
However, if gastrointestinal rupture or very advanced
gut necrosis are suspected, their confirmation by
abdominal paracentesis indicates the need for immedi­
ate euthanasia.
Characteristic changes to the peritoneal fluid in
horses with different categories of acute abdominal
disease are summarized in Table 2.2. Changes seen in
horses with peritonitis and abdominal neoplasia are
described in Chapters 1 1 and 17.
Carbohydrate absorption
tests
F Taylor
These tests assess the functional integrity of the small
intestine by measuring the efficiency of sugar absorption
from the intestinal lumen. They are indicated where
weight loss is occurring in the absence of an obvious
cause, despite an adequate food intake. Pathological
changes that interfere with cellular transport mecha­
nisms reduce sugar uptake into the bloodstream.
The most commonly used carbohydrate absorption
tests in the horse include the oral glucose absorption
test, the D ( + )-xylose absorption test, the starch toler­
ance test, and the oral lactose tolerance test.
THE ORAL GLUCOSE ABSORPTION TEST
The most useful of the carbohydrate absorption tests in
horses is the oral glucose absorption test (OGAT) . This
test is inexpensive, simple to perform, and offers good
20
empiric information on the efficiency of small intestinal
absorption.
Procedure
The horse's weight is estimated as accurately as possible
(e.g. using a girth weighband) and the animal is fasted
overnight on an inedible bedding. Access to water can
be allowed until 2 hours before the test begins.
One gram per kilogram bodyweight of anhydrous or
monohydrate D-glucose is weighed out and a fresh solu­
tion is prepared as 20 per cent weight/volume in warm
water. A 'fasting' sample of blood is taken immediately
before the test (time zero) . All samples that cannot be
processed within 1 hour must be collected into potas­
sium oxalate-sodium fluoride anticoagulant.
A nasogastric tube is passed and the entire solution is
delivered as a bolus into the stomach. Further blood
samples are taken at 30, 60, 90, 1 20, and 1 80 minutes
and submitted for glucose estimation. An absorption
curve is then plotted arithmetically. A modified test pro­
cedure employing a reduced number of sampling times
(time zero and 1 20 minutes) can also be used and has
the advantage of being more practical and economic to
use in the field.
Interpretation
Under normal conditions the absorption curve has two
phases. In the first 2 hours glucose is continuously
absorbed from the small intestine and the fasting
plasma glucose concentration doubles. The second
phase is insulin-dependent and shows a progressive fall
to a resting level which is achieved by 6 hours. The sam­
pling times suggested above should demonstrate these
features when absorption is not compromised. A late,
but normal-sized glucose peak may occur in cases of
delayed stomach emptying.
A flat line indicates a state of total malabsorption
and usually constitutes a grave prognosis. The principal
causes are progressive inflammatory or neoplastic cellu­
lar infiltrations of the gut wall. The diagnosis is defined
by histopathology.
An intermediate curve between normal absorption
and total malabsorption suggests a state of partial mal­
absorption that is more difficult to interpret. The cause
may be reversible, for example inflammatory change
associated with parasitism. In addition, some clinically
normal horses produce a partial malabsorption result
that may reflect a rapid gut transit time. Without know­
ing the precise nature of a lesion or functional distur­
bance, it is not possible to be certain that such cases will
not revert to normal given time and supportive treat­
ment. However, the test can be repeated at a later date
to monitor the patient's progress.

THE D(+)-XYLOSE ABSORPTION TEST
The D (+)-xylose absorption test is essentially the same
as the OGAT, but is considered to provide a more accu­
rate assessment of absorption. However, the shape of
the xylose absorption curve is influenced by factors that
can also cause anomalies in the glucose absorption
curve, i.e. the rate of gastric emptying, intestinal transit
time, intralumenal bacterial overgrowth, and immedi­
ate dietary history. In addition, the costs of xylose and
its assay are considerably more than those of glucose
and at present commercial laboratories do not process
the samples routinely. On balance, the practitioner is
advised to use the OGAT.
The peak plasma levels of xylose are reached 60-90
minutes after an oral dose of 0.5 or 1 .0 g xylose/kg body
weight, administered as a 1 0% solution by nasogastric
tube.
THE STARCH TOLERANCE TEST
The test is performed by administering 2 g corn­
starch/kg body weight as a 20% solution. This test
assesses both small intestinal absorptive and pancreatic
exocrine function.
THE ORAL LACTOSE TOLERANCE TEST
This test has been used to assess persistent non-systemic
diarrhea with malabsorption in the suckling foal, that is
associated with lactase deficiency caused by prior
intestinal epithelial damage. This may follow on from
other causes of diarrhea such as rotavirus infection. A
reduced tolerance curve may suggest the need to
restrict or prevent milk access for a short period until
small intestinal epithelial repair has occurred. The test
is performed by administering 1 .0 g lactose as a 20%
solution.
Endoscopy
MJ Murray
INTRODUCTION
Endoscopy is indispensable for making diagnoses or
ruling out several possibilities of alimentary tract disor­
ders. Endoscopy is used most commonly to examine the
esophagus, stomach, and proximal duodenum, but an
ADDITIONAL DIAG NOSTIC PROCEDURES 2
endoscope can also be inserted through an enterotomy
to view the lining of the small or large intestine.
Proctoscopy is feasible, but the rectum must be carefully
and thoroughly evacuated to be able to see the mucosal
surface adequately.
There is a great variety of endoscopic equipment
available that can be used for alimentary endoscopy.
The decision as to which endoscopic equipment to pur­
chase will be based on several factors, including
• the type of practice and its caseload
• whether the equipment will stay within a clinic or
be transported around
• equipment costs
• the interests of the practice owners.
ENDOSCOPIC EQUIPMENT 1*"�,ffi,yfMA' \W,'''"",",8lr"WWI'c>'''ii'«M", %"'';'"1',,,=, """NW""',"""O>'�'H�I�I,"'","!&" """oMB'Y'''',P,S",
This can be divided into two categories
• fiberoptic
• electronic (video) .
Fiberoptic endoscopic equipment uses glass fiber
bundles to transmit light to the area to be viewed and to
transmit the image to an eyepiece. Recently developed
technology uses a light-transmitting gel to deliver illu­
mination from the light source. The viewed image is
magnified by a lens system within the eyepiece. The
quality of an image viewed through a fiberoptic endo­
scope is determined by the number of fibers in the
endoscope and the intensity of the light source. The
more fibers the better the image resolution. High qual­
ity gastroscopes have approximately 30 000 fibers while
endoscopes of lesser quality may have as few as 1 2 000
fibers. The 60 W halogen lamps used in most portable
endoscope light sources provide poor illumination of
an adult horse's stomach. More powerful light sources
are available (up to 300 W xenon lamps), but these are
large and heavy and therefore less portable.
A video-endoscope system uses glass fiber bundles to
transmit light, with a charge-coupled-device (CCD)
chip on the end of the endoscope that transmits the
image. The light source (300 W xenon lamp) and pro­
cessing of the electronic signal generated by the CCD
are in the endoscope processor. With most video-endo­
scopic systems, a color image is obtained by transmit­
ting white light through a red-green-blue color wheel
that rotates approximately 30 times per second. The
processor combines sequential red, green, and blue
images generated by the CCD chip into a composite
red-green-blue image. Olympus utilizes a 'color' CCD
in which white light is transmitted through the endo­
scope, and red, green, and blue filters over the CCD
21
2 ADDITIONAL DIAGNOSTIC PROCEDURES
elements create post-illumination color. The number of
pixel elements per CCD varies from 32 000 to 500 000.
A CCD chip with more pixels provides a larger, but not
necessarily better, image. Enhancement of image
quality is achieved through processor electronics.
Because the image produced by a video-endoscope is
the result of processing electric signals from thousands
of pixel elements on the CCD chips, the appearance of
the image is, in many respects, artifactual. Color repre­
sented by different processors can be of varied hues.
Color artifacts are not unique to electronic endoscopes,
fiberoptic endoscopes tend to render an image with
more of a yellow hue than the true color of the object
being viewed.
Other characteristics of endoscopes to be consid­
ered include
• how the object is illuminated
• the field of view
• deflection of the endoscope tip
• ergonomics of the control section
• ease of cleaning and maintenance.
The surface being viewed should be illuminated
evenly, but many endoscopes do not accomplish this.
With some the center of the area being viewed is exces­
sively illuminated compared to the periphery, while
with other endoscopes one side of the area viewed is
excessively illuminated and the other side is under-illu­
minated. This results from the point where the trans­
mitting light bundles are configured on the tip of the
endoscope (along with the viewing lens or CCD, air­
water channel, biopsy channel, etc. ) . The standard field
Tabl. U A co",parlson ��Ptlclittl �. �. ���spttms
incllldlnl Jilht sO\:Ircf' a�:....r"or .· • . . . " . ..' . . " <.;
.. .
Feature Fiberoptic
(without camera)
Cost (new) $8000-$ 1 5 000
£5000-£ 1 0 000
Portabil ity Good
Image qual ity Fai r to very good
Image capture Poor
Teaching/client Poor
communication
Disinfection Good
Available accessories Good
22
of view for a gastroscope is 1 00 degrees, larger fields of
view are accomplished using lenses of greater convexity.
This can create a 'fish-eye' effect that distorts the image
being viewed. Most endoscopes manufactured today
can be completely immersed in cleaning and disinfect­
ing solution, facilitating cleaning and maintenance.
Other important considerations include the size or
availability of a biopsy channel, whether one needs an
extra biopsy channel, and the effectiveness of air-water
channels.
Fiberoptic and video-endoscope systems each have
characteristics that may be perceived as advantages or
disadvantages (Table 2.3) . Video-endoscope systems are
more expensive, but the cost difference between elec­
tronic and fiberoptic systems is based on the processor
and monitor rather than the endoscope. Video-endo­
scope systems are more cumbersome and are generally
poorly suited for transporting on a frequent basis.
Video-endoscope systems are advantageous, however, as
they include the client in the examination process, and
they facilitate documentation of endoscopic images.
Fiberoptic endoscopes can be used with a video­
endoscope processor by using an adapter with a CCD
chip. The adapter fits over the eyepiece of the endo­
scope and the image is returned to the processor and
displayed on a monitor. Analog cameras, such as those
used with arthroscopes, also can be used with a fiber­
optic endoscope for viewing on a monitor.
Finally, a paramount consideration in deciding which
endoscope system to purchase is its expected durability
and the company's ability and commitment to service
the endoscope. This also includes the availability of a
;
.
. ii , .
" .
Electronic
$20 000-$45 000
£ 1 5 000-£30 000
Poor to fair
Very good
Good
Good
Good
Good

loaned endoscope if one's endoscope requires extensive
repair work. The gastroscopic examination places con­
siderable strain on the endoscope, and a well-made
endoscope used extensively for that purpose will require
maintenance every 1-2 years. Many of the relatively inex­
pensive 2 to 3-meter endoscopes are not sufficiently
durable to withstand repeated gastroscopic procedures
and will require frequent maintenance. These issues
must be clarified in writing with the manufacturer prior
to any purchase. In most cases, it is advisable to purchase
an endoscope that is in the manufacturer's product line,
rather than one custom built. Finally, the likelihood of
endoscope damage, either from excessive wear and tear
or direct damage to the endoscope, is inversely propor­
tional to the experience of the endoscopist. An inexpe­
rienced endoscopist should expect that endoscope
damage will occur, and thus the manufacturer's main­
tenance agreement and availability of loaned endo­
scopes are critically important.
Endoscope dimensions
An important decision to be made in acquiring endo­
scopic equipment involves the dimensions of the endo­
scope. Flexible endoscopes are available from several
manufacturers in many lengths and diameters (Table
2.4) , and each length/diameter combination deter­
mines how the endoscope may be used. A working
length of 1 1 0 cm with an outer diameter of 1 0 mm
(standard human gastroscope) is usually sufficient to
reach the stomach of foals up to 30-40 days of age. A
length of 1 60-1 80 cm with a maximum outer diameter
Endoscope type Typical dimensions
(f = flberoptic, v = video) Working Outer
length diameter (o.d.)
Gastroscope, human (f,v) 1 00-1 1 0 em
Colonoscope, human (f,v) 1 55-1 70 cm
Small bowel endoscope (v) (Penta x) 250 em
Equine gastroscope (v) (Fujinon) 280 cm
Equine gastroscope (v) (Pentax) 300 cm
ADDITIONAL DIAG N OSTIC PROCEDURES 2
of 1 2.5 mm (human slim colonoscope) is required for
gastroscopy in weanling foals. For most equine gastric
endoscopy a minimum working length of 200 cm is
required. This length will usually permit adequate
observation of the squamous mucosa and much of the
glandular body, although examination of the antrum
and pylorus in standing adult horses will not be possi­
ble. An endoscope 200 cm long is usually sufficient to
examine the proximal duodenum in foals up to 6
months old. In older foals endoscopy of the proximal
duodenum may be possible using an endoscope 200 cm
long, with the foal placed in lateral recumbency under
general anesthesia. A 250-cm endoscope will permit
thorough examination of the stomach, including the
antrum and pylorus, of most adult horses, while a
length of 280-300 cm is required to perform duo­
denoscopy in adult horses.
TECHNIQUES FOR ENDOSCOPIC
PROCEDURES
Endoscopy of the esophagus is often performed in
emergency situations, for example cases of choke,
when there is little time for patient preparation. Horses
need to be properly sedated or anesthetized to pass
an esophageal obstruction safely and effectively.
Endoscopy is useful in identifYing the location and type
of obstructing material, but this material cannot usually
be removed by endoscopy. For elective esophagoscopy,
feed and water may be restricted for 2 hours. In many
Comments
9-1 0. 5 mm Gastroscopy in neonates.
1 1 .5-1 6 mm Not long enough for adult gastroscopy.
o.d. too great for passage through foal
nasal passages.
1 0 mm Suitable for all ages except adult
duodenoscopy.
1 4. 5 mm Large o.d. inappropriate for foals.
1 0 mm Suitable for all ages, including adult
duodenoscopy.
23
2 ADDITIONAL DIAGNOSTIC PROCEDURES
cases, it is useful to perform gastroscopy at the time of
esophagoscopy, because there may be both gastric and
esophageal disorders. The procedures described below
apply to gastroscopy and duodenoscopy.
Foals
I . Suckling foals not eating solid feed are allowed to
nurse until 2-4 hours before endoscopy.
2. Feed is withheld from foals eating solid feed for
8-12 hours, with nursing permitted until 2-4 hours
before endoscopy. Longer periods of fasting can be
used but the foal's hydration status should be
considered.
3. Sedation is not always required in neonatal foals,
although if the foal struggles excessively sedation
will facilitate the procedure for both the foal and
the endoscopist. Options for sedation include
• xylazine 0.5 mg/kg i.v.
• xylazine 0.5 mg/kg i.v. plus diazepam 0.1 mg/kg i.v.
• xylazine 0.5 mg/kg i.v. plus butorphanol
0.01-0.02 mg/kg i.v.
4. The procedure may be performed with the foal
standing or lying on a mat. To restrain a young foal
for standing endoscopy, a handler should hold the
foal around the chest and rump and the
endoscopist (if right handed) should bring the left
arm around the back of the foal's head so that the
poll rests in the crook of the left elbow. The right
hand advances the endoscope while the left hand is
used to guide the endoscope through the left nares.
Using this restraint, the typical response of foals to
jerk the head backwards can be controlled.
Adult horses
l . Feed is withheld for 8-12 hours, water for 2-4 hours.
Longer periods of fasting can be used to ensure
complete emptying of the stomach, but this is not
usually necessary. The person responsible for fasting
the horse should be instructed to remove hay and
bedding and to muzzle the horse. Horses will eat
straw, shavings, sawdust, their own manure (even
through a muzzle) if hungry enough. None of these is
conducive to a thorough examination of the stomach.
2. Sedation is required for a standing endoscopic
examination. Options for sedation include
• xylazine 0.5-0.7 mg/kg i.v.
• acepromazine 0.03 mg/kg i.v. then 20 minutes
later xylazine 0.5-0.7 mg/kg i.v. , this facilitates a
relatively longer examination, for example
duodenoscopy
• detomidine 0.02 mg/kg i.v., this facilitates a
relatively longer examination, for example
duodenoscopy.
24
3. General anesthesia may be elected to examine the
dependent portion of the stomach (glandular) or if
the antrum and pylorus must be observed using an
endoscope less than 240 cm long.
4. A nose twitch is useful in the restraint of many horses.
5. If delayed gastric emptying is suspected or known,
pre-treatment (45 minutes) with bethanechol,
0.025 mg/kg S.c., will facilitate advancing the
endoscope throughout the stomach.
ENDOSCOPIC PROCEDURE
The animal usually finds the passage of the endoscope
through the nares the most objectionable part of the
procedure. The endoscope is advanced to the rima glot­
tis, and into the esophagus. In older foals and adult
horses, swallowing can be facilitated by squirting water
through the endoscope air-water channel or the biopsy
channel onto the rima glottis. It is better to have the
horse swallow and then pass the endoscope than try
to force the endoscope into the esophagus, because
the endoscope may inadvertently and unknowingly
retroflex and then be advanced into the mouth.
If the horse coughs excessively during or immediately
after passing the endoscope into the esophagus, the soft
palate has probably been displaced dorsally. Inducing a
swallow or flexing the head will resolve this. Some horses
will use their pharyngeal muscles to grab the endoscope
as it is being passed, making it difficult to pass and to
withdraw. This requires patience by the endoscopist to
advance or withdraw the endoscope safely and effectively.
The esophagus should be carefully examined as the
endoscope is advanced. In an adult horse the lower
esophageal sphincter and entrance into the stomach is
typically 1 70-180 cm from the nares. Some resistance
may occur at the lower esophageal sphincter, but it
should be relatively easy to advance the endoscope into
the stomach.
The stomach is distended by insufflation of air
through the endoscope until the non-glandular and
glandular regions of the gastric surface can be
observed. Distention with air is tolerated by foals and
horses, and only rarely has been associated with signs of
abdominal discomfort in the patients examined by the
author. Gastric contents should be thoroughly rinsed
from the stomach surface using tap water flushed
through the biopsy channel. Excessive fluid within the
stomach may need to be aspirated; this may be accom­
plished through the endoscope biopsy channel, or
often more effectively using a nasogastric tube. If there
is a large volume of fluid or feed in the stomach and the
horse has definitely been fasted for an adequate period,
a gastric outlet obstruction should be suspected.
 ADDITIONAL DIAG N OSTIC PROCEDURES 2

When the endoscope first enters the stomach the
enrloscopist sees the right side and the greater curva­
ture of the stomach (Plates 2.5, 2.6) . As the endoscope
is advanced it travels against the right side of the stom­
ach and then dorsally. As it is advanced further toward
the caudal portion of the stomach the lesser curvature
and cardia can be seen (Plate 2.7) . When observing the
cardia the endoscope is pointing cranially, so that the
left side of the animal appears on the left side of the
endoscopist 's field of view.
In order to view the antrum and pylorus, the endo­
scope must be further advanced until it has passed
ventral to the ridge formed by the lesser curvature. The
endoscope will slide ventrally into the dependent por­
tion of the stomach as it is advanced toward the pylorus.
It then will become submerged in gastric fluid and the
remains of ingesta, and the endoscopist's view will be
obscured. It will be helpful to insufflate with air and
perhaps aspirate fluid, and then carefully advance the
endoscope until the antrum and pylorus can be seen.
This may require several minutes and it is important to
be patient. The endoscope usually cannot be advanced
to the pylorus without adequate gastric contractions.
Forcing the endoscope to advance can bow the endo­
scope inside the stomach. This can damage the endo­
scope and can cause discomfort to the horse as the
endoscope stretches the stomach wall. Make use of the
animal's intrinsic gastroduodenal motility to assist
advancing the endoscope to the pylorus and into the
duodenum. If motility is poor or absent, pre-treatment
with bethanechol, 0.025 mg/kg S.c., will often help.
With sufficient length the endoscope may be
advanced through the pylorus into the duodenum. It
will initially move into the duodenal ampulla and when
advanced further the lens will be pressed against
mucosa and the field of view will be a blurred red. As
the proximal duodenum extends past the pylorus it
makes a I SO-degree turn caudally; this is what the endo­
scope must do to continue to be advanced (Figure 2.9 ) .
I n most cases the endoscopist will b e able t o see t o the
major duodenal papilla, but not further, by advancing
the endoscope a few centimeters while rotating the
endoscope and maximally retroflexing the tip. In this
way the endoscopist is actually looking b<!ck at the

\
\

(a) (b)

Figure 2.9 Illustrations of the stomach depicting the path taken by the endoscope as it is advanced around the stomach to
the antrum, through the pylorus, and into the duodenum. The hash l ines represent the outline of the proximal descend­
ing duoden u m . a) In this illustration the left hemisphere of the stomach has been removed just to the l eft of midl ine.
Notice that the endoscope must travel along the c i rcumference of the stomach i n order to reach the gastric antrum. As the
endoscope is advanced around the circumference of the stomach it becomes i m mersed i n gastric contents. When the
endoscope is advanced into the duodenum the tip must be retroflexed to observe duodenal papi llae. Rarely the cli nician
might be able to advance the endoscope a borally into the duodenum, but the configuration of the duodenum with
respect to the stomach makes this very difficult. b) In this illustration the caudal hem isphere of the stomach has been
removed . In this view, the torque stresses placed upon the endoscope as it is advanced toward the pylorus and the duo­
denum can be appreciated. When the procedure is performed properly, the majority of these stresses are applied to the
cables controlling the tip deflection. Adva ncing the endoscope with excessive force or otherwise i m properly will cause
more of these forces to be applied to the endoscope insertion tube causing expensive damage to the instrument

25
2 ADDITIONAL DIAGNOSTIC PROCE D U R ES

duodenal papilla, rather than forward. One will notice should be available to optimally image the entire
that when the endoscope is first pulled back to leave the abdomen in horses of all ages and sizes. For evaluation
duodenum, it will appear as if the endoscope is advanc­ of the ventral body wall and peritoneal fluid, high fre­
ing into the duodenum. quency (6.5-10 MHz) transducers provide excellent
In some cases it may be desirable to obtain a biopsy resolution and adequate penetration in horses of all
through the endoscope. The biopsy channel diameter in types. In foals and small ponies, the deeper structures
gastroscopes is usually restricted to 2.8 mm, however in within the abdomen can be visualized satisfactorily with
large diameter colonoscopes the biopsy channel diame­ mid-frequency (4-6.5 MHz) transducers, while in the
ter can be 3.6-4.0 mm. Consequently most biopsies will mature horse, imaging depths in excess of 25-30 em
be very small. Biopsies of gastric squamous mucosa are may be required, thus low (2.25-3.5 MHz) transducers
usually unrewarding because very little mucosa can be are necessary. The ventral abdomen can be imaged
obtained. Gastric glandular and duodenal mucosal biop­ equally well with sector or linear transducers. For
sies are larger because mucosa can be torn away as the deeper abdominal imaging, sector transducers are
biopsy forceps is withdrawn. These biopsies are often suf­ required to provide flexibility to image between the ribs
ficient for diagnostic purposes. Biopsy sites will bleed, and around gas. The key requirement for examination
often impressively, but this is not a concern unless the of the caudal abdomen and pelvic contents per rectum,
patient has a severe bleeding disorder. is a transducer that is sufficiently small to be easily
When the endoscopic procedure is completed it is manipulated within the rectum, while still providing an
helpful to remove air from the stomach. Post-endoscopy adequate imaging field. Linear transducers are pre­
abdominal discomfort is unusual, but can be prevented ferred for most gynecological work because they are
by keeping the duration of the examination as short as
possible and removing the air insufflated into the stom­
ach. If discomfort does occur it will rapidly resolve after
treatment with flunixin meglumine, 0.5 mg/kg i.v.

CARE OF ENDOSCOPIC EQUIPMENT

ill'·.·:("''''U':"":'':"''"'"';I,"'::i:;i:'':i@;:'''i':>¢�I''M'':''"*''''='''lI©_I.""mli"'V!i
' kP_"':'''("*"''il:::U';'''''''M:8l£i�'''d''''Affi:"i:e;:"",:�,,<,:,'''""

The manufacturer should provide thorough written

instructions on the care and maintenance of the endo­
scope, and the sales representative should demonstrate
its operation, cleaning, and proper storage. After use,
the endoscope should be cleaned in an enzymatic solu­
tion (e.g. Endozime, Ruhof Corp., Valley Stream, NY)
that removes adhered mucus, blood, etc. The endoscope Figure 2.1 0 A transverse ultrasonogram of the right dorsal
biopsy channel should also be cleaned. After rinsing the abdomen from a normal horse: the d uodenum can be seen
endoscope in water it should be allowed to dry thor­ running ventral to the kidney a nd dorsal to the cecum
oughly, preferably by hanging vertically. A 3-m-long
endoscope may need to be dried by hand. For disinfec­
tion the endoscope should be immersed in a 2.4% solu­
tion ofglutaraldehyde (e.g. Cidex,Johnson andJohnson
Medical Inc. , Arlington, TX) for 1 5-30 minutes.

Ultrasonographic
examination of the abdomen
eM M arr, J Lyons, a n d 5 Freeman

Figure 2.1 1 A tra nsverse ultrasonogram of the caudoventral

Examination of the abdomen requires a range of imag­ abdomen from a normal horse: sma l l intestinal loops (51) are
ing depths and thus, ideally, a selection of transducers visible and there is a d istinct layer of retroperitoneal fat

26

easy to manipulate over the reproductive tract. In con­
trast, for examination of the caudal portions of the
intestine per rectum, the smaller microconvex trans­
ducers have the advantage that they can be positioned
to image in any direction, increasing the range of the
imaging field. For transcutaneous examination, sector
transducers are the most flexible and the area under
investigation may have to be clipped and the skin
cleaned. No specific preparation is necessary for rectal
examination. However, since the procedure may
involve prolonged examination periods and it is gener­
ally necessary to reach fairly far proximally into the
rectum, the operator should ensure that the horse is
adequately restrained and consider the use of drugs
sllch as probantheline or hyoscine to reduce rectal
straining and decrease the risk of inj ury to the rectum.
NORMAL ULTRASONOGRAPHIC
ANATOMY OF THE INTESTINE AND
PERITONEAL CAVITY
The stomach can be identified in the left cranial
abdomen. Typically it is recognized as an echogenic
curve caused by gas along the greater curvature. The
Figure 2 . 1 2 A transverse abdominal u ltrasonogram
obtained per rectum showing normal small i ntesti ne. The
wa l l (between arrows) is com posed of five discrete layers
that are normally measured in combination
Figure 2.13 A transverse ultrasonogram of the cranioven­
tral abdomen. Peritoneal fluid is visible between the sec­
tions of large intestine (LI) and could be sam pled in this site
ADDITIONAL DIAG N OSTIC PROCE D U R ES 2
stomach lies beneath the uniformly echogenic spleen.
Fluid is rarely visible within the stomach in normal
adults but occasionally a small amount of fluid will be
visualized within the ventral portion of the stomach in
the foal. The duodenum is a consistently recognizable
landmark, visible in most horses (Figure 2 . 1 0 ) . It can be
identified in the right dorsal abdomen, running cau­
dally, ventral to the liver and right kidney. The individ­
ual sections of the remainder of the small intestine
cannot be consistently identified in all animals. Motile
loops of small intestine, with small amounts of lumenal
contents, are visible in the caudoventral abdomen
(Figure 2. 1 1 ) in around 66 per cent of normal horses
and in the cranial abdomen in 25 per cent of horses.
The small intestine can also readily be assessed in the
mid-abdomen via rectal examination (Figure 2 . 1 2 ) . The
small intestinal wall is composed of five discrete layers,
however, the resolution of most ultrasonographic units
is such that the layers are usually measured in combina­
tion to define the total wall thickness (Table 2.5 ) .
Large intestine i s visible i n all quadrants of the
abdomen. It is recognized ultrasonographically by its
location, size, and the sacculated appearance of its con­
tour. The thickness of the large intestinal wall can be
documented (Table 2.5) but the gas within the colon
obscures the lumen so that it is not possible to deter­
mine the diameter of individual loops of large intestine
(Figures 2 . 1 3 , 2 . 1 4 ) . Waves of peristalsis within the
Figure 2.14 A transverse abdominal ultrasonogram
obtained with a 10 MHz l i near transducer i l l ustrating the
discrete layers of the abdo m i n a l wall
27
2 ADDITIONAL DIAGNOSTIC PROCEDURES

"

Table 2.5 Normal ultrasonographlc features of the in_tine

Region Recommended Strudures Subjedlve Quantitative

transducer examined assessments measurements
frequency (MHz) of Intestine of Intestine·

Cranioventral Foals: 1 0-5 Spleen Motility of colon and Colon:

sma l l i ntestine
Adu lts: 6.5-5 Large intestine wall thickness 0. 1 8 ± 0.04 cm
Presence/absence of
Small i ntestine sma l l i ntestine motility 2-6 contractions!
min
Volume and character
of peritoneal fluid

Ca udoventra I Foals: 1 0-5 Large intestine Motility of colon and Small i ntestine:
sma l l intestine
Adults: 6.5-5 Small intestine wall thickness 0 . 1 6 ± 0.05 cm
Presence/absence of
Bladder sma l l intestine diameter 1 .8 ± 0.8 cm

Volume and character motility 6-1 5 contractions!

of peritoneal fl uid min

Right dorsal Foals: 1 0-6.5 Liver Motility and nature Colonic and small intestinal
Kid ney of i ntestinal contents wall thickness
Adults: 5-2.25 Duodenum (see data above)
Cecum

Left dorsal Foals: 1 0-6.5 Spleen Presence/absence of

Kidney intestine in the
Adults: 5-2 .25 Large colon nephrosplenic space

Mid-abdomen Adults: 6.5-5 Aortoiliac Motility of colon and Colonic and sma l l intestinal
(transrectal quadrification smal l i ntestine wa l l th ickness
route) Bladder (see d ata above)
Small intestine
Cecum
Large colon
Small colon
�
*Freeman and Lyons, unpublished data

cecum run in a dorsal to ventral direction, while the
motion of the remainder of the large intestine runs in
the sagittal plane, so that it is possible to distinguish the
cecum from the right ventral and dorsal colon. Large
intestine should not normally be present within the
nephrosplenic space, and in most horses the entire left
kidney is readily visualized in the left caudodorsal
abdomen. Occasionally gas within the small colon is vis­
ible in the nephrosplenic area, but it is usually possible
to appreciate that this runs caudal, not cranial, from
the nephrosplenic space into the remainder of the
abdomen. Gas within the small colon can also
frequently b� identified as echogenic curves in the left
caudodorsal abdomen.
The ventral body wall is composed of subcutaneous,
muscle, and fat layers that can be distinguished ultra­
sonographically (Figure 2 . 1 4 ) . Peritoneal fluid can be
identified in the cranioventral abdomen in most horses
(Figure 2 . 1 3) , and ultrasonography is occasionally use­
ful to identifY a site for abdominal paracentesis when
unguided techniques have been unsuccessful. In smaller
horses and foals the bladder may be visible in the
caudoventral abdomen and in the mid- and late-term
mare the gravid uterus is identified in this location.

28
 ADDITIONAL D IAGNOSTIC PROCE D U RES 2

CLINICAL INDICATIONS FOR depending on the body position (Figure 2 . 1 5 ) . In the

ABDOMINAL ULTRASOUND IN HORSES
PRESENTING WITH COLIC
Ultrasonographic examination can be used to evaluate
the anatomical location, contents, wall thickness, and
motility of various regions of the intestine. This is par­
ticularly useful in foals, weanlings, or small ponies with
colic, when the size of the animal precludes rectal pal­
pation of the gastrointestinal tract. It is also useful in
horses presenting with clinical signs consistent with a
surgical lesion in which rectal examination has
proved inconclusive. In a study comparing the ultra­
sonographic and rectal detection of distended small
intestine as a criteria indicating that surgical inter­
vention was necessary in seventeen horses presenting
with signs of colic, ultrasonography had a sensitivity of
100 per cent with a specificity of 83 per cent, comparing
favorably to rectal examination which had a sensitivity
of 1 00 per cent and specificity of 75 per cent. With
ultrasonography, it is possible to evaluate portions of
intestine in the cranial abdomen that are out of reach
from the rectum. Ultrasonography is also valuable in
evaluating intra-abdominal masses and peritoneal effu­
sion and in horse with low-grade but persistent pain
where partial intestinal obstruction is suspected.
adult horse distended loops of small intestine are
occasionally visible in the left dorsal quadrant of the
abdomen although more frequently with small intesti­
nal obstruction, the abnormal small intestine is visible
in the right and ventral abdomen (Figures 2. 1 6, 2 . 1 7) .
Incarcerated segments of bowel are amotile and fre­
quently have extremely thickened walls reflecting intra­
mural edema. If this is severe the intestinal wall has a
low echogenicity, and in areas where there is no con­
current distention the intestine often has a corrugated
appearance ( Figure 2 . 1 8 ) . In foals small intestinal intus­
susception produces a characteristic bull's eye appear­
ance, with concentric rings formed by the walls of the
intussusceptum and intussuscipiens and fluid within
the intussusceptum. Ileocecal intussusceptions are not
visible because the gas within the cecum obscures the

CLINICAL INDICATIONS FOR

ABDOMINAL ULTRASOUND IN HORSES
PRESENTING WITH WEIGHT LOSS

The clinical indications for abdominal ultrasonography

in horses with weight loss are less specific.
Ultrasonography should be considered in horses with
palpable intra-abdominal masses or abdominal disten­
tion, and if there is laboratory evidence of hepatic,
renal, or intestinal disease, and in horses with abnormal
peritoneal fluid analysis. In horses with protein-losing
enteropathy and malabsorption, ultrasonography can
be a useful adjunctive aid to allow measurement of the
thickness of specific portions of the intestine and this
may be valuable in determining the response to
therapy.

SMALL INTESTINAL LESIONS

Obstructed intestine is heavy and tends to fall to the
ventral abdomen. If the examination is performed on a
recumbent foal, it is important to evaluate the most
dependent areas of the abdomen carefully, since small
intestinal intussusceptions and other localized lesions
will tend to fall to the lowest point of the abdomen
Figure 2. 1 5 A transverse abdominal ultrasonogram from a
4-week-old foal with sma l l intestina l volvulus i l lustrating a
distended. a motile segment of small intestine. The foal is
in lateral recumbency and this i m age has been obtained
from the ventral midline a nd therefore. because of
gravity. stationary ingesta i n the obstructed segment has
settled into horizontal layers

29
2 ADDITIONAL DIAGNOSTIC PROCE DURES
Figure 2 . 1 6 A longitudinal ultrasonogram of the left dorsal
abdomen from a 5-year-ol d sta l l ion with a right i nguinal
hernia. Multi ple distended loops of small intestine (51) are
visi ble
Figure 2.17 A longitudinal u ltrasonogram of the cranio­
ventral abdomen from an aged pony gelding with a n
obstruction of t h e sma l l i ntestine b y a pedunculated
lipoma. Flu id-filled distended small intesti n a l loops with
thickened walls are visible
Figure 2.18 A longitud inal ultrasonogram of the cranio­
ventral abdomen from a 1 5-year-old pony gelding with
smal l i ntestinal entrapment in the epiploic foramen. A
segment of non-d istended small intestine with hypo­
echoic, edematous wa l ls has a corrugated appearance
(arrows)
30
intussuscipiens. However, it is possible to visualize dis­
tended small intestine in the right and mid-abdomen
proximal to the obstruction. Adhesions are recognized
as portions of intestine that are stationary and remain in
consistent relationship to each other, or to other
abdominal structures that the intestine is adherent to,
such as abscesses, hernias, or the body wall (Figure
2 . 1 9 ) . The presence of both distended and collapsed
loops of intestine is strongly suggestive that there may
be an anatomical obstruction .
LARGE INTESTINAL LESIONS
Ultrasonography is the most sensitive tool available for
diagnosis of left dorsal displacement of the large colon
(nephrosplenic entrapment) . With this condition, large
colon is visualized in the nephrosplenic space obscur­
ing part or all of the left kidney. However, it is possible
for the large intestine to attain a position dorsal to the
left kidney or for small colon to enter the space without
entrapment. Therefore, to confirm the diagnosis of left
dorsal displacement, it is necessary to ensure that large
intestine can be identified running into the space from
a cranial location. Provided that the entrapped portion
is distended, gas shadowing creates a straight dorsal
border of the spleen and the most dorsal portions of the
spleen are obscured. In some horses fluid and ingesta
may be visible within the entrapped portion and this
can enable some of the more dorsal areas of the spleen
to be identified (Figure 2.20) . Cecocecal and cecocolic
intussusceptions can also be specifically identified and
have a bull's eye appearance, similar to that described
for small intestinal intussusception. Specific differentia­
tion of other surgical forms of large colon disease from
generalized tympany or large colon impaction is diffi­
cult. However, transrectal ultrasonography can be use­
ful in the identification of small colon obstruction
(Figure 2.2 1 ) . Most of the small colon is easily palpable
per rectum, however measurement of bowel wall thick­
ness can be useful to distinguish between simple
obstructions and those where the bowel wall is compro­
mised and edematous. The presence of gas free within
the peritoneal cavity, accompanied by particulate fluid
is consistent with gastrointestinal rupture and conse­
quently warrants a poor prognosis.
GENERALIZED INFLAMMATORY AND
INFILTRATIVE INTESTINAL DISEASES
Ultrasonography can be very valuable in distinguishing
between small intestinal distention due to enteritis, or
ileus from physical obstruction and strangulation. The
 ADDITIONAL DIAGNOSTIC PROCE D U RES 2

(a) (b)

(c) (d)

Figure 2. 1 9 Abdominal u ltrasonograms from a 1 5-year-old Shetland pony with m u ra l a bscessation and small i ntestinal
adhesions. I n longitud inal (al and transverse (b) i mages of the affected intest i ne, the walls are hypoechoic and extremely
thickened. The arrows indicate the area at which the two adjacent segments do not move relative to each other,
indicating that adhesions have formed. In other areas of the a bdomen, in longitudinal (cl and transverse (d) i m ages, both
distended and collapsed loops are visible, suggesting that there is intestinal obstruction

Figure 2.20 A tra nsverse ultrasonogram of the l eft dorsal

a bdomen from a 2-year-old g elding with left dorsal d is­
placement of the large colon. In this area the entrapped
portion of intestine is not tympanitic and therefore sound
penetrates the intestine so that the spleen is o n ly partially
obscured by acoustic shadows (arrows) caused by
intestinal gas

31
2 ADDITIONAL DIAGNOSTIC PROCEDURES

Figure 2.21 A transverse ultrasonogram of the caudal

abdomen obtained per rectum from a n aged gelding.
Thickened a reas of sma l l colon (SC) are due to obstruction
of the sma l l colon by a peduncu lated l i poma

wall thickness, diameter of the lumen, appearance of

the intestinal contents, and the intestinal motility
should be considered. Motility is assessed by observing
the intestinal walls and contents over a few seconds;
organized waves of motility should be apparent. Amotile
bowel may be completely motionless, or there may be
random bi-directional movement, particularly as the
abdomen moves in horses that are breathing heavily.
With physical obstruction the intestine is usually
amotile, whereas with enteritis some degree of motility
generally is retained, and in some cases, the motility is
increased. Small intestinal wall thickening is present
with strangulation and may also be seen with enteritis
and peritonitis, but the presence of intestinal motility
should help to distinguish these from cases of small
intestinal obstruction. With colitis the large intestinal
wall is thickened and fluid ingesta may be visualized.
Infiltrative bowel diseases produce focal or multi­
focal wall thickening in various segments of intestine.
Information on the distribution and extent of infiltra­
tion can be obtained with ultrasonography in these
cases (Figure 2.22) . In particular, differentiation of
small from large intestine is achieved and the wall
thickness documented. When combined with other
imaging modalities such as labeled granulocyte scintig­
raphy, ultrasonography is used to characterize individ­
ual areas of intestine in which there is scintigraphic
evidence of inflammation. However, intestinal wall
Figure 2.22 Tra nsverse ultrasonograms of the (a) cra nial,
thickening may extend beyond the primary site since
(b) mid-, (c) right ventral abdomen from a n 1 1 -yea r-old
protein-losing lesions may be associated with secondary mare with chronic eosinop h i l ic enteritis demonstrati ng
bowel edema leading to thickening and reduction in that the l a rg e colon varies i n thickness. In the most
the echogenicity of the bowel wall (Figure 2.23 ) . severely affected area (C), the five-layered a p pearance of
Regardless of its specific nature, infiltrated areas of the colon has been lost

32

(a)
(b)
Figure 2.23 Transverse abdominal ultrasonograms from a
6-year-old mare with plasmacytic-Iymphocytic enteritis,
affecting primarily the l a rge colon. a) In the caudal ventral
abdomen the large colon has irregular thickening of the
wa l l and loss of the five-layered appearance due to cel l u­
lar infi ltrate. b) In the cra n i a l ventral abdomen, the small
intestine is markedly thickened with hypoechoic wa lls due
to bowel edema secondary to i ntestinal protein loss
intestine are generally echogenic with irregular walls
and there may be loss of the normal five-layered appear­
ance. However, at present it is not possible to specifi­
cally differentiate the various forms of infiltrative
disease using ultrasonography (Figures 2.22-2.24) .
THE ABDOMINAL WALL IN THE
POSTOPERATIVE COLIC PATIENT
Ultrasonographic examination of celiotomy incisions is
an accurate means of identification of incisional infec­
tion. The technique is ea�y to perform and ultrasono-
ADDITIONAL DIAGNOSTIC PROCEDURES 2
(a)
(b)
Figure 2.24 Transverse ultrasonograms from a 1 6-year-old
gelding with i ntesti nal lymphosarcoma. a) The most
severely affected segment of small i ntestine has markedly
thickened walls, loss of the normal intestinal wall struc­
ture, and a reduced l u me n . b) In a less severely affected
proximal segment there is wall thickening and moderate
distention
graphic signs of infection may precede the onset of clin­
ical signs by up to 30 days. The presence of hyperechoic
foci with acoustic shadowing indicating gas, and accu­
mulation of anechoic or echogenic fluid within the sub­
cutis are indicative of incisional infection (Figure 2.25 ) .
I n a study o f 5 0 horses that had undergone exploratory
celiotomy, the accuracy of ultrasonography in the early
detection of incisional infection was assessed and the
sensitivity was 1 00 per cent with a specificity of 88 per
cent using these subjective assessment criteria. Horses
with ultrasonographic evidence of infection should be
observed for clinical signs of infection for at least 1
month following the ultrasonographic examination. In
33
2 ADDITIONAL DIAGNOSTIC PROCEDURES
addition the early introduction of antibiotic therapy or
removal of individual skin sutures may avert the devel­
opment of more serious complications. Hernia forma­
tion occurs occasionally following celiotomy. The
presence of distended loops of intestine suggests partial
Figure 2.25 A transverse ultrasonogram of the ventral
abdominal wall from a horse that has purulent drainage
from a cel iotomy incision performed 7 days previously. A
tract (a rrows) extends from a collection of hypoechoic
material resu lting from incisional infection
Figure 2.26 A longitud inal u ltrasonogram of the ventral
abdom inal wall from a horse that has developed deh is­
cence of the abdominal muscle 8 days after exploratory
cel iotomy. I ntestine is located between the muscle defect
(arrows) and had adhered to the subcutaneous tissue
34
or complete intestinal obstruction, while intestine
adhered to the incision or within a hernia is apparent
because adhered areas do not move relative to the
surrounding structures (Figure 2.26) .
Nuclear scintigraphy
-
R Wel ler a n d eM M a rr
INTRODUCTION
Gamma scintigraphy is a relatively new technique for
the diagnosis of abdominal disease in horses, whereas in
humans and small animals it is a well-established tool
for this purpose. Techniques used in humans and small
animals are described in Table 2.6.
In the horse scintigraphic techniques in gastro­
enterology involve the use of three types of agent.
1 . Radiopharmaceuticals, consisting of a radionuclide
and a carrier, whose biological activity causes it to
localize in specific tissues
• 99mTc-methylendiphosphonate (MDP) for dental
scintigraphy
• 99mTc-sulfur colloid for hepatic scintigraphy.
2. Radioactive agents which get entrapped in specific
cell populations
• 99mTc-hexamethyl propylene amine oxine
(HMPAO) and l l I In oxine to label leukocytes for
scintigraphic imaging of inflammation
• 99mTc-tetrofosmin and 99mTc-methoxy-isobutyl­
isonitrile (MIBI) for scintigraphic imaging of
neoplasia. These radiopharmaceuticals are
currently under investigation as unspecific
tumor-labeling agents in thoracic and abdominal
neoplasia in the horse.
3. Inert, non-toxic radioactive agents to assess motility
of the gastrointestinal tract
• 99mTc-sulfur colloid and Il I In-diethylene­
triaminepentaacetic acid (DTPA) to assess
gastric emptying. These techniques have been
used in experimental studies to investigate the
effect of prokinetics.
DENTAL SCINTIGRAPHY
In horses with suspected dental disease scintigraphy of
the head with 99mTc_MDP can provide substantial infor­
mation on the exact localization and extent of the prob­
lem. Skeletal scintigraphy with 99mTc_MDP is the most
commonly performed scintigraphic imaging procedure
 ADDITIONAL DIAG N OSTIC PROC E D U RES 2

Used for the diagnosis of Radiopharmaceutical

Dental disorders Technetium (99mTc) methylendiphosphonate (MOP)

Esophageal motil ity 99mTc-sulfur colloid

Gastric e m ptying 99mTc-sulfur colloid

99mTc-d iethylenetriaminepentaacetic acid (OTPA)

Gastric secretory function 99mTc-pertechnetate

Gastrointestinal bleeding 99mTc-labeled red blood cells

Gastrointestinal neoplasia 99mTc-methoxy-isobutyl-isonitrile (MIB!)

Inflammatory gastrointestinal conditions Technetium (99mTc), G a l l i u m (67Ga), Indium (1I I In) l a beled leukocytes

Hepatobiliary imaging 99mTc-sulfur colloid

99mTc-im inodiacetic acid (I DA)

in veterinary medicine. Bony abnormalities can be
detected before there are radiographic or ultrasono­
graphic changes. In cases of dental disease radiographs
are often inconclusive, especially in the early stages of
the disease. Bone scintigraphy has been proven to be a
sensitive and specific method to detect changes in the
alveolar bone surrounding the diseased tooth.
Principle
of increased activity. The teeth can be identified as
regions of decreased activity within the alveolar bone.
These anatomical structures get less distinct with age
and in old horses blend completely into the back­
ground activity. Horses with a tooth root abscess show a
focal increase of activity over the diseased tooth (Figure
2.27) , whereas horses with periodontal disease show a
linear increase over the involved arcades (Figure 2.28) .

The uptake of 99mTc-MDP depends on blood flow and

bone metabolism. In the case of dental disease there is
an increased bone turnover in the alveolar bone
adjacent to the tooth.

Indications
u dal
1 . I lorses with suspected den tal disease, in which
radiographs are inconclusive.
2. Horses with recurrent sinusitis to rule out an
underlying tooth problem.
3. Horses in which multiple dental disease is suspected.
right
Technique

Horses are injected intravenously with 1 0 MBq/kg ventral

99mTc_MDP. Three hours after injection left and right
lateral, and ventral and dorsal images of the teeth are
acquired, for 60 seconds, into a 256 x 256 matrix.
Interpretation
In the normal horse the alveoli, the vertical ramus of
the mandible, the zygomatic arch, the temporo­
mandibular joints, and th � ethmoids are seen as areas
ro tral
Figure 2.27 Tooth root abscess. A l eft lateral a n d a dorsal
scintigraphic image of the head of a 1 5-year-old
Warmblood gelding. The horse had a 6-month history of
recurrent swe l l i n g over the left maxi l l a . Radiog raphs were
inconclusive. Scintigraphy with 99mTc-M D P revealed a focal
uptake over the root of the second maxi l lary cheek tooth
on the l eft side, suggestive of a tooth root a bscess

35
2 ADDITIONAL DIAGNOSTIC PROCEDURES

audal

L G

l en.

yen aJ
fo tral

Figure 2.28 Periodontal disease. A left lateral scintigram,

3 hours after injection of 99mTc-MDP, of the head of a 2S­
year-old Connemara gelding that presented with progres­
sive weight loss. No evidence of dental disease was seen
on intra-oral examination or radiographs. The image
shows a linear increase of radioactivity over the upper and
lower arcade, suggestive of severe periodontal disease

Figure 2.29 Abdom inal abscess. A scintigram of the right

mid-abdomen of a 6-year-old gelding with a 3-week his­
tory of fever of unknown orig i n . An hour after injection of
99mTc-labeled leukocytes there was a circu lar increase of
activity caudal to the l u ng, suggestive of an abdom inal
a bscess

INFLAMMATION AND INFECTION 2. Identification or localization of inflammatory bowel

67Ga, I I IIn, and 99mTc-labeled leukocytes have been vali­
dated as a sensitive technique for the diagnosis of
abdominal abscesses in horses (Figure 2.29) . 99mTc_
labeled leukocytes have been used successfully for the
identification of focal or generalized intestinal inflam­
mation (Figure 2.30). It appears to be most useful in
acute inflammatory conditions and eosinophilic enteri­
tis. Variable results have been obtained imaging
lymphocytic-plasmacytic enteritis. The procedure is
particularly helpful for characterization of the distribu­
tion of lesions within the gastrointestinal tract.
Principle
99mTc-HMPAO is a lipophilic compound which gets
trapped within white blood cells. It labels a mixed
leukocyte population, of which granulocytes account
for around 75 per cent. The distribution of activity
reflects the distribution of granulocytes in the patient's
body.
Indications
1 . Identification or localization of abdominal
abscesses.
disease.
3. Evaluation of animals with fever of unknown origin.
4. Identification and localization of tooth root
abscesses.
5. Monitoring disease progression or response to
therapy.
Technique
The procedure can be divided into four steps.
1 . Isolation of leukocytes from peripheral blood
• 200 ml of venous blood is taken, using a 1 4-
gauge needle, into 40 m l acid-citrate dextrose
anticoagulant
• 20 ml is centrifuged at 2000 G for 10 min to
obtain cell free plasma
• the remaining blood is left at room temperature
for 60 min to allow the red blood cells to
sediment
• the leukocyte and platelet-rich plasma is
removed and centrifuged at 1 50 G for 5 min, the
resulting pellet contains a mixed population of
leukocytes
• the supernatant is centrifuged at 2000 G for 10 min
to produce cell-free plasma for washing the cells.

36

Figure 2.30 Inflammation of the small intestine. A scinti­
graphic image 1 hour after injection of 99mTc-HMPAO­
labeled leukocytes of the right caudodorsal abdomen of a
1 4-year-old Thoroughbred mare. The horse presented with
weight loss of 3 weeks duration. The scintigram shows two
linear reg ions of i ncreased activity in the right dorsal
abdomen, suggestive of inflammation of the small intestine
2. In vitro labeling
• to form 99mTc-HMPAO, 10 MBq/kg 99mTc_
pertechnetate is added to one vial, containing
0.5 mg HMPAO, 7.6 1lg stannous chloride
dehydrate, and 4.5 mg sodium chloride with
nitrogen and immediately mixed with the
isolated leukocytes
• after an incubation time of 10 min at room
temperature the labeling is stopped with 10 ml
of cell-free plasma
• the cells are centrifuged at 1 50 G for 5 min and
the resulting pellet resuspended in 5 ml cell-free
plasma.
3. Reinjection
• the labeled leukocytes must be injected back
into the horse immediately through a 1 2-gauge
catheter.
4. Examination with Gamma-Camera
• 1 hour after injection static images are acquired
of the area of interest for a minimum of 1 00 000
counts in a 256 x 256 matrix with a general all
purpose collimator and processed with
dedicated software.
Interpretation
In the normal horse there is activity in the liver, spleen,
salivary glands, and bone marrow reflecting the normal
ADDITIONAL DIAGNOSTIC PROCE D U R ES 2
distribution of granulocytes in the patient. In the horse
a high activity is seen in the lung, which may be caused
by the destruction of damaged labeled leukocytes by
pulmonary i ntravascular macrophages. Free 99mTc and
radiolabel byproducts are excreted via the urinary tract
accounting for a mild increase in uptake in the kidneys
and bladder. As leukocytes migrate into sites of inflam­
mation or abscessation there is an increase in activity
(Figures 2.29, 2.30) .
HEPATIC SCINTIGRAPHY
Hepatic scintigraphy with 99mTc-labeled sulfur colloid is
the only technique for visualizing the functioning
reticuloendothelial system of the liver in the horse. It is
used to determine hepatic size, shape, and intra­
abdominal location of the liver. Lesions greater than
2.5 em in diameter can be identified.
Principle
Colloid particles are readily phagocytized by stellate
cells of the liver (Kupffer cells) . Since these cells are
evenly distributed throughout the liver, the displayed
activity corresponds to the size and shape of the organ.
To avoid trapping of the 99tnTc-labeled sulfur colloid in
the reticuloendothelial system of the lungs, agents that
concentrate in the polygonal cells of the liver have to
be used (ethylenediamine-N-N-bis (a-2-hydroxy phenyl)
acetic acid derivatives EDBHA) .
=
Indications
1 . Assessmen t of the reticuloendothelial system of the
liver.
2. Determination of the size, form, and intra­
abdominal location of the liver.
3. Investigation of diseases of the biliary tract.
Technique
The procedure can be divided into four steps.
1 . Synthesis of EDBHA and 99mTc labeling of EDBHA
as described by Theodorakis et at. ( 1 982) .
2 . Preparation of 99mTc-labeled colloid using a
commercially available kit according to the
manufacturer's instructions.
3. Examination with Gamma-Camera, 3-50 minutes
after intravenous injection of the
radiopharmaceutical, dorsal, left and right lateral,
and lateral oblique views of the ventral thoracic and
dorsal abdominal areas are acquired.
37
2 ADDITIONAL DIAGNOSTIC PROCEDURES
Interpretation
The scintigrams show extensive uptake by the liver, with
less uptake by the kidneys and bladder; and slight
uptake by the lungs. Biliary secretion of radioactivity
into the intestines is evident. The right kidney appears
to be in contact with the caudal margin of the liver. The
separate liver lobes are readily discernible.
Breath hydrogen tests
T Mair
Breath hydrogen measurements can be used to investi­
gate gastrointestinal function in horses, although the
techniques and interpretation of results require further
refinement at the time of writing. These tests have
distinct advantages over other tests of gastrointestinal
function in being simple to perform, non-invasive, safe,
and well-accepted by patients. The technique is based
on the fact that, when carbohydrate comes in contact
with bacteria in the gastrointestinal tract, it is fermented
and hydrogen is produced as a by-product. A propor­
tion of this hydrogen diffuses from the intestinal lumen
into the portal circulation and is subsequently exhaled
in breath. Since relatively few bacteria are present in the
stomach and small intestine of healthy animals, hydro­
gen excreted in the breath originates almost entirely
from the large intestine. Using this knowledge, mea­
surement of breath hydrogen can be used to investigate
small intestinal carbohydrate malabsorption, small
intestinal bacterial overgrowth, and to assess oro-cecal
transit time.
Breath hydrogen tests are usually performed by
monitoring exhaled hydrogen concentration following
a test meal containing either an absorbable carbo­
hydrate (such as lactose or glucose) or a non­
absorbable carbohydrate (such as lactulose ) . Studies to
date in horses have shown variation between animals
following the ingestion of identical test meals. Further
research and modification of the technique are
required before it can be applied clinically.
'BIBLIOGRAPHY
Rectal biopsy
Lindberg R, Nygren A, Persson S G B ( 1 996) Rectal biopsy
diagnosis in horses with clinical signs of intestinal
disorders: a retrospective study of 1 1 6 cases. Equine Vet. )'
28:275-84.
38
Traver D S, Thacker H L ( 1 979) Malabsorption syndromes in
the horse: use of rectal biopsy in differential diagnosis.
Proc. Am. Assoc. Equine Pract. 24:487-98.
Fecal analysis
Morris D D, Whitlock R H, Palmer J E ( 1 983) Fecal leukocytes
and epithelial cells in horses with diarrhea. Cornell Vet.
73:265-74.
Abdominocentesis
Adams, S B, Fessler,j R, Rebar A H ( 1 980) Cytologic
interpretation of peritoneal fluid in the evaluation of
equine abdominal crisis. Cornell Vet. 70:232-46
Bach L G and Ricketts S W ( 1974) Paracentesis as an aid to
the diagnosis of abdominal disease in the horse. Equine
Vet. ). 6: 1 1 6-2 1
Coffman J R ( 1 980) Peritoneal fluid. Vet. Med. Small Anim.
Clin. 75: 1 285-8
Crowell R L, Tyler R D, Clinkenbeard K 0 and MacAllister
C 0 ( 1 987) Collection and evaluation of equine
peritoneal and pleural effusions. Vet. Clin. N. Am. Equine
Pract. 3:543-561
Tulleners E P ( 1 983) Complications o f abdominocentesis in
the horse. ]. Am. Vet. Med. Assoc. 1 82:232
White N A ( 1 990) Abdominal paracentesis. In The Equine
Acute Abdomen, N A White (ed. ) . Lea and Febiger,
Philadelphia. pp. 1 24-3 1 .
Analysis o f peritoneal fluid
Fischer A T ( 1997) Advances in diagnostic techniques for
horses with colic. Vet. Clin. N. Am. Equine Pract. 1 3:203- 1 9
Fischer A T , Lloyd K C K , Carlson G P ( 1 986) Diagnostic
laparoscopy in the horse . ). Am. Vet. Med. Assoc.
1 89:289-292
Frazer G S, Burba D, Paccamonti D ( 1 996) Diagnostic value
of peritoneal fluid changes in the postpartum mare. In.
Proc. Am. Assoc. Equine Pract. 42:266-7.
Grindem C B. Fairley N M. Uhlinger C A and Crane S A
( 1 990) Peritoneal fluid values from healthy foals. Equine
Vet. ). 22:359-61
Hanson R R. Nixon A J. Gronwall R ( 1 992) Evaluation of
peritoneal fluid following intestinal resection and
anastomosis in horses. Am. ). Vet. Res. 53:216-221
MalarkJ A. Peyton L C and Galvin MJ ( 1 992) Effects of blood
contamination in equine peritoneal fluid analysis. ). Am.
Vet. Med. Assoc. 201 : 1 545-8.
May K A. Cheramie H S and Prater D A ( 1 999)
Chyloperitoneum and abdominal adhesions in a
miniature horse . ). Am. Vet. Med. Assoc. 2 1 5:676-678
Santschi E M. Grindem C B. Tate L P and Corbett W T ( 1 988)
Peritoneal fluid analysis in ponies after abdominal
surgery. Vet Surg. 1 7:6-9
Schumacher J , Spano J S. McGuire J. Scrutchfield W L and
Feldman R G ( 1 988) Effects of castration on peritoneal
fluid constituents in the horse. ). Vet. Intern. Med. 2:22-25
Schumacher J , Spano J S and Moll H D ( 1 985) Effects of
enterocentesis on peritoneal fluid constituents in the
horse. ). Am. Vet. Med. Assoc. 1 86: 1 30 1 -1 303
Tulleners E P ( 1 983) Complications of abdominocentesis in
the horse. ). Am. Vet. Med. Assoc. 1 82:232-4.
Van Hoogmoed L. Snyder J R. Christopher M ( 1 996)
Peritoneal fluid analysis in peripartum mares.). Am. Vet.
Med. Assoc. 209 : 1 280-2.

Carbohydrate absorption tests
Dietz H H ( 1 98 1 ) D (+)-xylose absorption test in the horse. A
clinical study. Nord. Vet. Med. 33: 1 1 4-20.
Jacobs K A, Bolton] R ( 1 982) Effect of diet on the oral
glucose tolerance test in the horse. ]. Am. Vet. Med. Assoc.
1 80:884-6.
Loeb, W F, McKenzie, L D, Hoffsis, G F ( 1 972) The
carbohydrate digestion-absorption test in the horse.
Technique and normal values. Cornell Vet. 62:524-3 1 .
Murphy D , Reid S W], Love S ( 1 997) Modified oral glucose
tolerance test as an indicator of small intestinal pathology
in horses. Vet. Rec. 1 40:342-3.
Roberts M C, Hill F W G ( 1973) The oral glucose tolerance
test in the horse. Equine Vet.]. 5 : 1 7 1-3.
Roberts M C, Norman P ( 1 979) A re-evaluation of the
d (+)xylose absorption test in the horse. Equine Vet.]. 1 1
239-43.
Endoscopy
Adamson P, Murray M J . ( 1 990) Gastric endoscopy. In Equine
Endoscopy, ] L Traub-Dargatz, C M Brown (eds) .
C V Mosby, St Louis, pp. 1 1 9-37.
Knyrim K ( 1 989) Optical performance of electronic imaging
systems for the colon. Gastroenterology 96:776.
Lamar A M ( 1 997) Standard fiberoptic and video endoscopic
equipment. In Equine Endoscopy 2nd edn,] L Traub­
Dargatz, C M Brown (eds) . C V Mosby, St Louis, p. 13.
Ultrasonographic examination of the
abdomen in the gastrointestinal patient
Bernard W V, Reef V B, Reimer] M, Humber K A, Orsini] A
( 1 989) Ultrasonographic diagnosis of small-intestinal
intussusception in three foals.]. Am. Vet. Med. Assoc.,
1 94:395-397.
Klohnen A, Vachon A, Fischer A ( 1 996) Use of diagnostic
ultrasonography in horses with signs of acute abdominal
pain.]. Am. Vet. Med. Assoc., 209 : 1 597-1606.
Santschi E M, Slone D E, Frank W M ( 1 993) Use of
ADDITIONAL DIAGNOSTIC PROCE D URES 2
ultrasound in horses for diagnosis of left dorsal
displacement of the large colon and monitoring its
nonsurgical correction. Vet. Surgery, 22, 281-284.
Wilson D A, Badertscher R R, Boreo M], Baker G], Foreman
] H ( 1 989) Ultrasonographic evaluation of the healing of
ventral midline abdominal incisions in the horse. Equine
Vet. ]. (suppl. 7 ) , 1 07-1 1 0.
Nuclear scintigraphy
Butson R], Webbon P M, Fairbairn S M ( 1 995) Tc-99m­
HMPAO labeled leucocytes and their biodistribution in
the horse: a preliminary investigation. Equine Vet. ]. 27(4)
3 1 3-315
Hoskinson ] ], Tucker R L ( 1 996) Scintigraphic imaging of
inflammation and infection. In Handbook of Veterinary
Nuclear Medicine, R B Berry, G B Daniel (eds) . North
Carolina State University, Raleigh, NC, pp. 1 62-78.
Koblik P D , Lofstedt], ]akowski R M, ]ohnson K L ( 1 985) Use
of I I I In-labeled autologous leukocytes to image an
abdominal abscess in a horse . ]. Am. Vet. Med. Assoc.
186: 1 3 1 9-22.
Theodorakis M C, Bermudez A], Manning] P, Koritz G D,
Hillidge C ] ( 1 982) Liver scintigraphy in ponies. Am. ]. Vet.
Res. 43: 1 5 6 1 - 1565.
Weller R, Livesey L, Bowen I M, et al. (200 1 ) Comparison of
radiography and scintigraphy in the diagnosis of dental
disorders in the horse. Equine Vet. ]. , 33: 49-58.
Weller R, Weaver M, Livesey L, Bowen I M and Marr C M
(2000) Nuclear scintigraphy with 99mTc-HMPAO labeled
leucocytes in the assessment of horses with malabsorption.
Vet. Radiol. Ultrasound, 4 1 : 563.
Breath hydrogen tests
Bracher V and Baker S] ( 1 994 ) . Breath tests for investigation
of gastrointestinal disease. nquine Vet. Educ. 6: 1 73-6
Murphy D, Reid S W] and Love S ( 1 998 ) . Breath hydrogen
measurement in ponies: a preliminary study. Res. Vet. Sci.
65:47-51
39
 3
Laparoscopy
CA Ragle
Instrumentation
Laparoscopy can best be defined as abdominal explo­
ration employing a type of endoscope called a laparo­
scope. The word laparoscopy is derived from lapara,
meaning flank, and skopein, meaning to examine.
Laparoscopic procedures are desirable because they
allow improved viewing of the abdomen and are less
invasive than traditional operative techniques. The
number and variety of surgical procedures performed
in horses under laparoscopic guidance has steadily
increased during the last decade and many of these pro­
cedures are applicable to equine gastroenterology.
LAPAROSCOPIC EQUIPMENT
't"1"' W,H, '*' "",",�X�"', "A,,) wh", fcc " ee'),''''''
There is a paucity of laparoscopic equipment that is man­
ufactured specifically for use in the horse. Luckily, many
of the instruments intended for use in humans can be
used successfully in the horse. Equipment designed for
use in humans is often being used at the far limits of its
capacity in horses because of their larger size. The wide­
spread use of arthroscopy in equine hospitals paved the
way for the use of laparoscopy. Since many veterinary
hospitals already own a light source, light cable, video
camera, and a monitor for arthroscopy, laparoscopic
capability only requires the addition of a laparoscope,
insufflator, and operating instruments.
Laparoscope
Laparoscopes are available in various lengths, diame­
ters, and angles of view. Scopes longer than 50 cm are
recommended for use in the equine abdomen. A scope
length of 35 cm is adequate for use in foals and can be
used in adults when the structures to be viewed are near
the scope portal. Larger diameter laparoscopes offer
greater light transmission and are less likely to be dam­
aged; the most commonly used diameter for equine
applications is 10 mm. A 30 degree angled view scope is
preferred to a zero degree scope because an angled
view permits a more complete examination from a
single scope portal. Many surgeons also prefer the 30
degree scope because of its similarity to the 30 degree
arthroscope, which makes triangulation and instrument
manipulation more familiar. A 45 degree angle of view
laparoscope is also available. The laparoscope is
inserted into the abdomen via a previously placed
sheath and removable trocar. This sheath should be of
adequate length (10.5-15 cm) to extend through the
paralumbar fossa and be sturdy as to protect the laparo­
scope against the necessary torque and stresses encoun­
tered from manipulating the scope through this often
heavily muscled portal.
Insufflator
Insufflators are used to create and maintain pneumo­
peritoneum, which is necessary for clear viewing and
maneuvering the instruments and laparoscope in the
abdomen. Commercial insufflators permit careful
regulation of gas flow and intra-abdominal pressure.
Because of the large size of the equine abdomen, a
high flow insufflator (> 10 l/min) is recommended.
Alternative methods of insufflation include adaptation
of a flow meter to a carbon dioxide tank or using room
air via exhaust from a suction unit. Both of these
methods require use of in-line micropore filters and
close manual monitoring of intra-abdominal pressure.
Carbon dioxide (C02), nitrous oxide (N20) and
41
3 LAPAROSCOPY
helium (He) are the gases most commonly used for
laparoscopic insufflation. Currently carbon dioxide is
the most widely accepted because it is least likely to
cause gas emboli and it is affordable. The primary dis­
advantage is that it reportedly converts into carbonic
acid on moist peritoneal surfaces, and this can cause
postoperative discomfort to the patient.
Light source
Light sources provide illumination of the body cavity
during the laparoscopic procedure. For diagnostic and
operative techniques the 150 watt and 300 watt intensi­
ties are most commonly used. Although a 150 watt light
source is suitable for some procedures, a 300 watt light
source is well worth the added expense, especially when
video recording or digital image capture is used. Light
sources with xenon or halogen bulbs produce higher
intensity light and more heat than the standard tung­
sten light bulb. Photodocumentation (35 mm) is best
accomplished using a flash generator, but video record­
ing. digital images, or color thermal prints can be
accomplished with a 300 watt tungsten or a 150 watt or
greater xenon light source.
Video camera and mon itor
A video camera is essential for adequate viewing
because most operative laparoscopic procedures
require both hands for simultaneous manipulation of
instruments. This makes performing surgery under
direct viewing through an eyepiece difficult, if not
impossible. Use of a video camera and monitor also
decreases the risk of contamination of the surgical site
and allows recording of the procedure for later review.
Characteristics of a video camera most important for
use in equine laparoscopy are that it is immersible for
chemical sterilization and that it is compact in size with
sufficient resolution and color representation to pro­
vide true images. A camera with at least 300 lines of res­
olution is recommended. Newer 3-chip cameras have
over 800 lines of resolution. It is important to match the
light sensitivity of the camera with the intensity of the
light source to insure clear and bright images. Monitors
should provide a clear picture, have a minimum screen
size of 33 cm (13 in) (the larger the better and two mon­
itors are often helpful), and ample plug-in jacks to allow
addition of a video recorder, film recorder, digital
image capture unit, or thermal printer. A mobile cart
that can accommodate all the various components is
the best way to organize the video system. This facili­
tates easy setup and efficient connection of all cables
and tubing at surgery. A vertical stacking scheme allows
placement of the monitor on the top of the unit, pro­
viding unobstructed viewing of the screen. When
42
possible the gas source used for insufflation should also
be attached to the cart.
Instrumentation
Instruments for intra-abdominal use should be at least
30 cm in length. Whenever available the longer 43 cm
instruments should be obtained, as the greater length is
rarely a hindrance and very helpful when needed. The
most commonly available diameters are 5 mm and
10 mm, but well-designed, sturdy instruments are more
important than the actual diameter. Use of a cannula is
often omitted in equine laparoscopy, allowing use of
custom-made instruments of varying shapes and diame­
ters. A basic instrument set would consist of
• two tissue forceps (one grasping and one claw)
• scissors
• ligature introducer/knot advancer
• suction/irrigation cannula
• laparoscope cannula and trocar
• Knowles uterine forceps
• Chambers catheter
• 30 cm uterine catheter (Figure 3.1)
• biopsy instrument and injection needle.
Additional instruments for the complete kit include an
endoscopic clip applier and staplers.
Advanced laparoscopic techniques often include the
use of electrosurgery or laser. These require specialized
instrument� depending on the specific technique.
Intracorporeal suturing requires the use of laparoscopic
needle holders and assistant needle holders. An auto­
suture device (Figure 3.2) and specialized knots such as
the modified roeder, jamming anchor knot, and
Aberdeen knot can simplity an otherwise technically
challenging procedure. Tissue specimen retrieval bags are
helpful for intraoperative storage and subsequent removal
Figure 3.1 Endoscopy instruments (top to bottom): ligation
loop, suction/lavage tip, scissor, atraumatic grasping
forcep, Semm forcep
 LAPAROSCOPY 3

(Figure 3.3). The table is tilted using a tripod-style

hydraulic jack (Figure 3.4). The horse should be
secured with a chest brace and tail tie to allow the table
to tilt without the horse slipping forward (Figure 3.5).

Figure 3.2 Disposable auto suturing device (Endostitch®,

United States Surgical Corporation, Norwalk, CT)

of diseased tissues. Laparoscopy accessories are rapidly

being developed to minimize the infrequent but impor­
tant risks of endoscopy; one example is modified trocars
that are expanded radially after penetrating the abdomi­
nal wall. This creates portals with less trauma and helps to
avoid damage to epigastric abdominal wall vessels.

Surgery table
Figure 3.4 Hydraulic lift used to tilt the surgery table for
Several laparoscopic procedures are best performed endoscopy on a horse in dorsal recumbency
with the horse in dorsal recumbancy under general
anesthesia. For these procedures, putting the horse in
the Trendelenberg position (head down and hindquar­
ters raised) allows the viscera to displace cranially and
better expose the anatomy of the caudal abdomen.
Although it is possible to raise the end of a standard
surgical table and accomplish this, when the desired
degree of tilt is achieved, the table is usually too high for
the surgeon to operate comfortably without standing
on a stool. For these reasons we have constructed a
laparoscopy table that is low to the ground and when
tilted reaches an optimal height for performing surgery

Figure 3.3 A custom-designed tilt table allows the horse to Figure 3.5 A horse in dorsal recumbency is prepared to be
be positioned in the Trendelenberg position without tilted into the Trendelenberg position. A chest brace prevents
exceeding a comfortable operating height for the surgeon the horse from slipping forward when the table is tilted

43
3 LAPAROSCOPY
Indications for laparoscopy
Laparoscopy is a useful diagnostic tool to evaluate the
abdominal cavity. This evaluation is often aimed at
making a specific diagnosis or determining prognosis of
intra-abdominal disease. Direct viewing of the abdomi­
nal cavity using laparoscopy offers the clinician visual
access to areas which normally cannot be seen using
celiotomy techniques (e.g. epiploic foramen, nephros­
plenic ligament, duodenum, etc.) . This visual access
permits direct assessment of abdominal viscera, often
more informative and accurate than secondary imaging
or diagnostic techniques. In addition to increased diag­
nostic and prognostic ability, laparoscopy also can be
used to provide therapeutic intervention of intra­
abdominal disease. A balanced diagnostic approach
that uses laparoscopy in addition to clinical and labora­
tory methods offers the greatest opportunity for accu­
rate diagnosis, prognosis, and treatment.
The clinician needs to have a clear understanding of
the caveats of laparoscopy. For any meaningful exami­
nation of the abdominal cavity to take place adequate
free space between the viscera and body wall must exist.
For this reason laparoscopy is rarely indicated in horses
with significant abdominal distension. Adequate view­
ing cannot be achieved without adequate room inside
the abdominal cavity. When the intestines are full of
ingesta or gas adequate pneumoperitoneum cannot be
established. The more free space available in the
abdominal cavity the greater the viewing potential and
the lower the intra-abdominal pneumoperitoneum
inflation pressure that is needed. Lower intra-abdomi­
nal inflation pressures translates to less pain and better
cardiopulmonary function of the horse. Another con­
sideration is that standing laparoscopy should be
approached very cautiously in any horse in which
diaphragmatic hernia may be a differential. The poten­
tial for creating a pneumothorax must be appreciated
in such horses.
It is also important to note that complete examina­
tion of all intra-abdominal viscera and surfaces cannot
be achieved. It is an axiom of laparoscopy that 'what you
see, you see but what you don't, you don't'. Added to
that is 'if you don't look you will never see'.
Laparoscopy of the standing horse offers the best view­
ing of the dorsal aspect of the abdominal cavity while
the ventral aspects are best viewed using a ventral
abdominal approach with the horse in dorsal recum­
bancy.
Finally it must be emphasized that performing
exploratory laparoscopy on horses will affect the peri­
toneal fluid parameters. These have been reported as
an increase in mean leukocyte counts (mean leukocyte
44
count 31 960/IlI) and protein concentrations (mean
2.5 g/dl) of peritoneal fluid within 24 hours of
laparoscopy. As a comparison abdominal fluid collected
from ponies 24 hours after exploratory celiotomy had
mean leukocyte counts of 137 857/lll and mean protein
concentrations of 4.7 g/dl 24 hours postoperatively.
Peritoneal fluid cell counts have been reported to reach
their peak about 5 days after celiotomy in normal
horses. It is unknown how long peritoneal values take to
return to preoperative values after celiotomy or
laparoscopy. Operative complications directly related
to diagnostic laparoscopy are rare. The most common
complications are minor punctures of the spleen and
cecum or injury to the epigastric vessels during trocar
placement. These complications are minimized by
proper presurgical preparation of the horse and exer­
cising care during portal placement.
Diagnostic laparoscopy has been performed in
horses with chronic weight loss, chronic colic, intra­
abdominal hemorrhage, and peritonitis, and for diag­
nosing abdominal neoplasia, intestinal adhesions, and
evaluating the reproductive tract. The laparoscope has
been used to view and evaluate rectal tears, rectal pro­
lapses, mesocolic ruptures, gastric ruptures, abdominal
abscesses, splenic hematomas, retroflexion of the large
colon, vaginal and uterine tears, and uterine artery rup­
tures (Figures 3.6-3.12) An analysis of 105 diagnostic
laparoscopies in the horse revealed an overall sensitivity
of 75 per cent for diagnosis of disease with a specificity
of 18 per cent.
Biopsy of the liver, spleen, and kidney under laparo­
scopic viewing is also possible and allows selective sam­
pling of abnormal areas. It may also allow for a larger
and possibly more diagnostic specimen than is possible
with a true cut or biopsy gun. Laparoscopy can be used
Figure 3.6 Subcapsular splenic hematoma in a horse
viewed from a left paralumbar fossa portal during
standing endoscopy
 LAPAROSCOPY 3

following celiotomy to evaluate surgical results if they

are in question (e.g. integrity of an intestinal anastamo­
sis or bowel viability) . If a diagnosis indicates a need for
surgical correction, laparoscopy may also be useful;
many surgeries traditionally done via laparotomy or
celiotomy can be performed laparoscopically, including
removal of infected umbilical remnants, repair of
ruptured bladders in neonatal foals, repair of inguinal
herniation in stallions, cryptorchidectomy, ovariec­
tomy, granulosa cell tumor removal, hernia repair,
adhesiolysis, colopexy, and removal of cystic calculi.
Laparoscopy can also be used as an educational tool
in improving transrectal palpation skills. A systematic
and thorough approach to transrectal examination is
Figure 3.8 Laparoscopic cystotomy for removal of a S cm
necessary to assess normal as well as abnormal condi­ diameter urolith in a gelding
tions in the abdominal cavity; accurate mental images of
transrectally palpated structures are vital when evaluat­
ing conditions of the equine abdomen. Clinicians
cannot expand their palpation skills without a method
to develop accurate mental images and the ability to

Figure 3.7a Retroflexion of the large colon viewed left Figure 3.9 Exploratory laparoscopy for chronic colic

paralumbar fossa portal revealed a large melanoma tumor on the left dorsal body
wall of a mare. Smaller melanomas were visible
multifocally throughout the abdomen

Figure 3.7b Ventral colon in a dorsal pOSition. Diaphragm

(D), spleen (Sp), and stomach (St) are visible in the Figure 3.10 Laparoscopic-guided aspiration of a hepatic
periphery abscess

45
3 LAPAROSCOPY
Figure 3.11 Incarceration and adhesion of
mesentery in the inguinal ring. This occurred
complication of eventration subsequent to a cryptorchid
castration via an inguinal approach
Figure 3.12 Aspiration of a hematoma in the mesentery of
the small colon. A post-parturient mare was referred for
evaluation of colic and a mass in the caudal abdomen
link that visualization to a spatial orientation and tactile
sense. Videolaparoscopy performed during transrectal
palpation provides the opportunity to link visual, tac­
tile, and mental images of important structures in the
normal equine abdomen. Structures that can normally
be palpated transrectally and viewed with videoendo­
scopic imaging are: uterine body, uterine horn, ovaries,
bladder, left and right inguinal rings, spleen, nephro­
splenic ligament, left kidney, root of the mesentery,
aorta, duodenum, small colon, base and ventral band of
the cecum, and peritoneum. The left dorsal and left
ventral colon and the pelvic flexure may or may not be
palpahle.
46
Surgical procedures
PRESURGICAL PREPARATION FOR
LAPAROSCOPY
Reducing the quantity of ingesta in the gastrointestinal
tract is important prior to elective laparoscopic proce­
dures. This requires a minimum of 48-72 hours and is
accomplished by feeding reduced quantities of feed or
using a low bulk/residue diet such as a pelleted ration.
The degree to which the gastrointestinal tract needs to
be debulked depends on the procedure and the
amount of intra-abdominal body fat. Predicting the
amount of internal body fat can be difficult, as it does
not always correlate with the outward appearance of the
jejunal horse. Transrectal palpation can help determine the
as a amount of fat present in the mesorectum and caudal
abdomen. In the standing patient, adequate viewing of
the right cranioventral abdomen requires the greatest
amount of ingesta reduction. Reduced bulk is also more
important when the patient is operated on in dorsal
recumbancy with the rear quarters elevated
(Trendelenberg position) . In addition, the longer the
procedure is anticipated to last, the more important the
preoperative preparation. The horse should have a con­
cave shape to the paralumbar fossa when properly pre­
pared prior to laparoscopy. Laparoscopy is preceded by
12-24 hours of withholding feed to reduce stomach
contents; water intake is not restricted.
It is important to assess the tractability of the patient
when considering standing procedures. Immature and
untrained patients are better candidates for operation
under general anesthesia. A tilt table (end to end) and
ventilatory support should be available when
laparoscopy is performed with the horse under general
anesthesia. Restraining stocks for standing procedures
should have adjustable sides to allow unimpeded
manipulation of the scope and the instruments.
Preparation of the abdomen for aseptic surgery is a
necessary routine step prior to laparoscopy. The left
and right flanks from dorsal mid-line to the fold of the
flank ventrally, and from caudal to the tuber coxae to
the 15th rib cranially should be prepped for surgery.
When exploratory laparoscopy is performed with the
horse under general anesthesia and in dorsal recum­
bancy, the entire ventral abdomen is prepared for
surgery. It is important to shave and prepare 5-10 cm to
either side of the ventral midline for instrument portals.
Laparoscopy, whether performed standing or under
general anesthesia, requires the abdomen to be inflated
with gas. It is recommended that intra-abdominal
pressures he the minimum that allows adequate

viewing. This minimizes patient discomfort in standing
horses and the negative effects of increased pressure on
cardiopulmonary function in anesthetized horses.
Cardiopulmonary function is least affected when intra­
abdominal pressure is below 20 mmHg.
TECHNIQUE FOR DIAGNOSTIC
STANDING LAPAROSCOPY
The horse is sedated with either a combination of
xylazine (0.3-0.9 mg/kg i.v.) and butorphanol
(0.01-0.033 mg/kg i.v.) , or detomidine (0.025 mg/
kg i.v.) . Pre-operative placement of an intravenous
catheter facilitates further drug administration. The
patient's tail is raised and tied to the stocks or ceiling.
This adds to stability of the patient and improves safety
for equipment and personnel. Tying the tail up can pre­
vent the laparoscope or instruments from being
wedged between the patient and sidebar of the stocks if
the patient were to fall. Rectal palpation should
precede laparoscopy to confirm clearance in both
paralumbar areas for trocar placement. A sterile drape
is placed on the patient from head to tail. The drape is
placed over the dorsum covering the sides of the horse
and stocks. The drapes are attached to the patient
around the neck and tail using non-penetrating towel
clamps. It is important not to attach the drapes to the
stocks as they can easily be dislodged or torn when the
patient moves. Fenestrations are made bilaterally at the
flanks and sealed to the patient using adhesive strips or
film. Local anesthesia is obtained by injecting 20-30 ml
of mepivacaine (or an equivalent local anesthetic
agent) in the center of the paralumbar fossa through a
2.5 em, 20-gauge needle. Pneumoperitoneum is estab­
lished through a 30 cm x 5 mm metal uterine catheter
placed into the right paralumbar fossa through a 1.5 cm
incision in the skin. Use of a long metal uterine catheter
or Verse needle ensures that the gas is insufflating the
abdominal cavity and not being placed into the
retroperitoneal space. The catheter is subsequently
removed and the laparoscopic cannula with sharp tro­
car is placed through the same site.
Cannulas can be placed without pneumoperi­
toneum or after the abdominal cavity has been inflated.
The author prefers to inflate the abdomen first.
Abdominal distension should be adequate to prevent
collapse of the abdominal wall during trocar insertion.
The catheter used for insufflation is removed and the
same site is re-used as the scope portal. The cannula
with the sharp trocar should be inserted with a firm
twisting motion, being careful to prevent excessive pen­
etration of the abdominal wall. Directing the trocar in a
slightly ventral direction prevents i�ury to the
LAPAROSCOPY 3
sublumbar muscles and kidney. The trocar should not
be directed excessively cranially or caudally as damage
to the cecum or broad ligament of the uterus could
result. Gas will escape from the trocar/cannula when
the abdominal cavity is entered; the trocar is replaced
by the laparoscope and abdominal exploration begins.
Detailed descriptions of the laparoscopic abdominal
anatomy of the standing horse, the dorsally recumbent
horse, and the dorsally recumbent foal are available.
When performing laparoscopy in the standing horse it
is helpful to think of the abdominal cavity in terms of
regions and spaces (Figure 3.13) . Each of these regions
and spaces can be viewed by manipulation of the laparo­
scope from a single portal in the left and right flank.
The abdomen is divided at the level of the cecum into a
cranial and caudal region. The caudal region consists of
two spaces, right caudal and left caudal, that are on the
respective sides of the mesocolon of the descending
colon. The cranial region is divided into four spaces.
From the right side the right lateral and right medial
spaces can be accessed. The right lateral is viewed
between the cecum and the body wall. The right medial
is viewed between the root of the mesentery and the
cecum. The left cranial region is divided into left lateral
and left medial spaces. The left lateral space is between
the spleen and body wall. The left medial space is
between the mesocolon of the descending colon and
the spleen.
Laparoscopic examination from the right flank is
performed in a clockwise direction around the
abdomen. It is important to develop a consistent and
thorough sequence of examination. The following
structures can be seen and evaluated from the right
side: the base of the cecum, root of the mesentery,
descending duodenum, right lobe of the liver,
Figure 3.13 Standing laparoscopy allows a thorough
examination of the dorsal aspect of the abdominal cavity
47
3 LAPAROSCOPY
diaphragm, perirenal fat around the right kidney, parts
of the small intestine and large colon, small colon and
rectum, right ovary and horn of the uterus in mares,
and the right internal inguinal ring in males.
The left side of the abdomen is explored in an anti­
clockwise direction. Upon insertion of the scope, the
nephrosplenic ligament, perirenal fat, and the caudal
proximal border of the spleen can be seen. The scope
can be passed cranially past the spleen where the dorsal
surface of the stomach, the diaphragm, and the left lat­
eral lobe of the liver are seen. As the scope is angled
ventrally, parts of the small intestine, the large colon,
the mesentery of the small intestine and the small colon
can be seen. Usually peritoneal fluid can also be
obselVed. As the scope is angled caudally toward the
pelvic cavity, the left ovary and uterus can be evaluated;
in males, the left inguinal ring is seen. The bladder and
rectum may also be examined.
Depending on the horse's problem, entering both
sides of the abdomen with the laparoscope may not be
indicated. However, to completely evaluate the
abdomen in a horse with an unknown problem, enter­
ing both sides is necessary. Additional portals can be
established for instruments. These may be located in
the paralumbar fossa or in the 17th and 16th intercostal
spaces whichever offers the best access. A Chambers
catheter works well to atraumatically manipulate viscera
to allow more complete laparoscopic exploration.
Common procedures utilizing the standing laparo­
scopic approach include splenic, renal, hepatic, lymph
node, and abscess biopsies. When performing a splenic
biopsy the laparoscope is inserted into the left paralum­
bar fossa and the spleen is directly visualized and a
biopsy site selected. Biopsy of either the left or right
kidney is performed via a left or right flank approach
respectively. The caudal border of the kidney is the best
laparoscopic biopsy site. The hepatic biopsy is
approached from the right flank area and requires
longer instruments (uterine biopsy forceps) to obtain a
sample. Abdominal abscesses and lymph node
aspiration can also be performed under laparoscopic
guidance.
LAPAROSCOPIC TECHNIQUE FOR THE
VENTRAL ABDOMINAL APPROACH
Preoperative procedures include a thorough history,
physical examination, and a complete blood count.
Transrectal palpation should be performed in all horses
large enough to permit the examination. Horses are
withheld from feed or placed on a low residue diet (e.g.
complete pelleted feed) for 24-72 hours prior to the
operation. The aim is to reduce the amount of ingesta
48
in the large colon to provide adequate free space in the
abdominal cavity for viewing and manipulation of the
genital tract. This is especially important in obese
horses. Intraoperative anesthesia monitoring should
include arterial blood pressure, arterial blood gases,
end-tidal CO2 tension, and electrocardiography.
Ventilatory function should be supported by positive
pressure ventilation. Perioperative antibiotics (pro­
caine penicillin G, 22 000 IU /kg i.m. q. 12 h) are insti­
tuted prior to surgery and continued for 24 hours.
Horses are anesthetized, placed in dorsal recum­
bancy, and aseptically prepared and draped for abdom­
inal surgery. The patient's tail is secured to the
operating table and a padded rope is placed across the
front of the chest to prevent patient displacement dur­
ing tilting of the table. A urinary catheter is passed to
facilitate decompression of the bladder. A 1.5 cm inci­
sion is made with a number 11 blade, on the midline at
the level of the umbilicus and a teat cannula is placed
for abdominal insufflation. Insufflation is achieved by
use of a high-flow electronic laparoflator or by a CO2
cylinder equipped with a regulator, flow meter, and
pressure gauge. When insufflation reaches intra­
abdominal pressures of 20 mmHg, the teat cannula is
removed and the laparoscopic sleeve with sharp trocar
is placed through the abdominal wall. The abdomen
should be insufflated sufficiently to allow placement of
the sharp trocar without excessive collapse of the
abdominal wall. The sharp trocar is removed from the
sleeve and replaced by the laparoscope (10 mm x
57 cm, 30 degree angle). Videolaparoscopic viewing of
the abdominal cavity begins and the area of the pelvic
inlet is identified. At this point the table is tilted elevat­
ing the rear quarters of the patient and displacing the
abdominal viscera cranially. When the ventral surface of
the uterus is seen tilting of the table is stopped. The
angle of incline is approximately 30 degrees from the
horizontal.
Instrument portals can be established as needed dur­
ing the exploration. Portals are established by making a
1.5-cm skin incision followed by a 1-cm incision in the
external sheath of the rectus abdominis muscle. The
portals are completed by blunt penetration of the
remaining abdominal wall, using a 5-mm or 10-mm con­
ical tip trocar. Instruments are placed through these
portals without a cannula. A Chambers mare catheter
functions well to manipulate viscera to aid viewing and
provide tactile feedback. The surgeon can operate from
either side of the horse. If there are assistant surgeons
one is opposite the primary surgeon and the second is
with the primary surgeon. The video monitor is placed
opposite the primary surgeon (Figure 3.14). It can be
advantageous to have two video monitors, one on either
side of the horse. The surgical table can be tilted to

Figure 3.14 Horse undergoing laparoscopy in
Trendelenberg position. This approach allows better
access for operative procedures of the caudal abdominal
cavity
elevate either the head or the rear quarters to improve
viewing of the cranial and caudal aspects of the
abdomen respectively. When the exploration is com­
plete the operating table is returned to a horizontal
position. The abdomen is decompressed by allowing
the CO2 to escape through the laparoscopic sleeve.
After removal of the sleeve, the portal is closed with a
single simple interrupted suture of 3 polyglactin 910,
and skin is apposed using a subcuticular simple contin­
uous pattern of 0 polyglyconate. Instrument portals are
closed with a simple continuous subcuticular pattern of
o polyglyconate and the skin edges are secured by appli­
cation of cyanoacrylate. The portals are covered with
elastic tape for added protection in the early postopera­
tive period.
Phenylbutazone (4.4 mg/kg p.o. q. 12 h) is adminis­
tered for 1-3 days after surgery to reduce postoperative
inflammation. Discharge instructions suggest the horse
be confined in a stall or small paddock and walked in
hand for 2 weeks. Exercise or free turn out is permitted
thereafter. Feeding instructions are for a gradual return
to the horse's normal diet over the course of 1 week.
Intraoperative complications are minimal with
proper preoperative preparation of the horse.
Inadequate visualization of the genital tract can occur
LAPAROSCOPY 3
because of too much ingesta in the gastrointestinal tract
and/or marked distension of the urinary bladder if not
catheterized. These problems can be eliminated by
increasing the duration of feed withdrawal or using a
low residue diet (complete pelleted feed) preopera­
tively and maintaining a urinary catheter during the
operation. Damage to vessels of the ventral abdominal
wall (primarily the deep epigastrics) can occur during
portal placement. This is best avoided by using sharp
dissection only through the level of the external rectus
sheath. A conical obturator is adequate and safe for
completion of the portal. Commercial portal access
devices are available to minimize abdominal wall vessel
injury (InnerDyne, Inc., Sunnyvale, CA).
BIBLIOGRAPHY
Blackfordj T, Schneiter H L, VanSteenhouse Lj, et at. (19R6)
Equine peritoneal fluid analysis following celiotomy.
Equine colic research. Proceedings of the Second Symposium at
the University of Georgia, pp. 130-2.
Boure L, Marcoux M, Laverty S (1997) Laparoscopic
abdominal anatomy of foals positioned in dorsal
recumbency. Vet. Surg. 26:1.
the
Boure L, Marcoux M, Lavoie j P (1997) Laparoscopic
adhesiolysis in a standardbred filly. Vet. Surg. 26:258.
Boure L, Marcoux M, Lavoiej P (1998) Use of laparoscopic
equipment to divide abdominal adhesions in a filly.] Am.
Vet. Med. Assoc. 212:845.
Edwards R B, Ducharme N G, Hackett R P (1995)
Laparoscopic repair of a bladder rupture in a foal. Vet.
Surg. 24:60.
Embertson R M, Bramlage L R (1992) Clinical uses of the
laparoscope in general equine practice. Proc. Am. Assoc.
Equine Pract. 38:165.
Fischer A T (1991) Standing laparoscopic surgery, Vet. Ctin.
N. Am. Equine Pract. 7:641.
Fischer A T (1999) Laparoscopically assisted resection of
umbilical structures of foals.] Am. Vel. Med. Assoc.
214:1813.
Fischer A T,jr (1997) Diagnostic and surgical laparoscopy. In
Equine Endoscopy 2nd edn,j L Traub-Datgatz, C M Brown
(eds). C V Mosby, St Louis, pp. 217-31.
Fischer A Tjr, Vachon A M (1992) Laparoscopic
cryptorchidectomy in horses.] Am. Vet. Med. Assoc.
201:1705.
Fisher A T, Lloyd K C K, Carlson G P el al. (1986) Diagnostic
laparoscopy in the horse.] Am. Vet. Med. Assoc. lR9:289.
Fischer A T, Vachon A M, Klein S R (1995) Laparoscopic
inguinal repair in two stallions.] Am. Vet. Med. Assoc.
207:1599.
Galuppo L D, Snyderj R, Pascoe j R (1995) Laparoscopic
anatomy of the equine abdomen. Am. ] Vet. Res. 56:518.
Galuppo L D, Snyderj R, Pascoe j R et at. (1996)
Laparoscopic anatomy of the abdomen in dorsally
recumbent horses. Am.] Vet. Res. 57:923.
Gross M E,jones B D, Bergstresser D R et at. (1993) Effects of
abdominal insufflation with nitrous oxide on
cardiorespiratory measurements in spontaneously
breathing isoflurane-anesthetized dogs. Am.] Vet. Res.
54:1352.
49
3 LAPAROSCOPY
Hendrickson D A, Wilson D G (1997) Laparoscopic
cryptorchid castration in standing horses. Vet. Surg. 26:335.
HulkaJ F , Reich H (1994) Textbook of Laparoscopy. W B
Saunders, Philadelphia, p. 47.
Hurd W W, Pearl M L, DeLanceyJ 0, et al. (1993)
Laparoscopic injury of abdominal wall blood vessels: a
report of three cases. Obstet. Gynecol. 82 (4 pt 2, supp!.):
673-676.
Mehl M, RagleC, Mealey R (1998) Laparoscopic diagnosis of
subcapsular splenic hematoma in a horse. .J. Am. Vet. Med.
Assoc. 213:1171.
Palmer S E (1993) Standing laparoscopic laser technique for
ovariectomy in five mares . .J. Am. Vet. Med. Assoc. 203:279.
RagleC A (1999) Urinary tract surgery in the adult horse.
Proceedings of the 9th annual ACVS symposium, pp. 164-7.
RagleC A, Schneider R K (1995) Ventral abdominal
approach for laparoscopic ovariectomy in horses. Vet. Surg.
24:492.
RagleC A, Schneider R K, Southwood L L (1996) Abdominal
laparoscopy in horses. Compo Cont. Educ. Pract. Vet.
IS:1231.
RagleC A, Southwood L L, Galuppo L D (1997) Laparoscopic
diagnosis of small colon ischemic necrosis following rectal
50
prolapse and mesocolic rupture in two postpartum mares.
.J. Am. Vet. Med. Assoc. 210:1121.
RagleC A, Southwood L L, Hopper S A, Buote P L (1996)
Laparoscopic assisted granulosa cell tumor ovariectomy in
two mares. .J. Am. Vet. Med. Assoc. 209:1646.
RagleC A, Southwood L L, Howlett M R (1998) Ventral
abdominal approach for laparoscopic cryptorchidectomy
in horses. Vet. Surg. 27:138.
RagleC A, Southwood L L, Schneider R K (1998) Injury to
abdominal wall vessels during laparoscopy in three horses.
.J. Am. Vet. Med. Assoc. 212:87.
Santschi E M, GrindemC B, Tate L P, et al. (1988) Peritoneal
fluid analysis in ponies after abdominal surgery. Vet. Surg.
17:6.
Trostle S S, White N A, Donaldson L, et al. (1998)
Laparoscopic colopexy in horses. Vet. Surg. 27:56.
WalmsleyJ P (1999) Review of equine laparoscopy and an
analysis of 158 laparoscopies in the horse. Equine Vet. .J.
31:456.
Witherspoon D M, Kraemer DC, Seager S W J (1980)
Laparoscopy in the horse. In Animal Laparoscopy, L M
Harrison and D E Wildt (eds). Williams and Wilkins,
Baltimore, p. 157.
4
Parasite-associated gastroi ntesti na I
disease
S Love
This chapter focuses on clinical aspects of the principal
parasite infections of the horse, i.e. large strongyles,
small strongyles (cyathostomes), tapeworms, and
ascarids. Brief notes are included on some minor infec­
tions including bots, Coccidia spp., Cryptosporidium spp.,
Oxyuris pqui, and Strongyloides westeri.
INTRODUCTION
Parasite-associated gastrointestinal diseases are almost
certainly under-diagnosed. This may reflect a compla­
cent attitude on the part of veterinary surgeons and/or
owners based upon their over confidence in the efficacy
of modern anthelmintic products. However the princi­
pal reason for poor clinical recognition of parasitic
intestinal disease is the lack of availability of diagnostic
methods of sufficient sensitivity and specificity. Much of
what is known about the clinical aspects of parasitic
infections of the horse is derived either from general
observations undertaken during artificial infections
(large strongyles, cyathostomes, ascarids) or more
recently from quantitative epidemiological studies on
colic risk factors (cyathostomes, tapeworms). Although
the cumulative body of evidence supports a role for
various parasites in many types of colic, weight-loss
syndromes, and diarrhea, definitive information will
require detailed longitudinal, clinicopathological stud­
ies, ideally on both experimentally infected animals as
well as on cohorts of naturally infected animals. The
development of serodiagnosis of Anoplocephala perfoliata
has advanced the knowledge available on clinical
aspects of tapeworm infection by completion of
case-control studies on colic cases. Although it will be
technically complex to produce similar diagnostic
assays for cyathostome and large strongyle infections,
they are essen tial tools for objective studies on disease
prevalence, clinical effects, and therapy.
FEATURES OF EQUINE PARASITE
INFECTIONS
Occurrence of disease
The occurrence of parasite-associated disease depends
on three main factors
l. the abundance of parasite larvae and eggs in the
external environment
2. the numbers of parasites of one species within an
individual animal
3. the management of the horses.
The abundance of parasite larvae and eggs in
the external environment
This varies according to ambient temperature and
humidity so that there is variation with season and also
geographical region. In temperate climates, the highest
numbers of larvae on pasture usually occur in late sum­
mer or early autumn. Pasture larvae and eggs survive
best in wet, mild conditions but the larvae die quickly
in dry, hot weather. Both eggs and larvae are fairly
resilient to frosty conditions. Ascarid eggs (the infective
stage) are particularly adapted to survive for prolonged
periods of many months (even years) in the external
environment. The numbers of pasture eggs and larvae
are affected by the levels of worm egg output by grazing
animals, and this is intrinsically related to the intensity
of the adult worm burden (see below).
53
4 GASTROINTESTINAL PARASITES AND THEIR CONTROL
The number of parasites of one species within
an individual animal
This varies with
• the level of pasture contamination (see above)
• host immunity: this occurs as an absolute feature in
ascarid infections in animals greater than 2 years of
age but is much more variable in large strongyle,
cyathostome, and tapeworm infections
• individual propensity to infection: it is a fact that,
with any parasite infection, in all host species the
majority of worms are present within the minority
of animals, i.e. there is natural predisposition of
certain individuals to parasite infection.
Management of the horses
The likely exposure to parasite infection via contami­
nated pasture will be affected by the grazing practices
and the parasite control program applied on the pas­
ture, and also on any premises on which the animal(s)
were kept previously. It is always important to consider
this information as it pertains to the whole grazing
group, not just to the individual animal.
Summary of equine parasite biology
Understanding the timing of onset of clinical signs and
aspects of treatment!control requires a working knowl­
edge of the essential features of the biology of the main
pathogenic parasites.
Strongyles
The strongyles, synonym 'red worms', exist in two sub­
families.
1. Strongylinae (large strongyles), these are Strongylus
vulgaris, S. edentatus, S. equinus, and Triodontophorus
spp. The essential features of the large strongyles
include
a direct, migratory (intestinal arteries) lifecycle
•
(except for Triodontophorus spp.)
• a pre-patent period of 6-10 months
• the adult stages are large intestinal
• all stages are susceptible to modern
anthelmintics.
2. Cyathostominae (small strongyles/ cyathostomes)
There are 8 genera and 40 species of cyathostomes. The
essential features include
• a direct, non-migratory life cycle
• a pre-patent period of 6-20 weeks
• a propensity for arrested larval development within
the large intestinal mucosa (for as long as 2-3 years)
• the adult stages are large intestinal
54
• the luminal adults, luminal larvae, and developing
mucosal larvae (Plate 4.1) are susceptible to
modern anthelmintics
• arrested larvae are poorly susceptible to modern
anthelmintics (this varies with different products)
• resistance to benzimidazole compounds is common
• resistance to pyrantel salts is apparently increasing.
Ascarids
There is one species of ascarid - Parascaris equorum. Its
essential features include
• a direct, migratory (gut-liver-lung-gut) life cycle
• a pre-patent period of 3 months
• the adult stages are small intestinal
• prolific egg producers
adult and luminal larval stages are susceptible to
•
modern anthelmintics
migrating larval stages have low susceptibility to
•
modern anthelmintics.
Tapeworms
The three species of tapeworm that affect horses are
Anoplocephala perfoliata (common) (Plate 4.2), A. magna,
and Paranoplocephala mammillana. Their essential fea­
tures include
• an indirect life cycle with the oribatid mite as the
intermediate host
• a pre-patent period of 6-10 weeks
• the adult stages are either cecal (A. perfoliata) or
small intestinal (A. magna and P. mammillana); the
latter can also occur in the stomach
A. perfoliata and A. magna are susceptible to pyrantel
salts given at a high dose rate.
PATHOGENESIS OF PARASITIC
GASTROINTESTINAL DISEASE
Pathophysiological details of equine parasite infections
have only been studied at a superficial level. A consider­
ation of the existing facts and hypotheses is helpful in
understanding clinical parasitism.
Enteropathy is known to occur with large strongyle,
cyathostome, and tapeworm infections, but not with
ascarids. Particularly with cyathostomes, there is an
inflammatory reaction at the site of larval penetration
into and emergence from the large intestinal mucosa.
The severity of the typhlitis/colitis varies from a mini­
mal reaction to marked, diffuse lesions with edema,
discoloration and local lymph node enlargement. The
inflammatory lesion causes transmucosal protein

leakage. Foci of fibrous reaction occur where migrating
large strongyle lalVae re-enter the large intestine, and
there can be local intramural abscesses at these sites.
Adult large strongyles also feed on the mucosal surface
causing superficial damage. Tapeworms cause regions
of ulceration and edema at the ileocecal valve, the
severity depending on the numbers of tapeworms pre­
sent. Ascarids do not cause intestinal lesions but it is
thought that their presence is indicated by their con­
sumption of nutrients from the host's intestinal tract.
Intestinal motility changes have been documented
for both large strongyle and cyathostome infections.
Although the precise mechanisms of this effect are not
known, it has been hypothesized that these may result
from either pharmacological activity of substances
released from the parasites and/or a host response to
such substances. The proposed pharmacological sub­
stances may either exert their effect directly on intesti­
nal muscle or nelVes, or they may alter intestinal
motility via alteration to intestinal blood supply (see
below). It is possible that tapeworms produce similar
pharmacodynamic substance(s).
Altered mesenteric blood flow in animals with
Strongylus vulgaris infestations is a long-recognized patho­
genic event during lalVal migration, but the detailed
pathophysiology remains unclear. It may be a conse­
quence of substances produced by the parasite (see
above), but it is no longer considered to be the result of
physical thromboembolism from arterial lesions (Plate
4.3). Reduction in mesenteric blood flow can result in
either single or multiple areas of ischemic bowel wall, i.e.
the entity known as non-strangulating intestinal infarction.
CLINICAL FEATURES OF PARASITIC­
ASSOCIATED DISEASE 'ENTITIES'
Non-strangulating intestinal infarction
This is rare nowadays, reflecting the current low preva­
lence of Strongylus vulgaris infection. The preliminary
signs are the presence of either anorexia or fever, and
clinical signs include
• severe colic (sometimes recurrent bouts)
• cardiovascular compromise
• endotoxemia
• sanguinous peritoneal fluid
• reduced borborygmi
• nasogastric reflux
distended viscus palpable per rectum
•
occasional thickening or pain found on rectal
•
palpation of the mesenteric artery
• ischemic areas of either small and/or large
intestine found at exploratory laparotomy
PARASITE-ASSOCIATED GASTROINTESTINAL DISEASE 4
• mesenteric arterial thickening and/or thrombus at
post-mortem examination with possible grossly
visible S. vulgaris lalVae.
Mild strongyle-associated colic
This is suspected if there is non-specific mild colic and
often occurs if there is a sub-optimal parasite prophyl­
axis program and/or frequen t intake of new animals of
unknown worming history on the premises. It has been
proven to occur when there is poor control of cyatho­
stomes, i.e. it is not just a large strongyle disease.
Cecocolic intussusception
There is recent evidence of cecocolic intussusception
associated with heavy cyathostome infections, particu­
larly in young (less than 4-year-old) horses. The clinical
features are detailed in Chapter 14. There may be con­
current signs of other cyathostome entities (see below).
Larval cyathostomosis (see Chapter 21)
This is more common in Europe than in other regions.
Often an individual animal is affected but it can also be
a group condition. There is a seasonal prevalence with
the condition seen more during late winter and early
spring than at other times of the year, and there is also
an age prevalence, the condition being more common
in animals less than 6 years old. Clinical signs include
• sudden, rapid weight loss, possibly reaching
emaciation within 10 days
• diarrhea, sudden onset
• mild to severe colic
• variable demeanor, often fairly bright
• not usually endotoxemic
• peripheral edema
• fever
• cyathostome lalVae are often grossly evident on
close inspection of feces
• recent anthelmintic dosing may precipitate the
onset of disease by removing hypothesized
'feedback' of intestinal to mucosal cyathostomes,
and stimulating resumption of development of
lalVae arrested in development within the mucosa
• mucosal edema with gross thickening and a
'peppered' appearance on close examination of
cecal and/ or colonic surface at post-mortem
examination.
Cyathostome-associated weight loss in young
horses
This occurs in animals up to 6 years of age. It can affect
individuals or a group of animals and is indicated by
55
4 GASTROINTESTINAL PARASITES AND THEIR CONTROL
• rapid, marked weight loss
• peripheral edema
• fever.
Although large strongyles are now rare, mixed large
and small strongyle infections, i.e. 'strongylosis' will
produce similar clinical features.
Recurrent cyathostome-associated diarrhea
This occurs in aged ponies and is indicated by
• repeated bouts of diarrhea
• weight loss
• anorexia.
Autumnal cyathostome-associated weight loss
in weanlings
This affects foals 6-9 months old, i.e. older foals eating
significant quantities of grass, and affects both indivi­
duals and groups of animals. It is indicated by
sudden poor thrift, often in mild, damp conditions in
September and October.
Ascarid-associated ill thrift
This is a common condition indicated by non-specific ill
thrift or weight loss in older foals, weanlings and year­
lings, that can progress to emaciation unless treated.
Occasionally there are concurrent non-specific respira­
tory signs including a nasal discharge and cough.
Ascarid impaction (Plate 4.4) (see Chapter 13)
This rare condition occurs in older foals, weanlings,
and yearlings causing
• colic
• a distended small intestinal viscus that is detected
on radiography/ultrasonography or by palpation
per rectum if examination is feasible
• minimal cardiovascular compromise
• nasogastric reflux.
Tapeworm-associated colic
This is indicated by non-specific mild (spasmodic) colic
and ileal impaction together with serological!epidemio­
logical evidence of tapeworm infection. The clinical
features are detailed in Chapters 9 and 13.
INVESTIGATION OF SUSPECTED
PARASITE-ASSOCIATED DISEASE
There are no distinctive clinical features which enable a
definitive diagnosis of gastrointestinal parasitism, and
56
in only a few instances are there specific ancillary tests
by which confirmation of an entity can be achieved.
Clinical history
When a horse is presented with signs of weight loss
and/ or diarrhea and/ or colic it is appropriate to inves­
tigate the history relevant to parasitism. The key points
to consider are
• grazing management: is it full time, part time, or
not at all?
is it individual or shared?
if it is shared, how many are
in the cohort?
• anthelmintic dosing: what is the frequency and
product(s) used for both
individual diseased animal
and grazing cohort?
if known, what was the dos­
ing regimen in any previous
ownership (s)?
• previous evidence of parasite-associated disease on
premises and/or in grazing cohort?
It is easy to over-interpret and/or over-simplifY this
information. Certainly parasite-associated diseases com­
monly occur in animals which have been receiving
prophylactic anthelmintics. Common reasons for
failure of parasite control programs include
• anthelmintic resistance
• incorrect dosing intervals
• lack of synchronization of dosing of anthelmintics
in grazing cohort
• acquisition of horses infected with worm stages
unaffected by 'standard' anthelmintic dosing:
particularly cyathostomes arrested in development
in large intestinal mucosa and/or migrating ascarid
larvae. Cyathostome-associated illnesses can occur
years after the parasites were ingested (mucosal
arrested stages can survive multiple doses of
anthelmintics) so that evidence of good parasite
control applied to the current premises should not
be taken as conclusive evidence on which to
exclude parasitism.
Fecal tests
Large strongyle and cyathostome eggs
In clinical practice there is often too much diagnostic
emphasis given to the fecal worm egg count (FWEC). In
particular, negative counts are often inappropriately
used as the basis of excluding parasitism. It should be
borne in mind that the pathogenic stages of both large
strongyles and cyathostomes are larval, i.e. not egg-

laying stages. Also, it is notoriously difficult to correlate
the FWEC with the size of the parasite burden giving
further confusion to interpretation of test data. As a gen­
eral guideline, in an individual clinical case, a strongyle
fecal egg count of 200 epg or less is low, whereas more
than 1000 is high. Probably it is more meaningful to
obtain FWEC from at least half the grazing cohort and
use the data as an overall (but rather insensitive) index
of parasite challenge to the individual clinical case.
Certainly FWEC results for animals suspected of either
large strongyle and/or cyathostome-associated illnesses
should only be used as possible support of a positive
diagnosis, and never to rule out a diagnosis.
Ascarid eggs
The pathogenic stages of ascarids are the egg-laying
luminal adults. Therefore ascarid infection should be
strongly suspected in an animal less than 2 years old
with non-specific signs of ill thrift and a high ascarid
fecal egg count. Ascarids are prolific egg producers and
counts of several (or even tens of) thousands can occur.
Note that although FWECs have high sensitivity for
ascarid infection, they have low specificity, it is there­
fore possible that an ill thriven youngster could have co­
existing diseases.
Tapeworm eggs
Tapeworm infection is not readily detected by the
'routine' methods for FWEC utilized in most commer­
cial laboratories, but special centrifugation/flotation
methods have been developed and should be utilized
when tapeworm infection is suspected.
Cyathostome larvae
A simple fecal examination can be very useful for evi­
dence of cyathostome-associated illness: larvae are often
present in large numbers in the feces and can be
detected by careful visual inspection of samples and/or
microscopy. The larvae are very thin, about 0.5-1.5 em
in length and white, pink, or red. If not evident on
visual inspection, then dilution of the sample with tap
water in a petri dish and screening with a light micro­
scope is readily performed.
Hematology/blood biochemistry
There are no specific blood analysis results associated
with parasitic infections but both large strongyle and
cyathostome infections can result in
• neutrophilia
• hypoalbuminemia
• hyperglobulinemia (especially betaglobulinemia
detected by serum protein electrophoresis)
PARASITE-ASSOCIATED GASTROINTESTINAL DISEASE 4
• low albumin:globulin ratio
• increased serum alkaline phosphatase
• anemia
Hypoalbuminemia may be only minor in ascarid infec­
tions.
Serology
A quantitative serological assay has been validated for
tapeworm infection and successfully used to investigate
colic cases: it is commercially available in the UK.
TREATMENT
Symptomatic aspects
In parasite associated illnesses the likely principal clini­
cal symptoms to be addressed in the treatment plan will
be
1. Colic, treat with
• analgesics (and possibly surgery for either
ischemic intestine, Strongylus vulgaris or
ileal! cecal disorders, Anoplocephala perfoliata)
(see Chapters 13 and 14).
2. Diarrhea, typically cyathostome-associated, treat
with
• antidiarrheal agents; codeine phosphate elixir
given 'to effect', or guideline regimen is
3 mg/kg t.i.d. (days 1-9) then 2 mg/kg t.i.d.
(days 10-14) then 1 mg/kg t.i.d. (days 15-20)
• fluid/electrolyte support (details in Chapters 9
and 20); oral or stomach tube routes may be an
option for cases with moderate to mild severity
• anti-inflammatory treatment (of
typhlitis/ colitis); not NSAIDs (which could
exacerbate protein-losing enteropathy);
preferred protocol is oral prednisolone at
1 mg/kg s.i.d. (in the morning, days 1-20)
followed by 1 mg/kg every other day (in the
morning, days 21-40). It is hypothesized that in
addition to anti-inflammatory effects, the
corticosteroid renders mucosal cyathostomes
more susceptible to an anthelmintic via
reduction of the immune mechanisms which
contribute to mucosal arrested larval
development.
• nutritional support to counteract any weight
loss.
Anthelmintic aspects
In cases where parasitism is either confirmed or where
the index of suspicion of parasitism is high, then it is
usually appropriate to include anthelmintics in the
57
4 GASTROINTESTINAL PARASITES AND THEIR CONTROL

treatment plan. However, clinicians should consider • day 6 either ivermectin 0.2 mg/kg, or
the importance of potential side effects of anthel­ moxidectin 0.4 mg/kg
mintics when given in clinical disease. Specifically, • days 31-35 fenbendazole 7.5 mg/kg
there are reports which suggest possible associations • day 36 either ivermectin 0.2 mg/kg, or
between recent anthelmintic administration and onset moxidectin 0.4 mg/kg
of either parasite-associated colic or cyathostomosis. • day 61-65 fenbendazole 7.5 mg/kg
Therefore in a clinical situation, treatment with • day 66 either ivermectin 0.2 mg/kg, or
anthelmintics might either exacerbate the disease moxidectin 0.4 mg/kg
and/or induce overt signs of disease in apparently • days 91-95 fenbendazole 7.5 mg/kg
healthy grazing companions of the affected cases. • day 96 either ivermectin 0.2 mg/kg, or
It should be emphasized that the recommended moxidectin 0.4 mg/kg.
anthelmintic usage for treatment of clinical disease
states has a different basis from that of parasite control Ascarid-associated disease
programs (see below). Specific anthelmintic therapeu­ Ascarid-associated disease can be treated with either
tic regimens are preferred for the different parasite­
associated diseases. • oral ivermectin 0.2 mg/kg, or
• oral moxidectin 0.4 mg/kg, or
• oral fenbendazole 10 mg/kg on 5 consecutive days, or
Non-strangulating intestinal infarction
• oral levamisole 8.0 mg/kg (this drug is not licensed
This condition can be treated with in Europe).

• oral ivermectin 0.2 mg/kg, or Repeat treatment at 14-21 day intervals on three
• oral moxidectin 0.4 mg/kg, or targeted occasions.
• oral oxfendazole 10-50 mg/kg, or
• oral fenbendazole 7.5 mg-l0 mg/kg on Tapeworm-associated colic
5 consecutive days.
This condition is treated with either

Cyathostomosis and cyathostome-associated • oral pyrantel pamoate 13.2 mg/kg (in the US), or
conditions • oral pyrantel embonate 38 mg/kg (in Europe).

Affected clinical cases are treated with the following

regimen PARASITE CONTROL PROGRAMS
• days 1-5 fenbendazole 7.5 mg/kg on 5 Parasite-associated diseases are largely preventable by
consecutive days sustained control programs, but it should be empha­
• day 6 ivermectin 0.2 mg/kg or moxidectin* sized that no single parasite control program is recom­
0.4 mg/kg mended for every management situation. The strategy
• days 16-20 fenbendazole 7.5 mg/kg on 5 adopted should be custom designed with regard to age
consecutive days and type of animals, the local environment and climate,
• day 21 ivermectin 0.2 mg/kg or nil (if and the practicalities of available labor.
moxidectin" was given on day 6) The objective of a parasite control program is to
• days 31-35 fenbendazole 7.5 mg/kg on 5 minimize between-horse transmission of the infective
consecutive days stages. This is achieved mainly by preventing infective
• day 36 ivermectin 0.2 mg/kg or moxidectin larvae (strongyles) and eggs (ascarids) from contami­
0.4 mg/kg nating the pasture. The details of the life cycle of tape­
• thereafter follow the protocol for grazing cohorts worms are not known but they are controlled by
(see below). keeping their total numbers down.
*moxidectin has the potential for toxicity in thin, debilitated Knowledge about the parasites' life cycles and their
animals, and careful computation of dosage is required. susceptibility to anthelmintics is used to design control
**moxidectin has persistent action such that it is inappropriate programs.
to treat as often as the lO-day intervals suggested for ivermectin.
• Large strongyles have a long migration period
within the host when the parasites are readily
In-contact grazing cohorts are treated with the follow­
susceptible to modern anthelmintics.
ing regimen
• Hosts have a lifelong susceptibility to cyathostomes.
• days 1-5 fenbendazole 7.5 mg/kg • Hosts cannot be rendered 'worm free' by dosing

58
 PARASITE-ASSOCIATED GASTROINTESTINAL DISEASE 4

the larval stage of cyathostomes - every horse has
cyathostomes arrested in development within the
intestinal mucosa where they are protected from
anthelmintic action.
• Cyathostome populations readily develop
anthelmintic resistance - benzimidazole resistance
is ubiquitous and pyrantel resistance is becoming
increasingly common in the United States.
• Frequent dosing selects for anthelmintic resistant
parasite populations.
• Strongyle (large and small) eggs and larvae survive in
feces or on herbage for months in moist, temperate
climatic conditions.
• Ascarid eggs are highly resilient and can survive for
years in the external environment.
• Age immunity to ascarids occurs.
• Anthelmintic compounds are not all equally
effective against all parasite species.
• Parasite control programs should focus on
strongyles, especially cyathostomes.
• Ascarids will be controlled incidentally by cyathostomc
interval dosing programs but not by either strategic or
selective dosing options (see below).
• Twice yearly, double-dose pyrantel is considered
necessary for tapeworm control.
• Although bots are a common cause of concern to
owners, their control is not essential. Only
ivermectin, moxidectin, and organophosphates are
effective against bots. All bots exist within the host
during winter months.
• In many countries most horses graze for part or all
of the year, so year-round dosing is often required.
• Co-grazing horse pasture with sheep and/or cattle
can safely reduce the numbers of equine parasite
larvae on the grass.
The options for parasite control are listed in Table 4.1.
Piperazines, phenothiazines, and organophosphates
are drugs that are available but are used infrequently.
Additional guidelines for control programs include
• dose all horses from 6 weeks of age
• use the same product for an entire year, but with
incorporation of specific doses to deal with
tapeworms (pyrantel in April and October) and
bots (ivermectin or moxidectin in early winter)
• after one year's continuous use of one product,
change to an unrelated product the following year,
and change again in the third year, i.e. the
anthelmintic classes are used in a 3-year cycle
• emphasize the correct dosing interval (see Table
4.1) for different anthelmintic classes to the horse
owner
• screen for anthelmintic resistance using fecal egg
count reduction tests (FECRT) twice a year (the
FECRT establishes the efficiency of the
anthelmintic in reducing fecal egg output using

,.4;.1. "'1S\!�·,,"dIod,
Programs Guidelines Comments

1. Interval dosing Year round pro-/benzimadazoles, Synchronized dosing of all animals

4-6 weekly; ivermectin, 8-10 weekly;
pyrantel, 4 weekly; moxidectin 13 weekly.

2. Strategic dosing Spring/summer only using same Regional variations in pasture

anthelmintics as for interval dosing. cyathostome infectivity affect the
timing of dosing.
Synchronized dosing of all animals.

3. Targeted dosing Year round only dose animals that have Monthly worm egg counts on all
a positive FWEC using same anthelmintics animals.
as for interval dosing.

4. Continuous in-feed Year round pyrantel pamoate daily in Not available in Europe
feed.

5. Pasture hygiene Twice-weekly pasture fecal collection. Capital/labor expense high.

Effective if combined with 1, 2, or 3
above, especially 2.

6. Predacious fungi (fungi Year round daily in-feed administration. Not yet fully validated or licensed.
that are natural predators
for strongyle eggs)

59
4 GASTROINTESTINAL PARASITES AND THEIR CONTROL
FWEC results from one fecal sample taken pre­
treatment (day 0) and one sample taken on day
10-14 post-treatment); ideally the FWEC should be
reduced by 90 per cent at day 10-14, and failure to
achieve this level of reduction suggests anthelmintic
resistance
• anthelmintic resistance (only reported in
cyathostomes) is an irreversible feature - once it
has developed on a particular premises to a
particular class of drug, any product from that class
should not be included in the worm control
program again.
CLINICAL ASPECTS OF MINOR EQUINE
INTESTINAL PARASITES
Bots
The four main species of bots are Gasterophilus intesti­
rudis, G. nasalis, G. haemorrhoidalis, and G. pecorum
• the life cycle is direct - the Oy lays eggs on either
the legs or head of the host during the summer, the
host ingests the eggs and the larval stage is spent in
the host's stomach during the winter
• they are essentially non-pathogenic
• they can be controlled by early winter dosing with
either ivermectin 0.2 mg/kg, moxidectin
0.4 mg/kg, or organophosphates (not Europe).
Strongyloides westeri
This parasite occurs commonly in the foal, but it is not
found in adult horses
• it is rarely pathogenic but can cause diarrhea
• the life cycle is direct - the foal ingests the parasite
in the dam's milk or acquires it through
transcutaneous infection
• S. westen is treated with oral anthelmintics, but often
an increased dosage than that recommended for
strongyles is required (check package insert)
Oxyuris equi
This is the common large intestinal pinworm
• it is non-pathogenic other than causing pruritus
during egg laying, when adult stages protrude from
anus, resulting in tailhead excoriation
• treatment is oral anthelmintics with most classes
being effective (check package insert).
60
Habronema spp.
There are three species - Habronema muscae, H. majus,
and H. megastoma (synonym Draschia megastoma)
• they are common in the US but rare in Europe
• intermediate hosts are muscoid flies which deposit
infective larvae either around the mouth and
muzzle, or on wounds and skin leading to 'summer
sores'; the larvae are then swallowed by the host
• adult stages occur in the stomach where they may
result in increased mucus production and/or
formation of fibrous nodules but, although the
pathogenic importance of these parasites is unknown,
they are probably not associated with clinical disease
treatment is by either oral ivermectin 0.2 mg/kg, or
•
oral moxidectin 0.4 mg/kg.
Cryptosporidium spp. (see Chapter 27)
These parasites
• can cause diarrhea in immunocompromised foals
• infection can be detected using serum antibody or
fecal tests (specific techniques are required for fecal
detection) in apparently healthy individuals
• there are no known effective therapeutic agents.
Coccidia spp.
A few case reports describe Eimeria leukarti to be present
in diarrheic horses and several surveys report 40-60 per
cent prevalence of E. leukarti oocysts in the feces of
healthy foals
• fecal detection requires specific methods
• no disease occurred after experimental E. leukarti
infection studies
• overall coccidiosis does not appear to be a common
clinical entity in the horse.
BIBLIOGRAPHY
Austin S M, Oi Pietro]A, Foreman] H (1990) Paraswris
equarum infections in horses. Camp. Cant. Educ. Pract. Vet.
12:110-18.
Little S E, Moore] N, Oi Pietro]A (eds) (1999) Proceedings
of the conference on equine cyathostomes. Vet. Parasitol.
85:2,3.
Proudman C.J (1999) The role of parasites in equine colic.
Equine Vet. Educ. 11:219-24.
Southwood W, Baxter G M, Bennet 0 G, Ragle CA (1998)
Ascarid impactions in young horses. Camp. Cant. Educ.
Prart. Vet. 20: 100-6.
Herd, R P (1986) Parasitology, Veterinary Clinics of North
America: Equine Practice 2. W B Saunders, Philadelphia.
 5
Differential diagnosis and evaluation of
dysphagia

JG Lane

INTRODUCTION Pharyngeal phase of deglutition

Dysphagia literally means difficulty in eating and
although horses may be afflicted with a range of clinical
conditions that limit their ability to gain access to food,
ranging from blindness to disorders of the cervical
spine, for the purposes of these notes the discussion will
be limited to diseases which compromise the ability to
prehend, masticate, and swallow ingesta.
NORMAL DEGLUTITION
It is conventional to subdivide deglutition into oral,
pharyngeal, and esophageal phases.
Oral phase of deglutition
This phase of deglutition is under voluntary control.
The prehension of ingesta depends upon a normal
incisor dentition for grasping herbage, and lip mobility
with which to contain the ingesta in the mouth and to
help manipulate it toward the cheek teeth. For mastica­
tion. a healthy molar and premolar dentition and full
function of the temporomandibular joints are required.
The masticatory muscles which close the temporo­
mandibular joints are innervated by the mandibular
branch of the trigeminal nerve (V), with the caudal
belly of the digastricus muscle which opens the mouth
innervated by the facial nerve (VII). The function of the
tongue in deglutition is to assist in the movement of
food boluses around the mouth and to gather them up
onto the base of the tongue prior to the onset of the
pharyngeal phase. The tongue is suspended on the
hyoid apparatus and the lingual musculature is inner­
vated by the hypoglossal nerve (XII).
The presence of a food bolus on the base of the tongue
triggers a series of highly coordinated, split-second,
involuntary reflexes that collectively make up the
process of swallowing, and which include both pharyn­
geal and esophageal phases of deglutition. During
deglutition, respiration is suspended after inspiration,
and expiration follows immediately after swallowing is
completed. Contraction of the base of the tongue drives
the bolus caudally into the oropharynx. At the same time
the larynx dislocates from the intrapharyngeal ostium,
the soft palate is elevated, the apex of the epiglottis retro­
verts, and the arytenoid cartilages and vocal cords
adduct. The combined effect is to protect the nasal and
lower airways. The contraction of the levator palatini
muscles causes the ostia of the auditory tube diverticula
to shorten and dilate thereby allowing the exchange of
air for pressure equilibration across the ear drum.
The caudal movement of the bolus of ingesta is
accelerated by a wave of contraction of the constrictor
muscles of the pharynx, the pharyngeal stripping wave.
Liquid boluses tend to be squirted through the lateral
food channels on either side of the retroverted epiglot­
tis, whereas solid boluses pass directly over the closed
larynx. The upper esophageal sphincter formed by the
cricopharyngeus muscle is normally closed, but it must
relax to allow the passage of the bolus into the esopha­
gus. Following deglutition the larynx returns into the
intrapharyngeal ostium before respiration is resumed.
Esophageal phase of deglutition
After each bolus has passed into the proximal esopha­
gus primary peristaltic waves are initiated by closure of
the cricopharynx. Primary esophageal peristalsis carries

63
5 UPPER ALIMENTARY TRACT DISEASES
individual boluses to the cardia, but the process is not
completely eflicient and small quantities of ingesta are
left at variable levels in both the cervical and thoracic
esophagus even in normal horses. This ingesta is either
picked up in the bolus of a subsequent primary wave, or
by locally generated secondary peristalsis which is trig­
gered by segmental stretch responses.
DIAGNOSIS OF DYSPHAGIA
Clinical signs
The signs of dysphagia include
• an unwillingness to eat
• slow eating
• messy feeding
• rejection of semi-masticated food onto the ground
(quidding)
• productive coughing
• nasal reflux of saliva, ingesta, and fluids.
Horses that are unable to eat and swallow food lose
weigh t rapidly, and this process is accelerated if the
horse develops secondary inhalation pneumonia which
is not an uncommon sequel to dysphagia.
In addition to a clear case history recording the
circumstances and rate of onset of dysphagia, careful
observation of the patient's attempts to eat and drink
can be invaluable to deduce which phase of deglutition
is awry. Whenever a horse shows return of ingesta from
its mouth, the site of the lesion causing the dysfunction
must lie in the oral cavity or oropharynx, certainly no
further caudal than the epiglottis. Nasal reflux of
ingesta points to an abnormality of the pharyngeal or
esophageal phase of deglutition.
Physical examination
During the external assessment of the patient evidence
of systemic and/or toxic disease, including strangles,
botulism, grass sickness, rabies, upper motor neuron
disease, lead poisoning, and tick paralysis should be
noted. Thoracic auscultation (using a rebreathing bag)
should check for signs of inhalation pneumonia. Local
lymphadenopathies and firm distension of the esopha­
gus to the left side of the trachea are abnormalities that
might be found during palpation of the throat area.
Nasogastric intubation
Useful information can be obtained by attempting to
pass a nasogastric tube. This procedure should deter­
mine whether pharyngeal swallow reflexes are still pre­
sent, or whether the upper alimentary tract is physically
obstructed.
64
Oral examination
Under sedation and with a Hausmann gag or similar
mouth speculum in place, a detailed inspection of the
oral cavity should be carried out. In particular, one
should look for evidence of
• absence of teeth or dental malalignment
• enamel pointing of the cheek teeth
• fractures of the dental crowns
• periodontitis
• soft tissue lesions of the buccal cleft and palate
• oral foreign bodies
• lesions of the tongue.
The structures involved may require hands-on manipu­
lation to complete the examination, and a tell-tale foul
smell points to the presence of stale entrapped ingesta.
Most defects of the palate cannot be appreciated
from an examination of the mouth in a conscious
animal, because they are generally restricted to the soft
palate and the restricted opening of the equine jaws
prevents direct inspection of the more caudal oral
cavity. General anesthesia is necessary to complete
the inspection of the oral cavity, and the tendency of
the soft tissues to obscure the view, particularly toward
the base of the tongue, can be overcome by the use of
an endoscope passed through a polyethylene mare
speculum. Again, general anesthesia is required for a
more detailed manual examination of the caudal oral
cavity, especially in the region of the epiglottis and
aryepiglottic folds.
Endoscopy
Endoscopy per nasum is necessary to confirm whether
pharyngeal paralysis is present. The usual findings of
pharyngeal paralysis include
• a mixture of saliva and ingesta on the walls of the
nasopharynx
• persistent dorsal displacement of the palatal arch
• poor nasopharyngeal constrictor activity during
deglutition
• failure of dilation of one or both auditory tube
diverticulum ostia after swallowing.
Many horses where functional pharyngeal paralysis is
diagnosed are in fact afflicted with pharyngeal hemi­
plegia, i.e. unilateral glossopharyngeal neuropathy, for
example in cases of guttural pouch mycosis. However,
true pharyngeal paralysis may be seen in cases of botu­
lism. Whenever a neurological cause of dysphagia is sus­
pected, it is always correct to inspect the auditory tube
diverticula for evidence of mycosis or diverticulitis.
Inspection of the floor of the nasopharynx per
nasum for diagnosis of a palatal defect presents no
 DIFFERENTIAL DIAGNOSIS AND EVALUATION OF DYSPHAGIA
difficulties even in quite young foals if an endoscope
with a diameter of 8.0 mm or less is available. Not all
palatal clefts occur as simple midline linear defects,
although these are the most common form in younger
patients with nasal reflux. The various permutations of
unilateral hypoplasia of the soft palate and pseudo­
uvula formation can escape confirmation until the
patient is considerably older.
Other abnormalities which may cause dysphagia and
which can be confirmed by endoscopy of the pharynx
and larynx include
• epiglottal entrapment, with or without a sub­
epiglottic cyst
• epiglottal hypoplasia
• iatrogenic palatal defects after 'over-enthusiastic'
palate resection for dorsal displacement of the soft
palate
• fourth branchial arch defects
• evidence of sub-epiglottic foreign bodies, usually in
the form of unilateral edema in the region of the
aryepiglottic folds
• intrapalatal cysts
• nasopharyngeal cicatrix
• laryngeal chondropathy
• pharyngeal neoplasia
• pharyngeal distortion by external compressive
lesions such as neoplasia or abscesses.
Clearly it is helpful to obtain some impression of the
extent of tracheal aspiration of ingesta accompanying
the dysphagia, and tracheoscopy is useful in this context.
Esophagoscopy is often a less rewarding technique
than might be imagined in the investigation of dyspha­
gia, simply because physical or functional obstructions
of the esophagus invariably lead to a build-up of ingesta
and saliva in the lumen that, in turn, prevents a detailed
inspection of the area under suspicion. Prior to the
examination the patient should be starved for 3-4
hours. Examination of the esophagus is made easier by
passing the endoscope distal to the area of interest, and
by inflating the esophagus using the air channel of the
endoscope. Examination can then be performed dur­
ing retraction of the endoscope. Evidence of conditions
such as esophagitis, megaesophagus, stricture, rupture,
tracheoesophageal fistula, diverticulum, intramural cyst
dysautonomia, and neoplasia may be found.
Radiography
Radiography, particularly with fluoroscopic studies
using contrast media, provides a means for the dynamic
investigation of deglutition. Clearly it is preferable for
the patient to take up the contrast medium voluntarily
and, in the author's clinic, bran mash impregnated with
5
barium sulfate is offered to the horses. A variety of fla­
vorings are included to make the meal more palatable.
The shortcomings of the technique are that it is depen­
dent on the enthusiasm of the patient to eat and also it
takes no account of dysphagias that vary between differ­
ent food materials. Although it has been found that
sedation does not significantly distort the process of
deglutition, most horses will take part in the investiga­
tion without resentment, once they are familiar with the
ambient noises of the radiographic equipment. The
sequence of events that make up deglutition is very
rapid and facilities for video-recording of the fluoro­
scopic images for subsequent analysis, including slow­
motion replay, are invaluable. The forced introduction
of barium sulfate suspension into the mouth through a
syringe is far from satisfactory, but it can be helpful to
outline intra-oral, pharyngeal, and esophageal lesions.
CONDITIONS COMPROMISING THE
ORAL PHASE OF DEGLUTITION
Lip and tongue lesions
Facial paralysis inhibits the ability of the horse to pre­
hend and retain ingesta. Hypoglossal nerve injuries
with lingual paralysis are rare in the horse and trauma,
either in the form of lacerated wounds or tongue-strap
strictures, accounts for the majority of tongue lesions in
this species. Horses with a severely injured tongue may
be unable to maneuver ingesta around the mouth, and
are inclined to drop food or to collect it in the buccal
cleft. Foreign bodies may become buried in the lingual
tissues and the painful suppurative response can reduce
a horse's inclination to eat.
Dental disorders (see Chapter 6)
Those conditions that are associated with periodontitis,
which causes extreme discomfort, are most likely to
provoke quidding.
Temporomandibular joint disorders
These are rare in the horse but when they do occur they
cause marked pain and a rapid loss of bodily condition.
Disuse leads to obvious atrophy of the masticatory mus­
cles. Clinical examination shows resentment of attempts
to open the mouth, and even under general anesthesia
the range of opening may be severely reduced. The
diagnosis is confirmed by radiography of the area in two
planes. Ultrasonography may be more helpful.
Hyoid apparatus disease
Hyoid apparatus involvement usually accompanies
otitis media in the horse, and ankylosis of the temporo­
hyoid articulation is a likely result. Pathological fracture
65
5 UPPER ALIMENTARY TRACT DISEASES
of the stylohyoid bone follows and one of the effects of
this is a limited ability to move the tongue. Radiography
of the area and endoscopy of the guttural pouches con­
tributes to the diagnosis.
Oropharyngeal and tongue-hase foreign bodies
The most common foreign bodies at this site are bram­
bles which become lodged in the sub-epiglottal area,
causing acute-onset dysphagia. Endoscopy per nasum
will show edema in the aryepiglottic folds, even if the
j()]'(�ign body itself cannot be seen. Such an endoscopic
finding is an indication for an oral examination under
general anesthesia.
Oropharyngeal tumors
These are unusual in horses and they tend to cause
dysphagia simply by virtue of the space they occupy.
CONDITIONS COMPROMISING THE
PHARYNGEAL PHASE OF DEGLUTITION
Oropharyngeal and tongue-base foreign bodies (see
above)
These are discussed above in Conditions compromising
the oral phase of deglutition.
Congenital palatal defects (see above) (see
Chapter 6)
These are discussed in Chapter 6.
Iatrogenic palatal defects (see Chapter 6)
Excessive palatal resection in the treatment of DDSP is
a disastrous complication because it is irreparable.
Iatrogenic defects can usually be differentiated from
congenital palatal deformities because the end points
of the resection are generally visible and the margin of
the free border has a tighter, rounded appearance.
Epiglottal entrapment and sub-epiglottic cysts
These conditions cause dysphagia because of space
occupation and restriction of movement of the epiglot­
tis. However, horses with this condition are more likely
to be presented for the investigation of abnormal respi­
ratory noises and/or exercise intolerance.
Pharyngeal and intrapalatal cysts
These again cause dysphagia because of the space-occu­
pying lesion. However, horses with these conditions are
more likely to be presented for the investigation of abnor­
Illal respiratory noises and/or exercise intolerance.
Nasopharyngeal cicatrization
Nasopharyngeal cicatrization limits the efficiency of
pharyngeal constrictor function, but horses with this
66
disorder are more likely to present for the investigation
of respiratory noises and/or exercise intolerance.
Compromised glottic protection
Compromised glottic protection leading to the aspira­
tion of ingesta into the lower airways may arise sponta­
neously in cases of arytenoid chondropathy, or through
iatrogenic causes, such as complications of prosthetic
laryngoplasty or partial arytenoidectomy. The precise
cause of post-laryngoplasty dysphagia is not known, but
over-abduction of the arytenoid cartilage, cicatrization
associated with reactive implants, and nerve injuries are
among the possible causes.
Pharyngeal paralysis (see above)
The most common causes of pharyngeal paralysis are
guttural pouch mycosis, ATD diverticulitis, botulism,
and lead poisoning.
Fourth branchial arch defects
Congenital fourth branchial arch defects generally
include aplasia, or at least hypoplasia, of the cricopha­
ryngeal muscles, with the effect that the proximal
esophageal sphincter remains permanently open.
Horses with fourth branchial arch defects may cough
when eating and drinking, and show a nasal discharge.
Afflicted horses may swallow air involuntarily and may
also
be confused with stereotypic 'wind-suckers'.
Intralumenal pharyngeal neoplasia
Pharyngeal neoplasia is rare in horses, and most of
these proliferations turn out to be lymphosarcoma.
Retropharyngeal abscessation and neoplasia
Retropharyngeal space occupying masses, such as
enlarged lymph nodes occurring in horses with stran­
gles, cause dysphagia because of external compression
of the pharynx, and also because of the pain associated
with the movement of food boluses over the lesions.
CONDITIONS COMPROMISING THE
ESOPHAGEAL PHASE OF DEGLUTITION
Fourth branchial arch defects
See above Conditions compromising the pharyngeal
phase of degluttion.
Abscessation and neoplasia causing external compres­
sion (see above)
It is not uncommon for cases of intrathoracic lympho­
sarcoma to present with a degree of dysphagia caused
by esophageal compression by a mediastinal mass. In
some cases a mass of neoplastic tissue may protrude
 DIFFERENTIAL DIAGNOSIS AND EVALUATION OF DYSPHAGIA
through the thoracic inlet and be palpable at the base
of one or both jugular grooves.
Megaesophagus (see Chapter 7)
Megaesophagus has been reported sporadically in the
horse, sometimes as a primary congenital disorder and
sometimes secondary to other conditions causing
restriction of esophageal function, such as vascular ring
strictures. Coughing, nasal reflux of ingesta, and disten­
tion of the cervical esophagus may all be features.
Confirmation is by contrast radiography.
Esophageal impaction (choke) (see Chapter 7)
Obstruction by impacted, dry ingesta (,choke') is typi­
cally associated with the ingestion of inadequately
soaked sugar beet pulp in the UK. Horses with 'choke'
present in an acutely distressed state with copious reflux
of saliva to the nostrils. The cervical esophagus may be
palpably distended with firm ingesta and passage of a
stomach tube beyond the pharynx is generally not
possible.
Strictures of the esophagus (see Chapter 7)
Strictures are thought to be the sequel of episodes of
acute obstruction, and horses with this condition are
presented with recurring 'choke'. Confirmation of the
diagnosis is best achieved by contrast radiography.
Dysautonomia (grass sickness) (see Chapter 17)
Grass sickness produces dysphagia in its acute form but
colic in the sub-acute and chronic forms. The condition
is st'en in horses of all ages throughout the UK and
northern Europe, but has been reported only once
in Australia. Afflicted horses are generally severely
dt'pressed, with patchy sweating, elevated pulse rate,
and ileus. The dysphagia arises as a part of total gas­
trointestinal stasis, and nasal reflux of ingesta adds
to the pitiful appearance of the patients. There is
currently no reliable in vitro diagnostic test, but the radi­
ographic demonstration of esophageal stasis and the
endoscopic identification of ulceration of the
esophageal mucosa are helpful pointers to the likely
diagnosis.
5
Rupture of the esophagus (see Chapter 7)
Esophageal rupture carries a poor prognosis unless the
patient is presented for treatment soon after the injury
has occurred, because of the rapid advance of contami­
nation and cellulitis into the surrounding tissues. Most
ruptures are caused by obvious external trauma, but a
number of horses have been referred to the author's
clinic where rupture of the pharyngeal or esophageal
wall has occurred through excessively forceful attempts
to pass a stomach tube or, in one case, an endotracheal
tube.
Intramural inclusion cysts (see Chapter 7)
These may be encountered in young horses and cause
dysphagia through space occupation restricting the
passage of esophageal boluses. The lesions may be seen
as bulges in the esophageal wall at endoscopy, or be
demonstrated by ultrasonography or contrast radio­
graphy.
Intramural neoplasia of the esophagus (see Chapter 7)
Esophageal neoplasia is rare in the horse, but squamous
cell carcinoma at this site has been reported.
Many of the conditions outlined above are described in
greater detail elsewhere in this book, together with
explanations of their etiology, definitive diagnosis and,
when applicable, methods of treatment.
BIBLIOGRAPHY
Baker G] (1982) Fluoroscopic investigations of swallowing in
the horse. Vet. Radiol. 23:84.
Baum K H, Modransky P D, Halpern N E, Banish L D (1988)
Dysphagia in horses: the differential diagnosis. Parts 1 and
2. Compo Cont. Educ. Pract. Vet. 10:1301-7 and 1405-10.
Brown C M (1992) Dysphagia. In Current Therapy in Equine
Medicine3rd edn, N E Robinson (ed.). W B Saunders,
Philadelphia, pp. 171-5.
Freeman D E (1980) Diagnosis and treatment of diseases of
the guttural pouch. Parts 1 and 2. Compo Cont. nauc. Pract.
Vet. 2:S3-S11 and S25-S32.
Lane] G (1983) Fourth branchial arch defects. In
Proceedings of the 15th Bain-Fallon Memorial Lectures,
Australian Equine Veterinary Association, 209-212.
67
 6
Diseases of the oral cavity and soft
palate
Dental disease
BA Rucker
Equine dental disorders are quite common, a preva­
lence of 1 0-S0 per cent has been reported in the gen­
eral equine population. The author's review of 325
dental records revealed 30 per cent with normal denti­
tion. The remaining 70 per cent showed the following
distribution
• 3.4 per cent had mild-to-severe periodontal disease
• 6.4 per cent had worn out, broken, or missing teeth
• 8.9 per cent had exaggerated transverse molar
ridging
• 15.4 per cent had incisor malocclusion
• IS. l per cen t had oral ulceration secondary to
sharp molar points
• :�7.S per cent had other molar malocclusions.
The total exceeds 100 per cent because 30 per cent of
the horses had more than one problem. Eighty per cent
were presented without any history of dental difficulty.
DENTAL ANATOMY
The horse has evolved into an almost continuous
grazer. Forage is selected by the prehensile lips, cut off
with the incisors, and moved caudally with the tongue
for grinding by the molars. The rows of mandibular
cheek teeth are set 30 per cent closer together than the
maxillary cheek teeth (anisognathism) , and grinding
of forage is done with a side-to-side motion of the
mandible. Consequently, the mandibular teeth wear
more on the buccal side and the maxillary teeth wear
more on the palatial aspect, producing a slope to the
occlusal surface of 1 0-15 degrees.
The visible crown is comprised of layers of dentine,
cementum, and enamel, these layers wear at different
rates. The two prominences on the erupting cheek
teeth are worn down with occlusion to form an irregular
chewing surface. Except for the first cheek tooth, either
a slight undulation or transverse ridges ( two per tooth)
form on the occlusal surface. The six cheek teeth func­
tion as one long tooth and malocclusion or disease
involving individual teeth effects the function of the
entire arcade.
Pulp is soft, gelatinous material that fills the central
part of the tooth, the pulp cavity. Masticatory forces
cause the pulp to be replaced with secondary dentine
from the occlusal surface to the root. Dentine eventu­
ally fills the pulp cavity in old horses. The root elongates
with age by deposition of cementum. This extra root
helps to anchor the tooth in the alveolus in aged horses.
NOMENCLATURE
Traditionally teeth have been identified according to
their anatomic function. Each tooth is given a letter
designation: I incisor, C canine, P premolar, M
= = = =
molar. A lower case letter indicates a deciduous tooth;
an upper case letter indicates a permanent tooth. The
location of the tooth is indicated by the position of the
tooth number around the letter. The head is divided
into four quadrants represented by the four corners of
the letter. For example, the right second upper incisor
is connoted as 21. The anatomic system is more com­
monly used but is sometimes confusing as there is more
69
6 UPPER ALIMENTARY TRACT DISEASES

than one name for the same tooth, i.e. the right upper
third premolar is also the right upper second cheek
tooth.
The Modified Triadan System identifies teeth
numerically according to their location. Each tooth has
a three digit number describing its position. The first
digit of the number represents the quadrant of the
head. The first quadrant is the upper right, continuing
clockwise around the head, i.e. the upper left is quad­
rant 2, the lower left is quadrant 3, and the lower right
is quadrant 4. The next two digits identity the location
within the quadrant, with a maximum of 1 1 teeth in
each arcade. The central incisors are numbered 1 while
the last molars are numbered 1 1. The lower left second
premolar is 306. The Modified Triadan system allows
for the presence of a lower wolf tooth.
Deciduous teeth are indicated by substituting the
numbers 5 to 8 for the first digit beginning again with
the upper right side of the head, thus 807 designates
the deciduous right lower third premolar. This system
simplifies written and computer records.
DENTAL ERUPTION
Knowing the normal time when teeth erupt is essential
for practitioners to properly age and anticipate prob­
lems associated with eruption. Table 6.1 lists expected
eruption times for most horses, however times may vary
as much as 6 months.
AGE DETERMINATION
Age determination up to 8 years is based on tooth erup­
tion and incisor wear. From 8 years to the late teens or
early twenties age is determined on incisor wear, shape
of the incisor occlusal surface, and the incisor angle of
occlusion in profile. Mter 20 years molar wear may aid
in aging because the upper first molars (l09 and 209)
are beginning to wear to the root, which has no enamel,
causing these teeth to hollow out on the occlusal
. surface.
Age determination is accurate until all the per­
manent teeth are in wear, after this aging becomes
more an art than a science. Many factors affect wear
including
• management
• forage types
• breed
• dental care
• vices
• trauma
• malocclusion.
Soils with high silica content may cause the teeth to
wear more quickly. Horses kept stalled, getting minimal
grazing time, and consuming a diet of fine hay, will
chew with limited lateral excursion. Lack of lateral
excursion promotes molar malocclusion and affects
wear on both incisors and molars.

Teeth
Temporary Eruption
First incisor 6-8 days
Second incisor 4-8 weeks
Third incisor 5-9 months
Premolar Present at birth or first 2 weeks

Permanent Eruption In Wear

First incisor 2.5 years 3 years
Second incisor 3.5 years 4 years
Third incisor 4.5 years 5 years
Canine 3.5-5 years
First premolar (wolf tooth) 5-6 months
Second premolar 2 years 6 months 3-4 months later
Third premolar 2 years 8 months 3-4 months later
Fourth premolar 3 years 8 months 3-4 months later
First molar 9-14 months 2 years
Second molar 2 years 3 years
Third molar 3-3.5 years 4 years

70

Cups and stars
Incisors have an invagination of the enamel layer on
the occlusal surface that is partially filled with cemen­
tum. This invagination, called a cup or infundibulum,
is oval shaped and eventually wears off the tooth. The
cup is lost from the lower first incisors (301 and 401)
at 5-7 years, lower intermediate incisors (302 and 402)
6-9 years, and for the lower corner incisors (303 and
4(3) 7-10 years. Cup loss on 101 and 201 is at 9 years,
102 and 202 is at 10 years and 103 and 203 is at 11
years.
As the incisor wears, the cup becomes smaller, moves
distally and the dental star appears rostral to the cup.
The dental star is formed from secondary dentin that
has been deposited in the pulp (dental) cavity as the
tooth ages. Initially the dental star is wide but with wear
hecomes oval then round. The age range for the
appearance of the star is 6-7 years for the lower 01s, 7-9
years for the lower 02s, and 8-10 years for the lower 03s.
Star appearance for upper 01s, 02s, and 03s is 11, 12,
and 13 years, respectively.
Shape
The shape of the occlusal surface of the incisors
changes with age. When the permanent incisors erupt,
the occlusal surface is wider medial-to-lateral than ros­
tral-to-caudal. The shape changes to oval at 6-7 years,
then becomes rounded at age 9-12 years, and triangu­
lar at 14-1 7 years. After 20 years the incisors are wider
rostral-to-caudal than medial-to-lateral. Remember that
lack of incisor wear, seen in stabled horses, may inter­
fere with age determination.
Hooks
Hooks may form on one or both the upper corner
incisors from changes in occlusion. Sometimes called 7
and 11 year hooks, they may occur any time after 6 years
and are not very dependable for age determination.
Incisor hooks seldom remain after age 12-13 unless a
malocclusion is present.
Galvayne's groove
Galvayne's groove is a slight indentation of the tooth
material on the lateral aspect of the upper corner
incisors (03s). The groove is bilateral but the grooves
on either side may not appear at the same time. The
groove appears at around 10-11 years, is halfway down
the tooth at 15 years, and all the way down at 20 years.
The groove is seen only on the lower one half of the
teeth at 25 years and is completely gone at age 30
years.
DISEASES OF THE ORAL CAVITY AND SOFT PALATE 6
Incisor profile
In young horses the incisors meet at an obtuse angle,
almost vertically. The angle gets more acute with age.
The incisor profile is not an exact age determiner but it
helps in age approximation.
SIGNS OF DENTAL DISEASE
Signs of dental disease are diverse and may present in
many ways from subtle to obvious. A complete history,
coupled with presenting signs, and a thorough oral
examination with a full mouth speculum is needed to
reach a diagnosis. The oral cavity should be inspected
visually, and each tooth palpated during the examination.
Latex gloves should always be worn when performing
dental manipulations.
Signs of dental problems include:
• abnormal eating behavior (head tilt, quidding,
dropping grain)
• excessive salivation
• discharge or fetid odor from mouth
• refuses to eat, eats slowly, or eats hay but not grain
• long (greater than 0.6 cm) hay particles in feces
• poor body condition
• dorsal displacement of the soft palate
• swelling or bumps on the maxilla or mandible
• purulent drainage from fistulae over the maxilla or
mandible
• purulent nasal discharge
• resists bridling or rears when bridled
• head tilts while ridden or lunged
• sticks tongue out of the mouth or over the hit
• slightly opens the mouth when head is in a vertical
position
• refuses to maintain frame or vertical head carriage
• resists turns to one or both sides (may be very
subtle)
• head tossing or shaking
• unexplained or subtle lameness (oral examination
should he included in lameness examination)
• mouthing or chewing the hit
• slow in transitions
Nervous or fractious horses should be lightly sedated to
facilitate the examination. Most horses do not object to
the full-mouth speculum, but it can become a weapon
on an excitable horse. Horses 4 years old and under
object to a speculum because the incisor plate lip
pinches the gingiva behind the incisors. Grinding down
the lip will prevent pinching. To avoid pressing injured
cheek tissue into sharp molar points, lightly float the
maxillary arcade prior to using the speculum.
71
6 UPPER ALIMENTARY TRACT DISEASES
The author prefers not to pull the tongue out of the
mouth unless necessary. A 'tongue depressor' made
from PVC pipe is handy for pushing the tongue to the
side. Stainless steel wire inserts are available for
improved arcade visualization.
DEVELOPMENTAL DISORDERS
Mandibular and maxil lary brachygnathia
The most common developmental oral abnormality is
a mandible shorter than the maxilla or 'parrot
mouth'. If the mandible is longer than the premaxilla
(shortened premaxilla), the condition is called 'sow
mouth'. Both abnormalities are thought to be inher­
ited. Sow mouth is less common than parrot mouth
and is usually seen in small breeds, particularly minia­
ture horses. Foals may be normal at birth, but develop
these disorders by the time they are 2-6 months old.
The conditions may be partial with between 10-90 per
cent of the incisor occlusal surface in contact, or com­
plete, with no incisor contact. Assessment of severity
should be done with the nose pointed toward the
ground. Raising the head to a horizontal position lets
the mandible slide caudally and will exacerbate the
appearance of parrot mouth.
Parrot mouth has also been classified as an 'overbite'
or 'overjet' deformity. An 'overjet' is where the maxilla
protrudes further than the mandible, but the incisor
arcades are maintaining their usual anatomic positions.
An 'overbite' is an extreme protrusion of the upper
· passed through the hole. The wires are brought forward
incisors, and the incisors are deviated ventrally in front
of the lower incisors. Ove,:jet is seen more often in
Quarter Horses, and limited evidence suggests brachy­
gnathia may be an aspect of developmental ortho­
pedic disease. Overbite is more commonly seen in
Thoroughbreds and may have a familial predilection in
this and possibly other breeds. Overbite therapy in a
mature horse is palliative, however, horses are capable
of performing and maintaining themselves without dif­
ficulty. Routine correction for molar malocclusion and
occasional shortening of the incisors is required. With
overbite the lower incisors are in 'occlusion' with the
hard palate just caudal to the upper incisors. The
incisors should be examined annually and maintained
with a smooth, level surface.
Treatment
Treatment for parrot or sow mouth is more successful if
started while the horse is less than 6 months of age.
Conservative treatment for parrot or sow mouth in foals
utilizes one or more of the following.
72
1. For partial brachygnathia, eliminate any lip
formation on the rostral or caudal edge of the
incisors that arises from lack of wear.
2. Remove hooks or ramps occurring from molar
malocclusion and shorten exaggerated transverse
ridges on both upper and lower molar arcades.
3. Ensure there is no contact between the molar
arcades when the mouth is at rest. It is the author's
opinion that hooks, ramps, or transverse ridges tall
enough to make contact with the opposite molar
arcade (when at rest) may retard mandibular
growth.
4. The mandible in parrot mouths may be narrower
than normal, leading to a lip forming on the buccal
side of the upper premolars. This lip should be
floated off preserving the normal occlusal angle. If
the occlusal angle of the arcades is too steep,
restore it to 10-15 degrees.
A bite plate may be needed for horses with no incisor
contact. The plate attaches to a halter and projects
between the incisors beyond the lips. The plate provides
incisor contact preventing ventral deviation of the pre­
maxilla and upper incisors. The bite plate also separates
the molar arcades. This separation eliminates possible
opposing molar contact at rest.
Surgical therapy for overjet involves the application
of a premaxillary tension band restricting rostral devel­
opment of the maxilla. Under general anesthesia, a
hole is drilled through the alveolar bone between
deciduous upper 06s and 07s, with a 3.2 mm bit. Half of
a 30 cm length of stainless steel (18-20 gauge) wire is
and twisted together as they pass across the diastema.
One strand of the wire goes on the labial side of the
incisors, the other strand to the palatal side. A large
gauge needle inserted in the gingiva between the
contralateral first and second incisor is used to pass the
labial wire caudally. This wire is then passed between
the ipsilateral first and second incisors, re-emerging
on the labial side. The palatal wire is passed rostrally
between the central incisors and is then twisted with the
other wire on the labial surface of the ipsilateral first
incisor. The wires are cut off and covered with a small
amount of acrylic to minimize irritation to the lips. This
procedure is repeated on the opposite side of the
mouth.
Small notches may be cut into the teeth, as needed,
with a Dremel tool and a small-diameter burr to anchor
the wire at the gingival margin. Tension wires are left in
place for 2-6 months, and need to be checked daily by
the owner for failure, to flush out impacted food mate­
rial, and to observe improvement. Mandibular tension
bands can be used to treat sow mouth.

Application of tension wires for overbite correction
wilL instead, exaggerate this condition by further ven­
tral deviation of the premaxilla. A bite plate will need to
be applied until the ventral premaxilla deviation is cor­
rected. Simultaneous or alternating tension wiring and
bite plate application may be needed to correct foals
with severe overbite (2-3 cm shortening of the
mandible). Complete correction may not be obtained.
A bite plate applied after 6 months of age may have
limited correction on an overbite.
Surgical correction of a possible heritable disease is
open to ethical debate. Correction will improve grazing
ability and mastication, and will minimize complica­
tions from molar malocclusion. Owners should be
informed of the possible inheritable tendencies and
encouraged to not breed these animals.
Dental tumors
Odontomas, tumors with histologic presence of both
dentine and enamel, are rare in horses. Odontomas
originate from dental epithelium and four types have
been identified in the horse. These are ameloblastomas
(adamantinomas) and three types of odontomas:
ameloblastic, complex, and compound. Mesodermal
tumors, cementomas, and odontogenic myxomas, have
not been reported in the horse. Diagnosis is based
on radiographic and histologic examination. Amelo­
blastomas are usually seen in mature horses and
odontomas are commonly found in younger animals.
Ameloblastic odontomas usually present as a con­
genital, firm, non-painful, 2-3 cm nodule. Foals are
otherwise normal. The mass slowly enlarges during the
next weeks or year to reach a size of 15 cm, involving
vital structures. Treatment is surgical eXCISIOn.
Odontogenic tumors generally do not metastasize, but
they are invasive and successful removal depends on
location and extent of bony, sinus, and soft tissue
involvement. If extensive tumor involvement prohibits
removal, affected animals may live for months or years
before euthanasia is required.
Dentigerous cysts
Dentigerous cysts (heterotopic polyodontia), also
known as ear teeth or aural fistulae, are odontogenic
cysts frequently containing stratified squamous or gob­
let cell epithelium. They are commonly found at the
base of the ear, other locations include the mandible,
maxilla, and maxillary sinus. These cysts may have a
seromucous or purulent discharge. Careful excision
usually results in complete resolution. Radiographs are
needed to differentiate between tumors, dentigerous
cysts, and fluid cysts.
DISEASES OF THE ORAL CAVITY AND SOFT PALATE 6
Cysts
Fluid filled cysts occasionally occur in the mandible,
maxilla, and paranasal sinuses. They produce a variable
degree of facial deformity and present as a smooth,
firm, non-painful, gradually enlarging swelling.
Aspiration of a pale yellow clear to turbid fluid coupled
with a radiolucent center is indicative of a cyst. Surgical
removal is the treatment of choice.
Polyodontia
Supernumerary teeth are considered congenital
because they arise from abnormal differentiation of
tooth germinal tissue. The condition is only recognized
after tooth eruption. Incisors are the teeth most often
affected. One extra tooth or an entire incisor arcade
may be present. Extra molars may appear within the
molar arcades, from the hard palate or as an extra last
molar. Customary treatment is to maintain the length of
any extra teeth that do not wear. Removal is seldom
indicated.
Oligodontia
Too few teeth are more frequently encountered than
too many teeth. Congenital oligodontia may involve
deciduous or permanent incisor or molars. Acquired
oligodontia is usually from trauma and subsequent
damage to existing teeth or to developing tooth buds.
Treatment is directed at maintaining the proper height
of teeth that are unopposed and not wearing properly.
Retained deciduous teeth
Retained 'caps' may occur in either the incisor or molar
arcades. The erupting permanent tooth normally dis­
rupts the circulation to the root of the deciduous tooth.
The deciduous tooth loosens and separates as the per­
manent tooth reaches the gingiva.
Incisor caps
Incisor caps frequently are retained because the perma­
nent tooth erupts caudally to the deciduous root. In
most cases the root is vestigial and the cap slips off eas­
ily. Loose caps should be extracted prior to using a full
mouth speculum as the incisor plate can pinch soft
tissue between the cap and permanent tooth beneath.
Occasionally caps are firmly held in place by 1-2 cm of
root. Removal requires sedation and local anesthesia.
The gingiva is incised over the root and the root ele­
vated with a curved bone chisel. The mucosa may be left
to granulate in with daily flushing with a mild disinfec­
tant by the owner. Incisor caps should be removed if the
opposing cap is gone and the permanent tooth is in
73
6 UPPER ALIMENTARY TRACT DISEASES
wear. Sometimes 702 and/or 802 overlap the erupting
302/402, impacting these permanent teeth. Removal or
trimming off the impacting part of the deciduous tooth
is indicated.
Premolar caps
Removal of the cap is indicated if the cap is loose, trap­
ping food, or causing maleruption of the permanent
tooth. If the permanent tooth can be palpated above
the gingiva, the caps should be removed. A deciduous
premolar, still securely attached, should be extracted if
a putrid odor is detected on the operator's gloved
hand. This indicates that forage is fermenting around
the cap or between the cap and the permanent tooth.
The associated gingivitis may lead to early periodontal
disease. Starch fermentation between the cap and per­
manent tooth may lead to early infundibular necrosis.
The fourth premolar is the last permanent tooth to
erupt and is most often impacted or deviated.
Infectious dental disease
Infectious disease involving the cheek teeth may be
divided into three categories
• infundibular necrosis
• periodontal disease
• periradicular disease.
These terms do not identifY the cause and one classifi­
cation may progress to another.
Infundibular disease or necrosis
Dental caries or decay is the destruction of the cemen­
tum, enamel, and dentin secondary to fermentation of
carbohydrates. Baker observed infundibular necrosis at
an incidence of 80 per cent in horses over 15 years. The
first upper molar is the most common site.
Hypoplasia of cementum in the enamel invagination
(infundibulum) of the upper cheek teeth allows food to
pack into these pockets. Carbohydrate fermentation
and resulting acid production dissolves and weakens
the tooth material. Cementum hypoplasia may not be
visible until some crown wear exposes the defect
• grade I disease is restricted to cement erosion
• grade II involves both cement and surrounding
enamel
• grade III includes the dentin.
Although the mandibular cheek teeth do not have
infundibula, fracture of the exposed crown may lead to
decay.
Lesions may be innocuous in some horses. Apical
and lateral extension may not produce pulpitis because
74
secondary dentine production preserves the pulp cav­
ity. Progression of the necrosis leads to coalescence of
the rostral and caudal infundibula into a single large
pocket. Sequelae include pulpitis, with or without frac­
ture, apical migration and infection (periradicular dis­
ease or apical periostitis), sinusitis and nasal discharge.
Endodontic treatment for pulpitis has been
described. Sinusitis is treated with lavage and drainage.
Extraction may be done intra-orally, via sinus trephina­
tion and repulsion, or through lateral buccostomy and
elevation of the tooth intact or in sections.
If a coalesced pocket is present but there is no pulpi­
tis or alveolar infection, the occlusal surface of the
opposing tooth should be maintained level with the
other teeth in that arcade. The opposing tooth may
develop a hump corresponding to the defect in the
damaged tooth. This malocclusion predisposes the
arcade for wave or step formation, fracture of the dis­
eased tooth, periodontal disease, and loss of additional
teeth.
Periodontal disease
Periodontitis is
• inflammation of the gingiva with progression to
formation of gingival pockets in the interproximal
spaces
• resorption of alveolar bone
• loss of gingival attachment
• destruction of the periodontal ligament
• tooth loosening.
Periodontal disease has been described as the most
common dental disease of horses. The normal shearing
forces of mastication are essential for sustaining healthy
periodontium. Molar malocclusion interferes with nor­
mal lateral excursion and proper grinding of forage.
Periodontal disease is often secondary to malocclu­
sions. The initial stages of periodontal disease (regres­
sion of inflamed gingiva, small pockets of trapped
forage) may locate acljacent to a minor malocclusion. A
minor malocclusion may be a single tooth with a flat­
tened table angle or exaggerated transverse ridges.
Animals exhibiting dysmasesis: quidding, dropping
grain, head tilt, and excessive salivation should be
examined closely for early periodontal disease. The first
lesions are caused by trapped forage in the gingival sul­
cus at molar junctures, this may be unilateral. Retained
premolar caps trap food, leading to periodontitis, but
this usually resolves after normal grinding resumes. The
only clue may be a subtle putrid odor requiring a
thorough digital and visual examination to identify the
location of the lesion. Gingival hyperemia and swelling
are usually present. The pocket enlarges via a cycle of
 DISEASES OF THE ORAL CAVITY AND SOFT PALATE 6

irritation, inflammation, and erosion of the periodontal • maxillary sinusitis

ligament, gingiva, and alveolar bone. The erosion of the • sinus empyema
periodontal ligament creates a gap in the interproximal • signs associated with painful chewing.
space and the tooth loosens. Severe alveolar sepsis even­
Painful bony swellings (pseudocysts) appear secondary
tually causes tooth loss.
to eruption of permanent premolars. Retained decidu­
Treatment for early periodontitis includes correc­
ous premolars impede normal permanent tooth erup­
tion of any malocclusion, and routine (every 6 months)
tion. The fourth premolar is most commonly affected
dental maintenance. This may prevent or slow the dis­
because it is erupting between two permanent teeth. A
ease progression. Flushing out the trapped food and
radiographic change seen with pseudocysts is lysis of
packing the pockets with metronidazole tablets may
surrounding bone. The alveolar periostitis seen with
restore the gingiva when minimal pocketing is present.
pseudocysts typically resolves after the permanent tooth
This can be repeated every other day until resolution
is in wear.
or until it is decided that therapy is unsuccessful.
Hematogenous bacteria may infect the hyperemic
Additionally, the owner should flush out the mouth
tooth root, leading to periapical abscess formation. This
twice daily with an appropriate disinfectant. Grinding
is called anachoretic pulpitis and results in periradicu­
the opposing tooth out of occlusion, using a rotary
lar disease. Treatment is the removal any retained caps,
burr, will aid in minimizing food packing into the sul­
malocclusion, or abnormal wear. Radiographs are indi­
cus. The opposing tooth is shortened 2-3 mm.
cated to assess tooth placement and root involvement.
Treatment of advanced periodontitis consists of cor­
Rostral upper second premolar hooks put caudal
recting any malocclusions and evaluation of the dis­
pressure on the lower premolars, crowding the perma­
eased tooth for extraction. If the tooth wiggles easily
nent teeth. Permanent teeth may be impacted or
and is painful, extraction is indicated. Affected animals
displace medially during eruption. The teeth that are
with advanced periodontitis are usually over 15 years
impeding the eruption may need their mesial surfaces
old. Extraction is generally easy because of the shorter
ground off. This can be done with a diamond cut off
reserve crown and minimal periodontal ligament
wheel or end cut rotating burr with appropriate guard.
attachment. Grasp the tooth with a cap extractor, move
Antibiotic and anti-inflammatory therapy should be
the handles side to side and then rotate the occlusal
initiated and continued for 2-4 weeks.
surface lingually (palatally).
When several teeth are involved, usually the second,
Apical abscess formation may produce a draini g �
tract. This more severe form has been termed chronIC
third, and fourth cheek teeth, only one tooth may
ossitying periostitis. Contrast radiology will help deter­
appear loose enough to extract. Extraction of this tooth
mine tooth involvement and extent of the fistula.
will frequently reveal advanced periodontitis of the
Typical treatment is extraction of the diseased tooth.
other two, requiring their extraction. Probe the alveo­
Complications from removal of a tooth with an intact
lus for tooth fragments and flush with antibiotics or dis­
periodontal ligament are frequent. Medical treatment
infectants after extraction. Packing the alveolus with
in the form of 4-8 weeks of appropriate antibiotics,
gauze is generally not necessary. The alveolus gra �u­
immune stimulants, and weekly intravenous sodium
lates in and covers with gingiva in 2-3 weeks. GlVe

.
�
systemic an tibiotics effective against anaero i � and
.
iodide (2-3 treatments of 25 0 ml, 20% solution) has
been successful in saving abscessed teeth.
gram-negative bacteria when widespread gmglVItlS or
Endodontic treatment with exposure of the affected
regional lymph nodes are enlarged.
alveolus, removal of the apices and pulp, and filling the
Slightly unstable teeth should be left in situ as long as
possible. Removing occlusion by grinding down th � pulp cavity has had limited success. Mandibular teeth
are better candidates than maxillary teeth because of
opposing tooth will enable the diseased tooth to stabI­
their simpler root structure.
lize in some cases.
Antibiotic therapy
Peri radicular disease
Mixed bacteria are most commonly cultured from
Periradicular disease is infection or inflammation of the
periodontal pockets and dental abscesses. Antibiotics
pulp and surrounding tissue. Synonymous ten s ar � � should be broad spectrum. Trimethoprim-sulfa,
alveolar periostitis, periapical osteitis, and chrOnIC OSSI­
30 mg/kg p.o.q. 12 h, may be used singly or in combi­
tying periostitis. One text defines periodontal disease as
nation with procaine penicillin G, 22 000-44 000 IU/kg
alveolar periostitis. Signs include
Lm. q. 12 h. Potassium penicillin, 22 000-:-44 000 �l!
l.kg
• painful bony swelling Lv. q. 6 h can be substituted for procame penICIllin.
• external or intra-oral fistula formation If Bacteroides Jragilis is suspected, penicillin may be

75
6 UPPER ALIMENTARY TRACT DISEASES
combined with metronidazole, 1 5-20 mg/kg p.o. q.
6-8 h. Ceftiofur, 2-4 mg/kg i.v. or i.m. q. 8-1 2 h, is also
effective. Sodium iodide 20%, 250 ml/500 kg i.v. weekly
for 2-3 weeks can resolve apical infections that do not
appear to be responding to antibiotics.
Malocclusions
The incidence of incisor and particularly cheek teeth
malocclusions is quite high. Detection and correction
of malocclusions is often done after periodontitis or
severe abnormalities of wear have developed. Many
malocclusions are easily recognized, for example ros­
tral upper and caudal lower hooks. Thorough exami­
nation can reveal small, but significant, abnormalities.
It is sometimes necessary to carefully evaluate the
height of the exposed crown on all teeth in order to
determine abnormal dentition. Proper correction of a
molar malocclusion includes restoring the normal
table angle.
Correction of hooks, ramps, and wave or step mouth
has traditionally been done with cutters and hand tools.
Cable grinders and reciprocating electric or air floats
have eliminated the need for these tools. Power tools
are safer and quicker than cutters.
Molar malocclusions can be indicated by pain
response with lateral excursion, or by incisor malocclu­
sions, f()r example
• offset mandible
• rostral lip on the upper 01 and 02 incisors
• unilateral hook on upper or lower 03 incisors.
Normal incisors will be level and parallel to the ground
when viewed at eye level. Deviations from this require
incisor reduction or alignment. Incisors should be
repaired after molar corrections unless a full mouth
speculum cannot be applied to the incisors.
Incisor malocclusions can be treated with hand tools
for minor problems. Treatment of abnormalities need­
ing more than 2 mm removed from the surface of the
tables should be done with power tools. After 1 or 2 mm
has been removed excursion to molar contact is deter­
mined. When lateral excursion to molar contact is
shortened to 5-6 mm, stop removing incisor height.
Even if the table surface is not level, stop at this point
and recheck the animal in 6 months time when further
correction can be made.
Hooks and ramps
Upper 06 hooks may be secondary to overjet of the
upper premolars, erupting into wear ahead of the lower
06s, or shaping of the lower 06s without corresponding
upper 06 shaping (iatrogenic hooks). After hook
removal, the affected teeth should be viewed from both
76
sides of the mouth, assuring removal of excess tooth
material from the occlusal surface. Lower 06 ramps may
be secondary to eruption into wear ahead of the upper
06 or oveIjet of the lower premolars.
Rear hooks are usually found on the last lower
molars (1 1s) and secondary to upper 06 hooks. As
upper front hooks get longer, they also get thicker, forc­
ing the mandible caudally. Caudal mandibular dis­
placement pushes the lIs out of occlusion causing a
hook to form.
Hooks and ramps are best removed with guardeu
rotary grinders.
Tall teeth
Tall teeth consist of dominant cheek teeth that are
taller than the other teeth in the arcade. One to three
teeth may be involved and determination of which
teeth have excess crown requires experience.
Observation of the contralateral arcades is beneficial
because the condition frequently is unilateral. The
occlusal angle on the affected tooth is often too flat.
Dominant teeth are often lower 06s with or without
07s and 08s, lower 08s, 09s, and lIs. Upper teeth
involved are 06s, 09s, and lOs. It is common to have a
tall upper 10 on one side and tall lower 07 or 08 on
the other side of the mouth. Correction is achieved by
shortening the affected tooth to the level and angle of
the rest of the arcade.
Step mouth
Step mouth is an abrupt difference in tooth height and
results from untreated dominant teeth. Tall teeth grad­
ually increase in height, while the opposing tooth is
worn too short. If treated before the short tooth is worn
to the root, the mouth can be restored to normal. Step
mouth can be secondary to permanent tooth extraction
when the unopposed tooth is not maintained properly.
Correction is achieved by grinding down the taller teeth
or cutting through these teeth, thereby restoring them
to the arcade height.
Wave mouth
Wave mouth is the gradual excessive increase in tooth
height on both arcades causing an'S' shape on the
occlusal surface. Correction is initially done with a
grinder and then finished by shaping by hand. There
will be minimal or no occlusion at the spot where a wave
is corrected. The teeth that were too tall, prior to cor­
rection, will again be too tall in 6 months, but the exces­
sive height will be only 1-2 mm. The correction should
be repeated every 6 months until both arcades are nor­
mal in exposed crown height and angle.
 DISEASES OF THE ORAL CAVITY AND SOFT PALATE 6

Table ang les

The normal tilt to the cheek teeth occlusal surfaces is

from 10-15 degrees. Animals under 3 years of age may
normally have steeper angles. The angle decreases
when all permanent cheek teeth are in wear.
Shear mouth is an extreme type of excess angle,
caused by mandibular arcades that are too narrow or by
severe chronic incisor tilt. Animals with shear mouth
can chew on one side of the mouth until the sheared
mandibular teeth reach the hard palate.
Flattened table angles occur secondary to lack of
lateral excursion. Horses chewing more up and down,
rather than side to side, wear the taller side of the teeth
(buccal upper and lingual lower) more than the lower Figure 6.1 Ridges block rostral-caudal motion. Occlusal
side. The primary cause of lack of lateral excursion, or forces are directed along the lines indicated
side-to-side chewing motion, is oral pain. The oral pain c) open arrows = abnormal occlusial forces
can be caused by malocclusions, periodontitis, peri­ -t thin arrows = normal forces
radicular disease, or trauma. The table angles may be
flatter than normal or the upper cheek teeth may have
a slight hollowed out appearance or depression in the
center of the tooth, running the length of the upper axis of the reserve crown. Periodontal pocketing
arcade. Decreased angles are also found on teeth worn appears when a groove is worn down to the gingiva.
down to the root. Unilateral exaggerated transverse ridges can hold the
Correction is made by restoring the angle, but this mandible to one side, while one exaggerated transverse
may be difficult in old horses because there may be very ridge can wedge apart teeth in the opposing arcade.
little exposed crown left. When the decreased table Correction is achieved by shortening the ridge
angle is unilateral, the incisors will not separate as much height to a point where there is no contact between the
on the affected side during lateral excursion. arcades when the mouth is at rest. Usually one-half of
the excessive height is shortened on both arcades.
Listening to occlusion while pushing the mandible lat­
Exaggerated transverse ridges erally will produce a more uniform, even sound after
the ridges have been shortened. Also the rostral move­
Cheek teeth have a slight buccal-to-lingual (palatal) ment of the mandible, when the nose is pointed toward
undulation to the occlusal surface. Each tooth, except the ground, will increase.
for the first, has two of these transverse ridges. The posi­
tion of the maxillary ridges is equidistant between the
Deviated teeth
cingula. The crests have a smooth rounded top and
match the rounded depression on the opposing tooth. Buccal or lingual deviation is secondary to impaction or
The height difference of the low and high spots is trauma. Common sites of tooth deviations are
normally 1-2 mm.
• lingual deviations - lower 07s, 08s and 09s
Exaggerated transverse ridges are present when the
• buccal deviations - upper 07s and 09s, lower lOs.
ridge height exceeds the distance between the molar
arcades in the resting mouth (see Figure 6.1). Deviations of 1-2 mm do not usually cause problems.
Exaggerated transverse ridges may affect the entire Deviations of more than 3 mm allow food to pack
pair of arcades or just one pair of teeth. Exaggerated between the teeth leading to periodontitis and eventual
transverse ridges accentuate the buccal points on the tooth loss. Treatment is removal of the deviated portion
cingula. The crests of the ridges become less rounded of tooth preventing soft tissue irritation.
and more angular, like a row of saw teeth. The caudal
ridge on maxillary teeth wears an exaggerated groove in
Geriatric malocclusions
the juncture between the mandibular teeth.
Exaggerated transverse ridges interfere with lateral Treating malocclusions in horses over 20 years old is
excursion and the normal rostral-caudal movement of usually palliative. Teeth worn to the roots can no longer
the mandible. The shearing force of chewing is directed grind. Loose teeth are extracted and tall teeth are
to the sides of the ridges i nstead of parallel to the long shortened enough to prevent soft tissue damage.

77
6 UPPER ALIMENTARY TRACT DISEASES

Disorders of the mouth 2. Blisters, ulceration, or cellulitis may affect the

MA Ball
INTRODUCTION
Disorders of the mouth most frequently result in saliva­
tion and/or failure to prehend, masticate, or swallow
food properly. Acute salivation (ptyalism) may be
caused by the inability to swallow normal saliva or from
excessive production of saliva. To determine the cause
of ptyalism a thorough physical examination and history
are necessary to differentiate between local causes and a
more generalized disease. In adults, the most common
causes of excessive salivation are choke and red clover
poisoning. In foals the commonest cause is esophagitis
secondary to gastroduodenal ulcer syndrome.
PHYSICAL EXAMINATION
Disorders of the mouth and palate may be diagnosed by
oral examination in some cases. The entire oral cavity
should be evaluated looking in particular for
• lacerations
• ulcerations
• vesicular disease
• foreign bodies
• abscesses of tooth roots or soft tissue
• fractured teeth
• injury to the palate
• evidence of chemical injury.
tongue.
3. Burrs or grass awns may be stuck in the mouth and
cause salivation. This may occur as an outbreak or
a farm problem.
4. Patients that have licked mercury blister
compounds are prone to severe oral erosions.
5. Most vesicles are idiopathic, but consider vesicular
stomatitis, which appears most commonly in the
US in New Mexico and Colorado, occurring every
3-7 years.
6. Immune-mediated pemphigus can result in vesicle
formation in the oral cavity but is rare.
7. Actinobacillus lignieresii can cause wooden tongue
in the horse (see Figure 6.2).
8. Sialadenitis, fractured teeth, or fractured bones of
the mouth may cause excessive salivation.
9. Primary pharyngitis or epiglottiditis,
retropharyngeal lymphadenopathy, guttural
pouch empyema, pharyngeal edema, improper
mastication and swallowing, and choke are other
frequent causes of ptyalism.
10. Fracture or inflammation of the hyoid apparatus.

Sedation (e.g. detomidine with butorphanol) and the

careful use of an equine mouth speculum may be
needed to examine the mouth. Without proper seda­
tion, the mouth speculum becomes dangerous both to
the examiner if the patient 'throws' its head, and to the
patient as excessive biting on it may cause a fractured
tooth or even a fractured mandible.

ETIOPATHOGENESIS OF ORAL CAVITY

DISEASE AND PTYALISM

Factors causing oral cavity disease and ptyalism are

listed below.
1. The most common foreign body found in the
mouth of a horse is a wooden stick large enough
to become lodged between the upper arcade of
teeth, or a smaller stick penetrating the soft tissue Figure 6.2 Wooden tongue (Actinobacillus Jignieresii
of the pharyngeal cavity or soft palate. infection)

78
 DISEASES OF THE ORAL CAVITY AND SOFT PALATE 6

DIAGNOSIS

Ancillary diagnostic tests include radiography, ultra­

sonography, and endoscopy of the mouth, guttural
pouch, and/or pharyngeal area. If the temporohyoid
articulation is being evaluated, both lateral and
dorsoventral radiographic views may be required.
Ultrasonography may elucidate an area that can be
aspirated for cytology and culture. The horse should be
observed carefully from a distance to ascertain whether
the ability to prehend, masticate, and swallow is
retained. In some cases, a complete oral examination
under general anesthesia may be necessary before a
cause can be determined.
Figure 6.3 Weight loss and dysphagia due to squamous cell
carcinoma of the oral cavity

TREATMENT

Treatments may include

• removal of foreign bodies
• tooth extraction
• antibiotic therapy for infectious causes
• intravenous fluids to replace and maintain fluids
and electrolytes
• non-steroidal anti-inflammatory drugs (NSAIDs)
• other symptomatic treatment, e.g. 0.2% potassium
permanganate as a mouth disinfectant or
furacin/prednisolone spray for pharyngeal edema
and inflammation.
Penicillin is often the initial choice for an antibiotic
since many commensal oral organisms are sensitive to
it. Some cases may require a tracheotomy if laryngeal!
pharyngeal swelling is compromising the airway.
Regarding equine fluid therapy, it is important to
remember that the anion of highest concentration in
saliva is chloride, with a relatively low concentration of
bicarbonate. When an equine develops an acid-base
disturbance as a result of salivary loss, it is typically
hypochloremic metabolic alkalosis although with pro­
gressive dehydration metabolic acidosis may occur.
Cleft palate
SA Semevolos and NG Ducharme
INTRODUCTION
Congenital cleft palate in horses is an uncommon
deformity affecting approximately 0.05-0.2% of the
equine referral population. Most defects affect the cau­
dal aspect of the soft palate, and more rarely extend to
the hard palate. In addition midline clefts are more
common than lateral defects. This disease leads to nasal
regurgitation of milk and, later on, feed material, pre­
disposing a horse to tracheal aspiration and aspiration
pneumonia. Mfected animals therefore often have
recurrent lower airway infection and stunted growth.
Treatment is achieved through surgical repair, but the
anesthetic episode is complicated by the status of the
lower airway. Success, defined as sufficient closure to
prevent nasal regurgitation and aspiration, is obtained
in 50-70 per cent of animals, but multiple revisions are
often needed. Aquired cleft palates are usually caused
iatrogenically following surgery to the soft palate.

Oral tumors in horses are rare (see Chapter 5).

Odontopathic tumors such as odontomas are most
ANATOMY, EMBRYOLOGY, AND
common in the maxillae of young horses while
PHYSIOLOGY
ameloblastomas primarily affect the mandible of older
horses. The most common soft tissue tumor of the
The hard and soft palate function to
horse's oral cavity is squamous cell carcinoma (Figure
6.3). These tumors can involve any region of the • prevent feed contamination of the nasal cavity and
mouth, occur in older horses, and produce a character­ nasopharynx while eating
istic fetid smell. • maintain an appropriate size and stability to the

79
6 UPPER ALIMENTARY TRACT DISEASES
nasal cavity and nasopharynx so that upper airway
impedance is minimized during exercise.
The hard palate separates the nasal cavity from the oral
cavity. Anatomically, the hard palate is formed by the
fusion of the palatine processes of the incisive and max­
illae bones and the horizontal plates of the palatine
bone. These palatine processes normally fuse during
embryological life in a rostral-to-caudal plane around
day 47 of gestation. These bones are covered by pseudo­
stratified columnar ciliated epithelium on the nasal
aspect and keratinized stratified squamous epithelium
with a lamina propria submucosa continuous with the
fibrous periosteum on the buccal aspect.
The soft palate separates the nasopharynx from the
oropharynx. Anatomically, the soft palate consists of an
oral mucous membrane continuous with the hard
palate, the palatine glands, the palatine aponeurosis,
the palatinus and palatopharyngeus muscles, and a
nasopharyngeal mucous membrane resembling the
nasal mucosa. The caudal free margin of the soft palate
continues dorsally on either side of the larynx to form
the palatopharyngeal arch. The coordinated function
of four muscles determines the soft palate position
• the tensor veli palatini muscle tenses the rostral
aspect of the soft palate during exercise
• the levator veli palatini muscle elevates the soft
palate during swallowing to close the choanae
• the palatinus muscle shortens the soft palate and
depresses it toward the tongue
• the palatopharyngeus muscle also shortens the soft
palate.
The innervation of the soft palate is through the
pharyngeal branch of the vagus nerve, mandibular
branch of the trigeminal nerve, and the glossopharyn­
geal nerve.
ETIOLOGY
There are two forms of cleft palate: congenital and
acquired. Hard palate cleft results from a failure of the
lateral palatine processes of these bones to fuse during
embryonic development. Since palate fusion occurs in a
rostral-to-caudal plane, one can assume that the cleft
extends caudally from the cleft origin where it is identi­
fied in the hard palate. The etiology of soft palate con­
genital cleft is unknown, but the condition is heritable
in other species such as Charolais cattle and Abyssinian
cats. Other factors implicated include exposure to
toxic, nutritional, and metabolic abnormalities in utero.
Acquired cleft palates are a complication of dental
or upper airway surgery. Hard palate clefts, perhaps
80
better defined as oronasal fistulae, result from inadver­
tent fracture of the palate by a tooth punch during
repulsion of upper cheek teeth. Soft palate clefts can
result from using a hook knife through a nasal
approach during axial division of the aryepiglottic
folds. A nasal approach with this instrument is no
longer recommended for that specific reason. Excessive
resection of the caudal free edge of the soft palate for
treatment of dorsal displacement of the soft palate can
also result in a soft palate cleft.
PATHOPHYSIOLOGY
Regarding the digestive function, the hard palate has a
static role while the soft palate dynamically closes the
choanae during swallowing, predominately through the
action of the levator veli palatini. Failure of this strict
separation between airway and digestive tract leads to
contamination of the nasal cavity and tracheal aspira­
tion of feed material. The degree of nasal and airway
contamination is dependent on the size and location of
the cleft. Any cleft rostral to the levator veli palatini
muscle on the soft palate results in nasal or naso­
pharyngeal contamination. Clefts caudal to levator veli
palatini muscles cause less consistent and significant air­
way contamination and therefore result in less or no
lower airway disease.
The respiratory role of the palate is mainly a func­
tion of the soft palate. A cleft soft palate (in addition to
the resulting tracheal contamination) leads to dorsal
displacement of the soft palate during exercise and,
therefore, an increase in expiratory impedance . This
expiratory resistive load appears to be caused by the soft
palate'S inability to form a proper laryngo-palatal seal
around the epiglottis and arytenoid cartilages. During
exhalation, this results in airflow being directed to the
oropharynx, thus lifting the soft palate into the
nasopharynx and partially occluding its lumen, causing
an expiratory obstruction.
SIGNALMENT AND HISTORY
There is no breed or gender predisposition for congen­
ital cleft palate, and the condition is discovered in most
cases in the first few weeks of life because of the obvious
clinical signs. The appearance of milk at the nostrils
(Figure 6.4) and coughing after nursing are distressful
for both the foal and for its carers. Some horses with
more caudal and shorter clefts go unnoticed for many
months and present with a history of recurrent lower air­
way infection, stunted growth, and an occasional obser­
vation of feed material at the nostrils. The authors have
also observed cleft palate in association with wry nose.

Figure 6.4 The most common clinical sign of congenital
cleft palate in the horse is milk or feed material exuding
from both nostrils (note: milk appears at the left nostril)
Acquired cleft palate usually presents with a history
of observation of clinical signs shortly after a surgical
procedure for treatment of upper airway disease or,
more rarely, after treatment of dental disease.
CLINICAL SIGNS
The clinical signs observed with cleft palate vary depend­
ing on the location and length of the cleft and include
• milk, water, or food exuding from both nostrils
• coughing while nursing or eating
• un thriftiness
• stunted growth
• purulent nasal discharge
• fever
• depression
• chronic pneumonia.
It is unclear whether the stunted growth is a result of
loss of caloric intake associated with nasal regurgitation,
ill effects of chronic lower airway disease, or both these
conditions. The severity of the most common complica­
tion of this disease, chronic infection of the lower air­
ways, will significantly influence the survival rate.
INVESTIGATION AND DIAGNOSIS
A presumptive diagnosis of congenital cleft palate can
be made based on clinical signs alone. A definitive
DISEASES OF THE ORAL CAVITY AND SOFT PALATE 6
diagnosis is made by a combination of oral examination
and endoscopic evaluation of the nasal cavity and
nasopharynx. In young foals an oral examination with
digital palpation can assess the integrity of the hard
palate and, with adequate illumination, the most rostral
aspect of the soft palate. Therefore, endoscopic exami­
nation of either the oral or nasal cavity is essential to
diagnose the presence and extent of cleft palate. Given
the risk of damage to the endoscope during an oral
endoscopic examination, and accepting the fact that
most equine veterinarians have a greater familiarity
with examining the nasal cavity and nasopharynx, a
nasal endoscopic examination is recommended. Oral
endoscopic examinations should only be undertaken
under general anesthesia. It is surprising how often a
diagnosis of cleft palate is missed, but reasons for the
difficulty in making this diagnosis are related to the
quality of equipment used, the endoscopic field-of-view
size (i.e. small pediatric endoscope) , and, of course, the
rarity of this condition. It is imperative that an endo­
scope with adequate illumination and a large field of
view be used. Pediatric endoscopes have a small field of
view and are a reason for failing to identify a cleft
palate. Whenever possible, a regular endoscope (8-
10 mm) should be used to examine the nasal cavity and
nasopharynx. The endoscopic diagnosis of cleft palate
is made if a lack of palate continuity is observed, or by
observation of other oral structures that are not
normally visible from the nasopharynx (Figure 6.5).
Figure 6.5 The caudal midline of the soft palate is the most
commonly affected area in horses with congenital cleft
palate (note: the oropharynx mucosa can be seen during
nasal video endoscopy)
81
6 UPPER ALIMENTARY TRACT DISEASES
Congenital hard palate cleft is always on the midline,
while soft palate cleft may be on the midline ( axial) or
to one side (abaxial) . The presence of a cleft will allow
observation of the structures on the floor of the
nasopharynx. The most obvious is the 'white' oro­
pharynx mucosa with its numerous folds and rounded
elevations containing the tonsils and the glossoe­
piglottic fold at the base of the epiglottis (Figure 6.5).
Because saliva often obscures the floor of the orophar­
ynx, one can mistakenly assume the soft palate is intact
if it is covered with mucus or other secretions. These
secretions must be removed to determine if the palate is
intact underneath.
TREATMENT
The treatment of choice for cleft palate is one-stage
surgical correction of the defect, but the high compli­
cation rates ( dehiscence of the repair site, chronic
nasal discharge, and high mortality rates) and frequent
need for revisions have limited the number of horses
receiving surgical treatment. The status of the lower
airway influences the anesthetic risk to the patient.
Delay in repair greatly increases the chance of lower
airway infection and poor growth, but the size of the
oral cavity and nasopharynx in young foals limits the
surgical manipulation that can be performed.
Therefore, the ideal age for repair is unknown. The
authors prefer operating on an animal between 2-4
weeks after birth.
Surgical .pproach Adv.nt.....
Transhyoid Allows surgical access to caudal
pharyngotomy two-thirds of the soft palate.
Animal Is more comfortable
postoperatively.
Mandibular Allows surgical access to the hard
symphysiotomy palate and rostral third of the
soft palate.
82
Surgical approaches
Mandibular symphysiotomy and/or transhyoid pharyng­
otomy are the most widely described surgical
approaches, and their respective values and disadvan­
tages are indicated in Table 6.2. Although neither
approach gives exceptional access for unhindered
manipulations, they allow acceptable access with long
instruments so that primary repair of the cleft palate is
possible. Good exposure can be attained via the trans­
hyoid pharyngotomy for defects affecting the caudal
two-thirds of the soft palate. In fact, the exposure is bet­
ter than that attained by a mandibular symphysiotomy
for this region of the soft palate. However, a transhyoid
pharyngotomy is insufficient when the entire soft palate
or both the hard and soft palates are affected.
For both procedures the animal is anesthetized and
placed in dorsal recumbency with nasotracheal intuba­
tion or intubation via tracheostomy. Whenever possible,
nasotracheal intubation is preferable to prevent com­
plications associated with tracheostomy and to mini­
mize postoperative pain caused by multiple incisions.
Appropriate broad-spectrum antibiotics and non­
steroidal anti-inflammatory drugs are given preopera­
tively.
Mandibular symphysiotomy ( Figure 6.6)
Mter aseptic preparation of the ventral mandibular
area, a ventral midline incision is made from the basi­
hyoid bone extending rostrally to the lower lip. The
skin incision in the ventral mandible area is extended
DI••dv.nt.....
Illumination must come from
. surgeon's headlight or placement of a
flexible oral light.
Possible damage to hyoepiglotticus
muscle leading to exercise intolerance
because of epiglottic retroversion.
Invasive procedure.
More discomfort to animal.
Requires orthopedic instrumentation
for fixation of the mandible.
Higher morbidity associated with
fixation (e.g. pin migration, draining
tracts)
 DISEASES OF THE ORAL CAVITY AND SOFT PALATE 6

through the mylohyoid muscle. The lower lip is not the intended site for screw fixation after the symphys­
incised, but a horizontal incision is placed at its base to iotomy. The symp hysis is separated longitudinally using
allow the lip (Figure 6.7) to be placed orally (Figure an osteotome. A more abaxial dissection is made on
6.8) so the ventral aspect of the symphysis is exterior­ approximately 1.5 cm of the medial wall of one of the
ized. A 3.2 mm drill hole is placed in the symphysis at mandibles. The geniohyoid (Figure 6.9) and genioglos­
sus tendon insertions on the mandible are transected
and tagged. The incision is bluntly extended on the
lateral edge of these muscles toward the oral mucosa
avoiding the sublingual salivary gland and the duct of
the mandibular salivary gland (Figure 6.10 ) . Care must
be taken to avoid damaging the hypoglossal and lingual
nerves at the caudal and medial aspect of the incision.
The oral mucosa is incised to allow separation of the
Basihyoid
mandible and access to the palate.
bone
The incision is closed as follows: the oral mucosa is
sutured from caudal to rostral with an absorbable
monofilament suture (no. 0) in a simple continuous
pattern. The geniohyoid and genioglossus tendons are
reattached using an absorbable suture material (no. 1)
in a simple interrupted or cruciate pattern. The
mandible is fixed with an appropriate length 4.5 mm
screw placed in lag fashion. Alternatively cross pinning
Thyroid Incision can be used instead of screw fixation. The lip is replaced
cartilage site in its proper anatomical position and the oral mucosa
closed as described earlier. The stromal tissue of the lip
Figure 6.6 Mandibular symphysiotomy - note the incision is closed with absorbable suture (no. 0) in a simple
site extends from the basihyoid bone rostrally to the
mandi bular symphysis

Figure 6.7 At the base of the

lower lip a transverse incision
is made in the subcutaneous
tissue and extended to the oral
mucosa

83
6 UPPER ALIMENTARY TRACT DISEASES
interrupted pattern. The mylohyoid muscle and sub­
cutaneous tissues are re-apposed separately with an
absorbable suture (no. 0) in a simple continuous
pattern. The skin is closed in a routine manner.
Transhyoid pharyngotomy
An approximately 8-10 em ventral midline incision is
made extending from the caudal extent of the thyroid
84
Figure 6.8 The lip can be placed
orally to expose the mandibular
symphysis so the lip is spared a
vertical incision
Figure 6.9 After the symphys­
iotomy has been performed.
the tendon of insertion of the
geniohyoid muscle is transected
in its mid-body
cartilage to the rostral extent of the basihyoid bone.
The incision is extended by bluntly separating the
sternohyoid muscle on the midline. The basihyoid bone
is separated longitudinally using an osteotome. The
incision is extended deeper by blunt dissection of the
loose fascia between the pharynx and basihyoid bone. It
is crucial that the fascia encircling the hyoepiglotticus
muscle be identified and retracted laterally so it does
not damage this muscle or its innervation. The pharyn-

Incision line Palatine artery
/
) periosteum and mucosa using monofilament absorb­
Cleft Ridge in hard
palate
Figure 6.10 A mucosa-periosteaI-sliding flap is made by
incising the mucosa and periosteum lateral to the defect
and sliding the flaps axially (note: position of the palatine
artery in order to avoid it)
geal mucosa is tented and incised with curved scissors
on the midline. Four stay sutures are placed at each cor­
ner of the pharyngeal mucosal incision and retracted
out of the incision. A Gelpi retractor is placed in the
pharyngeal mucosa to obtain exposure to the soft
palate. Additionally, an army-navy retractor or a 2.5 cm
malleable retractor is needed to retract the base of the
tongue rostrally.
Closure is obtained by re-apposing the oral mucosa
using an absorbable monofilament suture (no. 0) in a
simple continuous pattern. The basihyoid suture is re­
apposed with a wire suture, and the soft tissues over the
basihyoid bone are re-apposed using a few absorbable
sutures (no. 0) in a simple interrupted pattern. The
sternohyoid muscle is partially re-apposed using three
or four absorbable sutures (no. 0) in a simple inter­
rupted pattern, leaving the rest of the incision to heal
by second intention.
Cleft palate repair
The use of long instruments and an intra-oral light
source greatly improve the visibility and accessibility of
the palate and are a necessary part of cleft palate repair.
Hard palate repair
A mucosa-periosteal sliding flap is used to close the
hard palate. Using a no. 1 2 curved Parker-Kerr blade,
the nasal and oral mucosa at the axial edge of the cleft
are incised to the hard palate, thus separating the nasal
mucosa-periosteal flap from the oral mucosa­
periosteal flap. An incision parallel to the long axis of
DISEASES OF THE ORAL CAVITY AND SOFT PALATE 6
the cleft is performed through the mucosa and perios­
teum of the hard palate as abaxial as possible but still
axial to the palatine artery (Figure 6.10). Using a curved
blunt periosteal elevator, a mucosa-periosteal flap is
freed from the underlying hard palate on both sides of
the cleft. The flaps are slid axially toward each other
and sutured together in one layer through both the
able suture (no. 0 or no. 1 ) . The defect at the donor site
is left to heal by second intention.
Soft palate repair
Transection of the insertion of the tensor veli palatini
tendon or fracture of the hamulus of the pterygoid
bone are no longer recommended. These procedures
were originally performed to reduce tension on the ros­
tral aspect of the soft palate. However, they result in
instability of the rostral aspect of the soft palate during
exercise and increase upper airway impedance.
Therefore, these procedures should not be performed
in horses intended for athletic performance.
If adequate soft palate tissue is available for repair with
minimal tension on the incision site, the standard
method for closure of the soft palate in horses involves
a three-layer closure of the defect using a combination
of vertical and horizontal mattress patterns. Using a
long-handled curved Metzenbaum scissor, a 2 mm sec­
tion of palate is removed at the periphery of the cleft
palate. The nasal and oral mucosa are separated using a
no. 12 curved Parker-Kerr blade, exposing (when pre­
sent) the palatinus muscle (Figure 6.11a). The nasal
mucosa is then apposed using a monofilament
absorbable suture material (no. 00) in a simple contin­
uous pattern (Figure 6.11 b ) . Interrupted vertical mat­
tress sutures penetrating the oral mucosa and stromal
tissue (palatinus muscle, levator veli palatini muscle, or
aponeurosis of tensor veli palatini) are then placed
1.25 cm lateral to the cleft using monofilament
absorbable suture material (no. 0) creating the strength
layer of the closure (Figure 6.11c). Finally, the everted
oral mucosal layer is apposed using a monofilament
absorbable suture material (no. 00) in a simple contin­
uous pattern (Figure 6.11d) . Another technique, the
double opposing Z-plasty, first developed in humans to
improve speech and allow adequate maxillary growth
following surgery, has been used by the authors with
some success in horses but appears to have no advan­
tage over the standard method.
If significant soft palate tissue is missing and palate
repair without tension is impossible, then buccal
mucosal flaps are used (Figure 6.12) . This technique
can only be done via a mandibular symphysiotomy. The
object of this technique is to create two buccal mucosal
85
6 UPPER ALIMENTARY TRACT DISEASES

a) b) Cleft palate

Nasal mucosa - =.=,.:".

.- . ---,--".,--'T-rr-ri7'''(...
Stromal tissue

c)

Soft palate

Hard palate

Figure 6.11 Closure of the soft palate. a) The nasal and oral mucosa are separated using a no. 1 2 curved Parker-Kerr blade.
b) The nasal mucosa is apposed using a monofilament absorbable suture material (no. 00) in a simple continuous pattern.
c) Interrupted vertical mattress sutures penetrating the oral mucosa and stromal tissue are placed 1 .25 cm lateral to the
cleft creating the strength layer of the closure. d) The everted oral mucosal layer is apposed using a monofilament
absorbable suture material (no. 00) in a simple continuous pattern

flaps with their base on the palatoglossal arch. Starting
at the palatoglossal arch, an incision is made sharply
extending rostrally. The incision length must match the
width of the soft palate defect. The width of the flap
must match the length of the soft palate (Figure 6 . 1 2a) .
Using submucosal dissection and appropriate hemo­
stasis, the flap is dissected free up to the palatoglossal
arch. Care is taken to avoid the deep fascial vein. The
mucosal flap is rotated so its mucosal side is facing the
nasopharynx and sutured to the nasal mucosa free edge
of the cleft palate. The same procedure is repeated on
the contralateral side. The second flap is placed over
the sutured flap so its mucosa is facing the oropharynx.
The edge of this second flap is sutured to the oral
mucosa of the free edge of the cleft palate. The donor
sites are left to heal by second intention.
Postoperative care
Postoperatively, the animal is treated with appropriate
antibiotics, with the duration depending on the
presence and severity of lower respiratory infection.
Appropriate analgesics are needed if a symphysiotomy
has been performed. A non-steroidal anti-inflammatory
drug should be used for 5-7 days to minimize swelling
and, therefore, increase the likelihood of healing.
Because of the pre-existing airway infection, monitor­
ing the patient after surgery is critical.
It is not known what the best postoperative feeding
technique is to allow the palate to heal. Ideally, par­
enteral nutrition for 7-10 days would give the greatest
protection to the surgery site. However, this treatment
is expensive and alternative feeding regimes can be
used with acceptable results. The authors recommend
feeding young foals through a nasogastric tube and
feeding a soft gruel to adult horses.
PROGNOSIS
The overall morbidity rate for complications after cleft
palate repair approaches 1 00 per cent. However, the
rate of successful healing of a repaired cleft palate may
be as high as 70 per cent after one or more surgeries. It
is not uncommon for one or two revisions to be needed
to obtain sufficient healing to resolve clinical signs.
Short-term morbidity is higher for the mandibular
symphysiotomy approach than the transhyoid pharyn­
gotomy, probably because of the technique required to
repair the symphysiotomy as well as its associated soft
tissue trauma. Reported complications associated with
mandibular symphysiotomy include dehiscence of the

86

a)
Figure 6.12 Schematic of how buccal mucosal flaps are used. a) Starting at the palatoglossal arch, an incision is made
sharply extending rostrally. The incision length must match the width of the soft palate defect. The width of the flap must
match the length of the soft palate. b) The mucosal flap is rotated so that its mucosal side is facing the nasopharynx and
sutured to the nasal mucosa free edge of the cleft palate. The procedure is repeated on the other side.
lip, osteomyelitis of the mandibular pin tracts, and sub­
mandibular abscesses. In addition, tongue paralysis can
result from damage to the hypoglossal or lingual nerves
during surgery.
One potential long-term complication following
transhyoid pharyngotomy is epiglottic retroversion at
exercise, because this approach has the potential to
cause trauma to the hyoepiglotticus muscle and/or its
innervation. Previous studies have identified pharyn­
geal surgery and intermandibular abscesses as predis­
posing factors for developing epiglottic retroversion.
Local anesthesia of the glossopharyngeal and hypoglos­
sal nerves has also reproduced epiglottic retroversion.
There are no reports concerning respiratory func­
tion of the soft palate during exercise following cleft
palate repair. Dorsal displacement of the soft palate was
not found in one cleft palate repair case where the
authors were able to perform video endoscopic exami­
nation 1 year after surgery, in this case the nasopharynx
appeared stable.
PREVENTION
Because the etiology is not well understood prevention
may be difficult. However, because of heritability con­
cerns, it is recommended that owners should neither re-
DISEASES OF THE ORAL CAVITY AND SOFT PALATE 6
b)
breed the same dam and sire who have produced off­
spring with congenital cleft palate, nor breed from
horses affected with congenital cleft palate.
BIBLIOGRAPHY
Signs of dental disease
Baker G] ( 1 99 1 ) Disease of the teeth. In Equine Medicine and
Surgery 4th edn, vol 2, P T Colahan,] G Mayhew, A M
Merritt,] N Moore (eds) . American Veterinary
Publications, Santa Barbara CA, pp. 550-70.
Baker G] ( 1 970) Some aspects of equine dental disease.
Equine Vet. ] 2 : 105-10.
Baker G] ( 1 971 ) Some aspects of equine dental radiology.
Equine Vet. ] 3:46-5 1 .
Baker G ] ( 1 974) Some aspects o f equine dental decay. Equine
Vet.] 3 : 1 27-30.
Baker G] ( 1 985) Oral disease of the horse. In Veterinary
Dentistry, C E Harvey (ed. ) . W B Saunders, Philadelphia,
pp. 203-35 .
Baker G] ( 1 99 1 ) Dental morphology, function and
pathology. In Proceedings o/the 3 7th Annual Convention o/the
American Association 0/Equine Practitioners, San Francisco,
.
pp. 83-93.
Dixon P M ( 1 997) Dental extraction and endodontic
techniques in horses. Comp. Cont. Educ. Pract. Vet.
19:628-38.
Dixon P M ( 1 997) Dental extraction in the horse: indications
and preoperative evaluation. Comp. Cont. Educ. Pract. Vet.
19:366-75.
87
6 UPPER ALIMENTARY TRACT DISEASES
Easley K] ( 1 996) Equine Dental Development and Anatomy.
In ProceedinKs oJ the 42nd Annual Convention oJ the American
Association oj Equine Practitioners, Denver CO. pp. 1 - 1 0.
Easley K] ( 1 99 1 ) Recognition and Management of the
Diseased Equine Tooth . In Proceedings oJ the 37th Annual
Convention oj the American Association ojEquine Practitioners,
San Francisco CA. pp. 1 29-139.
Easley] E ( 1 996) Dentistry and Oral Disease. In Smith, B.P.
(ed.) Large Animal Internal Medicine. Mosby, St Louis,
pp. 688-97.
Gaughan E M and Debowles R M (eds) ( 1 998) Vet. Clin. N.
Am. Equine Pract. Dentistry. W B Saunders, Philadelphia,
August, 1 4 ( 2 ) .
Gaughan E M and Debowles R M ( 1 993) Congenital diseases
of the equine head. In Vet. Clin. N. Am. Equine Pract. The
Equine Head. W B Saunders, Philadelphia, April,
9 ( 1 ) :93- 1 10 .
Gift LJ, DeBowles R M, Clem M F, Rashmir-Raven A, Nyrop
K A ( 1 992) Brachygnathia in horses: 20 cases ( 1 9 79-1989)
.f. Am. Vet. Med. Assoc. 200 ( 5 ) : 7 1 5-71 9 .
Hance R S and Bertone A L ( 1 993) Neoplasia. In Vet. Clin. N.
Am. Equine Pract. The Equine Head. W B Saunders,
Philadephia, April, 9 ( 1 ) :2 1 3-34.
Hawkins] F, Dallap D L ( 1 997) Lateral buccostomy for
removal of a supernumerary tooth . .f. Am. Vet. Med. Assoc.
2 1 1 ( 3 ) :339-340
Kilic S, Dixon P M, Kempson S A ( 1 997) A light microscopic
and ultrastructural examination of calcified dental
structure of horses. The occlusal surface and enamel
thickness. Equine Vet. .f., 29(3) : 1 90-197
Kilic S, Dixon P M, Kempson S A ( 1997) Ultrastructural
enamel findings. Equine Vet. ]. , 29 (3) : 1 98-205
Kilic S, Dixon P M, Kempson S A ( 1 997) Dentine. Equine Vet.
.f., 29 (3) :206-2 1 2
Kilic S , Dixon P M , Kempson S A ( 1 997) Cement and the
amelocemental junction. Equine Vet. .f. , 29(3) : 2 1 3-21 9 .
Lane ] G ( 1 994) A review o f dental disorders o f the horse,
their treatment and possible fresh approaches to
management. Equine Vet. Educ. , 6 ( 1 ) : 1 3-21 .
Mueller P O E ( 199 1 ) Equine dental disorders: cause,
diagnosis, and treatment. Compo Cant. Educ. Pract. Vet. 1 3,
pp. 14 5 1-1 460.
Rucker B A ( 1 996) Incisor procedures for field use. In
Proceedings oJ the 42nd Annual Convention oJ the American
Association oj Equine Practitioners, Denver CO, pp. 22-5.
Scrutchfield W L and Schumacher] ( 1 993) Examination of
the oral cavity and routine dental care. In Vet. Clin. N. Am.
iI'quine Pract. The Equine Head. W B Saunders, Philadelphia,
April, 9 ( 1 ) : 1 2 3-32.
88
Scrutchfield W L, Schumacher], Martin M T ( 1 996)
Correction of abnormalities of the cheek teeth. In
Proceedings oJthe 42nd Annual Convention oJthe American
Association ojEquine Practitioners, Denver CO, pp. 1 1-2 1 .
Uhlinger C ( 19 9 1 ) Common abnormalities of premolar and
molars I n Proceedings oJ the 3 7th Annual Convention oJ the
American Association ojEquine Practitioners, San Francisco,
pp. 1 23-7 .
Cleft palate
Bowman K F, Tate L P , Evans L G, et al. ( 1 982) Complications
of cleft palate repair in large animals. ]. Am. Vet. Med.
Assoc. 1 80:652-7.
Bowman K F, Tate ]r L P, Robertson ] T ( 1 990) Cleft
palate. In Current Practice oj Equine Surgery, N A White
and ] N Moore (eds) . ] B Lippincott, Philadelphia,
pp. 277-80 .
Furlow L T ( 1 986) Cleft palate repair by double opposing Z­
plasty. Plastic &constr. Surg. 78:724-33.
Gaughan E M, DeBowes R M ( 1 993) Congenital diseases of
the equine head. Vet. Clin. N. Am. Equine Pract. 9:93-1 1 0.
Grossman B S, Brinkman ] F, Grant B: A new approach for
intra-oral surgery in the horse: a lip-sparing
modification of mandibular symphysiotomy.]. Equine
Vet. Sci. 1 : 1 07-9.
Holcombe S], Derksen F], Stick] A, Robinson N E ( 1 997)
Effects of bilateral hypoglossal and glossopharyngeal nerve
blocks on epiglottic and soft palate position in exercising
horses. Am. .f. Vet. &s. 58(9) : 1 022-1026.
Holcombe S], Derksen F], Stick] A, Robinson N E ( 1 997)
Effect of bilateral tenectomy of the tensor veli palatini
muscle on soft palate function in horses. AJVR 58
( 3 ) : 3 1 7-32 1 .
Mason T A, Speirs V C, Maclean A A, Smyth G B ( 1 997)
Surgical repair of cleft soft palate in the horse. Vet. Rec.
100:6--8.
Nelson A W, Curley B M, Kainer R A ( 1 97 1 ) Mandibular
symphysiotomy to provide adequate exposure for intraoral
surgery in the horse . .f. Am. Vet. Med. Assoc. 1 59 : 1 025-3 1 .
Sager M , Nefen S ( 1 998) Use of buccal mucosal flaps for the
correction of congenital soft palate in three dogs. Vet.
Surg. 27:358-63.
Semevolos S A, Ducharme N G ( 1 998) Surgical repair of
congenital cleft palate in horses: 8 cases ( 1 979- 1 997) .
Proceedings of the 44th annual conference of the
American Association of Equine Practitioners, Baltimore,
pp. 267-8.
 7
Esophageal diseases

SL Fubini

ANATOMY AND PHYSIOLOGY
The cranial cervical esophagus is on the median plane
just above the trachea. At the level of the proximal one­
third of the neck, the esophagus passes to the left, rarely
to the right, of the trachea and becomes more super­
ficial. Dorsolaterally the esophagus is in proximity to
the common carotid artery, vagosympathetic trunk and
recurrent laryngeal nerves. At the mid-cervical region,
the esophagus inclines steeply to the thoracic inlet.
From there, it passes to the right of the aortic arch and
enters the diaphragm to the left of the midline. In the
abdominal cavity, the esophagus enters the cardia of
the stomach at the level of the 14th rib.
The cranial two-thirds of the esophagus consists of
two helical layers of striated muscle. The distal third is
composed of smooth muscle. The esophageal mucosa is
made up of moderately keratinized stratified squamous
epithelium arranged in longitudinal folds. The esopha­
gus is unique to other hollow viscera of the gastro­
intestinal tract in that only the abdominal portion of
the esophagus has a serosal covering. The remainder is
covered by the tunic adventitia which is rich in blood
supply, nerves, and elastic fibers. The blood supply of
the cervical esophagus originates from the carotid arter­
ies and the thoracic part is supplied by the esophageal
artery and a branch of the gastric artery. A combination
of the central nervous system, intrinsic and extrinsic
nerves, and myogenic factors act to integrate
esophageal peristalsis and lower esophageal sphincter
relaxation. Horses are prone to gastric rupture, and it is
unknown exactly why this is so. One theory has been
that there is a powerful caudal esophageal sphincter
that prevents vomiting in response to intragastric pres­
sure. However, this has not been shown to be the case
experimentally. It is more likely that the vomiting reflex
is poorly developed in horses.
ESOPHAGEAL DISORDERS
Clinical signs
Obstruction of the esophagus (,choke') in the horse is
typically manifested by feed and water appearing at the
nostrils and mouth, and is associated with salivation,
dysphagia, and flapping of the lower lip. Early in the
condition, when feed is offered affected horses will
show interest but do not eat. Coughing may occur, and
affected horses appear anxious and may show some
retching as they attempt to swallow. As time progresses,
affected animals will become dehydrated and inappe­
tent.
Diagnosis
Physical examination
The horse's hydration status is evaluated by assessing
skin turgidity, mucous membrane color, and capillary
refill time. The neck and laryngeal area should be
palpated for any subcutaneous emphysema or mass
lesions. A detailed oral examination should be per­
formed to look for abrasions and to rule out cleft palate,
dental disease, or other foreign bodies in the mouth.
The lower ailWay should be examined by auscultation
with a rebreathing bag to detect any evidence of adven­
titious lung sounds compatible with aspiration pneu­
monia. Thoracic radiographs should be taken if there is
any suspicion of lower ailWay pathology. Nasogastric
intubation is essential in most instances to determine

89
7 UPPER ALIMENTARY TRACT DISEASES

the location of the esophageal obstruction. Minimal

laboratory tests include packed cell volume (PCV), total
plasma protein (TPP), and plasma electrolyte concen­
trations to determine the horse's metabolic and hydra­
tion status. It should always be remembered that rabies
and other causes of dysphagia must be on a differential
diagnosis list when dealing with a suspected esophageal
obstruction (see Chapter 5).

Esophagoscopy

When examining the esophagus by esophagoscopy, it is

ideal to have the animal sedated and if possible pass the
endoscope distal to the area of interest and examine
the site as the endoscope is moved in an oral direction.
The esophagus is continuously insufflated with air to
dilate it and allow better observation of lesions. The
normal esophagus has off-white colored longitudinal
mucosal folds. To view the entire esophagus, a 3 m
endoscope is necessary in an adult horse, and if an area
of suspicion is seen, it should be examined repeatedly
to rule out an artifact. If the esophageal lumen is
obstructed, esophagoscopy may be useful to help
evaluate the nature of the obstruction.

Radiographic examination

Most esophageal obstructions occur in the cervical area.

Diagnostic radiographs of this area can be obtained
with portable radiographic equipment. Examination of
lesions in the thoracic esophagus requires high power
equipment with a good ability to penetrate (increased
kVp and rnA capacity.) Plain or survey radiographs
demonstrate lesions such as radio-opaque foreign Figure 7.1 Survey radiograph showing an esophageal
bodies or peri-esophageal gas (Figure 7.1). For a com­ obstruction due to a feed impaction
plete esophageal study, positive contrast esophagogra­
phy is necessary. A radiograph taken after
administration of barium paste (e.g. Novopo-que,
entire area of interest should be fully distended when
Alcon Laboratories, Lafayette, IN) will allow evaluation
contrast radiography is performed.
of mucosal folds. An aqueous-based contrast agent (e.g.
Gastrografin, ER Squibb and Sons, Inc., Princeton, r-.u)
should be used if there is suspected esophageal perfo­
GENERAL SURGICAL CONSIDERATIONS
ration. An esophagogram is especially useful when
esophageal strictures and fistulae are suspected. The
Restraint and anesthesia
study is performed by administering positive-contrast
material under pressure through a cuffed nasogastric Some esophageal procedures can be performed in the
tube. Double-contrast radiography, simultaneous standing sedated animal. These include esophagotomy
administration of air, and a positive contrast agent, of the cervical esophagus or exposure of the esophagus
allows examination of the mucosa in a distended esoph­ and manipulation. If extensive surgical procedures are
agus. This technique is useful to evaluate the extent of necessary general anesthesia is recommended. For
mucosal injury following foreign body obstruction. surgical procedures involving the thoracic esophagus,
Esophageal radiography is a useful technique but general anesthesia and positive pressure ventilation is
artifacts are common. To avoid the appearance of arti­ required.
facts during swallowing, xylazine should be adminis­ When operating on the esophagus it is imperative to
tered 5 minutes before the radiographs are taken. The use gentle tissue handling, strict aseptic technique, and

90

the prevention of any undue tension on the sutures.
Perioperative antibiotic therapy is appropriate as are
non-steroidal anti-inflammatory drugs. It is absolutely
essential that a nasogastric tube be placed before induc­
tion of anesthesia because passage is very difficult once
a horse is anesthetized. The tube should extend past the
level of obstruction.
Surgical approaches
Cranial cervical esophagus
The cranial one-third of the cervical esophagus can be
approached from either side of the neck. The skin inci­
sion is made dorsal to the jugular vein. The cutaneous
coli muscle is reflected caudally, the sternocephalicus
muscle and jugular vein are retracted ventrally, and
the brachiocephalicus muscle is retracted dorsally. The
incision is then extended through the omohyoideus
muscle.
Mid-cervical esophagus
In the middle one-third of the cervical esophagus, the
ventral midline approach is preferred. The sternothyro­
hyoideus muscles are separated, and the trachea is
retracted to the right of midline.
Caudal cervical esophagus
In the caudal cervical region, the esophagus is located
dorsal to the trachea. A ventrolateral approach is used.
A skin incision is made ventral to the left jugular vein.
The sternocephalicus and brachiocephalicus muscles
are retracted, and the deep cervical fascia is incised to
expose the esophagus. The vagosympathetic trunk and
recurrent laryngeal nerve must be avoided. Retractors
should be adequately padded.
Thoracic esophagus
For lesions in the thoracic esophagus, a rib resection is
generally performed from the left side. A skin incision is
made directly over the rib. Subcutaneous tissues, cuta­
neous trunci, latissimus dorsi, and external abdominal
oblique muscles are incised. Subperiosteal dissection is
continued to isolate the rib. The rib is transected
dorsally with Gigli wire or a saw and disarticulated at
the costochondral junction. The pleura is incised and a
thoracic retractor is placed to spread the adjacent ribs.
The carotid sheath and vagosympathetic trunks should
be identified and retracted.
Esophageal layers
When the esophagus is incised it separates easily into
two distinct layers. The first layer is the outer, relatively
ESOPHAGEAL DISEASES 7
inelastic muscle layer and adventitia. The elastic inner
layer composed of mucosa and submucosa contains the
greatest amount of fascia and greatest tensile strength
during esophageal closure. Traditionally, when operat­
ing on the esophagus these two distinct layers are closed
separately. When mucosa and submucosa are being
closed together it has been recommended that the
knots be tied within the esophageal lumen to prevent
contamination of the wound with ingesta migrating
along the suture tract. The muscle and adventitia are
then closed separately. A wide variety of suture patterns
are appropriate. Typically, a non-absorbable, non­
reactive monofilament suture such as polypropylene or
nylon is recommended, or a long-lasting absorbable
monofilament such as polyglyconate. There has been
debate in the last few years whether the mucosa or the
submucosa are the true functional holding layers of the
esophagus. In 1988 Dallman reported that the submu­
cosa had the greatest strength, and that including the
mucosa in the closure did not enhance the repair.
Some advocate a one-layer closure of the esophagus
with an absorbable monofilament suture using the sul:r
mucosa as the strength layer and not penetrating the
mucosa.
Incisional closure
In the cervical area the incision is closed by re-apposing
each layer incised with absorbable suture material,
given the potential contamination of the surgery site.
Drains are generally placed to
• minimize dead space
• allow evacuation of contaminated fluids.
The lack of a serosal covering may contribute to com­
plications following surgery, including leakage and
dehiscence.
Closure of the left hemithorax following a thoraco­
tomy for exposure of the thoracic esophagus is carried
out as follows
• using long acting local anesthesia the intercostal
nerves of the resected rib as well as the two adjacent
ribs cranial and caudal are desensitized
• a 28th French chest drain is then placed in the
chest at the 8th intercostal space and secured to the
skin with a non-absorbable suture
• the intercostal muscles are closed in a simple
continuous pattern using no. 3 polyglactin 910
suture material
• at this time continuous low pressure suction is
applied to the chest drain to reduce the
pneumothorax
• the latissimus dorsi is then closed in a simple
continuous pattern using the same material
91
7 UPPER ALIMENTARY TRACT DISEASES

• the subcutaneous tissue and cutaneous trunci are

closed together with no. 1 polyglactin 910 suture
material
• the skin is closed with staples and an impervious
impregnated drape is applied over the incision and
drain site
• the drain is closed with a syringe case glued into
place
• on recovery a Heimlich valve is applied to the drain.

SPECIFIC DISORDERS

Esophageal obstruction

A lumen obstruction is very common following inges­

tion of feed or foreign material. Foreign bodies such as
carrots, apples, and wood chips may obstruct the esoph­
agus, as well as feed impactions. Impactions can be
secondary to a narrowing of the esophagus from some
other pathology. Feed impaction has been associated
with greed and poor dentition, and is known to be com­
mon in Shetland ponies. The most common sites of
obstruction have been reported to be the cranial cervi­
cal esophagus, the esophagus at the thoracic inlet, and
the caudal esophagus sphincter in the hiatal area.
However, in this author's experience, obstructions are
also common in the cranial and mid-cervical region.
Rarely, extralumenal compression of the esophagus can
occur secondary to neck trauma and subsequent fibro­ Figure 7.2 Lavage of an esophageal obstruction using a
sis, mediastinal abscessation and neoplasia, or vascular stomach tube placed through a larger cuffed tube in an
anomalies. effort to prevent aspiration of feed material

Treatment

Medical management
Because of the risk of aspiration pneumonia, a horse
with suspected esophageal obstruction should be kept
in a stall and not allowed to eat or drink until treatment
is initiated. All bedding should be taken away or a
muzzle applied to prevent any oral intake. Spontaneous
resolution of esophageal obstruction may happen with
sedation only. If resolution is not apparent in several
hours, the horse should be sedated and a nasogastric
tube should be passed to the level of the obstruction.
Esophagoscopy can be performed as well, although
sometimes it is difficult to be precise about a diagnosis
if the proximal esophagus is distended with gas and
fluid.
If spontaneous resolution does not occur, tissue han­
dling and manipulation should be gentle to help pre­
vent any further damage to the esophagus. The horse's
head is lowered with the use of sedation, and repeated
lavage at the site of the obstruction is performed
(Figure 7.2). Some clinicians like to pass a large diame­
ter malleable endotracheal tube through the nose into
the esophagus, and then pass a small lavage tube
through the lumen of the endotracheal tube. This tech­
nique allows the lavage fluid and food to drain through
the larger diameter tube, thereby minimizing the risk of
aspiration. Patience is required as it may take several
attempts to -dislodge the impaction with lavage. If
repeated attempts are unsuccessful to dislodge the
impaction or foreign body, the horse can be anaes­
thetized and these procedures repeated with the horse
relaxed under general anesthesia and with a endo­
tracheal tube with inflated cuff in place.
Surgical therapy (esophagotomy)
If it is impossible to relieve an obstruction with medical
management, an esophagotomy is indicated. Ideally,
the incision is made in a healthy area of esophagus adja­
cent to the foreign body. If the esophageal wall appears

92

to be without compromise, a primary closure can be
attempted which should allow for rapid healing.
Following surgery, food and water are withheld initially
for 48 hours, and the horse is kept hydrated with
intravenous fluid therapy. Following this time, small
amounts of feed are introduced, usually in the form of
a pelleted slurry. In 1982, Stick recommended a pel­
leted diet (7 g/kg in 5 liters of water t.d.s.). Studies have
shown that hay may predispose wound dehiscence.
Different recipes exist for feeding horses via stomach
tube, and these are noted in the reference list (Orsini
and Divers, 1 998). If the esophageal wall is not normal
and the surgeon elects to leave the wound open to heal
by secondary intention, placement of an esophageal
feeding tube until the wound contracts is advocated. If
an esophagostomy tube is elected, the current recom­
mendation is to position the caudal end of the tube in
the stomach. If left to heal by secondary intention, a
traction diverticulum is likely to result, however usually
these are asymptomatic.
Once the obstruction is relieved, the integrity of the
mucosa of the esophagus should be checked via
esophagoscopy. Circumferential mucosal defects are
prone to stricture.
Esophageal rupture
Esophageal rupture can be a catastrophic lesion.
Ruptures of the cranial esophageal sphincter can be
very difficult to visualize with esophagoscopy. The most
likely cause for such a perforation is repeated naso­
gastric intubation. The more distal esophageal ruptures
are easier to see using esophagoscopy. Diagnosis can be
aided by radiography and ultrasound examination.
Horses with closed cervical esophageal perforation
quickly develop subcutaneous emphysema and cellulitis
around the area. Unfortunately the cellulitis can extend
down fascial planes toward the mediastinum and
thoracic cavity. The horse may be so dyspneic that a
tracheotomy is required.
Treatment
Most esophageal perforations will have to heal by sec­
ondary intention. Adequate ventral drainage is essential
to prevent migration of the infection to the thoracic
inlet, and the wound is allowed to heal by contraction
and epithelialization. The horse can be fed by placing
an esophagotomy tube through the rupture site and
allowing tissues to contract down around the tube.
Alternatively it can be fed through a tube placed distally
to the esophageal perforation in a normal area of the
esophagus. Typically, although these horses have a
long-drawn-out hospital course, they do well with
aggressive wound care. However, some horses take a
ESOPHAGEAL DISEASES 7
long time to granulate the wound and allow migration
of esophageal mucosa over the granulating bed.
Intermittent fluid therapy may be necessary.
Mucosal disease
Mucosal disease is most commonly caused by ulceration
secondary to an obstruction. For this reason all horses
that have had resolution of an obstruction should be
checked with esophagoscopy. If a mucosal defect is pre­
sent, current recommendations are to feed a pelleted
ration, and administer broad-spectrum antibiotic and
anti-inflammatory drugs. Surgical management should
be delayed for 60 days until the lumen of the stricture
site is of maximal diameter and mucosal healing is com­
plete. It is possible that in the future 'bougienage' or
inflation of a cuffed tube or balloon at the site of a stric­
ture might be feasible. However at this point, there are
no published reports of using these techniques in
horses, although there are anecdotal reports of success
expressed on a popular equine server (ECN - equine­
clinicians' network).
Esophageal stricture
Esophageal strictures can be congenital or acquired.
Acquired strictures can result from either external
trauma such as a kick or from internal trauma, i.e.
foreign body or feed impaction. Strictures can also
result following mucosal disease or esophageal surgery.
Prognosis varies with the nature of the stricture. There
are three types of annular lesions which are categorized
depending on which layers of the esophagus are
involved
1. mural lesions that involve only the adventitia and
muscularis
2. esophageal rings or webs that involve only the
mucosa or submucosa
3. annular stenosis that involves all layers of the
esophageal wall.
Treatment
Clinical and experimental studies indicate that stricture
formation can occur as soon as 15 days after circumfer­
ential mucosal loss, but there is little change in lumen
diameter for the next 15 days. Between 30-60 days post­
injury, the lumen diameter increases with the largest
change occurring between days 30-45. Therefore, as
mentioned earlier, surgical incision of a stricture
should be delayed until 60 days after the traumatic
incident. Pelleted mash has been found to be the most
palatable feed. Other alternatives include intravenous
total parenteral, or partial parenteral nutrition, or
extra-oral alimentation using an esophagostomy tube.
93
7 UPPER ALIMENTARY TRACT DISEASES

Surgical management

The surgical management of an esophageal stricture

will depend on the layer of the esophagus that is
involved, although this may not be known prior to the
start of surgery. Surgery should be performed under
general anesthesia, and once again a stomach tube
should be passed to the level of the obstruction prior to
induction of the anesthesia.

Esophagomyotomy
An esophagomyotomy is indicated for an esophageal
stricture confined to the muscularis and adventitia. The
esophagus is exposed and gently freed from surround­
ing tissue. Once the esophagus is isolated a longitudinal
incision is made through the adventitia and muscle
allowing mucosa and submucosa to bulge through the
incision. The stomach tube is gently advanced to deter­
mine if the lumen will allow passage easily across the
strictured site. The muscle should be separated from
the mucosa around the entire circumference of the
esophagus. In most instances, the myotomy is left open
and the rest of the surgical incision is drained and
sutured in a routine manner.
Partial esophageal resection
This procedure is most appropriate for lesions confined
to the mucosa and submucosa. Once again the esopha­
gus is approached and freed from surrounding tissues.
The muscularis and adventitia are incised in a longitu­
dinal manner, and the strictured area of mucosa and
submucosa dissected free and resected (Figure 7.3).
The mucosa is closed only if possible to do so without
excessive tension. It is ideal to close the muscularis
because it serves as a muscular tube upon which the
mucosal defect can regenerate. It may be necessary to
feed the horse through a separate esophagotomy site or
via extra-oral alimentation.
Complete esophageal resection
A resection and anastomosis of all layers of the esopha­
gus is an option if all layers are involved or the muscu­
lature is damaged and is not useful as a scaffold for
mucosal regeneration. Minimizing tension and good
apposition of tissue layers are necessary. It is suggested
that prior to surgery the horse is trained to tolerate an
elastic martingale that prevents elevation of the head.
The esophagus is approached and isolated. Rubber
tubing rather than clamps may be less traumatic when
manipulating the esophagus. Transection is performed
in healthy tissue cranial and caudal to the lesion, and a
two-layer anastomosis is performed. Past recommenda­
tions are to close the mucosa and submucosa in simple
continuous or interrupted pattern followed by closure
Figure 7.3 Esophagomyotomy and resection of a
mucosal stricture via a ventral incision
of the muscular layer in a simple interrupted pattern
(see General surgical considerations). If necessary, ten­
sion relieving incisions adjacent to the anastomosis can
be performed. Extra-oral alimentation or feeding by
esophagostomy after surgery may be advantageous.
Esophagoplasty
Esophagoplasty is a longitudinal incision in the esopha­
gus closed in a transverse manner. This has had limited
applicability in the horse and is only recommended for
lesions less than 2 cm in length.
Esophageal replacement
In small animals and humans, other tissues have been
used to create a feeding tube to replace a diseased
esophagus. These include jejunum, colon, stomach,
and skin. These pedicle grafts have limited applicability
in the horse.
Muscular patch grafting
There is one successful report in the literature using a
muscular patch graft of the sternocephalicus tendon. In
this case, the esophagus was exposed and the lesion was
identified and resected. Both sides of the mucosal
defect were apposed to the muscle body of the tendon
using pre-placed mattress sutures. Again, this proce­
dure requires appropriate drainage and the same feed­
ing instructions mentioned above.
Fenestration through a cicatrix
The final procedure reported for esophageal stricture is
the one currently employed in our hospital. The esoph­
agus is isolated and an esophagotomy is performed

94
 ESOPHAGEAL DISEASES 7

through the strictured area followed by fenestration of Treatment

the mucosal and submucosal cicatrix. This may need to
be done in several places until one is able to pass a stom­ Treatment of traction diverticulum is rarely necessary.
ach tube past the strictured segment easily. Following Treatment of a pulsion diverticulum involves isolation
this, an esophagostomy tube is placed through the of the esophagus and either inversion of the redundant
defect and the horse is fed through the tube until the mucosal sac into the lumen of the esophagus or resec­
site constricts down enough for the tube to be removed tion of the sac.
and the horse can eat again normally. As this incision
heals a traction diverticulum is formed. The hope is Esophageal fistula
that a large enough lumen diameter will be created to Esophageal fistulae can result from healing of
make a second procedure unnecessary. esophagotomy incisions or after esophageal perfora­
tion. They can be diagnosed clinically or by contrast
Esophageal diverticulum radiography when barium is administered under pres­
There are two types of diverticulum. sure. Most fistulae will heal once ventral drainage is
I. Traction or true diverticulum, resulting from
established (Figure 7.5). If healing does not occur, it
may be necessary to perform a resection of the sinus
contraction of periesophageal fibrous scar tissue
tract and closure of the stoma.
often secondary to wound or previous surgery. This
condition is usually asymptomatic and appears as a
wide neck on a barium swallow esophagogram.
2. A pulsion or false diverticulum, resulting from
protrusion of mucosa and submucosa through a
defect in the esophageal musculature (Figure 7.4).
These diverticulae may be caused by external
trauma or by some fluctuation in esophageal
intralumenal pressure and overstretch damage to
esophageal muscle fibers by impacted feed stuff. A
pulsion diverticulum appears spherical and flask­
like on an esophagogram. They may enlarge over
time and become evident as a large swelling in the
neck resulting in dysphagia.

Figure 7.5 Secondary healing of an esophagotomy site.

Figure 7.4 Pulsion diverticulum viewed via This horse had previous esophageal surgery and the tube
esophagoscopy was placed to permit extra-oral feeding

95
7 UPPER ALIMENTARY TRACT DISEASES

Figure 7.6a Positive contrast esophagogram showing a

filling defect typical of an intramural esophageal cyst

Intramural esophageal cysts

Cysts have been found within the wall of the esophagus,

that are consistent histologically with a keratinizing
squamous epithelial inclusion cyst. These cysts can be
diagnosed on the basis of clinical examination and
radiography (Figure 7.6a). Clinical signs include Figure 7.6b Intramural esophageal cyst removed at
surgery (top). Incision of the cyst shows the creamy cyst
• dysphagia contents (bottom)
• regurgitation
• a palpable soft tissue mass in the neck (in some cases).
possible early in the disease process but the prognosis is
Filling defects are present on contrast radiography.
poor.
Surgical treatment recommendations include removal
of the cyst 'in toto' by gently dissecting it free following
Megaesophagus
esophagomyotomy, or marsupialization (Figure 7.6b).
The advantage of the latter is that there is less risk of Primary megaesophagus is also very rare in the horse. It
entering the esophageal lumen. is most likely caused by a generalized motor dysfunction
similar to that reported in dogs. However mega­
Other anomalies esophagus secondary to gastric ulceration in foals is
more common. Presumably repeated gastroesophageal
Congenital abnormalities reflux, impaired peristalsis, and partial obstruction of
the cardia contribute to the development of mega­
Congenital abnormalities of the esophagus are rare.
esophagus. Therapy involves treatment of the primary
There have been occasional reports of tubular duplica­
problem, i.e. the gastric ulcerations, and if necessary
tion in young animals; the signs include dysphagia and
surgical correction of gastric outflow obstructions.
regurgitation. Congenital esophageal dilatation (ecta­
sia) was reported in a 4-month-old foal with a history of
intermittent milk regurgitation.
COMPLICATIONS OF ESOPHAGEAL
SURGERY
Esophageal neoplasia

Reports of esophageal neoplasia are also very rare. There Unfortunately, complications including dehiscence are
have been two horses mentioned in the literature with common following esophageal surgery for a number of
squamous cell carcinoma. Resection and anastomosis is reasons.

96

I. It is difficult to work on the esophagus without
having resulting tension on the tissues.
2. The esophagus is in constant motion due to
swallowing and diaphragmatic movement, and
there is constant irritation by food and saliva.
3. The lack of a serosal covering may contribute to a
delay in healing. The serosa is believed to contribute
to a fibrin seal following incision and to provide
alignment of apposed tissue layers after suturing.
4. The horse with an esophageal obstruction suffers
electrolyte abnormalities because of the loss of
large amounts of saliva and subsequent
dehydration, hyponatremia, and hypochloremia,
and initial transient metabolic acidosis due to the
loss of bicarbonate. Later, progressive metabolic
alkalosis results because of progressive
hypochloremia.
5. Because of the proximity of the recurrent laryngeal
nerves to the esophagus it is possible to damage
these structures during surgical manipulation.
Careful attention to atraumatic tissue handling is
necessary.
Other complications include
• extension of infection down fascial planes to the
thoracic cavity and mediastinum resulting in
pleuritis and mediastinitis
• aspiration pneumonia is the most common lower
airway complication
• Horner's syndrome has been reported secondary to
esophageal surgery
• laminitis can develop from some of the dietary
management processes that are necessary.
Prognosis
Many complications can be dealt with by careful tissue
handling, perseverance, and sophisticated medical
management. In surgery, efforts to minimize tension
and use of strict aseptic technique lessen the likelihood
of incisional problems. Adequate ventral drainage and
careful apposition of tissues to prevent dead space
following surgery is also ideal. Feed impactions and
foreign body obstructions have been reported to have a
short-term survival rate of 78 per cent, although 37 per
cent are reported to have some problems with recurring
obstruction. Mural strictures involving only the muscle
and adventitia of the esophagus have a good prognosis.
If the mucosa and submucosa are involved, penetration
of the esophageal lumen is necessary, making the prog­
nosis more guarded. In most instances, esophageal per­
f'orations can be managed successfully with adequate
ventral drainage and long-term wound care. In our
experience, cranial esophageal perforations are
exceedingly difficult to manage.
ESOPHAGEAL DISEASES 7
BIBLIOGRAPHY
Aanes WA (1975) The diagnosis and surgical repair of
diverticulum of the esophagus. Proc. Am. Assoc. Equine
Pract. 21:211.
Bowman KF, Vaughan] R, Quick C B, et al. (1978)
Megaesophagus in a colt.] Am. Vet. Med. Assoc. 172:334.
Craig D R, Shivy D R, Pankowski R L, et al. (1989) Esophageal
disorders in 61 horses - results of nonsurgical and surgical
management. Vet. Surg. 18:432.
Craig D R, Todhunter R] (1987) Surgical repair of an
esophageal stricture in a horse. Vet. Surg. 16:251.
Dallman M] (1988)Functional suture-holding layers of the
esophagus in the dog.] Am. Vet. Med. Assoc. 192:638.
Freeman D E, Naylor] N (1978) Cervical esophagotomy to
permit extra oral feeding in the horse.] Am. Vet. Med.
Assoc. 172:314.
Fubini S L, Starrak G S,Freeman D E (1999) Esophagus. In
Equine Surgery 2nd edn,]A Auer and]A Stick (eds.). W B
Saunders, Philadelphia, pp. 199-209.
Hackett R P, Dyer R M, Hoffer R E (1978) Surgical correction
of esophageal diverticulum in a horse.] Am. Vet. Med.
Assoc. 173:998.
Hoffer R E, Barber S H, Kallfelz FA, et al. (1977) Esophageal
patch grafting as a treatment for esophageal stricture in a
horse.] Am. Vet. Med. Assoc. 171:350.
Moore] N, Kintner L D (1976) Recurrent esophageal
obstruction due to squamous cell carcinoma in a horse.
Cornell Vet. 66:589.
Murray M], Ball M M, Parker GA (1988) Megaesophagus
and aspiration pneumonia secondary to gastric ulceration
in a foal.] Am. Vet. Med. Assoc. 192:381.
Oakes M G, Hosgood G, Snider III T G, Hedlund C S,
Crawford M P (1993) Esophagotomy closure in the dog.
Vet. Surg. 22:451-6.
Orsini]A, Divers T] (1998) Manual ofEquine Emergencies 1st
edn. W B Saunders, Philadelphia, pp. 658-63.
Orsini]A, Donawick W] (1986) Surgical treatment of
gastroduodenal obstructions in foals. Vet. Surg. 15:205.
Peacock E E, Van Winkle L (1984) Healing and Repair of
Viscera Wound Repair 3rd edn. W B Saunders, Philadelphia,
p. 451.
Roberts M C, Kelly W R (1979) Squamous cell carcinoma of the
lower cervical esophagus in a pony. Equine Vet.] 11:199.
SamsA E, WeldonA D, Rakestraw P (1993) Surgical
treatment of intramural esophageal inclusion cysts in
three horses. Vet. Surg. 22:135-9.
Scott EA (1982) Surgery of the equine oral cavity. Vet. Ctin.
N. Am. Large Anim. Pract. 4:3.
Scott E R, Snoy P, Prasse K W, et at. (1977) Intramural
esophageal cyst in a horse.] Am. Vet. Med. Assoc. 171:652.
Shamir M H, Shahar R,]ohnston D E, Mongil C M (1999)
Approaches to esophageal sutures. Camp. Cant. Ed.
21:414-20.
Sisson S (1975) Equine digestive system. In Sisson and
Grossman's Anatomy of the Domestic Animals 5th edn, R Getty
(ed.). W B Saunders, Philadelphia, p. 454.
Stick]A, DerksenF], McNitt D L, et al. (1983) Equine
esophageal pressure profile. Am.] Vet. Res. 44:272.
Stick]A, DerksenF ], Scott GA (1981) Equine cervical
esophagostomy: Complications associated with duration
and location of feeding tubes. Am.] Vet. Res. 42:727.
Stick]A, Krehbiel] D, Kunze D], et at. (1981) Esophageal
healing in the pony. Comparison of sutured vs.
nonsutured esophagotomy. Am.] Vet. Res. 42:1506.
97
7 UPPER ALIMENTARY TRACT DISEASES
Stick] A, Robinson N E, Krehbiel] D (1981) Acid-base and
electrolyte alterations associated with salivary loss in the
pony. Am.]. Vet. R£s. 42:733.
Stick]A, Siocombe RF, Derksen R], Scott EA (1983)
Esophagotomy in the pony: Comparison of surgical
techniques and form of feed.Am.]. Vet. R£s. 44:2123.
Stick J H (1982) Surgery of the equine esophagus. Vet. Clin. N.
Am. Large Anim. Pract. 4:33.
98
Todhunter RJ, Stick] A, Siocombe RF (1986) Comparison of
three feeding techniques after esophageal mucosal
resection and anastomosis in the horse. Cornell Vet. 75:16.
Todhunter RJ, Stick]A, Trotter G W, et al. (1984) Medical
management of esophageal stricture in seven horses.
]. Am. Vet. Med. Assoc. 185:784.
 8
Etiology, risk factors, and
pathophy siology of colic
Factors associated with
increased risk of colic
NO Cohen
Colic is considered by horse owners and equine veteri­
narians to be one of the most important (if not the most
important) medical problems of horses. The term colic
comprises nearly 100 conditions recognized to result in
abdominal pain. Because a comprehensive review of the
determinants of the many disorders that cause colic is
beyond the scope of this chapter, factors known to con­
tribute to the development of colic will be described
here. Despite the magnitude of the problem of equine
colic, relatively little is known about factors that cause it,
particularly those forms of colic examined in the field
by veterinarians.
SIGNALMENT
Age, sex, and breed have been associated with increased
risk of colic. Some forms of colic appear to be more
prevalent in younger animals (e.g. intussusception in
younger horses, larval cyathostomosis in horses less
than 6 years old) while strangulating lipomas, for exam­
ple, are more common in older horses. Colic can affect
horses of any age. Risk of colic, risk of requiring surgical
treatment for colic, and prognosis for survival appear to
be higher in older horses than in younger horses.
Some forms of colic are gender-specific (e.g. uterine
torsion or scrotal herniation). Although not substanti­
ated by an epidemiologic study, colonic torsion appears
to be more prevalent among mares. Sex has not been
consistently associated with the general complaint of
colic.
The Arabian breed has been identified in multiple
epidemiological studies to be associated with increased
risk of colic. The meaning of this observation remains
unknown. The association may be related to differing
management practices for Arabians, increased concern
for management of colic among owners and caretakers
of Arabians, or a genetic predisposition to gastrointesti­
nal disorders among Arabians. Alternatively, Arabians
may have been less likely to be selected for the control
populations for these epidemiological studies. Feca­
liths and impactions of the small colon appear to be
more prevalent in younger miniature horses while
Standardbreds appear to be at increased risk of scrotal
hernias.
Discrepancies in observations made between studies
with regard to age, sex, and breed can be confusing to
veterinarians wanting to apply the results of epidemio­
logical studies of colic. These discrepancies may result
from differences between studies such as the outcome
used for analysis (e.g. colic in general form versus a spe­
cific form), or the population studied, also the relation­
ship for a given factor may be more complex than a
simple bivariate comparison allows (e.g. effects of
management may vary with age). Those observations
that are repeatable should be considered to have
greater credibility.
MEDICAL HISTORY
History of previous colic has been repeatedly identified
as a risk factor for colic. In one study the effect was mod­
ified by the caretaker - the risk of colic for horses with
101
8 COLIC
previous colic nearly doubled if the horse was cared for
by a non-owner. Horses with history of previous surgery
for colic are at increased risk of colic. The association of
previous colic or previous surgery for colic with future
colic is important information for horse owners and
farm managers.
FARM MANAGEMENT FACTORS
Management practices are of particular importance
because they can be changed and, consequently, can
reduce the incidence of colic. Dietary factors can pre­
dispose to colic, however, epidemiological studies have
yielded conflicting results. Some studies have impli­
cated the type (e.g. corn) or amount (i.e. increased risk
with increased amount) of concentrate fed, whereas
others have implicated change in diet, particularly a
change in the type, quality, or batch of hay/forage fed.
It is reasonable to believe that many types of concen­
trate can be fed safely to horses - although excessive
amounts may predispose to colic, laminitis, and endo­
toxemia - and that changes in diet, particularly changes
in forage/hay predispose to colic. Because diet is widely
regarded as an important risk factor for colic, dietary
practices may be modified to decrease the risk.
However, little reliable information is available and it is
apparent that further epidemiologic studies of diet and
colic are much needed.
Management practices have been associated with
increased risk of colic but few studies have been con­
ducted. It is likely that management factors vary
between regions and countries. Factors associated with
colic in one area may not be relevant in other areas.
Despite this limitation, some management factors are
consistently associated with colic or are sufficiently
plausible to merit discussion.
Constant access to water is important to prevent
colic, and it is likely that the quality and palatability of
the water is also important. Horse owners and farm
managers should be advised about the importance of
continuous access to fresh water.
Housing practices contribute to colic. The greater
the density of horses per unit area, the greater the risk
of colic. Changes in stabling, particularly a change from
being kept on pasture to being kept in a stall, predis­
pose to colic. A greater proportion of time grazing at
'pasture is associated with lower risk of colic; however,
access to lush pasture predisposes to colic. Although as
yet ill-defined, activity level seems likely to play a role in
colic. Changes in activity level have been shown to pre­
dispose to colic, although specific types of changes in
activity or types of activity have not been demonstrated.
There is a lack of consistent evidence to show that any
102
particular activity or level of activity predisposes to colic;
however, it has been suggested that brood mares may be
at increased risk of colic, and strenuous exercise may
predispose to ileus and dehydration resulting in colic.
PREVENTATIVE MEDICINE FACTORS
Surprisingly, there is little epidemiologic evidence of an
association between preventative medical practices and
colic. Although no association between colic and fre­
quency of dental care has been documented, dental dis­
orders are thought to predispose to certain forms of
colic (e.g. choke, large colon impaction). It would be
advisable to conclude that routine dentistry is impor­
tant for equine health.
With regard to parasite control, limited and conflict­
ing evidence has been reported. In general, good
parasite control programs will decrease the risk of colic.
One example would be a program designed to mini­
mize herd average fecal egg counts. Because tapeworms
are associated with spasmodic colic and ileal impactions
in the UK, specific targeting of tapeworms may be nec­
essary for some farms. Administration of anthelmintics
effective against larvae of cyathostomes should decrease
the incidence of colic. Consistent epidemiologic
evidence is lacking to show that any particular
anthelmintic either predisposes or prevents colic rela­
tive to other anthelmintics. Recent deworming, how­
ever, may predispose to colic, particularly larval
cyathostomosis and ascarid impaction in foals and
weanlings. Parasite-associated colic probably varies
between geographic regions and between farms, and it
is worth emphasizing the importance of parasite con­
trol to horse owners and farm managers.
WEATHER
There are conflicting reports of an association of colic
with weather-related factors. Some investigators report
an increased incidence of colic during warmer months
of the year (possibly associated with increased dehydra­
tion from sweating) and some report an increased
incidence during cooler months (possibly because of
decreased water intake in cold weather). Investigators
have failed to find an association between incidence of
colic and ambient temperature, change in ambient
temperature, change in barometric pressure during the
24 hours prior to colic, mean monthly temperature,
mean monthly rainfall, or mean monthly rainfall
weighted for temperature. Recently, a significant
change in weather during the 3-day period prior to
examination was significantly associated with colic.
 E TIOLOGY, RISK FACTORS, AND PATHOPHYSIOLOGY OF COLIC
Although clinical experience would suggest an associa­
tion of colic with weather-related factors, these factors
have not been confirmed.
Clearly much work remains to determine the many
causes of colic. It is likely that colic results from a com­
bination of multiple predisposing factors. Although no
single cause is likely to be sufficient or necessary to
result in colic, efforts to alter factors that predispose to
colic and to characterize horses at increased risk for
colic should be made by veterinarians and those respon­
sible for the care of horses. Confirmation of the benefit
of interventions to decrease colic are rare, but vitally
important. Because risk factors are likely to vary by type
of colic, studies of risk factors for specific types of colic
are needed.
Pathophysiology of
intestinal obstruction
DE Freeman
PATHOP HYSIOLOGY OF INTESTINAL
DISTENTION
Intestine proximal to an obstruction becomes dis­
tended with secretions, gas, fluid, and digesta, and the
bowel wall and mesentery become stretched resulting in
abdominal pain. Veins in the small intestinal wall are
compressed as lumenal pressure increases, and capil­
lary hydrostatic pressure and capillary filtration rate
increase. If capillary filtration into the interstitium over­
whelms fluid removal through lymph flow, then tissue
edema and a net secretion of fluid into the intestine
develops.
Four hours of experimentally induced intralumenal
pressure of up to 18 cmH20 (13.2 mmHg) induced
mild edema in the lamina propria of equine jejunal
villi. Experimentally induced intralumenal pressure in
pony jejunum to 14 cmHp ( 10 mmHg) increased
vascular resistance but without an effect on oxygen
consumption or viability. Experimentally induced
intralumenal pressures of 25 cmH20 (18.4 mmHg) for
120 minutes in equine small intestine caused shorten­
ing of villi, loss of mesothelial cells, neutrophil infiltra­
tion, seromuscular edema, and a decreased number of
vessels in the seromuscular layer and, to a lesser extent,
in the mucosa. Decompression of distended small intes­
tine caused progression of morphologic lesions in the
seromuscular layers and mucosa, perivascular hemor­
rhage in the seromuscular layer, and an increased
8
vascular density, but to less than control values. These
changes could contribute to formation of serosal adhe­
sions.
PATHOPHYSIOLOGY OF INTESTINAL
ISCHEMIA
Ischemic changes in the metabolically active mucosa can
be graded in severity from Grade I (development of a
subepithelial space, called Gruenhagen's space, and
slight epithelial lifting at the villus tip), through pro­
gressive loss of the epithelial layer in sheets, starting at
the villus tip, to Grade V (complete loss of the villus archi­
tecture, with severe mucosal hemorrhage and loss of the
lamina propria). Sensitivity of villus tip cells to anoxia is
not caused by the countercurrent mechanism in small
intestinal capillaries because anoxic injury to equine
jejunum in vitro causes the same progression of epithe­
lial damage. In the equine colon, unlike the small intes­
tine, complete ischemia causes cellular necrosis and
detachment of small clusters of surface epithelial cells.
In experimental models of colonic ischemia and in clin­
ical cases of colonic volvulus in the horse, ischemic vas­
cular injury causes capillary plugging and thrombosis.
Intestinal smooth muscle is more resistant to
hypoxia than is mucosa, and crypt cells are more resis­
tant than are villus cells, factors that can play a part in
recovery from an ischemic insult. The early stages of
mucosal repair involve restitution, whereby the villus
contracts to reduce the size of the defect and adjacent
viable cells cover the exposed villus stroma. This repair
process can cover pony jejunum with stunted villi lined
with cuboidal epithelium within 12 hours after a Grade
IV ischemic i�ury.
ENDOTOXEMIA
When ischemia or inflammation destroys the integrity
of the intestinal epithelial barrier, the lipopolysaccha­
ride component of the outer wall of enteric gram­
negative microorganisms gains access to the circulation
(Figure 8.1). Clinical and laboratory signs of endotox­
emia are more pronounced in horses with colitis than
in horses with strangulating lesions (see Chapter 11).
Circulating and tissue-fixed mononuclear phagocytes
release the cytokines, lipid-derived mediators, and coag­
ulation/fibrinolytic factors that are critical to genera­
tion of responses to endotoxin. The cytokine, tumor
necrosis factor (TNF a)' induces synthesis of other
cytokines (such as the interleukins), prostaglandins,
and tissue factor, and initiates an acute-phase response
and fever. The most important lipid-derived mediators
103
8 COLIC

are cyclooxygenase-derived metabolites of arachidonic MOTILITY DISTURBANCES IN

acid, and these are responsible for the early hemo­
dynamic responses to endotoxin. Thromboxane � and
prostaglandin F2a cause vasoconstnctlOn and
prostaglandin 12 and prostaglandin E2 cause vasodila­
tion. Another important lipid-derived mediator is
platelet-activating factor (PAF), which aggregates
equine platelets and increases thromboxane B2 produc­
tion from equine peritoneal macrophages. Horses with
endotoxemia also develop a hypercoagulable state and
consumptive coagulopathy, presumably secondary to
synthesis of tissue factor by mononuclear cells. The
response to endotoxin influences survival in horses with
gastrointestinal tract diseases.
INTESTINAL OBSTRUCTION
Non-strangulating occlusion of pony jejunum causes
loss of gastric contractile activity in the distended stom­
ach and immediate continuous spiking activity in intes­
tine proximal to the obstruction. Jejunal distention in
ponies increases the amplitude of rhythmi� contrac­
tions in the distended segment. Occlusion of blood sup­
ply to the pony ileum decreases motility in the ischemic
bowel, increases motility in the more proximal seg­
ment, and has no effect on the distal segment. Ileus
is a common postoperative complication of intestinal
surgery in horses, and adrenergic and dopaminergic

Cytokines, lipid-derived mediators,

coagulation/fibrinolytic factors

�
Changes in cardiovascular and
MEDIATORS
OF CELL
respiratory systems, motility,
DAMAGE
and coagulation

�
Endothelial cell
iCytosolic .
calcium � Calpaln
ATP Xanthine
[H�2 2J0 2 0 o� ·
dehydrogenase

Xan hine

ypoxanthine
+H +02 0
oxidase

Uric acid Fe3+

�===02==

Ischemia =======�> Reperfusion ========�>

Figure 8.1 Pathways and mechanisms in the pathophysiology of ischemia and reperfusion injury in the intestine.
Increased shading in the mucosal epithelium represents increased cell damage. A T P = adenosine triphosphate;
SOD = superoxide dismutase; O2 = superoxide radical; OH = hydroxyl radical; HP2 = hydrogen peroxide; Fe3+ = ferric iron;
O2 = oxygen; HOCI = hypochlorous acid; PAF = platelet activating factor; LTB4 = leukotriene B4; TXA2 = thromboxane A2;
PGI2 = prostaglandin 12; PGE2 = prostaglandin E2; PGF2a = prostaglandin F2u; PGD2 = prostaglandin O2; fMLP = formyl­
methionyl-Ieukyl-phenylalanine

104
 ETIOLOGY, RISK FACTORS, AND PATHOPHYSIOLOGY OF COLIC
stimulation appears to occupy a central role in its
pathogenesis (see Chapter I I).
Continuous infusions of prostaglandin E I (PGEI)
decreased motility in pony stomach, left large colon,
small colon, left dorsal colon, and jejunum (more
than in the ileum). Also, intravenous infusion of
prostaglandin E2 (PGE2), but not prostaglandin F2"
(PGF2,,) mimicked the disrupted motility patterns
induced by endotoxin in the stomach, small intestine,
and large intestine of ponies. Nitric oxide from
myenteric neurons also appears to act as an inhibitory
neurotransmitter to circular smooth muscle of equine
jejunum and could be released from macrophages in
inflamed small intestine.
REPERFUSION INJURY
Reperfusion i�ury is the exacerbation of tissue damage
that occurs when ischemic tissue is reoxygenated
(Figure 8.1). The most widely accepted explanation for
reperfusion injury is initiation of tissue damage by reac­
tive oxygen metabolites (ROMs) and exacerbation by
neutrophils (Figure 8.1). Initiation of reperfusion
injury depends on conversion of xanthine dehydrogen­
ase to xanthine oxidase (Figure 8.1), and activity of
these enzymes is high in equine small intestine but not
in equine colon. Neutrophil accumulation in equine
colonic mucosa peaks during the first 10 minutes of
reperfusion after low flow ischemia, and this coincides
temporally with mucosal necrosis.
Attempts to demonstrate reperfusion injury in
equine intestine have met with varied success. The
intestinal model that allows more complete display of
the expected paradigms of reperfusion injury is the seg­
mental hypoperfusion or low flow model, which causes
mild tissue damage during the ischemic period. The
clinical equivalent to this is intestine subjected to
decompression or to hypoperfusion. In contrast with
laboratory animals, pharmacologic manipulation of
reperfusion injury is unrewarding in equine intestine.
PATHOGENESIS OF ADHESION
FORMATION
Peritoneal ischemia and inflammation (trauma, disten­
tion, bacteria, and foreign material) are thought to pre­
dispose to adhesions by causing an imbalance between
fibrin deposition and fibrinolysis in the peritoneal
cavity. If fibrin is not removed, the ingrowth of fibro­
blasts and subsequent deposition of collagen converts
fibrinous adhesions to fibrous adhesions.
Plasmin, antithrombin III, and protein C are
8
responsible for fibrinolysis. Plasminogen is converted to
plasmin by tissue plasminogen activator (tPA) , which is
a key regulator of fibrinolysis. Inhibitors of fibrinolysis
include plasminogen activator inhibitor-l (P AI-I) and
alpha- 2 anti plasmin which inhibit tPA and plasmin,
respectively. PAI-l increases in inflammation and
ischemia possibly explaining the decreased activity of
tPA in these disease conditions. Concentration of tPA
decreases in peritoneal fluid following peritoneal
trauma.
BIBLIOGRAPHY
Factors associated with increased risk of colic
Cohen N D (1997) Epidemiology of equine colic. Vet. Clin. N
Am. Equine Pract. 13:191-201.
Proudman C] (1991) A two year, prospective survey of equine
colic in general practice. Equine Vet.] 24:90.
Reeves M (1992) Risk and prognostic factors in colic. In
Current Therapy in Equine Medicine, 3rd edn, N E Robinson
(ed.). W B Saunders, Philadelphia, pp. 206-10.
White NA (1990) Epidemiology and etiology of colic. In The
Equine Acute Abdomen, NA White (ed.).Lea and Febiger,
Philadelphia, pp. 49-64.
Pathophysiology of intestinal obstruction
Allen D, White NA and Tyler D E (1988) Morphologic effects
of experimental distension of equine small intestine. Vet.
Surg. 17:10-14.
Dabareiner R M, Sullins K E, Snyder] R, et al. (1994)
Evaluation of the microcirculation of the equine small
intestine after intraluminal distension and subsequent
decompression. Am.] Vet. Res. 54:1673-82.
Davies] V and Gerring EL (1985) Effects of experimental
vascular occlusion on small intestinal motility in ponies.
Equine Vet.] 17:219.
Freeman D E, Cimprich R E, Richardson D W, et aL (1988)
Early mucosal healing and chronic changes in pony
jejunum after various types of strangulation obstruction.
Am.] Vet. Res. 49:810.
Gerring EL and Hunt] M (1986) Pathophysiology of equine
postoperative ileus: effect of adrenergic blockade,
parasympathetic stimulation and metoclopramide in an
experimental model. Equine Vet.] 18:249.
Granger D N, Kvietys P R, Mortillaro NA, et al. (1980) Effect
of luminal distension on intestinal transcapillary fluid
exchange. Am.] Physiol. 239:G516--G523.
Hunt] M and Gerring EL (1985) The effect of prostaglandin
E] on motility of the equine gut.] Vet. Pharmacol. Therap.
8:165.
Johnston] K, Freeman D E, Gillette D, et al. (1991) Effects of
superoxide dismutase on injury induced by anoxia and
reoxygenation in equine small intestine in vitro. Am.] Vet.
Res. 52:2050.
King] Nand Gerring EL (1989) Observations on the colic
motor complex in a pony with a small intestinal
obstruction. Equine Vet.] Supplement 7:43-5.
King] Nand Gerring EL (1991) The action of low dose
endotoxin on equine bowel motility. Equine Vet.] 23:11.
Moore] N and Barton M H (1998) An update on
105
8 COLIC
endotoxemia Part 1: mechanisms and pathways. Equine.
Vet. Educ. 10:300-6.
Moore R M, Muir W W and Granger D N (1995) Mechanisms
of gastrointestinal ischemia-reperfusion injury and
potential therapeutic intelVentions: a review and its
implications in the horse.] Vet. Int. Med. 9: 115-32.
Parks A H, Stick] A, Arden W A, et ai. (1989) Effects of
distension and neostigmine on jejunal vascular resisitance,
oxygen uptake, and intraluminal pressure changes in
ponies. Am.] Vet. Res. 50:54-8.
106
Rakestraw PC, Snyder] R, Woliner M], et ai. (1996)
Involvement of nitric oxide in inhibitory neuromuscular
transmission in equine jejunum. Am.] Vet. Res. 57:1206.
Snyder] R (1989) The pathophysiology of intestinal damage:
effects of luminal distension and ischemia. Vet. Clin. North
Am. Equine. Prac. 5:247-70.
SouthwoodLL and Baxter G M (1997)Current concepts in
management of abdominal adhesions. Vet. Clin. N. Am.
Equine Prac. 13:415.
�9
Clinical evaluation of the colic case

Clinical signs of colic painful; slowly developing tension may be painless.

____I1If_____
T Mair
MECHANISMS OF ABDOMINAL PAIN
Abdominal pain can be differentiated into visceral pain,
parietal (somatic) pain, and referred pain. Visceral pain
is most commonly observed in colic, and refers to the
dull, non-specific, poorly localized pain resulting from
visceral disease. The horse's response to this pain is to
move about excessively in an attempt to remove the dis­
comfort. In contrast, parietal pain is more localized and
may occur in response to diseases affecting the parietal
peritoneum. Referred pain is rarely recognized in the
horse.
Painful stimuli activate free nerve endings of small
A-delta and C afferent nerve fibers. Tissue hormones
such as bradykinins, histamine, leukotrienes and
prostaglandins can either activate pain receptors or
lower the threshold for other stimuli. A-delta fibers
mediate sharp, sudden, well-localized pain that follows
some forms of injury. C fibers mediate dull, poorly
localized painful sensations; these fibers are found in
muscle, periosteum, parietal peritoneum, and viscera.
Since A-delta fibers are not present in the viscera, cut­
ting, crushing, or tearing pain sensation is not per­
ceived at this site. However, visceral nociceptors are
sensitive to stretching or tension caused by distention,
traction (e.g. from a neoplasm) , or forceful muscular
contraction (e.g. oral to a bowel obstruction) . The pari­
etal peritoneum and mesentery are sensitive to pain,
but the visceral peritoneum and omentum are insensi­
tive. Tension must develop rapidly to be perceived as
Inflammation can also cause visceral pain by direct
mechanisms or indirectly by lowering nerve-ending
thresholds. Ischemia causes pain by increasing the
tissue concentrations of metabolites around sensory
nerves, and by lowering the threshold of noxious
stimuli.
CLINICAL SIGNS OF COLIC
The horse affected by colic due to gastrointestinal pain
may behave in a variety of ways. To a large extent the
signs will be determined by the severity of the pain, but
it must be recognized that there is a wide variation
dependent on the personality of the individual horse.
Some horses appear to be more stoical and tolerant of
pain than others.
Despite this variation in signs, it should be possible
to classify the degree of pain exhibited by the horse into
one of several groups
• no pain
• mild pain
• moderate pain
• severe pain
• depression.
The horse with mild pain may demonstrate one or
more of the following signs
• occasional pawing
• turning the head to the flank
• stretching out
• lying down for longer than usual ( Figure 9. 1 )
• quivering of the upper lip

107
9 COLIC

• inappetence • dropping to the ground

• backing up to the wall • extreme restlessness
• 'playing with' or 'nosing' water. • other signs of pain listed above.

With moderate pain the following may be seen The stage of depression may be seen after a severe bout
of colic as advanced intestinal necrosis and endo­
• restlessness
toxemia produce a state of indolence. Alternatively,
• pawing
depression may be seen as an early sign of other
• cramping with attempt� to lie down
diseases that produce colic, especially inflammatory
• crouching
diseases such as colitis and peritonitis. Depression is
• kicking at the abdomen
also common in horses affected by anterior (proximal)
• lying down
enteritis after nasogastric decompression of the
• rolling ( Figure 9.2)
stomach.
• turning the head to the flank
In general terms, the more severe the disease, the
• dog-sitting position
greater the severity of pain. Strangulating obstructive
• groaning.
diseases usually cause more severe pain than simple
The horse in severe pain will show one or more of obstructions. However, early in the course of strangulat­
the following ing diseases the pain may not be as severe, and late in
• sweating the course of these conditions depression takes over as
• violent rolling the predominant sign. Severe pain that is continuous
may be more likely in cases of severe tympany or in
strangulating diseases where there is bowel wall stretch­
ing or tension on the mesentery. When pain changes
rapidly from severe and uncontrollable to total relief
or depression, gastric or bowel rupture should be
considered.
The horse that presents with signs of depression
(especially animals that are found like this first thing in
the morning) should be evaluated for 'tell-tale' signs of
previous pain. In particular, skin abrasions and swelling
around the eyes, abrasions over the tuber coxae, and
marks on the walls of the stable indicate violent rolling
by the horse.

Figure 9.1 Mild colic cha racterized by restlessness and lying

down more often than usua l

Figure 9.2 Moderate colic in a foal that is rolling repeat­ Figure 9.3 Stretched out ('trestle table') appearance in a
edly horse with a jejunojejunal intussusception

108

In some diseases the clinician may notice character­
istic clinical signs suggesting the presence of a particu­
lar disease, for example
• a dog-sitting position is seen in horses with gastric
distention
• a stretched-out (,trestle table') position is seen in
horses with small intestinal intussusceptions (Figure
9.3) and sand impactions
• foals that roll onto their backs and lie in dorsal
recumbency for long periods may be affected by
gastric ulceration.
It should be noted that these signs are not specific for
these diseases and not all animals with these conditions
will demonstrate these signs. However, their observa­
tion can help raise the index of suspicion for a particu­
lar disease.
Physical examination of a
horse with colic
PD Van H a rreveld and E M Gaughan
A physical examination of a horse with colic should be
performed in a quick, thorough, and systematic fash­
ion, so that a working diagnosis can be established and
proper treatment initiated. Information gathered dur­
ing the physical examination will allow the attending
veterinarian to make the appropriate decisions about
disease severity, prognosis, and course of therapy.
Because of the possible need for surgical intervention it
is important to consider diagnosis of obstructive disease
as early as possible.
HISTORY
An accurate history will provide valuable information
regarding current and past health and colic concerns.
This can be very beneficial in determining the specific
cause of abdominal pain. The initial history should
include
• signalment
• duration of clinical signs
• severity and frequency of pain
• the time when the horse was last observed to be
normal.
An accurate history can also help determine if a horse's
colic is acute, chronic, or recurrent. Nutritional history
can help determine if feed materials or feeding practices
CLINICAL EVALUATION OF THE COLIC CASE 9
could predispose to colic (e.g. poor quality hay may pre­
dispose to impaction; grain overload predisposes to colic
and laminitis). Certain geographic locations or previous
housing locations can also be important, for example
in horses predisposed to sand accumulations and
enterolith formation. Availability of water and drinking
habits should be reviewed. Acute changes in water intake
from defects in automatic watering systems or freezing
temperatures can lead to obstructive colic (impaction
can occur secondary to decreased water intake) . An
understanding of the parasite control program, date of
last deworming, and agent used can be especially impor­
tant for younger horses. In mares, breeding history and
pregnancy status should be documented. A complete
description of treatments administered prior to and
after the onset of colic, including medications, is impor­
tant for assessment. Manure production, volume, and
character should be determined.
CLINICAL EXAMINATION
For the physical examination of a horse with colic, a con­
sistent, effective, and systematic examination of the var­
ious body systems should be routinely completed. It is
important to use a similar system of examination for each
horse to ensure complete evaluation and comparison
between one horse and others. Routine equipment to
perform a complete examination includes thermome­
ter, stethoscope, nasogastric tube, pump, rectal sleeve,
and lubricant. Instrumentation for abdominocentesis
and diagnostic ultrasound can also be very helpful.
Initially, an affected horse should be evaluated
quickly from a distance. This can provide information
regarding
• the type and severity of pain
• the animal's general condition
• signs of colic
• mentation
• the presence of wounds or lacerations
• the degree of abdominal distention
• any other external signs.
Assessments of fecal output can also be made.
Rectal temperature
The body temperature should be determined prior to
performing a rectal examination because a pneumo­
rectum can lead to a reduced temperature. The normal
temperature range for horses is 37.5-38.5°C. Increases
in body temperature can occur after anxiety, excite­
ment, or exertion. Temperatures greater than 39.5°C
may suggest an inflammatory or primary infectious
109
9 COLIC
process, such as colitis, proximal enteritis, peritonitis,
or pleuritis. Body temperature elevation can also occur
early after stomach or intestinal rupture, leading to sep­
tic peritonitis. Decreased temperature (hypothermia) ,
in addition to tachycardia, is indicative of the develop­
ment of circulatory compromise and potential shock.
Respiratory rate
The respiratory rate of a horse with colic will usually be
elevated because of pain or metabolic acidosis. Dyspnea
or shallow breathing can result from pressure applied
to the diaphragm by severe gastric or intestinal disten­
tion. The rate and character of respiration should be
noted, but these do not usually provide any direct
insight into the causes of colic.
Heart rate
A horse's heart rate can usually be obtained by auscul­
tation of the heart at the thorax, it can also be obtained
by palpation of the facial artery or other peripheral arter­
ies. Palpation of a peripheral pulse can offer a reflection
of cardiovascular function and tissue perfusion. The
absence of a palpable pulse may indicate cardiovascular
compromise . In relation to gastrointestinal origins, it
may be wise to palpate the digital arteries in order to
detect the potential early development of laminitis.
The normal equine heart rate is 24-40 bpm.
Elevations of heart rate in horses with colic are usually
the result of anxiety, pain, and hypovolemia. Heart rate
elevation is a good indicator of the severity of pain and
indirectly, the original intestinal disorder. Pulse assess­
ment should always be used in addition to other physi­
cal examination data to determine the potential presence
of a surgical condition. Horses with a functional or mild
intestinal obstruction can have intermittent heart rate
spikes, whereas horses with strangulating lesions usually
have sustained heart rate elevations up to 80-90 bpm. A
sustained elevation in heart rate is critical to a more com­
plete understanding of the diagnosis and prognosis.
Mucous membranes and jugular vein filling
The character and color of mucous membranes can
reflect the circulatory status of the patient. Normal
mucous membranes are moist and pink. Physiological
capillary refill time is usually 1 .5 seconds or less. When
peripheral vascular circulation is impaired capillary
refill time is prolonged, this is considered severe when
increased to 4 seconds or more. The moisture of the
mucous membranes can reflect the overall hydration
status of the patient. Dry mucous membranes can indi­
cate systemic dehydration. Pale mucous membranes
can occur with shock from hypovolemia or pain. Dark
1 10
mucous membranes or a toxic line are usually
associated with septic or endotoxic shock, following
resorption of bacterial endotoxins from intestinal com­
promise or enteritis. Skin elasticity is maintained
through water content in the tissues. A fold of skin can
be pinched over the cervical region or eyelid to evaluate
hydration. The skin fold should flatten within 1-2 sec­
onds in normally hydrated skin, however, this should
only be assumed to be a crude assessment. Manual
occlusion of the jugular vein can be useful in determin­
ing the state of venous blood pressure and circulating
fluid volume. With substantial hypovolemia, jugular fill­
ing is either prolonged or absent.
Abdominal auscultation (see Chapter 1 , General
physical examination and auscultation)
Intestinal motility can be evaluated subjectively by
auscultation of the abdomen using a stethoscope. The
frequency, duration, intensity, and location of intestinal
sounds should be noted. Normally, organized inter­
mittent peristaltic sounds can be heard. Auscultation
should be performed on both the right and left flanks
as well as the ventral abdominal wall, or over all four
quadrants, dorsal/ventral and left/right. Colonic and
small intestinal sounds can best be heard at the left
flank, whereas cecal sounds can be heard at the right
flank. The presence of sounds associated with sand in
the large colon are best detected on auscultation of the
ventral abdominal wall. Excessive frequency of sounds
or intestinal hyperactivity is associated with conditions
such as enteritis or spasmodic colic. The absence of
intestinal sounds over a prolonged period of time may
indicate ileus or obstructive disease. Abdominal per­
cussion during auscultation can reveal gas-distended
bowel when a high-pitched resonant sound (ping) is
present.
NASOGASTRIC INTUBATION (see Chapter 1 ,
Passage of a nasogastric tube should be performed for
all horses presenting with colic. The inability of a horse
to regurgitate means that the stomach may rupture if it
becomes overloaded or distended. It is important to
detect and alleviate fluid or gas distention from the
stomach as early as possible. Reflux into the stomach
usually occurs with small intestinal obstruction or
enteritis, it can also occur secondary to colonic
displacement leading to compression of the duode­
num. The stomach should be decompressed with a
nasogastric tube and a siphon established allowing fluid
contents to drain. Removal of gastric contents can be

challenging, and repeated efforts to create a siphon by
moving the stomach tube back and forward may be
necessary. In cases where increased pressure of the
stomach causes complete closure of the cardia, blowing
air into the tube while moving it into the stomach may
allow the tube to move forward. Introducing a local
anesthetic agent (lidocaine hydrochloride 2%, 60 ml)
into the esophagus through the tube can also be
attempted. In healthy horses, only small amounts of
fluid « 500 ml) can be retrieved from the stomach. The
pH of normal stomach contents is 5 or less. In cases of
small intestinal obstruction or enteritis, many liters of
fluid can be removed from the stomach. In these cases
the fluid pH is increased as a result of bicarbonate-rich
pancreatic and intestinal secretions.
RECTAL EXAMINATION (see Chapter 1 ,
Rectal examination and Chapter 9, Rectal examination
for the acute
Rectal examination may be the most revealing compo­
nent of the physical examination of a horse with colic
and should be performed in all cases when possible.
This is especially important if surgical therapy is being
considered. Only 40 per cent of the abdomen can rou­
tinely be explored by examination per rectum. Prior to
performing a rectal examination the patient should be
properly restrained. It may also be necessary to use anal­
gesics or sedatives such as xylazine (0.2- l .1 mg/kg Lv.
or Lm. ) to relieve anxiety. A twitch can also be applied
for restraint, and this may help to reduce straining. The
use of a local anesthetic (lidocaine hydrochloride
2%, 120 ml) enema can help reduce rectal straining.
Voluminous use of a lubricant such as K-Y jelly or
methyicellulose is usually required. The rectum should
be entered slowly and feces carefully evacuated. The
arm should then be carefully advanced as the tension in
the rectal wall diminishes. Relaxation can take up to 30
seconds in many horses. It is important to keep the
examination hand and fingers cone shaped and not
force entry against rectal peristaltic waves. Feces recov­
ered during rectal examination should be examined for
the presence of sand or blood. The presence of sand
can be detected by placing feces in a container of water
and looking for sand separating away from the ingesta.
If fresh blood is present at the end of the examination,
a rectal abrasion or tear should be suspected and
further evaluated. Normal structures palpable during
examination per rectum include the spleen, left kidney,
nephrosplenic ligament, root of mesentery, cecum,
medial cecal band, pelvic flexure, the small colon, and
the bladder when distended. The inguinal canals can be
felt in stallions, and the uterus and ovaries in mares.
CLIN ICAL EVALUATION OF THE COLIC CASE 9
ABDOMINOCENTESIS (see Chapter 2,
Abdominocentesis and Analysis of peritoneal fluid)
WIl���!Il!W�_W'11f
Abdominocentesis can provide useful information
when other examination techniques fail to reveal a
clear diagnosis, or when further determination is
required of the severity of the lesion. It is also indicated
in cases where rectal examination does not yield defini­
tive findings and the signs of colic persist. This proce­
dure can be performed using a hypodermic ( I8-gauge)
needle or a blunt cannula (bitch catheter or teat can­
nula) . The most dependent site of the abdomen, to the
right of midline, should be selected to avoid the spleen
and stomach. Abdominocentesis should probably be
avoided in any foal with abdominal distention or small
intestinal distention. The cannula technique is pre­
ferred in foals as trauma to the thin intestinal walls can
be minimized, however, ultrasonographic evaluation is
preferred in foals. Peritoneal fluid should be evaluated
grossly for volume, color, turbidity, and food particles.
The fluid can be examined microscopically for leuko­
cyte and erythrocyte counts as well as total protein
determination. Normal peritoneal fluid is clear or straw
colored, with a protein concentration up to 2.5 g/dl
(25 gil) and total white blood cell count (WBC) of less
than 5000 cellS/ill (5.0 x 1 0 9/1), consisting mostly of
macrophages and neutrophils. The presence of food
particles or bacteria in the peritoneal fluid can indicate
loss of bowel integrity and a poor prognosis. Prior to
euthanasia, abdominocentesis findings should be con­
firmed by repeating the technique in at least one differ­
ent site to rule out enterocentesis. Blood-tinged fluid is
consistent with advanced intestinal disease such as
intestinal strangulation. Neutrophil counts can increase
in inflammatory conditions such as long-standing
impaction or strangulation and can exceed 1 00 000/111
(l00 x 1 09/1) . Neutrophil counts greater than 50 000
cellS/ill (50 x 1 09/1) can be suggestive of an intra­
abdominal abscess or of primary bacterial peritonitis.
ULTRASOUND EXAMINATION (see Chapter
Ultrasound examination of the
Ultrasonography can provide additional information in
the examination of a horse with colic, especially in foals
and small horses where rectal examination cannot be
performed. Abdominal ultrasound can be performed
transcutaneously or per rectum. Abnormalities com­
monly detected with ultrasonography include peri­
toneal effusion, adhesions, masses, small intestinal
distention, ileus, intussusception, and left dorsal dis­
placements of the large colon.
111
9 COLIC
CLINICAL PATHOLOGY
For many horses, laboratory assessment of blood is not
essential for treatment success. However, with severe or
changing cases WBC, packed cell volume ( PCV) and
total plasma proteins (TPP) are often helpful. The PCV
and TPP are useful for assessment of the degree of
dehydration, and are necessary to monitor the efficacy
of volume replacement. Normal PCV values range
between 32-46 per cent, but may vary slightly according
to the horse's age, breed, and athletic condition.
Splenic contraction following transport and anxiety
may raise the PCV values above normal. Packed cell vol­
ume can be of use in determining the prognosis of a
colic case. The higher the PCV, the greater the rate of
mortality, with values greater than 65 per cent associ­
ated with a poor prognosis. Normal total protein levels
range between 5.5 and 7.5 gldl (55-75 gil) . Plasma
protein in a colic patient is usually increased as a result
of dehydration. Plasma proteins can be decreased by
sequestration of protein into the abdominal cavity as a
result of peritonitis or into the intestinal lumen as a
result of enteritis. Neither the PCV nor the TPP can be
used as specific indicators of a surgical lesion, but can
help determine the severity of the lesion, the degree of
shock, and the response to treatment.
The total WBC is useful in determining conditions in
which surgery is contraindicated. White blood cell count
elevations are often observed in horses with proximal
enteritis or intra-abdominal abscesses. Severe leukope­
nia « 3000 celliIll, < 3.0 x 109/1) can indicate gram-neg­
ative sepsis or endotoxemia as a result of salmonellosis
or severe acute peritonitis from intestinal rupture.
Blood gases and electrolytes can show changes in a
horse's metabolic state and can be of limited value in
determining the prognosis or diagnosis for a horse with
colic. They are valuable in preparation for anesthesia
and in monitoring a horse's postoperative recuperation.
Rectal examination for the
acute abdomen
POE Mueller
INTRODUCTION
A complete and thorough rectal examination is an
essential component of a diagnostic evaluation when
examining horses with abdominal pain. Rectal exami­
nation findings should always be considered in con-
1 12
junction with the results of the physical examination,
nasogastric intubation, abdominocentesis, and labora­
tory evaluation. A rectal examination should always be
performed before abdominocentesis in order to recog­
nize an extremely gas-distended or ingesta-filled cecum
or large intestine. If these abnormalities are identified,
extreme care must be taken when performing an
abdominocentesis to avoid accidental enterocentesis.
Occasionally, rectal examination findings clearly
indicate the specific disease, such as a renosplenic
entrapment, early ileal impaction, or herniation of
small intestine through the inguinal ring in a stallion.
More often, however, rectal examination does not yield
a specific diagnosis, but gives information regarding the
severity of the problem and the need for surgical inter­
vention. Abnormal rectal examination findings include
• abnormal positioning of the intestine
• distention of the intestine with gas or ingesta
• excessive mural thickness
• the presence of intra- or extralumenal masses.
The size and depth of the peritoneal cavity in the
horse limit palpation to the caudal 30-40 per cent.
Because of the inability to examine the entire peri­
toneal cavity, subtle abnormalities identified on exami­
nation are often used to make inferences concerning
the more cranial regions of the peritoneal cavity.
Consequently, the lack of abnormal rectal examination
findings does not completely rule out an intestinal
abnormality.
The technique for rectal examination is described in
Chapter 1 . When performing a rectal examination in
horses with colic, proper restraint is even more impor­
tant than normal to ensure the safety of the horse and
the examiner. Horses with signs of unrelenting abdom­
inal pain should be sedated with xylazine (0.3-0.5 mgl
kg i.v. ) , detomidine (7-10 Ilglkg i.v. ) , or romifidine
(40-120 Ilg/kg i.v. ); these drugs can be administered
with butorphanol (20 Ilg/kg i.v.) to provide stronger
analgesia and more profound sedation.
Absence of fecal material on initial insertion of the
hand into the rectum, or the presence of dry, fibrin­
and mucus-covered feces is abnormal and is consistent
with delayed intestinal transit. Fetid, watery fecal mater­
ial is often present in horses with colitis. Large amounts
of sand within the feces may indicate a sand impaction
or sand-induced colitis.
In general, palpable characteristics of the abdominal
contents and viscera are often helpful in identifying the
particular segment of the intestine involved and the

severity of the condition. Severe gas-filled or ingesta-dis­
tended intestine, tight mesentery or tenia (bands ) , or
thickened or turgid intestine are indicative of intestinal
obstruction or strangulation. Free peritoneal gas or
crepitus within the intestinal wall is usually indicative of
intestinal rupture. A gritty or granular texture to the
peritoneal cavity is indicative of intestinal rupture with
contamination of the serosal and peritoneal surfaces
with ingesta.
Because the majority of the body and apex of the
cecum are beyond the examiner's reach the tautness
of the ventral and medial cecal tenia is used as an
indicator of the amount of ingesta within the cecum.
Normally the cecal tenia should be loose and easily
movable (Figure 9.4) . With increased amounts of
ingesta in the cecum the tenia become more taut. Pain
elicited on palpation of the ventral or medial cecal tenia
may be associated with tension of the ileum or its
mesentery. This has been associated with pain originat­
ing from the ileum and its vasculature, such as that
occurring with entrapment of the ileum in the epiploic
foramen.
Figure 9.4 Caudal view of a sta nding horse demonstrating
abdom inal structures that are palpable in the normal
horse during rectal exa m inatio n . Starting i n the left dorsal
abdom inal quadrant, and progressing in a clockwise direc­
tion, palpable structures include: caudal border of the
spleen, renosplenic l igament, ca udal pole of the left kid­
ney, ventral cecal tenia, cecal base, and the pelvic flexure.
Thel Melton, CAD special ists, Department of Educational
Resources and Dr IN Moore, Department of Large Animal
Medicine, U n iversity of Georg ia, Athens, GA 30602, with
permission
CLINICAL EVALUATION OF THE COLIC CASE 9
RECOGNITION OF INTESTINAL
ABNORMALITIES
Small intestine
Palpable small intestinal distention is always an indica­
tion of small intestinal obstruction. The obstruction
may be a physical obstruction such as an ileal impaction
or small intestinal strangulation, or it may be a func­
tional obstruction such as ileus secondary to enteritis or
non-strangulating intestinal infarction. The small intes­
tine is of a similar diameter to the descending colon.
The small intestine is distinguished from the descend­
ing colon by the absence of both an anti-mesenteric
band and fecal balls. During early obstruction, one to
two loops of easily compressible small intestine may be
identified (Figure 9.5). As the disease progresses the
distention increases and multiple loops of tightly dis­
tended, fluid-filled intestine are palpable side by side
(Figure 9.6) .
Non-specific small intestinal distention is the most
common finding in horses with small intestinal lesions.
However, specific findings identified on rectal examina­
tion will occasionally lead to a diagnosis. An ileal
Figure 9.5 Caudal view of a sta n d i n g horse demonstrating
a n ileal i m paction with early small intestinal distention.
The ileum may be palpable as a firm, tubu lar structure in
the center of the abdomen coursing toward the cecum.
Thel Melton, CAD specialists, Department of Educational
Resources and Dr IN Moore, Department of Large Animal
Med icine, U n iversity of Georg i a , Athens, GA 30602, with
permission
1 13
9 COLIC
Figure 9.6 Caudal view of a standing horse demonstrating
severe sma l l i ntesti nal distention. Multiple loops of gas­
and fluid-distended sma l l intestine are pal pable. Thel
Melton, CAD specialists, Department of Educational
Resources a nd Dr IN Moore, Department of Large An imal
Med icine, U n iversity of Georgia, Athens, GA 30602, with
permission
impaction, detected early in the disease process, may be
palpable as a firm, tubular structure in the center of the
abdomen coursing toward the cecum (Figure 9.5 ) .
Herniation of small intestine through the inguinal ring
in a stallion is palpable as small intestinal distention
with a segment of small intestine or mesentery coursing
into one of the inguinal rings. If the herniated loop of
small intestine is not distended, the specific diagnosis of
inguinal herniation may not be evident. In these cases
the inguinal rings often feel asymmetric, and gentle
traction on the mesentery associated with the affected
ring elicits a painful response. Jejunojejunal intussus­
ception causes generalized small intestinal distention,
but the intussusceptum is occasionally palpable as an
extremely thickened, edematous, tubular structure in
the caudal aspect of the abdomen. Ileocecal intussus­
ception is difficult to identifY per rectum, but early in
the disease process is occasionally identified as a turgid
mass in the right dorsal abdomen and sometimes it can
be appreciated that it is within the cecum.
Rectal examination findings in horses with proximal
enteritis may mimic those of a physical obstruction.
With enteritis, however, the small intestinal distention is
often less severe and easily compressible. With naso-
1 14
gastric decompression and intravenous fluid therapy
the intestinal distention often decreases.
Obstruction of the small intestine causes absorption
of fluid from the ascending colon and rapid dehydra­
tion of the ingesta in the ascending colon. The colon
becomes hard and indurated and feels as if it were vac­
uum sealed. In a horse with an early small intestinal
obstruction, and little or no palpable small intestinal
distention, the inexperienced examiner may interpret
this finding as a primary large colon impaction. The
tenia and haustra of an ascending colon that is secon­
darily dehydrated contour to the ingesta within the
intestinal lumen and are easily palpable. This is in con­
trast to a primary large colon impaction, where the
tenia and haustra become less distinct with increasing
colonic distention (see below, Large colon ) .
Cecum
Cecal distention may be a primary problem, such as
impaction of the cecum with ingesta or fluid, or more
commonly secondary to obstruction of the large or
small colon. Early in the development of a cecal
impaction, the apex of the cecum becomes distended
with ingesta, but is beyond the reach of the examiner.
Therefore, palpation of the ventral cecal tenia is used as
an indirect indicator of cecal filling. Normally the
cecal tenia should be loose and easily movable. With
increased filling of the cecum with ingesta, the tenia
become more taut and the cecum displaces toward the
midline. As the cecum becomes further distended, the
weight of ingesta in the apex pulls the cecal base cra­
nially within the abdomen, and the ventral tenia, which
normally courses from the right dorsal to right ventral
quadrant, crosses diagonally across the caudal
abdomen, from the right dorsal to left cranioventral
quadrant. As the cecum fills above the cecocolic orifice,
complete obstruction occurs and the cecal base fills
with fluid and gas (Figure 9.7) . The distended cecum
fills the right dorsal and ventral abdominal quadrants.
In cases of severe cecal tympany, either primary or sec­
ondary to a large colon obstruction, the cecal base feels
like a tightly distended balloon in the right dorsal quad­
rant. With marked cecal mural edema, the haustra
between the tenia become more prominent. The pres­
ence of severe cecal mural edema or emphysema is an
indicator of intestinal compromise and possible cecal
rupture, and is associated with a poor prognosis for
survival.
Cecal impaction and right dorsal displacement of
the large colon may be difficult to distinguish during
rectal examination. In cases of right dorsal displace­
ment of the large colon, the cecal base and tenia are dif­
ficult to feel, and the examiner's hand can palpate the

Figure 9.7 Ca udal view of a standing h orse demonstrating
a primary cecal impaction. With i ncreased fi l l i ng of the
cecum with i ngesta , the ten i a become more taut and the
cecum displa ces toward the midline. As the cecum fills
above the cecocolic orifice complete obstruction occurs
and the cecal base fills with fluid and gas. Thel Melton,
CAD special ists, Department of Educational Resou rces and
Dr IN Moore, Department of Large Animal Med icine,
U niversity of Georgia, Athens, GA 30602, with permission
dorsal aspect of the distended colon cranially and
another structure (cecum and its attachment) can be
felt medial to the colon. While in cecal impaction, cra­
nial palpation qf the dorsal aspect of the distended
cecum is limited by the dorsal attachment of the cecum.
Large colon
Abnormalities of the large colon have a variety of intesti­
nal positions and degrees of intestinal distention, and
include large colon impaction, left and right dorsal colon
displacement, and colon volvulus. Impaction of the large
colon usually occurs at the pelvic flexure and may be felt
in the left or right caudal abdominal quadrants. The
colon is enlarged and easily identifiable on palpation
(Figure 9.8) . The two free tenia of the ventral colon
course in a cranial-to-caudal direction, from the left
cranial abdomen to the left caudal abdomen. As the
impaction enlarges, the tenia may continue to the right
caudal abdomen, with the pelvic flexure lying in the right
caudal abdomen,just cranial to the pelvic rim . The con­
sistency of the ingesta forming the impaction may vary
CLIN ICAL EVALUATION OF THE COLIC CASE 9
Figure 9.8 Ca udal view of a standing horse demonstrating
impaction of the ventral colon and pelvic flexure. The
colon is enlarged and easily identifiable on palpation. The
two free tenia of the ventral colon course i n a cranial­
to-caudal d i rection, from the left cra nial abdomen to the
left caudal a bdomen. Thel Melton, CAD special ists,
Department of Educational Resources and Dr IN Moore,
Department of Large Animal Med icine, University of
Georgia, Athens, GA 30602, with permission
from soft and indentable to firm and indurated. With
severe impaction, the colon may fill the entire caudal
abdomen, and the haustra of the ventral colon become
indistinct. It is imperative that the examiner ensures
that the colon is not displaced. Primary large colon
impactions are usually treated medically, whereas horses
with colon displacements and secondary impaction
require surgery for resolution of the impaction.
Horses with impactions or obstructions (enteroliths)
of the right dorsal colon and transverse colon most
often present with generalized cecal and large colon
tympany. Occasionally, however, the lesion may be
identified on rectal examination. In these cases, the
impaction or enterolith may be ballotted with the exam­
iner's fingertips, but cannot be palpated in its entirety.
Abdominal surgery is generally necessary to confirm the
diagnosis.
Left dorsal displacement of the large colon (reno­
splenic entrapment) can be diagnosed by rectal exami­
nation if the colon is not markedly distended. The left
dorsal and ventral colon become entrapped within the
renosplenic space, between the spleen and left kidney
1 15
9 COLIC
(Figure 9.9 ) . The majority of the colon is palpable on
the left side of the abdomen with the tenia coursing
from the left craniodorsal abdomen to the left caudo­
ventral abdomen and if sufficiently enlarged to the
right caudoventral abdomen. Following the tenia cra­
nially and dorsally, the examiner can feel them enter
the renosplenic space. When moving the hand from left
dorsal abdomen to the dorsal midline, the examiner
should feel the head of the spleen, large colon and asso­
ciated tenia, renosplenic ligament, and left kidney to
confirm the diagnosis of left dorsal colon displacement.
With increased duration, the cecum often becomes sec­
ondarily distended with gas. If the colon is severely dis­
tended, the colon may fill the left caudal abdomen and
preclude examination of the renosplenic region. In this
case, left dorsal displacement may be suspected but
should be confirmed with percutaneous ultrasonogra­
phy. Displacement of the spleen medially and ventrally
may be associated with left dorsal displacement, but this
finding alone does not confirm the diagnosis of left
dorsal displacement.
Figure 9.9 Caudal view of a sta nding h orse demonstrating
a left dorsal displacement of the large colon. The left ven­
tral and dorsal colon are entrapped within the renosplenic
space. The colon is palpable on the left side of the
abdomen with the tenia coursing from the left cran iodor­
sal abdomen to the l eft caudoventral abdomen. Following
the tenia cranially and d orsa lly, the examiner can feel the
tenia enter the renosplenic space. Thel Melton, CAD spe­
cialists, Department of Educational Resources and Dr IN
Moore, Department of Large Animal Med icine, U n iversity
of Georg ia, Athens, GA 30602, with permission
116
Right dorsal displacement of the large colon may
assume a variety of anatomic configurations, but the
common finding for all right dorsal displacements is
displacement of the left ventral and dorsal colon lateral
to the cecum (Figure 9 . 1 0 ) . The colon retroflexes on
itself and passes between the cecum and right body wall.
The colon and associated tenia are felt immediately cra­
nial to the pelvic canal, coursing from the right caudal
abdomen, transversely across the abdomen , and then
continuing toward the left cranial abdomen. The pelvic
flexure usually comes to lie in the left cranial abdomen
beyond the reach of the examiner. The colon displaces
the cecum medially, and cranially, making it difficult to
palpate. With increased duration, the cecum often
becomes secondarily distended with gas. The degree of
intestinal distention is variable and severe gas disten­
tion of the colon will preclude complete examination of
the abdomen .
Torsion o r volvulus of the large colon i s easy to diag­
nose in the later stages of the disease. The horse's
abdomen is visibly distended and the large colon fills
Figure 9.10 Caudal view of a standing h orse demonstrat­
ing a right dorsal displacement of the large colon. The left
ventral and dorsal colons a re displaced lateral to the
cecum. The colon and associated tenia are felt immedi­
ately cranial to the pelvic can a l , coursi ng from the right
caudal abdomen, transversely across the abdomen, and
then conti n u ing toward the left cranial a bdomen. Thel
Melton, CAD special ists, Department of Educational
Resources and Dr IN Moore, Department of Large Animal
Med icine, U n iversity of Georg ia, Athens, GA 30602, with
permission

the entire abdomen (Figure 9.11) . In extremely
advanced cases, the examiner cannot introduce the
hand beyond the pelvic rim. The marked colonic dis­
tention causes the colon to fan-fold (pretzel) within the
limited space of the abdominal cavity. This is often evi­
dent as colonic tenia coursing transversely across the
caudal abdomen. With intestinal compromise, colonic
mural edema develops and is characterized by a thick­
ened colon wall and mesentery, and haustra between
the tenia becoming more prominent.
In the early stages of colon volvulus colonic disten­
tion may not be severe. Often the pelvic flexure and left
colons will be evident in the left abdominal quadrant.
The pelvic flexure may be moderately distended with
gas, displaced cranially, and appear to be suspended
within the middle left abdomen. The haustra and tenia
of the ventral colon may be palpated dorsal to the dor­
sal colon, indicating malpositioning of the colon. The
rest of the colon and the entire cecum are displaced cra­
nially and beyond the reach of the examiner. In these
cases, persistent abdominal pain and progressive colonic
distention are often evident on sequential examinations.
Figure 9.11 Caudal view of a standing h orse demonstrat­
ing a volvu lus of the l a rge colon. The large colon fills the
entire abdomen. The marked colonic distension causes the
colon to fan-fold with i n the l i m ited space of the abdomi­
nal cavity. This is often evident as colonic tenia coursing
transversely across the ca udal abdomen. Thel Melton, CAD
special ists, Department of Educational Resources and
Dr IN Moore, Department of Large Animal Medicine,
U n iversity of Georgia, Athens, GA 30602, with permission
CLIN ICAL EVALUATION OF THE COLIC CASE 9
Descending colon and rectum
Rectal examination of the horse with obstruction of the
proximal descending colon (fecalith or enterolith) is
usually characterized by generalized cecal and colonic
tympany, and marked rectal mucosal edema. Impaction
of the middle to distal descending colon has additional
findings of continuous, solid, ingesta within the
descending colon. This forms a uniform, smooth tube
of variable length in the central caudal abdomen
(Figure 9.12) . Individual fecal balls and haustra of the
descending colon are not usually evident in horses with
descending colon impaction. The ingesta is most often
soft and easily indentable, in contrast to large colon
impactions. In severe cases the entire descending colon
becomes impacted with ingesta. When this occurs, the
rectal ampulla may be pulled ventrally and to the left of
midline, because of the weight of the ingesta in the
descending colon and tension on the mesentery. This
makes complete examination of the rest of the
abdomen difficult if not impossible.
Figure 9.12 Caudal view of a standing h orse demonstrat­
ing an impaction of the descend ing colon with secondary
cecal and colonic tympany. I ndividual fecal balls and
ha ustra of the descending colon are not usua l ly evident in
h orses with descending colon impaction. The rectal
ampulla is pul led ventrally a n d to the left of mid line,
because of the weig h t of the ingesta in the descending
colon and tension on the mesentery. Thel Melton, CAD
specialists, Department of E duca tiona l Resources and
Dr IN Moore, Depa rtme n t of Large Animal Medicine,
U n iversity of Georgia, Athens, GA 30602, with permission
1 17
9 COLIC

Defects in the rectal mucosa, abnormal rectal
mucosal thickening, or frank blood on the sleeve after
rectal examination are indications of possible rectal
perforation. If a rectal perforation is suspected, a thor­
ough digital evaluation of the distal descending colon
and rectum should be performed with adequate
restraint and a bare hand. The distal descending colon
and rectum are circumferentially examined, moving
from a cranial-to-caudal direction. If a tear is identified,
the horse owner should immediately be informed of the
situation, and emergency first aid procedures should be
initiated (see Chapter 1 6) .
intestinal disease. These conditions are commonly
known as 'false' colics.
A differential diagnosis list of the more common
causes of 'false' colic are listed in Table 9. 1 .
Differentiation between ' true' and 'false' colics
depends upon obtaining an accurate history and per­
forming a careful physical examination coupled, where
appropriate, with further diagnostic procedures such
'
as clinical pathology. Although not always true, horses

SUMMARY Female reproductive tract Uterine torsion

Dystoclas
Rectal examination is an essential component of the Uterine hematoma
diagnostic evaluation of horses with abdominal pain. Uterine perforation
Proper restraint of the horse during rectal examination Retained placenta
Granulosa cell tumor
is of the utmost importance to insure the safety of the
Ovulation
horse and the examiner. The examination should be
performed in a consistent, systematic manner to ensure Male reproductive tract Orchitis
a complete and thorough examination and to minimize Seminal vesiculitis
the chance of missing a lesion.
Most often rectal examination does not yield a spe­ Urinary tract Cystic calculi
Renal calculi
cific diagnosis, but yields information regarding the seg­
U reteral calculi
ment of intestine affected, the severity of the problem,
Urethral calculi
and the need for surgical intervention. In general, dis­
Pyelonephritis
tention of any segment of intestine, large intestinal Cystitis
tenia coursing horizontally across the abdomen, or R uptured bladder
intra- or extra-lumenal masses are abnormal findings
and indicate intestinal obstruction and/or malposition­ Liver Acute hepatitis
ing. Rectal examination findings should always be con­ Cholangiohepatitis
Choledocholithiasis
sidered in conjunction with the results of the physical
examination, nasogastric intubation, abdominocente­ Spleen Splenic abscess
sis, and laboratory evaluation. Serial rectal examina­ Splenomegaly
tions are often necessary to determine resolution or
progression of the disease and the need for surgical Respiratory tract Pleuritis
intervention (see Decision for surgery) . Pleuropneumonia

Cardiovascular system Aortoiliac thrombosis

Aortic rupture
False (non-gastrointestinal) Acute hemorrhage
Myocardial infarction
colics Pericarditis

Musculoskeletal system Laminitis

T Mair
Acute exertlonal
rhabdomyolysis
Colic is not a specific disease or diagnosis, but simply
represents a clinical syndrome related to abdominal Nervous system Tetanus
pain. Although colic is generally associated with dis­ Botulism
eases of the gastrointestinal tract, conditions of other Seizures
body systems can sometimes cause abdominal pain, and Hypocalcemic tetany
Equine motor neuron
other painful diseases may produce clinical signs that
disease
are difficult to differentiate from pain due to gastro-

1 18
 CLINICAL EVALUATION OF THE COLIC CASE 9

exhibiting colic caused by disorders of systems other • agents to normalize intestinal contractions during
than the gastrointestinal tract generally paw and lie adynamic ileus
down for prolonged periods, but rarely roll violently. • therapy for ischemia-reperfusion injury
• antimicrobial drugs
• anthelmintics.

Medical therapies for colic Analgesic therapy

Relief of visceral pain in horses with colic is essential

T Ma i r
both on humane grounds and to minimize injury to the
horse and attending personnel during evaluation and
INTRODUCTION therapy. Even in mild cases owner distress over animal
pain is an important consideration.
The majority of colic cases encountered in practice are The most satisfactory method of pain relief is to cor­
associated with mild and non-specific signs. In one sur­ rect the cause of increased intramural tension resulting
vey, carried out over a 2-year period in general practice from distention or spasm. This may take time however,
in the UK, colics were categorized as and it is often necessary to provide temporary pain relief
chemotherapeutically to allow a thorough clinical exam­
• spasmodic and undiagnosed colics - 72 per cent
ination without risk of injury to the horse and personnel.
• pelvic flexure and other impactions 14.5 per cent
-
It is important to select a drug that will accomplish the
• surgical lesions (including strangulating
desired effect without creating complications such as
obstructions) - 7 per cent
depressing gut activity, predisposing to hypovolemia and
• flatulent colic 5.5 per cent
-
shock, or, most important, masking the signs of develop­
• colitis 1 per cent.
-
ing endotoxemia. The commonly used analgesic drugs,
The majority of colics encountered in first opinion prac­ their dosages, and relative efficacy for the control of
tice will, therefore, be amenable to medical therapy. In abdominal pain are summarized in Table 9.2.
many cases the response (or lack of response) to simple
medical treatments will also be helpful diagnostically.

AIMS OF MEDICAL TREATMENT

The aims of medical therapy in equine colic are to

• relieve pain Drug Dosage Efficacy

• restore normal propulsive motility of the gut Dipyrone 10 mg/kg poor to
• correct and maintain hydration and electrolyte or moderate
acid-base balance Phenylbutazone 2.2-4.4 mg/kg poor to
• treat endotoxemia moderate

• treat bacterial or parasitic infections (if present) . Flunixin meglumine 0.25-1.1 mg/kg good to
excellent
The first two aims given above need to be accomplished
Ketoprofen 1.1-2.2 mglkg good
without masking the clinical signs that must be moni­
Xylazine hydrochloride 0.2-1.1 mg/kg excellent
tored for proper assessment of the horse 's condition
Detomidine hydrochloride 10-4011g/k9 excellent
and progress.
A wide variety of therapeutic agents are used to treat Romifidine hydrochloride 40-80 1lg/k9 excellent

colic. These include Acepromazine 0.034J.1 mg/kg poor

Morphine sulfate 0.3-0.66 mg/kg* good

• analgesics to control visceral pain
Pethidine 2.0 mglkg poor
• agents to soften and facilitate the passage of ingesta
Butorphanol tartrate 0.05-0.075 mg/kg** good
(laxatives)
• fluids and electrolytes to improve cardiovascular Pentazocine 0.3-0.6 mg/kg poor to
moderate
function during endotoxic and hypovolemic shock
'Use only with xylazine or another alpha2 adrenoceptor agonist
• anti-endotoxin therapy
to avoid eNS excitement
• anti-inflammatory drugs to reduce the adverse "Doses in the upper range may cause ataxia
effects of endotoxin

1 19
9 COLIC
Walking
Walking the horse with mild colic frequently appears to
be beneficial, and in some cases may be the only treat­
ment necessary. Walking appears to have an analgesic
effect in addition to stimulating intestinal motility. It
also helps to prevent injury to the horse caused by
falling to the ground and rolling.
Gastric decompression
Gastric distention frequently occurs secondarily to
small intestinal obstruction or small intestinal ileus.
Since horses do not vomit, nasogastric intubation is nec­
essary to determine if gastric distention is present and
to provide relief. Decompression of the stomach is nec­
essary to relieve pain, and to prevent gastric rupture
and death. Large volumes of reflux ( 1 0-20 liters) may
be obtained in some cases and if necessary an
indwelling nasogastric tube may left in place to allow
frequent (approximately every 2 hours) decompres­
sion.
Non-steroidal anti-inflammatory drugs
(NSAIDs)
Among the most useful analgesics for both surgical and
non-surgical disease are the non-steroidal anti-inflam­
matory drugs. The therapeutic and adverse effects of
these drugs result from inhibition of cyclooxygenase
(COX) enzyme-mediated biosynthesis of prosta­
glandins. The NSAlDs non-selectively block both COX-
1 and COX-2 enzymes. Prostaglandins directly and
indirectly stimulate nerve endings. These drugs are
most effective as analgesics when some degree of
inflammation is present. The NSAlDs commonly
employed (dipyrone, phenylbutazone, flunixin meglu­
mine, and ketoprofen) differ greatly in efficacy in the
treatment of visceral pain in horses.
Dipyrone
Dipyrone is a very weak analgesic drug that can provide
only short term relief in cases of mild abdominal pain.
Combined with hyoscine N-butylbromide it is effective
in relieving intestinal spasm. It� failure to help reduce
or stop pain in individual cases should signal that a con­
dition exists that is more serious than a simple intestinal
spasm or tympanitic colic.
Phenylbutazone
Phenylbutazone provides no greater relief from visceral
pain than does dipyrone. However, the toxic side effects
of phenylbutazone are numerous and include gastro­
intestinal ulceration and nephrotoxicity. For this reason
the dosage should not exceed 4.4 mg/kg every 1 2
120
hours. Phenylbutazone has been shown to be superior
to flunixin meglumine in maintaining gastric motility
during endotoxemia, but this is likely to be of only
minor importance in horses being treated for abdomi­
nal pain.
Flunixin meglumine
Flunixin meglumine is the most effective of the NSAIDs
used to control visceral pain in horses. It has been
shown to block the production of prostaglandins,
specifically thromboxane and prostacyclin, for 8-12
hours after a single dose ( 1 . 1 mg/kg) . The duration of
analgesia produced varies from 1 hour to more than 24
hours depending on the cause and severity of the pain.
Although this drug has basic side effects similar to
phenylbutazone, there is a greater risk associated with
its use in its ability to mask clinical signs of intestinal
strangulation or obstruction by reducing heart rate,
relieving pain, and improving mucous membrane
color. If administered to horses in which the precise
cause of colic has not been ascertained, it is essential to
monitor closely rectal examination findings, nasogas­
tric reflux, peritoneal fluid, and heart and respiratory
rates over the following few hours. It should be admin­
istered to control severe pain and to diminish the
effects of endotoxins in horses needing transport to a
referral center for surgery.
Ketoprofen
Ketoprofen blocks both the cyclooxygenase and lipo­
oxygenase pathways. It is not as effective as flunixin in
alleviating abdominal pain.
RamiJenazone
This is another non-steroidal anti-inflammatory drug
sometimes used in combination with phenylbutazone.
Eltenac
Eltenac is a potent non-steroidal anti-inflammatory
drug with anti-pyretic and anti-edematous properties. It
is a relatively weak analgesic, but the anti-edema prop­
erties may make it useful in the postoperative colic
patient.
Sedatives
Alpha2 agonist sedative drugs include xylazine, detomi­
dine, and romifidine. These agents are effective anal­
gesics in horses affected by abdominal pain, but they
have the disadvantage of decreasing gastrointestinal
motility for the duration of the period of sedation.
Xylazine
Xylazine produces both sedation and visceral analgesia
by stimulating alpha2 adrenoceptors in the CNS,

thereby decreasing neurotransmission. At a dose rate of
1 . 1 mg kg-I i.v., the visceral analgesia provided by
xylazine appears to be similar to that of flunixin and the
narcotics. The duration of effect of xylazine is much
shorter (usually 1 0-30 minutes) than that of flunixin
making xylazine more useful for controlling pain
during evaluation of the cause of colic and its specific
therapy.
Potentially detrimental side effects of xylazine
include bradycardia, decreased cardiac output, tran­
sient hypertension followed by hypotension, ileus and
decreased intestinal blood flow; these may affect its
use in horses in shock. In contrast to the bradycardia,
hypertension, and intestinal hypotension which last
only a few minutes, the ileus and hypotension can be
prolonged. A reduced dosage of 0.2-0.4 mg/kg i.v.
can be administered in an attempt to reduce the sever­
ity and duration of the side effects. Alternatively it can
be used at the lower dosage in combination with a
narcotic agonist such as butorphanol.
Detomidine
Detomidine, another alpha2 adrenoceptor agonist, is a
more potent sedative and analgesic than xylazine. The
same complicating effects are likely to be present for
detomidine as for xylazine. Detomidine will reduce
intestinal motility similarly to xylazine and can mask
many of the signs that assist the clinician in diagnosing
the cause of the colic. Since it is such a potent drug, any
signs of colic observed within an hour of administration
are an indication that a severe disease that requires
surgery is present. Therefore it is a useful drug when
used with caution and preferably at the low dose rate of
10 rg/kg i.v. Potentiated sulfonamides should not be
given to horses sedated with detomidine.
Rnmifidine
Romifidine has a similar action to xylazine and detomi­
dine. At a dose rate of 40-80 Ilg/kg i.v. it provides
potent analgesia lasting 1-3 hours.
Acepromazine
Phenothiazine tranquilizers have a peripheral vasodila­
tory effect which is contraindicated in horses with
reduced circulatory volume because they block the life­
saving vasoconstriction that maintains arterial blood
pressure and insures, within limits, perfusion of vital
organs.
Narcotic analgesics
The analgesic and sedative effects of these drugs result
from interaction with central and/ or peripheral opioid
receptors.
CLINICAL EVALUATION OF THE COLIC CASE 9
Morphine
Morphine and pethidine are opioid receptor agonists.
They are potent analgesics, but morphine in particular
can cause excitement in horses unless used in combina­
tion with drugs like xylazine. Morphine is known to
reduce progressive motility of the small intestine and
colon while potentially increasing mixing movements
and increasing sphincter tone. The disadvantages of
morphine are sufficient to discourage its use in most
horses with abdominal disease.
Pethidine
Pethidine is a narcotic agonist with few side effects and
provides slight to moderate analgesia of relatively short
duration in horses with abdominal pain. Used repeat­
edly it can potentiate obstructions caused by impactions
by reducing colon activity.
Butorphanol
Butorphanol is a partial agonist and antagonist which
gives the best pain relief of the drugs in this group, with
the fewest side effects. It can be used in combination
with xylazine or the other alpha2 adrenoceptor agonists
in horses with moderate to severe abdominal pain to
increase the level of analgesia. The dose can vary from
0.05-0.075 mg/kg. Doses exceeding 0.2 mg/kg can
cause excitement. Butorphanol reduces small intestinal
motility but has minimal effect on pelvic flexure activity.
It is potent enough to stop colic for short periods of
time when it is caused by severe intestinal disease but
the pain from large colon torsion or small intestinal
strangulation may not be altered. When administered
without xylazine or another alpha2 adrenoceptor ago­
nist, even small doses of butorphanol may occasionally
cause head jerking.
Pentazocine
Pentazocine is a partial agonist which is slightly more
effective than dipyrone but less effective than xylazine
and flunixin in relieving visceral pain.
Spasmolytics
Increased frequency of intestinal contractions, for
example in spasmodic colic or spasms occurring oral to
intralumenal obstructions, cause pain which can be
relieved by spasmolytics. Spasmolytic drugs include
cholinergic blockers such as atropine and hyoscine N­
butyl bromide.
Atropine
Atropine is not recommended for use in horses with
colic because its effect in relaxing the intestinal wall and
preventing contractions can last for several hours or
121
9 COLIC
even days creating tympany and complicating the initial
problem with ileus.
Hyoscine
Hyoscine has a shorter muscarinic cholinergic blocking
effect compared to atropine and is effective in relaxing
the bowel wall. It is available in Europe combined with
dipyrone and is administered intravenously in doses of
20-30 m!.
Laxatives
Laxatives are commonly used in horses with colic to
increase the water content and softness of ingesta
thereby facilitating intestinal transit. The most common
indication for their use is in the treatment of large
colon impactions. In severe impactions, the effective­
ness of laxatives is increased by administering oral and
intravenous fluids concurrently. These medications
should never be administered orally in horses with naso­
gastric reflux.
Mineral oil (liquid paraffin)
Mineral oil (liquid paraffin) is the most frequently used
laxative in equine practice. It is a surface lubricant and
is administered at a dosage of 5-10 ml/kg once or twice
a day by nasogastric tube. Its effects are considered mild
and it is safe for prolonged use. It is commonly admin­
istered with water or saline and is considered by many
clinicians as the lubricant of choice for mild colonic
impactions.
Psyllium hydrophilic mucilloid
Psyllium hydrophilic mucilloid is a bulk-forming laxa­
tive which causes the fluid and ion content of feces to
increase by absorbing water. It has been considered to
be particularly useful for treating sand impactions. A
dose of 1 g/kg can be administered per os up to four
times a day. As a long-term treatment, it may be admin­
istered daily for several weeks to help eliminate sand
from the large colon. Recently the efficacy of psyllium
hydrophilic mucilloid in treating sand impactions has
been questioned.
Osmotic laxatives
Magnesium sulfate (Epsom salt) and sodium chloride
(table salt) can be used as osmotic laxatives in horses.
Research has shown that magnesium sulfate also stimu­
lates water secretion in the colon by a reflex action
immediately on administration. Undiluted osmotic lax­
atives will cause enteritis by osmotic damage to the
mucosal cells, so each dose of 0.5-1.0 gm/kg should be
diluted in 4 liters of warm water and administered by
nasogastric tube once or twice a day. Epsom salt should
122
not be administered longer than 3 days because of
severe enteritis and possible magnesium intoxication.
Dioctyl sodium succinate (DSS)
DSS is a surface-active agent with wetting and emulsifying
properties. It reduces surface tension and allows water
and fat to penetrate the ingesta. A dose of 1 0-20 mg/kg
can be administered as a 5% solution by nasogastric tube
every 48 hours. DSS can cause damage to the mucosa and
increases fluid permeability of colon cells, this can result
in mild abdominal pain and diarrhea.
Fluid therapy and cardiovascular support
Fluid, electrolyte, and acid-base imbalances commonly
occur in equine gastrointestinal diseases. While univer­
sally employed to support horses with severe intestinal
obstructions requiring surgery, the value of fluid ther­
apy for colic in a field situation has not been widely
appreciated. Fluid therapy is rarely, if ever, contraindi­
cated in adult horses with colic. The type of fluid and
rate of administration will change from the initial ther­
apy, which is designed to replace the deficits, to mainte­
nance therapy, which is designed to keep pace with
ongoing requirements. Detailed descriptions of fluid
therapy in the horse are provided elsewhere (see
Chapter 9) .
Intravenous administration of polyionic-balanced
electrolyte solutions (e.g. Hartmann's solution) will
help to maintain the intravascular fluid volume and aid
tissue perfusion. Normal saline (0.9% sodium chloride)
may also be used initially for rehydration, but should
not be used long term without evaluation of serum elec­
trolytes and acid-base balance because it tends to pro­
mote acidosis, hypokalemia, and hypernatremia. The
hydration status of the horse should be assessed by clin­
ical observations and measurement of packed cell vol­
ume and total serum/plasma protein. The percentage
dehydration of the patient can be estimated, and this is
used to calculate the volume of fluid necessary to cor­
rect the horse's fluid deficit. Horses with severe colonic
impactions may benefit from overhydration in an
attempt to hydrate and break up the impaction; a bal­
anced electrolyte solution can be administered continu­
ously at a rate of approximately 4-5 l/h for a 500 kg
horse. Horses with continued fluid loss by gastric evacu­
ation and sequestration of fluid into the bowel have
increased maintenance fluid requirements. The packed
cell volume and plasma protein levels of such cases
should be regularly monitored to assess the degree of
dehydration. If available, measurements of serum elec­
trolytes and blood gases are also helpful in determining
the type and quantity of fluids to be given, and to mon­
itor the effects of treatment.

In severe hypovolemic and hypotensive shock,
hypertonic saline (7% sodium chloride, 4 ml/kg) can
be administered initially to provide a rapid improve­
ment in cardiovascular function. However, this treat­
ment must be followed within 2 hours by isotonic fluid
therapy to replace the volume deficit.
The bicarbonate deficit and replacement require­
ments are based on the volume of the extracellular fluid
compartment, body weight, and base deficit as deter­
mined by arterial or venous blood gas analysis. The
following formula is used to calculate this deficit
bicarbonate deficit (mEq) = 0.3 x body weight (kg)
x base deficit (mEq/l)
One half of the deficit should be replaced over the first
several hours, and then the blood gas analysis repeated.
If the plasma protein concentration is low (less than
45 gil) and the horse is dehydrated, administration of
plasma (minimum of 2 liters given slowly intravenously)
will help to maintain plasma oncotic pressure and avoid
inducing pulmonary edema during rehydration with i.v.
fluids. Plasma is also helpful in treating horses with
en do toxemia (see below) .
Anti-endotoxin therapy
Endotoxin is the toxic lipopolysaccharide component
of the outer cell envelope of gram-negative bacteria.
Entry of endotoxin into the circulation occurs when the
intestinal mucosal barrier is damaged, for example in
strangulating and ischemic bowel disorders, and this
initiates a series of deleterious events involving the syn­
thesis and release of numerous inflammatory media­
tors. Severe endotoxemia frequently results in death.
The treatment of endotoxemia is discussed in greater
detail in Chapter 1 1 .
Purified endotoxin-specific IgG containing antibod­
ies against lipopolysaccharide extracts of a variety of
gram-negative bacteria is available in the UK This treat­
ment aims to promote the clearance of endotoxins
from the circulation prior to its interaction with inflam­
matory cells and the subsequent production of pro­
inflammatory mediators. Treatment early in the course
of the disease is therefore necessary.
Active immunization of horses with mutant core
polysaccharide vaccines is available in the US, although
the duration and degree of protection afforded by these
vaccines is uncertain. Hyperimmune plasma directed
against gram-negative core antigens provides antibodies
with cross-reactivity against a wide range of bacteria.
Normal equine plasma (2-10 liters) administered
slowly intravenously may also be beneficial, supplying
protein, fibronectin, complement, antithrombin III,
and other inhibitors of hypercoagulability.
CLINICAL EVALUATION OF THE COLIC CASE 9
Anti-inflammatory treatment of endotoxemia
Flunixin meglumine has been shown to suppress
prostaglandin and thromboxane production, and to
improve the clinical signs in equine endotoxemia.
Flunixin appears to be more effective than phenylbuta­
zone and other NSAIDs in this respect. A low dose of
f1unixin (0.25 mg/kg i.v. q. 8 h) effectively suppresses
endotoxin-induced CYclooxygenase-derived products
without masking the clinical manifestations of endotox­
emia. This treatment is valuable in the postoperative
management of many colic cases.
Drugs that alter intestinal motility
Postoperative ileus is the most common indication for
pharmacological manipulation of intestinal contractile
activity. Ileus may also occur in association with proxi­
mal duodenitis-jejunitis (anterior enteritis) and peri­
tonitis. There are two general methods by which drugs
may correct ileus caused by any disease. First, drugs may
directly stimulate contraction of intestinal smooth mus­
cle. Second, certain agents block the mechanisms by
which the disease inhibits motility, thereby restoring
normal contractions. Continuous or repeated gastric
decompression must be provided in addition to drug
therapy. The management of postoperative ileus is dis­
cussed in greater detail in Chapter 1 1 .
Neostigmine methyl sulfate
Neostigmine is an acetyl-cholinesterase inhibitor that
directly stimulates intestinal contractions. Doses of
0.0044 mg/kg (2 mg for an average sized adult horse)
can be administered subcutaneously or intravenously.
The duration of effect is very short ( 1 5-30 minutes) and
up to five doses may be given at 20-60 minute intervals.
If there is no response to this dose rate, and assuming
that the horse is not showing any evidence of side
effects, the dose of neostigmine can be increased by 2-
mg increments up to a total of 10 mg per treatment.
Neostigmine induces disorganized segmental contrac­
tions, and can actually decrease propulsive motility of
the jejunum and delay gastric emptying. It can also
cause abdominal pain by stimulating spasmodic
regional contractions. For these reasons many clini­
cians do not favor its use in clinical cases. However,
studies have shown that neostigmine can improve cecal
and colonic motility.
Metoctopramide
Metoclopramide is a non-specific dopaminergic antago­
nist that also augments the release of acetylcholine
from intrinsic cholinergic neurons and has adrenergic­
blocking activity. It is a potent gastrointestinal stimulant
when given at a dosage of 0.25 mg/kg i.v. ( diluted in
1 23
9 COLIC
500 ml of saline and administered over a period of
30-60 minutes ) , but in some cases has proved unsuit­
able because it can produce severe CNS side effects
(excitement, sweating, and restlessness) . However, it
may be safely administered to most horses as a continu­
ous infusion at 0.04 mg kg-1 h-1 •
Domperidone
Domperidone, a newer dopaminergic antagonist does
not cross the blood-brain barrier and at a dose rate of
0.2 mg/kg i.v. has been shown to block dopaminergic
receptors and prevent postoperative ileus induced
experimentally. It has potential for use in clinical cases.
Cisapride
Cisapride is a substituted benzamide with gastrointesti­
nal prokinetic properties. The mode of action is
believed to be enhancement of release of acetylcholine
from postganglionic intramural interneurons leading
to increased calcium flux. Cisapride does not have any
dopamine-blocking activity. In normal horses cisapride
has been shown to augment the amplitude of gastric
contractions, stimulate jejunal activity coordinated with
gastric contractions, enhance contractile activity of the
large and small colons, and stimulate coordinated activ­
ity at the ileocecocolonic junction. An injectable prepa­
ration of cisapride is no longer available but 1 0 mg
tablets, available for the treatment of motility disorders
in humans, can be administered orally in horses.
Although there is anecdotal evidence that cisapride is
also effective when administered rectally (0.2 mg/kg) ,
offering advantages in horses with gastric reflux, recent
studies have demonstrated that it cannot be detected in
the blood of horses after administration by this route.
Lidocaine (lignocaine)
Lidocaine has been used in horses with colic primarily
to treat ileus, but recently it has been found to be an
effective analgesic as well. Lidocaine exerts its analgesic
properties by decreasing afferent traffic through small
C fibers. In addition, it has anti-inflammatory proper­
ties and decreases the influx of inflammatory cells. The
plasma levels necessary for analgesia are much lower
than those required to block normal peripheral nerve
conduction. Lidocaine has also been shown to decrease
reperfusion injury by inhibiting the release of free radi­
cals and decreasing the migration of neutrophils at the
site of i�ury. Preliminary studies suggest that the proki­
netic effect of lidocaine may be useful in postoperative
ileus. An initial intravenous bolus at a dose rate of
1 .3 mg/kg (administered slowly over 5 minutes) can be
followed by a continuous intravenous infusion at a rate
of 0.05 mg kg-1 min-1 (diluted in saline or lactated
Ringer's solution) . Signs of toxicity include muscle
1 24
fasciculations, ataxia, and possible seizures. These signs
are more likely to happen if the initial bolus is adminis­
tered too rapidly.
Erythromycin lactobionate
Erythromycin is a macrolide antibiotic that appears to
have a prokinetic action on the intestine that is inde­
pendent of its antimicrobial action. It acts on enteric
cholinergic neurons through motilin and/or 5-HT3
receptors to stimulate the release of acetylcholine. A
dose of 2.2 mg/kg diluted in 1 liter of saline and
infused over 60 minutes may be administered every 6
hours. Alternatively it may be administered as a contin­
uous intravenous infusion at a rate of 0 . 1 mg kg-l h-1 • A
recent study in normal horses determined that a lower
dose of 1 .0 mg/kg is effective in stimulating both cecal
and small intestinal propulsive activity. Doses higher
than 10 mg/kg can potentially disrupt propulsive activ­
ity. There has been some concern that the prokinetic
response may diminish with repeated treatments
because of down-regulation of motilin receptors. An
association between erythromycin therapy and the
occurrence of colitis induced by Clostridium difficile in a
small number of horses has led some clinicians to ques­
tion the safety of this therapy.
Acetylpromazine (acepromazine) and yohimbine
These drugs are a-adrenergic antagonists. Their use is
based on the assumption that sympathetic hyperactivity
contributes to postoperative ileus. Norepinephrine
inhibits the release of the excitatory neurotransmitter
acetylcholine by stimulating alpha-2 receptors located
presynaptically on cholinergic neurons. Acepromazine
facilitates small intestinal transit in normal ponies. The
drug can also produce hypotension via antagonism of
alpha-l adrenergic receptors, so it is essential that the
horse should be well hydrated prior to administration.
Yohimbine hydrochloride is a competitive antago­
nist that is selective for alpha-2 adrenergic receptors.
When administered at a dose rate of 0 . 1 5 mg/kg intra­
venously it can reduce the severity of postoperative
ileus especially when used in combination with
bethanecol.
Bethanecol
Bethanecol is a muscarinic cholinergic agonist, which
stimulates gastrointestinal smooth muscle cells causing
them to contract. At a dose rate of 2.5 mg/kg, subcuta­
neously, bethanecol was shown to improve gastrointesti­
nal motility in an experimental model of postoperative
ileus when administered in combination with yohim­
bine. Bethanecol has also been shown to increase the
rate of gastric and cecal emptying in normal horses. A
common use of be thane col in horses is in the treatment

of gastric atony following correction of an outflow
obstruction in foals with duodenal ulcers. Side effects,
including abdominal cramps, diarrhea, salivation, and
gastric secretion, arise from enhanced parasympathetic
tone.
Spasmodic colic
illl !
T Mair
Spasmodic colic is the most common type of colic
encountered in adult horses. It probably accounts for
some 40 per cent of colic cases seen in general practice.
ETIOLOGY AND PATHOGENESIS
Spasmodic colic is believed to arise from spasms, or
abnormal and uncontrolled contractions, of the small
intestine. These dysfunctional contractions do not con­
tribute to aboral movement of ingesta through the
intestinal tract but result in pain to the horse due to
stimulation of mural stretch receptors. It is a func­
tional disorder that is rarely associated with any
morphological changes of the intestinal wall. It is
attributed to an increase in peristalsis and a propensity
to spasm.
Numerous causes of spasmodic colic have been pro­
posed, for example
• excitement
• physical exertion and fatigue
• parasitic migration through the bowel wall or
vessels
• moldy feed
• excessive grain or insufficient fiber
• weather changes
but none of these has been proven. An individual pre­
disposition to spasmodic colic occurs in some horses
resulting in recurrent bouts of colic.
The intestinal spasms are invariably transient and do
not persist long enough to cause significant bowel
obstruction. It is possible, however, that these abnormal
movements may predispose to a malposition of the
intestine that could then lead to a strangulation
obstruction.
CLINICAL SIGNS AND DIAGNOSIS
Uncomplicated spasmodic colic is characterized by
intermittent mild to moderate abdominal pain,
CLIN ICAL EVALUATION OF THE COLIC CASE 9
increased small intestinal and colonic sounds, and
increased heart rate (see below) . The paroxysmal
attacks of colic usually last from 5-10 minutes and are
separated by pain-free intervals during which the
horse's appearance and behavior are normal. There are
usually no metabolic derangements or changes in the
peritoneal fluid. The respiratory rate and heart rate
increase mildly during bouts of pain, but quickly return
to normal when the horse is quiet. The heart rate is
rarely elevated to more than 60 bpm.
The clinical signs of spasmodic colic include
• intermittent pain
• mild to moderate abdominal pain indicated by
pawing, flank watching, recumbency, and rolling
• increased borborygmi
• semi-liquid feces.
The hyperperistaltic activity is often audible at some
distance from the horse, and frequently has a 'metal­
lic' sound. Feces may be passed frequently and in small
amounts, and may have a soft to semi-liquid consis­
tency.
Rectal findings are often unremarkable, however
one or more spastically constricted loops of small intes­
tine may be palpable; these loops may subsequently be
felt to relax. In other cases mild gaseous distention of
the duodenum or cecum may be palpable.
Nasogastric intubation does not reveal any gastric
reflux and results of abdominal paracentesis are
routinely normal.
The diagnosis of spasmodic colic is usually made on
the basis of the characteristic clinical signs, the absence
of other significant findings on rectal examination, and
the response to treatment with analgesic and spas­
molytic drugs.
TREATMENT
Many horses with mild spasmodic colic improve sponta­
neously and require no treatment. However, if the
animal is in pain at the time of examination, some form
of analgesia should be provided. The administration of
a spasmolytic and analgesic drug combination such as
hyoscine and dipyrone will quickly abolish the spasms
and thereby relieve the pain. Xylazine, detomidine,
romifidine, and non-steroidal anti-inflammatory drugs
are also effective treatments. The treatment may be
repeated after several hours if necessary, but most cases
show no recurrence of colic when the effects of the
initial medication wears off.
The prognosis for recovery is excellent provided
there is no subsequent or associated malpositioning of
the bowel.
125
9 COLIC
Acute colic - the decision to
refer
T Mai r
The primary aim of the initial evaluation of the horse
affected with acute colic is to attempt to distinguish
horses with mild or uncomplicated disease processes
from those with potentially life-threatening diseases.
Referral of the colic case to an equine hospital may be
required to permit further evaluation and monitoring,
surgery and/or intensive care.
The initial assessment of the horse with acute colic
on the farm is fraught with difficulties, even for the
most experienced equine clinician . Distraught owners,
absence of competent lay assistance, and inadequate
facilities for handling and restraint are just a few of the
problems that the veterinarian may encounter. An
accurate diagnosis of the cause of acute colic may be dif­
ficult or impossible to achieve in such circumstances.
However, the clinician should not be too concerned
about the inability to reach a specific diagnosis in all
cases. Careful assessment and appropriate management
of acute colic cases are of much greater importance
than reaching a specific diagnosis. Indeed, in many
cases of acute colic, a specific diagnosis of the cause will
never be reached.
The past few decades have seen dramatic improve­
ments in survival rates of horses undergoing surgical
treatment for a variety of diseases causing colic. These
improvements have been associated with better under­
standing of the diseases, their pathophysiology and
methods of treatment, and greater availability of surgi­
cal facilities. However, despite improvements in survival
rates, many horses with intestinal ischemia and other
surgical diseases of the abdomen still die in spite of sur­
gical intervention. A delay in making the decision to
refer the case can represent one of the most critical fac­
tors that impacts upon the chances of survival. Early
referral is therefore of vital importance, and the pri­
mary veterinarian needs to address the question of
whether or not the case should be referred to a surgical
center (whether this be part of his or her own practice,
another private practice, or an academic institution) as
a matter of priority.
The decision to refer a horse with acute colic should
be regarded separately to the decision to perform
surgery. In some cases, the diagnosis of a surgical lesion
may be made at the initial assessment of the patient,
and immediate referral must, therefore, take place.
However, in many other cases, the decision to perform
surgery (see Colic - decisions for surgery) is only made
after re-assessment of the case over time and after eval-
126
uating the response to medical treatments. By the time
that the decision to perform surgery is reached in such
cases, the horse should already be located at the surgi­
cal facility so that surgery can be undertaken immedi­
ately. It is imperative, therefore, that referral of such
cases should have taken place before the final decision
to undertake surgery is reached.
Referral of a horse with acute colic should never be
regarded as unnecessary, even if the horse recovers
without surgery. Early transport of horses in abdominal
pain to a surgical facility does not constitute a decision
to perform surgery; it serves only to transfer the horse to
a location where it can be re-assessed (using further
diagnostic procedures that might not be available in the
field) and where immediate surgery can be undertaken
as and when deemed necessary. The surgeon is the
most qualified person to decide whether or not surgery
should be performed. The referring veterinarian need
not feel embarrassed or inadequate if the surgeon
decides that surgery is unnecessary - most owners will
be only too pleased to learn that their horse does not
require major (and expensive) surgery.
EVALUATION OF THE PATIENT
The evaluation of the horse with acute colic is under­
taken as described in other sections in this chapter. The
veterinarian should then be in a position to make a
qualified judgment about the necessity to refer the
horse to a surgical clinic. This judgment may need to be
constantly re-evaluated if initial referral is not deemed
necessary but the abdominal pain persists or recurs. It is
important that the results of examinations are carefully
documented so that accurate comparisons at different
times can be made. In this way important trends in the
course of the illness can be identified. This is particu­
larly important if a subsequent examination is carried
out by a different veterinarian in the practice. A printed
colic sheet listing the various procedures and providing
spaces for recording the findings at each examination is
of considerable value. In some cases the need for imme­
diate referral will be obvious without the necessity of
undertaking all components of the evaluation.
Factors which are helpful in determining the need
for referral include
• signalment
• geographical location
• medical history (especially relating to previous
episodes of colic)
• management and deworming history
• severity of pain and progression of colic since its
onset

• fecal production
• response to medical therapy (see Medical therapies
for colic)
• results of physical examination (see Physical
examination of a horse with colic)
• hematocrit (PCV) and total plasma protein (TPP)
estimations
• results of nasogastric intubation
• results of rectal examination
• appearance of peritoneal fluid.
Signalment
Age, sex, and breed may be important clues indicating
the possibility of certain diseases (e.g. meconium
impaction in foals less than 48 hours of age, inguinal
herniation in stallions and Standardbreds, strangulat­
ing lipomas in horses over 1 5 years of age, colonic tor­
sion in recently foaled mares, etc. ) . Miniature horses
with marked abdominal pain are likely to have a small
colon impaction, and it may be wise to assume that this
is the cause of colic in such animals unless proven
otherwise. Although the signalment will not necessarily
indicate the presence of a certain disease, it can be use­
ful information that should be kept in mind during the
rest of the evaluation.
Geographical location
Geographical location can be important, since some
diseases have a much higher incidence in certain loca­
tions, for example enterolithiasis in California.
Medical history
A history of previous illness may be helpful in making a
decision about the case or in guiding the veterinarian
toward specific diagnostic procedures. For example, a
history of strangles ( Streptococcus equi subsp. equi infec­
tion) in a horse with chronic or recurrent colic may sug­
gest the possibility of an abdominal abscess; a history of
infrequent, recurrent bouts of mild spasmodic colic
may suggest the likelihood of a further bout of spas­
modic colic.
Management and deworming history
Factors relating to the general management and
deworming history that can be helpful include
1. general history
• housed or at grass
• type of feed
• use of the animal
• daily routine
• parasite control
CLI NICAL EVALUATION OF THE COLIC CASE 9
2. recent history
• when the last feed was given
• consumption of feed and water
• recent changes in feeding, bedding, housing, or
routine
• recent deworming
• pregnancy
• recent exercise.
Some diseases, such as tympanitic (distention) colic, are
more likely to affect pastured horses than stabled
horses. Horses subjected to changes in diet or exercise
regime, or decreased water consumption because of
cold weather, may be more prone to develop colonic
impactions. Appearance of colic following administra­
tion of an anthelmintic drug may suggest the possibility
of larval cyathostomosis or intestinal obstruction by
ascarids (in young horses) .
Severity of pain and progression of colic since
onset
The most important factors of the recent history are the
time that has elapsed since the onset of clinical signs
and the severity of pain. The duration of colic may be
known precisely if the horse was observed at the onset
of clinical signs, but is often unknown, especially in
horses that are found with colic first thing in the morn­
ing. Skin abrasions around the eyes and over the tuber
coxae are indicative of recent rolling and other violent
behavior caused by severe pain. Marks on the stable
walls caused by the horse's kicking and excessive distur­
bance of the bedding, or flattening of an area of grass at
pasture, are further evidence that the horse is in severe
pain.
In general terms, horses showing signs of having
been in severe abdominal pain are more likely to have a
surgical lesion than horses showing signs of mild
abdominal pain. However, horses with a strangulating
intestinal lesion that has been in existence for more
than 4-6 hours may not currently show signs of pain
because of advanced necrosis of the affected bowel wall.
Such cases usually show signs of severe depression
(standing quietly with the head low and showing no
interest in the surroundings) , and there is likely to be
evidence of previous periods of severe pain as outlined
above. This stage of indolence is associated with severe
endotoxemia and may be mistaken by the owner as an
indication that the horse's condition is improving.
Although the degree of behavioral pain that the horse is
demonstrating is important, it must be remembered
that some horses are more stoical than others. Also, old
horses and ponies affected by strangulating lipomas
may sometimes not demonstrate the severe signs of
pain that might be expected.
1 27
9 COLIC

Fecal production the time of the re-evaluation, the horse may be found to
have either improved, to have developed conclusive signs
The nature and quantity of feces passed by the horse
indicating the need for referral, or to have remained
since the onset of colic can be useful information.
unchanged. A decision as to whether or not referral is
Decreased or absent fecal production is likely in horses
necessary can be made at the time of re-examination.
affected by intestinal obstruction. Soft, 'cow-pat' or diar­
Alternatively, referral may be considered at the time of
rheic feces might indicate colitis.
the first examination, especially if the horse is showing
any signs of dehydration or poor peripheral perfusion.
Response to medical therapy

Failure to eliminate abdominal pain or the recurrence Additional factors to evaluate

of abdominal pain following administration of appro­
For a detailed discussion of
priate analgesic and other drugs (see Medical therapies
for colic) may raise the index of suspicion of a surgical • results of the physical examination
lesion. However, certain factors must be taken into con­ • hematocrit ( PCV) and total plasma protein (TPP)
sideration when interpreting the response to therapy. estimations
Wherever the cause of colic is uncertain, and especially • results of nasogastric intubation
in horses where referral at some point in the future is • results of rectal examination
considered possible, administration of potent non­ • appearance of peritoneal fluid
steroidal anti-inflammatory drugs, such as flunixin meg­
see Physical examination of a horse with colic, and
lumine, should be avoided. Such agents may mask the
Colic - decisions for surgery.
early clinical signs of endotoxemia, thereby delaying the
A systematic clinical examination should be per­
decision to refer the horse or to undertake surgery until
formed to include the cardiovascular system, abdomen
extensive irreversible tissue damage has taken place. The
and state of peripheral circulation (Table 9.3 ) .
use of other, short-acting analgesic agents is therefore
recommended in cases of uncertain etiology. Good
clinical response to a weak analgesic, such as dipyrone,
suggests that the horse is very unlikely to be affected by
a lesion that requires surgical intervention.
Following the initial evaluation of the horse, it
Cardiovascular system
should be possible to classity the problem into one of Heart rate
three categories Pulse qual ity
I . a relatively benign problem requiring medical Appearance of mucous membranes

therapy Examination of the abdomen

2. a problem requiring surgical correction Abdominal d istention
3. a problem which might require surgery, but for Auscultation
which there is at present no conclusive evidence. External palpation
Rectal examination
Horses affected by conditions falling into the first cate­
Abdominal paracentesis
gory should receive appropriate medical therapy. This Nasogastric intubation
will usually involve the administration of an analgesic
agent, possibly with other drugs such as laxatives. In State of peripheral perfusion and hydration
many cases such treatment can be adequately per­ Capillary refill time
formed in the field and referral to a hospital is unnec­ PCV
TPP
essary. However, in horses with medical problems that
may require intensive therapy (such as colitis, peritoni­
tis, etc . ) , then referral to an equine hospital should be
considered early in the course of the condition.
Horses with diseases in the second category require FACTORS WHICH MIGHT INDICATE A
prompt referral to a surgical facility after appropriate NEED FOR REFERRAL
preparation before transport (see Horse preparation
for referral transport) . The decision to refer the horse affected by acute colic is
Horses with problems fitting the third category may frequently made as a result of a combination of factors
be treated on the farm with an appropriate analgesic and rather than one single observation. Some of these
re-examined after a period of approximately 2 hours. At factors are listed in Table 9.4.

128

Severe unrelenting pain
Absence of response to a n a l gesics
Rapid recurrence of pain following administration
of analgesics
Persistently elevated heart rate (especially over
60 bpm)
Progressively rising heart rate
Positive rectal findings
Large quantities or persistence of gastric reflux
Persistently reduced or absent borborygmi
Serosanguinous peritoneal fluid with i ncreased total
protei n and nucleated cell count
Exudative peritoneal fluid indicating peritonitis
Progressive cardiovascular d eterioration with rising
PCV (> 55%), TPP, i njected or cyanotic mucous
membranes, and prolonged cap i llary refill time
(> 2 sec)
Progressive abdominal d istention
Profuse watery d i a rrhea
Recurrent bouts of colic over a period of days or
weeks, especially if the frequency of bouts or
severity are increasing
Chronic colic persisting > 24 hours where no
diagnosiS has been reached
Colic - decisions for surgery
EM Gaughan and PD Van H a rreveld
INTRODUCTION
Although the decision for general anesthesia and surgi­
cal treatment of horses with colic should not be made
lightly, early surgical intervention often results in the
best outcome. Although the vast majority of horses with
signs of colic do not require surgical therapy, when
signs do suggest the need for surgery, performing it
early in the course of the disease leads to greater suc­
cess. This may also imply that some horses may have sur­
gical exploration performed when more conservative
care may have allowed survival. However, surgery may
reduce the morbidity of some colic cases and return
horses to normal in a more satisfactory fashion.
Therefore, straightforward, timely decisions, based
most often on physical examination findings generally
provide the greatest success rate for horses with colic.
In deciding the need for surgery in an individual
horse there is no single criterion that can be relied on.
Many horses with acute abdominal pain will require
CLIN ICAL EVALUATION OF THE COLIC CASE 9
repeated reassessments over a period of time before a
decision to perform surgery is reached. A change in one
or more clinical parameters may determine the need
for surgical or medical therapy. In other cases a deci­
sion can be made at a single examination. Careful con­
sideration of the horse's pain, response to analgesic
therapy, cardiovascular status, rectal examination find­
ings, amount of gastric reflux, and abdominocentesis
are necessary in determining the need for exploratory
surgery. Some of the more important indications for
performing exploratory laparotomy (celiotomy) in
horses with acute abdominal pain are
• severe, unrelenting abdominal pain
• pain that is refractory to analgesics or that shows
only temporary improvement with analgesics
• persistently elevated heart rate
• large quantities of gastric reflux
• absence of borborygmi
• abnormalities on rectal examination
• serosanguinous abdominal fluid with increased
total protein and total nucleated cell count
• progressive abdominal distention that is becoming
life threatening.
See also Table 9.5.
PHYSICAL EXAMINATION
Many horses with colic have physical examination find­
ings which directly indicate that surgical treatment is
required for survival. A thorough physical examination
may be the most important aspect of the management
of horses with colic, and it can certainly lead to appro­
priate and timely decisions for medical care and
surgery. Components of the physical examination that
are useful in assessing the need for surgery are
• heart rate
• respiratory rate
• rectal temperature
• degree of pain
• rectal examination
• nasogastric intubation.
Heart rate, respiratory rate, and rectal
temperature
Determination of vital signs should be completed for
every horse with colic. Respiratory rate may be the least
useful vital sign in assessing colic but the character of
breathing may be supportive in the final assessment.
Body temperature determination can be very important
in the cascade of decision making. Fever should be just
cause to re-examine a decision for surgery. A fever can
1 29
9 COLIC
Diagnostic examination Signs that suggest surgical
exploration
Temperature Normal
Heart rate Elevated
Abdominal pain Severe unrelenting
Rectal examination Multiple distended loops of small intestine
Tight tenia and haustra of the large colon
Thickened edematous i ntestinal wall
Nasogastric Intubation Reflux greater than 1 liter and pH > 5
Appearance of abdominal fluid Opaque and dark to orange or brown/green
be an indication that inflammation or sepsis may be the
cause of the colic pain, and that surgical manipulation
may not appropriately address the primary lesion.
However, some febrile horses can have abdominal pain
severe enough to warrant surgical intervention.
A horse's heart rate is the vital parameter that can
provide the most insight into current systemic status
and prognosis for survival. A sustained, elevated heart
rate can indicate deterioration in the cardiovascular sta­
tus related to progression of the gastrointestinal tract
disease, and the requirement for emergency surgical
treatment. In general, a heart rate which has risen to
60-70 bpm within 6 hours of the onset of colic gives rise
for concern, particularly if it remains high during quiet
interludes and in the face of adequate analgesia.
Degree and nature of pain
Pain is likely to be the most consistent indication for
surgical treatment of horses with colic. Horses with
severe, unrelenting colic that is unresponsive to anal­
gesics usually require emergency surgical management.
If pain is readily modified and managed with analgesic
medications or physical manipulation, surgery may not
be imminently necessary. Episodic, moderate to severe
abdominal pain usually indicates the need for aggres­
sive treatment and often surgery. Recurrent or chronic
pain, in the face of appropriate conservative manage­
ment and additional diagnostic findings quite often
indicates that surgery will be required to reach a suc­
cessful outcome.
Rectal examination
Abnormalities in intestinal location, texture, and con­
tent that are palpable per rectum can also provide
1 30
Signs that suggest further
monitoring and medical
management
Elevated
Normal
Mild
Clear yellow color
distinct indications for surgery. Small intestinal disten­
tion which is palpable on rectal examination and is pre­
sent without fever usually requires emergency surgery.
The magnitude of distention and tympany should be
assessed, for multiple loops of small intestine and very
tight tenia and haustra of the large colon usually indi­
cate that surgical treatment will be necessary. Intestine
which has a thickened or edematous texture on rectal
examination may justify surgical exploration of the
abdomen. Heavy, non-indentable intestine, believed to
be filled with impacted ingesta may also be an indica­
tion for surgery when conservative treatment fails. If the
impacted ingesta is in the cecum, early surgical inter­
vention should be strongly considered.
Nasogastric intubation
Passage of a nasogastric tube can be a diagnostic aid as
well as therapeutic in the evaluation and treatment of
horses with colic. Because of the normal function of the
cardiac sphincter, horses do not vomit and spontaneous
reflux of small amounts of gastrointestinal contents has
been associated with a grave prognosis. A nasogastric
tube should be passed very early in the course of the
evaluation of any horse with severe unrelenting colic
pain. This procedure should probably be a part of the
total baseline examination of any horse with colic.
Placing a nasogastric tube into the gastric lumen can
reveal the magnitude and nature of fluid and ingesta
sequestered or refluxed into the stomach. The pres­
ence of a substantial volume (> I liter) of easily obtain­
able gastric reflux and fluid with an increased pH (> 5)
have been associated with the potential need for surgi­
cal treatment. Reflux as a single abnormal finding does
not necessarily indicate a need for surgery. The results

of passing a nasogastric tube should be interpreted in
combination with the systemic physical examination,
including body temperature and rectal examination.
Horses with proximal enteritis can have very large vol­
umes of basic fluid reflux from the stomach via a naso­
gastric tube. Horses with proximal enteritis, however,
are frequently febrile and the colic pain associated with
the disease is often palliated with decompression of the
stomach through a nasogastric tube. With this response,
surgery may not be essential. Pain again becomes the
determining factor, in combination with nasogastric
reflux, whether or not surgery is required to treat
affected horses.
EVALUATION OF PERITONEAL FLUID
Results of peritoneal fluid evaluation can lend evidence
that surgery may be indicated for horses with colic. The
results of abdominocentesis may not be as essential in
decision making when a horse is located at the surgical
venue, as it may be when decisions are being made for
referral to the surgical site. Most physical examination
findings override a requirement for abdominocentesis.
However, peritoneal fluid can be readily and safely har­
vested, and some quick information can be determined
without extensive laboratory evaluation (see Chapter
2) . When the normally clear yellow color of peritoneal
fluid changes to opaque and dark, to orange or
brown/green, then substantial compromise of bowel
integrity is likely and the decision for referral for
surgery is well grounded or arguably too late. The total
protein content of peritoneal fluid can be readily
obtained from a refractometer and elevations in pro­
tein can also support decisions for surgery. However, a
total protein content of less than 2.5 g/ dl (25 gil) does
not always mean that vascular compromise is absent.
Brown/green fluid with particulate matter present can
indicate that the intestine has ruptured. It must also be
recalled that an inadvertent tap of the bowel lumen
can confuse the diagnostic picture and, therefore,
abdominocentesis results should continue to be inter­
preted in close conjunction with the physical examina­
tion findings.
ULTRASONOGRAPHY
Ultrasonographic examination of the abdomen per rec­
tum and from a ventral, percutaneous approach can
provide additional information that may lead to a deci­
sion for surgery (see Chapter 2 ) . The percutaneous
examination is especially helpful for foals with colic,
and can be helpful in the assessment of adults as well.
CLINICAL EVALUATI ON OF THE COLIC CASE 9
Volumes of peritoneal fluid and some indication of its
nature can be determined with ultrasonography. Small
intestine, when distended, can be examined in cases
that are not suitable for rectal palpation, and therefore,
earlier decisions for surgery may be appropriately
made. Motility patterns and texture of bowel may also
be assessed with careful ultrasound examination.
Thickened intestinal wall, occasionally with gas patterns
in the submucosa, and protracted ileus can also support
decisions for surgery. Specific diagnoses are not
commonly determined with ultrasound, but some are
possible. Left dorsal displacement of the large colon
(nephrosplenic entrapment) can be diagnosed by ultra­
sonographic examination from a percutaneous site at
the dorsal aspect of the left side of the abdomen and
surgery may be necessary if other management tech­
niques fail. Occasionally, intra-abdominal masses can
be detected by ultrasound examination from an exter­
nal or rectal approach, and when associated with colic
signs, surgery may be indicated. Intussusceptions in
foals can often be diagnosed by ultrasound examina­
tion.
RESPONSE TO MEDICAL THERAPY
Another indication that a horse may require surgical
treatment is when appropriate medical or conservative
therapy has failed to resolve colic signs. Surgery may be
necessary with recurrent pain, especially if it is severe.
Low grade pain can also become an indicator of surgi­
cal need when typical management with analgesic med­
ication and physical manipulation do not succeed in an
acceptable time course. Repetitive and frequent admin­
istration of non-steroidal anti-inflammatory drugs can
be problematic, in that a confused and inappropriate
assessment of colic signs can be made and time lost
when surgery may be required. The high dose of flu­
nixin meglumine ( 1 .0 mg/kg) is best administered at
1 2 hour intervals. More frequent administration is not
indicated and can only serve to delay more appropriate,
aggressive treatment. At times, failure of conservative
management to improve the conditions found on rectal
examination can also be an indication for surgery. This
is most common when managing large intestinal
impactions. Some large colon impactions and many
cecal impactions require surgical decompression
because of continued mild colic signs and a lack of
improvement in the original status of the affected intes­
tine.
The concept of recurrent signs and possible failure
to respond as expected to conservative management
techniques is also historically important. Surgery may
be an earlier consideration in case management if a
131
9 COLIC
chronic course is already known at the first examina­
tion. This is also an important time to review previous
medication with clients. All physical examination and
ancillary diagnostic findings must be interpreted in
light of current and previous medications.
CLINICAL PATHOLOGY
Occasionally, laboratory tests can lead decision making
toward surgery. Laboratory results alone are rarely the
sole indications for surgery. Complete blood count
(CBC ) , electrolyte, and blood gas determinations are
solid support for physical examination indications for
surgery. An elevated white blood cell count may support
a diagnosis of an intra-abdominal abscess and a need
for surgery. Elevation in hematocrit, anion gap, and
deterioration from normal electrolyte and blood gas
profiles are consistent with cardiovascular compromise
resulting from the progression of an intestinal lesion
that requires surgical treatment. Laboratory data may
also be a helpful diagnostic tool in the rare case of colic
not caused by intestinal disease, for example liver
disease.
CONCLUSIONS
Many factors must be considered when making the
decision to perform surgery. Sometimes surgical explo­
ration of the abdomen is necessary before a diagnosis
can be made. Most pre-surgical diagnoses are not defin­
itive of a precise lesion but suggest which anatomic
aspect of the intestines is involved. At times the source
of colic pain is not apparent and surgical exploration is
indicated for diagnostic and potentially therapeutic
purposes. This approach should not be undertaken
lightly but should be considered in a timely manner as
case management progresses. Timely, as early initiation
of surgical treatment is a major factor in the successful
outcome for horses that need surgery.
Preparation of the horse for
referral transport
_r I _7 r ?FUJIi IMIIII 711 J r
A Worster
INTRODUCTION
The objective of preparing a referral patient is to
improve or stabilize the hemodynamic status of the
132
patient and reduce morbidity during transport. Early
aggressive treatment aims to
• stabilize hypovolemia
• provide adequate analgesia
• counteract endotoxemia
• provide gastric decompression.
Because of sweating, decreased water intake, increased
intestinal secretions, and decreased intestinal absorp­
tion, hypovolemia can be significant in both large colon
and small intestinal disorders. A large colon can pool
up to 40 liters of fluid with additional loss of sodium
and protein through the compromised mucosal wall.
Small intestinal ileus, obstruction, and anterior enteritis
create pooling of fluids in the intestinal tract and reflux
in the stomach. Hypovolemia from third-space fluid loss
is exacerbated with intestinal strangulation or volvulus.
Endotoxemia from compromised bowel causes further
hypovolemia by maldistribution of blood and an
increase in endothelial permeability.
MANAGEMENT OF HYPOVOLEMIA
A large gauge catheter should be placed for intravenous
administration of fluids and medications. A 10- to 1 4-
gauge catheter should be used in an adult horse, while
smaller foals may require a 1 6- or I S-gauge catheter.
The catheter length used should be greater than S.5 cm
(3.5 in) for a foal and 14 cm (5.5 in) for an adult. The
jugular vein is the most common site for aseptic
catheter placement. The catheters should be as non­
thrombogenic as possible. Catheter materials ranked
according to their decreasing reactivity are polypropy­
lene, Teflon, silicon, rubber, nylon, polyvinykhloride,
and polyurethane. The more commonly used 14 cm
(5.5 in) , 1 4-gauge catheters are made of Teflon or
polyurethane and tend to cycle at the insertion site.
Teflon is a short-term catheter material and should be
replaced after 2-3 days of use. The polyurethane
catheter is less reactive and may maintain functionality
without morbidity for 1 0-21 days. Therefore, a
polyurethane, central venous catheter (20 cm/S.O in,
16-gauge, e.g. Mila International, Inc, Erlanger, KY) is
often used as a long-term catheter. This over-the-wire
catheter is more flexible and less prone to cycling at the
insertion site. The central venous catheter also has a
one-way intralumenal valve, that prevents blood loss or
air embolism if the fluid administration set becomes dis­
connected during transport. Wrapping the catheter site
prior to transportation helps prevent inadvertent
removal.
Isotonic fluids such as lactated Ringer's solution or
plasmalyte are appropriate to replace a deficit within

Body weight
deficit (%)
Mild 5-7
Moderate 8-10
Severe >10
the interstitial spaces. To estimate replacement volume
of fluids needed, use
per cent dehydration x body weight (kg) = liters of fluid
(see Fluid and electrolyte therapy and acid-base bal­
ance in horses with abdominal pain ) . Therefore, a
500 kg horse that is 5% dehydrated would require
25 liters of fluid to become normovolemic (see Table
9.6) . Isotonic fluids expand the interstitial space but do
not maintain the vascular volume; so with ongoing
endotoxemia and hypovolemic shock, hypertonic solu­
tions or colloids may be more appropriate for pro­
longed transport. These solutions may be followed with
isotonic fluids during transport, provided the horse's
degree of pain and movement is adequately controlled.
Hypertonic saline 7.5% ( 1 -4 ml/kg) may be admin­
istered to maintain vascular volume for up to 60 min­
utes. Hypertonic saline will draw fluid from the
interstitial and intracellular space and should be fol­
lowed by isotonic fluids within 1-2 hours. Hypertonic
saline may be combined with dextrans to prolong the
effect. Synthetic colloids also help maintain the intravas­
cular volume (dextrans for 2-6 hours or hetastarch for
up to 24 hours) . Plasma administration should be con­
sidered in cases of hypoproteinemia « 4.0 g/dl) or sep­
sis. Plasma is the most physiologic fluid and may help
maintain intravascular oncotic pressure for 2-3 days.
Plasma has anti-endotoxin effects as well as macro­
globulins, antithrombin III, and fibronectin.
MANAGEMENT OF PAIN
Adequate analgesics are critical to control the patient
during transport. This is especially important if a horse
is transported while receiving intravenous fluids; it is
important to have it confined and adequately con­
trolled. Adequate analgesics, such as alpha2 adrenergic
agonists and anti-inflammatory drugs, are important for
mediation of pain. Alpha2 adrenergic agonists have been
shown to have the most immediate and potent effect on
gastrointestinal pain. Xylazine (0.2-l .0 mg/kg) has a
CLINICAL EVALUATION OF T H E COLIC CASE 9
Liter deficit Clinical signs
(SOO.kg horse)
25-35 Decreased skin turgor
40-50 Sunken eyes, depression
>50 Cold extremities, recumbency
profound analgesic effect for 1 5-30 minutes and deto­
midine (0.006-0.02 mg/kg) for 30-60 minutes. When
there is mild visceral pain, a prolonged analgesic effect
may be apparent for up to 4 hours. Xylazine and deto­
midine worsen hypotension and decrease gastrointesti­
nal motility. Although xylazine has a shorter duration of
action, its use is preferable since it has less pronounced
hypotensive effects and decreased gastrointestinal
motility compared to detomidine. Butorphanol
(0.01-0.02 mg/kg) may potentiate the analgesic effects
of the alpha2 agonists for up to 4 hours. Therefore,
xylazine in combination with butorphanol is commonly
administered intramuscularly for a prolonged effect.
Flunixin meglumine ( 1 . 1 mg/kg) is commonly used
for visceral pain and is a potent anti-inflammatory drug
which acts by inhibiting the cyclooxygenase pathway.
Flunixin has a 2-hour delayed onset and duration of
action of 1 2-24 hours. Gastrointestinal ulceration and
masking of surgical colic are potential risks when multi­
ple flunixin doses are given.
MANAGEMENT OF ENDOTOXEMIA
AND HEMODYNAMIC DISTURBANCES
A low dose of flunixin (0.25-0.5 mg/kg) is beneficial in
endotoxemic shock because it inhibits prostaglandin-I­
mediated vasodilation and minimizes hypotension.
Ketoprofen ( 1 . 1 mg/kg) inhibits both the cyclooxygenase
and lipooxygenase pathways. It is less ulcerogenic but also
has decreased analgesic properties compared to flunixin.
Other drugs frequently used to decrease endotoxin
include polymyxin B (6000 IU/kg i.v.) , antiserum
( Salmonella typhimurium) 1 .5 ml/kg i.v., dimethylsulf­
oxide (DMSO) 0.5-1.0 g/kg i.v. b.i.d., and pentoxi­
fylline (8.5 mg/kg p.o. b.i.d. ) . Both polymyxin B and
hyperimmune antiserum bind lipid A, the core
lipopolysaccharide of circulating endotoxin. Polymyxin
B has been shown to decrease the effects of endotoxin
in foals. Conversely, the use of hyperimmune antiserum
in one study increased endotoxic effects in foals. DMSO
is an oxygen-free radical scavenger and may be useful in
preventing damage from cell membrane peroxidation
1 33
9 COLIC
that can accompany endotoxemia. Interestingly,
numerous studies have shown no benefit in intestinal
reperfusion injury with DMSO administration.
PentoxifYlline decreases tumor necrosis factor and
interleukin-5 release by macrophages, decreases throm­
boxane B2 release by platelets, increases red blood cell
deformability, and causes vasodilation. The decreased
thrombin formation and vasodilation may be beneficial
for treatment of laminitis as well as endotoxemia. The
hemodynamic effects may make pentoxifYlline use
more appropriate in postoperative colic or after stabi­
lizing hypotension in medical cases.
GASTROINTESTINAL PREPARATION
Nasogastric intubation with a large diameter ( 1 .5 cm or
5/8 in) tube is essential in horses with small intestine
Figure 9.13 Nasogastric intubation . The nasogastric tube
should be secured to the halter prior to transportation
1 34
disease. Nasogastric intubation is recommended for
horses being transported for over 3 hours, a heart rate
more than 50 bpm, or signs of progressive small intes­
tine disease. Although nasogastric intubation has not
been proven to prevent gastric rupture, the high
esophageal sphincter tone in horses can cause signifi­
cant gastric distention from small intestinal disease.
The nasogastric tube should be secured to the halter
(Figure 9 . 1 3 ) and the distal limbs should be wrapped
prior to transport.
CONCLUSION
Early referral and aggressive treatment are particularly
important for any condition involving strangulated
bowel that can become irreversibly compromised
within 5 hours. A good preoperative physical status is
directly correlated to an improved prognosis following
surgery. The recent increase in long-term survival rates
in small intestine disease from 50-80 per cent may be
attributed to earlier referral and better patient stabiliza­
tion techniques. Early, aggressive medical therapy with
referral has helped decrease the morbidity and mortal­
ity of colicky horses.
Intravenous catheterization
and complications
T Divers
INTRODUCTION
Intravenous catheter placement is performed in virtu­
ally all horses and foals that are hospitalized for any
gastrointestinal disorder. Intravenous catheterization is
performed in a smaller percentage of horses treated on
the farm. There are many things to consider when plac­
ing or evaluating an intravenous catheter in the horse
• how long the catheter will be needed
• cost
• ease of placement
• type of medication to be administered
• volume and rate of administration
• venous access.
Once the catheter is placed, questions that arise include
• when to replace it
• whether or not to bandage
• the frequency of heparinization
• signs of complications.

Signs of complications and management of the
catheter is particularly relevant since the horse with gas­
trointestinal problems has the greatest complication
rate of any critical care equine.
CATHETER TYPES
There are three basic types of catheters in general use
1 . over-the-needle
2. through-the-needle
3. over-the-wire (Seldinger) .
Most intravenous catheters that are commercially avail­
able are made of either Teflon or polyurethane. Silastic
or silicone catheters are infrequently used by equine
practitioners and are not readily available. With the
widespread availability of long polyurethane over-the­
wire catheters, there is currently very little indication
for silastic catheters.
Teflon over-the-needle catheters
These are less expensive and easier to place than
polyurethane over-the-needle or over-the-wire catheters
and through-the-needle catheters. Therefore, Teflon
catheters are frequently used when
• intravenous catheterization time is expected to be 2
days or less
• speed of catheter placement is critical (e.g. in cases
of severe abdominal pain, septic shock, etc.)
• placement of the catheter is expected to be difficult
because of either restraint problems or difficulty in
visualizing the vein
• help is minimal.
Teflon catheters are generally stiffer and more throm­
bogenic than polyurethane catheters. Because of their
stiffness they are also at greater risk of kinking at the
skin-vein junction than softer catheters. Their stiffness
may also cause increased movement at the skin-vein
junction resulting in a seemingly greater incidence of
cellulitis at this site in comparison to over-the-wire
polyurethane catheters. On very rare occasions, a
Teflon catheter may break off at the kink site. Another
disadvantage of Teflon over-the-needle catheters is that
if there is repeated manipulation of the needle within
the catheter during a difficult placement, fraying of the
catheter tip may occur enhancing thrombogenecity.
Polyurethane catheters
Polyurethane catheters can be purchased as over-the­
needle or over-the-wire types. Polyurethane over-the­
needle catheters are more expensive than Teflon
over-the-needle catheters but are less thrombogenic
CLIN ICAL EVALUATION OF THE COLIC CASE 9
and can be left in place for longer. Polyurethane over­
the-needle catheters are indicated when
• the time of catheterization is expected to be more
than 2 days
• the medical condition, for example sepsis and/or
protein-losing enteropathy, make the horse more
prone to thrombosis
• adequate help is not present to place an over-the­
wire catheter.
Polyurethane over-the-wire catheters
These are the most commonly used catheters for
horses and foals in intensive care. The over-the-wire
polyurethane catheters are longer and more flexible
than over-the-needle polyurethane or Teflon catheters
and are, therefore, more likely to float in the middle of
the vein, have less contact with the vessel wall and are,
therefore, less thrombogenic. In neonatal foals, the
catheter tip is generally in the anterior vena cava or the
right heart which further decreases any chance of
thrombosis. If the catheter is found by X-ray (all com­
mercial catheters are radio-opaque) to be in the right
ventricle, it should be backed out to prevent damage to
the ventricular wall. The catheter tip may reside in the
anterior vena cava in some adult horses if placed low in
the neck and may, therefore, be used to measure cen­
tral venous pressure. The over-the-wire polyurethane
catheters have the following disadvantages
• more than one person may be needed to place the
catheter
• flow rate is generally a maximum of 3-4 liters/hour
• increased expense.
Additionally these catheters are available as single,
double, or multi-lumen catheters. The multi-lumen
catheters are especially useful for critical care foals
receiving parenteral nutrition, antibiotics, crystal­
loids/ colloids, and other medications. Some
polyurethane catheters have silver sulfadiazine and/or
chlorhexidine impregnated into the catheter material
which reduces catheter-related infections. Although the
initial investment is an added expense, these catheters
are often left in place for several days to several weeks.
Like all catheters, they may occasionally become
occluded or displaced by horses rolling in the stall or
the recovery room, excessive rubbing at the catheter, or
by the mare chewing on the foal' s catheter.
Polyurethane through-the-needle catheters
These catheters are also available in different lengths.
These are excellent catheters but some veterinarians
find the peel-off-needle more awkward than the over­
the-wire method.
1 35
9 COLIC
In the great majority of horses and foals catheters are
placed down the jugular vein. The upper middle cervi­
cal area is most often selected and the area clipped and
scrubbed. A local anesthetic is used in many foals and
also in a few 'needle shy' horses prior to needle place­
ment. If an over-the-needle catheter is used, the
catheter should be filled with heparinized saline prior
to jugular puncture. The over-the-wire method is
demonstrated in Figures 9.14, 9 . 1 5, and 9.16. After
Figure 9.14 The l-wire is pushed through the adaptor and
needle into the lumen of the jugular vein
Figure 9.15 The polyurethane catheter is fed over the wire
into the jugular vein
1 36
placement of the catheter, a short extension set is
attached to the catheter and a cap placed at the end.
The catheter and extension set are then sutured (occa­
sionally glued) to the skin. The catheters are generally
left unwrapped for most adult horses, but foals may
require wrapping as they are more prone to scratch the
catheter with their hind feet or the mare may chew at
the catheter. On rare occasions it may be necessary to
place the catheter in a vein other than the j ugular vein.
Cellulitis of the neck, unilateral or bilateral j ugular vein
thrombosis ( partial or complete) , and severe head
edema, are some of the reasons for choosing another
site. The cephalic and lateral thoracic veins are alterna­
tive sites. Over-the-wire catheters have remained func­
tional in these sites for at least 3 weeks. If a venous site
cannot be located in a foal, i ntra-osseous fluids should
be considered.
CATHETER REPLACEMENT
There is no set time that a catheter must be replaced.
Teflon catheters are generally replaced every 2-3 days.
Polyurethane over-the-needle catheters may be left in
for several more days if there is no local swelling or pain
and there is no evidence of developing occlusion as
determined by resistance to medication flow. Using the
same criteria, over-the-wire catheters are commonly left
in place for 1-2 months if needed.
Figure 9.16 The catheter placement is complete and the
wire i s withdrawn. The catheter hub and the attached
extension can now be sutured to the skin

COMPLICATIONS
Complications are common in horses with gastrointesti­
nal disorders for a number of reasons
• colicky signs such as rolling increase the chance of
the catheter kinking and contamination at the
skin-vein junction
• rapid placement in an emergency situation
increases the chance of contamination
• rapid intravenous fluid flow rates as required for
many horses with abdominal pain or diarrhea
increase turbulence at the tip of the catheter and
further damage the endothelial wall increasing the
chance of thrombosis.
Additionally, horses with sepsis resulting from ischemic
or inflammatory bowel disease have excessive stimula­
tion of procoagulants, and horses with protein-losing
enteropathy have loss of anticoagulants.
The two most common complications are thrombo­
sis and phlebitis/cellulitis. Thrombosis may be either
septic or aseptic. If the thrombi form initially at the
catheter tip, it is most commonly aseptic thrombosis,
although if the patient has been bacteremic, septic
thrombi may form at this site. If the thrombus begins at
the catheter-skin junction, cellulitis is often present
and the thrombosis is most commonly septic. Fever and
moderate to severe pain on palpation are generally pre­
sent with septic thrombi. Ultrasound examination
(7 MHz linear probe) will allow visualization of the
thrombus and help determine that an abscess is pre­
sent. Severe head edema may occur from jugular
thrombosis if the opposite vein is abnormal and/or the
patient keeps its head abnormally low for a prolonged
time. Nasal edema may be so severe that a tracheostomy
must be performed.
Another complication is physical kinking of the
catheter preventing flow. If this occurs the catheter
should be replaced and not simply repositioned. On a
rare occasion the catheter may break into the vein. If
the broken catheter can be trapped in the j ugular vein
it should be surgically removed. If the broken catheter
passes into the lung, as determined by radiographs, it
should be left alone where, based upon a limited num­
ber of cases, it does not appear to cause a problem. If
the catheter is lodged in the heart it must be removed.
TREATMENT OF THROMBOPHLEBITIS
If a thrombus forms at the tip of the catheter the
catheter should be removed, a sonogram performed on
the vein, and the horse monitored for signs of sepsis. If
there is evidence that the thrombus might be infected,
CLINICAL EVALUATI O N OF THE COLIC CASE 9
fever, extreme pain on palpation, or thrombus forming
in a septic patient, the catheter tip should be cultured
and the patient treated with antibiotics. Initial anti­
microbial therapy might be a combination of intra­
venously administered penicillin and aminoglycoside,
or a third generation cephalosporin if a catheter can be
placed in another vein. If oral antimicrobials are
needed, enrofloxacin would provide good coverage
against gram-negative organisms which are most com­
mon with catheter-tip septic thrombosis. Antimicrobials
should be continued until the vein is not painful on pal­
pation, the sonogram shows a solid thrombus, and the
neutrophil count 'has returned to normal. In a rare
refractory case, the vein might need to be surgically
removed.
If cellulitis is noted at the skin-vein junction the
catheter should be removed immediately and any
serum or exudate present at the opening should be
carefully aspirated and cultured ( aerobically and anaer­
obically) . The most common organisms at this site are
Staphylococcus spp. Antimicrobial therapy, trimetho­
prim-sulfonamides, enrofloxacin, cefazolin or ceftiofur,
or a combination of penicillin and aminoglycoside
should begin immediately. The skin opening might
need to be nicked slightly to help guarantee outward
drainage. The area should be hot-packed frequently
and ichthammol may be applied to the area. If the cel­
lulitis has caused only a partial occlusion of the vein,
aggressive therapy might allow the vein to return to
normal. If the vein is not entirely thrombosed and the
gastrointestinal tract is functional, anti-platelet therapy
(aspirin 0.25 g/kg p.o. every other day) should be
administered.
CATHETER MANAGEMENT
The site of catheter placement should be kept as clean
and dry as possible. The area is better visualized if it is
not bandaged, but in foals and adult horses that are fre­
quently recumbent, bandaging is preferred. Immediate
flushing of any irritating medication, for example
phenylbutazone, should be performed with either
isotonic crystalloids or heparinized saline. If no fluids
are being administered, heparinized saline should be
administered after each intravenous medication and at
least twice daily. Ideally, the catheter should not be used
for blood collection, although this is often not practical
in some foals. If the catheter has become occluded for
whatever reason, or accidentally disconnected from the
fluids such that blood backs up into the line, replace­
ment of the catheter should be considered based upon
economics, potential degree of contamination, and
availability of other veins.
1 37
9 COLIC
Fluid and electrolyte
therapy and acid-base
balance in horses with
abdominal pain (Figure 9.1 7)
Jii&
T Divers
EXPECTED ABNORMALITIES
Horses with abdominal pain may have a variety of fluid,
electrolyte, and acid-base disturbances. In milder cases
of abdominal pain there are usually minimal fluid and
electrolyte abnormalities, including an occasional
mildly diminished serum calcium concentration. In
more severe disorders, interstitial and intravascular vol­
ume is depleted as fluid accumulates in an obstructed
bowel. Serum sodium and chloride usually remain nor­
mal since the accumulating intralumenal fluid is nearly
isotonic. Serum chloride may be abnormally low if there
has been profuse sweating and/or gastric reflux. If
endotoxemia develops, additional fluids are lost from
the intravascular compartment because neutrophil and
platelet margination on capillary membranes causes
'leaky membranes' . Endotoxin also stimulates cytokine
production and arachidonic acid metabolism which can
decrease cardiac output and vascular tone, and cause
'maldistribution' of blood, further diminishing blood
pressure and perfusion to organs. Either localized
bowel ischemia and/or a more general perfusion
abnormality result in enhanced anaerobic metabolism
and generation of lactic acid causing a decrease in
plasma bicarbonate and a corresponding increase in
the anion gap. Dehydration and/or diminished perfu­
sion of the kidneys results in azotemia. If there is
enhanced portal absorption of endotoxin, sorbitol
dehydrogenase is frequently elevated.
Fluid losses are further aggravated by lack of oral
intake which should be between 30-60 ml kg-I day-I.
Although the initial loss in body fluid is extracellular
fluid, considerable intracellular fluid may be lost with
more prolonged abdominal pain and lack of fluid
intake. This may be particularly true for impaction colic
of several days' duration. Because of the movement in
intracellular fluid, the packed cell volume and protein
may be relatively normal in spite of severe dehydration,
and hypertonic saline would be a poor choice of fluid
therapy. Sweating causes loss of chloride, potassium,
and calcium, and may result in the loss of considerable
amounts of body fluids and electrolytes. Alkalosis with
an increased anion gap (mixed alkalosis, acidosis) may
be present if severe sweating has caused hypochloremia.
1 38
Although serum sodium and chloride are generally nor­
mal and calcium low in the great majority of horses with
abdominal pain, potassium is more variable. It may be
low if there is prolonged anorexia or high if there
is pronounced azotemia. Total body potassium can
become severely depleted because of anorexia and con­
tinuing urinary losses. Intravenously administered
fluids are likely to cause further urinary loss of potas­
sium, even when potassium is added to the fluids.
Magnesium may be abnormally high and clinically
important if a dehydrated horse has been given
magnesium sulfate per os.
An estimate of the liters of fluid to be given in order
to correct dehydration can be made by estimating per
cent dehydration and multiplying this by the body
weight in kilograms. The percentage of dehydration is
best determined by the change in body weight but this
is often not possible. Clinical and laboratory findings
that help estimate per cent dehydration include
• dryness of mucus membranes
• speed of distention of the occluded jugular veins
• skin turgor
• elevations in blood urea nitrogen and creatinine
• packed cell volume
• plasma protein concentration
• urine specific gravity.
A 1 gil increase in plasma protein suggests a 7-8 per
cent loss in extracellular fluid.
THERAPY - INTRAVENOUSLY
ADMINISTERED FLUIDS
-------.;;..;;.;
.;;. .;;;.",.
;;. -- , --...-.
The basic goals of fluid therapy in horses with abdomi­
nal pain are to
• restore intravascular volume
• promote tissue perfusion
• initiate urination
• help correct electrolyte and acid-base disturbances
without promoting tissue edema.
The most important aspect of fluid therapy in horses
with strangulating lesions of the intestine is to quickly
increase intravascular volume such that cardiac output
and perfusion pressures are normalized. In many cases
a 2-4 ml/kg bolus of hypertonic saline is the initial
treatment of choice. This is the safest and most rapid
method of increasing perfusion pressure without pro­
moting tissue edema. Hypertonic saline also promotes
diuresis and lowers pulmonary hypertension caused by
prostanoid or neutrophil-released mediators. It must be
followed by appropriate amounts of isotonic fluids
(generally a commercial polyionic crystalloid contain-
 Horse appears dehydrated· Horseappears dehydrated but no Impaction Colic Horse appears dehydrated
and has proof perfusion+ obvious perfusion abnormalities Perfusion pressures normal

2-4 mllkg Hypertonic saline followed Estimate % dehydration and replace Administer 3-12
/ �
Reflux present No reflux
by polyionic crysta lloid 3-10 mllkglhr deficit over 6-12 hours; provide for mllkglhr of polyionic

I
maintenance and additional losses crystalloid until plasma

/1 I
/�
protein is maintained
between 4.0-4.5 g1dl.
No urine produced within hr Adequate urine produced Give 5% x BW (kg) = L Give 5% X BW (kg) = L
Continue fluids to

I
Check CVP± , PCV,
protein, jugular
distention and rectal
exam, ultrasound or
catheterize bladder to
Horse PCV, protein, of polyionic crystalloid of polyionic crystalloid
maintain protein in that
deteriorates heart rate, plus losses equal to over 6-12 hours if
range until impaction is
Protein and PCV remain reflux over 6-1 2 hrs
/'
perfusion normal desirable - oral fluids
relieved
within normal range, blood may be used here
pressure returns to normal, Protein drops below normal,
peripheral pulses normalize, PCV remains high which
heart rate decreases, color suggests leaky membranes, Continues at 1.5 x Reassess

determine (urine and CRT of membranes protein-losing enteropathy maintenance (60-120

production) improved or peritonitis; perfusion mllkglday) and

I�
pressure low, increased additional losses

anion gap, persistently high

heart rate
CVP high CVP normal or Continue with
andlor low and no polyionic crystalloids n
evidence of signs of 4-10 mllkglhr C
overhydration depending upon
Z
overhydration
and I ittle or
no urine
losses and physical
parameters, blood
Add colloids (plasma
�
r-
and/or Hetastarch), m

�
pressure and lab
continue crystalloids,
findings
reassess need for surgery r­
C

�
Continue with * decreased skin turgor, dry mucous
Stop IV fluids
Treat for
polyionic membranes �
crystalloids 1 0 � o
Urine produced + slow CRT, cold extremities, discolored mucous
oliguric renal
mllkglhr and z
membranes, high heart rate
failure
add colloids o
"T1
-I
::I:
m
Figure 9.1 7 Guide for intravenous fluid therapy i n horses with abdominal pain
n
o
r-
R

�
m

W
ID U)
9 COLIC
ing sodium, chloride, potassium, and calcium with
acetate) . Hypertonic saline should not be used in
horses with more chronic dehydration.
Crystalloids should be administered at 4-10 ml kg-I
h-I until the patient is stabilized and estimated dehydra­
tion is one and one-half times corrected. Maintenance
fluids should be 40-100 ml kg-I day-I plus additional
fluids to compensate for excessive loss from gastric
reflux. Calcium borogluconate (22 mg/kg) can be
added as needed to the crystalloid fluid in order to
maintain ionized calcium within the normal range
(> 1 .4 mmol/l) . Maintaining ionized calcium within the
normal range may help promote normal intestinal
motility and cardiac function. It should be used cau­
tiously or not at all if cardiac arrhythmias are present
and if reperfusion injury of ischemic bowel is a possibil­
ity. Additional potassium ( 20-40 mEq KCI/l) may be
required in horses that have normal renal function and
are experiencing a pronounced diuresis from the
crystalloid therapy. Potassium should not be used in
Quarter horses believed to be positive for the HYPP
gene. Sodium bicarbonate is rarely indicated in horses
experiencing abdominal pain. The acidosis that is pre­
sent is virtually always a high anion gap/lactic acidosis
which should be corrected by improving perfusion and
oxygenation and by surgical repair of devitalized bowel.
Colloid therapy is synergistic with crystalloid therapy
in promoting the goals of fluid therapy. Without ade­
quate oncotic pressure, crystalloids quickly move from
the intravascular space and may cause tissue edema
and/ or unnecessary loss of fluids in the urine. This loss
of intravascular fluid may be particularly pronounced
if the horse is experiencing systemic inflammatory
response and has ' leaky membranes' . In horses with
strangulating intestinal lesions, plasma protein should
be maintained at 50 gil (5.0 g/dl) or greater to have
maximal effect of the intravenously administered fluids
without promoting tissue edema. Equine plasma is the
ideal fluid for those horses since it has crystalloid prop­
erties, colloid properties, and contains many additional
proteins that can have anti-inflammatory and anti­
thrombotic properties. Hydroxyethyl starch is an excel­
lent synthetic colloid that can be administered to horses
in addition to isotonic or hypertonic crystalloids.
Colloid oncotic pressure changes with either plasma,
hydroxyethyl starch, or concentrated albumin can be
measured with a colloid osmometer (Wescor Co.,
Logan, UT) .
An exception for maintaining oncotic pressure
would be in the use of intravenous fluids for treating
impactions of the large intestine. In this case, crystal­
loids should be given at a fast rate, 8 ml kg-I h -I without
colloids such that plasma protein decreases to
< 4.5 g/ dl. The increase in hydrostatic pressure and
140
drop in oncotic pressure should cause movement of the
fluids into transcellular fluid sites, i.e. intestinal lumen,
such that the impaction is softened. This can generally
be done without harm to other body organs assuming
there is no generalized capillary disorder, and cardiac,
renal, and respiratory function are normal. When large
amounts of fluids are given to horses, the fluids should
ideally be warmed to near body temperature prior to
administration .
Some horses with abdominal pain may need only
oral fluids, or oral fluids in addition to intravenously
administered fluids. Horses with large bowel impac­
tions often benefit from orally administered fluids. If
there is no abnormal gastric reflux 1 g/kg magnesium
sulfate mixed in 8 ml/kg of warm water should be given
via nasogastric tube. The magnesium sulfate may cause
an almost immediate reflex secretion of fluid into the
large intestine. The magnesium sulfate should not be
administered more than twice daily in order to avoid
hypermagnesemia. If the horse tolerates the initial oral
fluids, up to 8 1/450 kg of either isotonic or slightly
hypertonic fluids may be given every 4 hours to an adult
horse. Granular sodium chloride, potassium chloride,
or sodium bicarbonate may be added to water if elec­
trolytes are desirable. Tonicity can be determined by
remembering that
• 1 g of sodium chloride equals 1 7 mEq or 34 mmol
• 1 g of potassium chloride equals 1 4 mEq or
28 mmol
• 1 g of sodium bicarbonate equals 1 2 mEq or
24 mmol.
Oral fluids are ideally administered via gravity flow
rather than by pump. On rare occasions, gravity admin­
istration of isotonic fluids may be given per rectum.
This would only be indicated for horses with colonic
impactions when oral fluids can not be given and eco­
nomic considerations prevent administration of intra­
venous fluids.
Preoperative preparation
P Rakestraw
INTRODUCTION
One of the most important components of preoperative
patient preparation is correction of fluid, acid-base,
and electrolyte abnormalities to improve the patient's
cardiovascular status prior to induction of general
anesthesia (see Fluid and electrolyte therapy and

acid-base balance in horses with abdominal pain) .
Another important area to attend to is pain manage­
ment. Most horses referred for colic have already been
treated with varying amounts of analgesics such as
xylazine, detomidine, romifidine, and butorphanol.
Depending on how severe the pain is at the time of
admission, these drugs are likely to be given in the
immediate preoperative period. Most of these drugs
have certain undesirable side effects such as brady­
cardia seen with xylazine, detomidine, or romifidine
administration, and respiratory depression seen with
butorphanol administration. Consequently it is impor­
tant that these drugs be used only when necessary, and
that their use in the preoperative period is recorded for
the information of the anesthesia personnel. Flunixin
meglumine, in addition to its analgesic properties,
should be given prior to surgery to abate the adverse
effects of endotoxemia.
PRE-OPERATIVE THERAPIES
Thirty minutes prior to induction of anesthesia, the
author routinely initiates broad spectrum antibiotic
therapy such as aqueous penicillin G (22 000 IV/kg Lv.
q.i.d.) and gentamicin (6.6 mg/kg i.v. s.i.d. ) . We have
not seen any detrimental effects using the once daily
dose of gentamicin as long as the horse is well hydrated.
Antibiotics are discontinued 24 hours after surgery in
most cases that do not require intestinal resection.
Horses with severe large colon distention may have
compromised venous return and excessive respiratory
excursions. In these cases, when rectal examination
indicates a gas-distended large colon adjacent to the
body wall, percutaneous decompression can be per­
formed by placing a 1 4-gauge catheter through the
flank (after sterile preparation and local anesthesia)
and into the colon.
Prognosis for acute
abdominal pain
P Rakestraw
Because of the significant economic and emotional
strains placed on the owner when their horse is treated
for acute abdominal pain, it is important that the vet­
erinarian supplies them with as accurate a prognosis as
possible for the animal's survival. In certain instances
this is difficult to do without surgical exploration.
However, numerous studies have attempted to identify
CLI NICAL EVALUATIO N OF THE COLIC CASE 9
specific preoperative prognostic indicators to deter­
mine the probability of short term survival in horses
with acute abdominal crisis. Some of the factors that
can be helpful in predicting the prognosis are
• heart rate
• capillary refill time
• packed cell volume
• total plasma protein
• blood lactate.
Many of these factors are indirectly related to the
degree of intestinal ischemia which leads to cardio­
vascular compromise. In several studies heart rate has
been found to be a valuable prognostic indicator. In
one study horses with heart rates of 40, 80, 1 00, and
1 20 bpm had survival probabilities of 0.90, 0.50, 0.25,
and 0.10 respectively. Capillary refill time above 4 sec­
onds has been associated with a poor prognosis in sev­
eral studies. Packed cell volumes (pev) of 56 per cent,
60 per cent, 64 per cent, and 68 per cent were associ­
ated with survival rates of 0.46, 0.44, 0.44, and 0.23
respectively. Horses with both an elevated pev and
hypoproteinemia (Total protein < 50 gil or 5 g/dl)
have a poorer prognosis than those with a similarly ele­
vated pev and normal serum protein. Blood lactate
levels, a measure of peripheral tissue hypoperfusion, in
the range of 0-75, 76-- 1 00, and greater than 1 0 1 mg/dl
were associated with 0.93, 0.33, and 0.25 survival proba­
bilities respectively.
Other laboratory parameters that have been used as
prognostic indicators include
• systolic blood pressure
• blood urea nitrogen
• white blood cell and protein concentration in
peritoneal fluid
• activity of antithrombin III in blood and peritoneal
fluid
• fibrinolytic activity in blood and peritoneal fluid
• procoagulant activity in blood.
In most cases use of these single variables, or multi­
variate predictive models based on several of these
variables have limited value in improving the clinician's
ability to predict the outcome over clinical experience,
which takes into account both the above variables as
well as variables unique to the individual case.
Another strategy to predict outcome is to base the
prognosis on the outcome of horses with similar lesions.
Retrospective studies have been performed to evaluate
outcome for the majority of different types of acute
abdominal crises. In reviewing these, the clinician
should realize that cases in retrospective studies have
been collected over a series of years, and consequently
changes in surgical and medical treatment, and/or
141
 Lo�tlon of lesion elllsslflc.tlon of I.slon Sltort term survlv.1 (,,) ...

STOMACH U lcers and associated obstructions Insufficient data

SMALL INTESTINE (non-ileal) Strangulating and non-strangulating i nfarction 85

SMALL INTESTINE (non-ileal) Simple obstruction 90

SMALL INTESTINE (ileum) Strangulating and non-strangulatlng i nfarction 68-70

SMALL INTESTINE (ileum) Simple obstruction 90-100

CECUM Strangulating and non-strangLllating i nfarction 60

CECUM Simple obstruction 80-90

LARGE COLON Strangulating or non-strangulating i nfarction 40-50

LARGE COLON Simple obstruction 80-90

LARGE COLON Agenesis o r atresia poor

SMALL COLON Non-strangulating or non-infarctin g 65

SMALL COLON Simple obstruction 75

SMALL COLON Agenesis/atresia poor

PERITONEUM Septic Inflammation 50

"The information in this table is given as a guideline only, many other risk factors such as status of cardiovascular disease, extent of
lesion, degree of peritoneal contamination, and experience of the surgeon and anesthetist, must also be considered
"" Long term survival rate can be estimated at 5-10% less than short term survival

changes in the timing of referral and surgical decisions
may have improved the prognosis of similar cases at the
current time. For example, one frequently quoted study
determined that only 49 per cent of horses with
strangulating small intestinal lesions were discharged.
However, in a more recent study, 87 per cent of horses
with strangulating small intestinal lesions were dis­
charged. The prognosis for horses with strangulating
lesions of the large colon varies dramatically depending
on the degree of intestinal compromise as well as how
much of the large intestine is involved, i.e. can the large
colon be resected back to healthy bowel? Most horses
with non-strangulating lesions such as impaction colic
that has failed to respond to medical treatment, or large
colon displacement, have a very good prognosis with
surgical intervention. The expected short term survival
rates for horses with surgical lesions affecting different
parts of the intestinal tract are shown in Table 9.7.
In general, the prognosis for horses with acute
abdominal pain has improved significantly over the last
20 years. In a recent survey of equine veterinary special­
ists, delays in initiating surgery are believed to be the
most common cause of surgical failure. Increases in the
survival rates of horses undergoing colic surgery are
thought to result from early recognition and referral of
these cases by the primary care veterinarians. The
timely identification of these cases occurs through judi­
cious use of analgesics and increased awareness of signs
indicating that the horse needs to be referred for more
intensive care. It is also critical that the referral center
makes the appropriate decision whether to treat a horse
medically or to intervene surgically.
BIBLIOGRAPHY
Clinical signs of colic
Hardy J ( 1 999) Failure of body organ systems.
Gastrointestinal system. Proceedings of Bluegrass Equine
Medicine and Critical Care Symposium, October 24-27 1999,
Lexington, Kentucky.
White N A ( 1 990) Examination and diagnosis of the acute
abdomen. In The Equine Acute Abdomen, N A White (ed. ) .
Lea and Febiger, Philadelphia. pp. 1 02-42.

1 42

Physical examination of a horse with colic
Ragle C A ( 1 999) The acute abdomen: diagnosis,
preoperative management, and surgical approaches. In
Equine Surgery 2nd edn,] A Auer,] A Stick (eds) . W B
Saunders, pp. 224-32.
White N A ( 1 990) Examination and diagnosis of the acute
abdomen. In TheEquine Acute Abdomen, N A White (ed. ) .
Lea and Febiger, Philadelphia, pp. 1 02-42.
Rectal examination for the acute abdomen
Kopf N ( 1 997) Rectal examination of the colic patient. In
Current Therapy in Equine Medicine 4th edn, N E Robinson
(ed. ) . W B Saunders, Philadelphia, pp. 1 70-4.
Mueller P O E ( 1 995) Diseases of the large intestine causing
colic. In The Equine Manual, A] Higgens, I M Wright
(eds) . W B Saunders, Philadelphia, pp. 482-95.
Mueller POE, Moore ]N ( 1 998) Classification and
pathophysiology of colic. In Manual ofEquine Emergencies,
Treatment and Procedures, ] A Orsini, T] Divers (eds) , W.B.
Saunders, Philadelphia, pp. 1 5 6-64.
White N A ( 1 990) Examination and diagnosis of the acute
abdomen. In White N A (ed ) : The Equine Acute Abdomen,
Lea and Febiger, Philadelphia, pp. 1 1 6-24.
White N A ( 1 998) Rectal examination for the acute abdomen.
In White NA, Moore]N (ed) : Current Techniques in Equine
Surgery and Lameness, 2nd edn, W B Saunders,
Philadelphia, pp. 262-70.
Medical therapies for colic
Barton M H ( 1 995) . Treatment of equine endotoxemia.
Proceedings 41st Annual Convention of the American
Association ofEquine Practitioners Lexington, Kentucky,
4 1 : 1 1 2-16.
Clark E S ( 1 992). Pharmacologic management of colic. In
Current Therapy in Equine Medicine 3rd edn, N E Robinson
(ed. ) . W B Saunders, Philadelphia, pp. 201-6.
Hardy] ( 1 999) . Failure of body organ systems.
Gastrointestinal system. Proceedings ofBluegrass Equine
Medicine and Critical Care Symposium, October 24-27,
Lexington, Kentucky.
Murray R ( 1998). Endotoxemia in horses. Vet. Rec. Suppl. In
Practice 20: 88-94.
Proudman C] ( 1 991 ) . A two-year prospective survey of colic
in general practice. Equine Vet. ]. 24:90-3.
Seahorn T L and Cornick-Seahorn ] ( 1 994) Fluid Therapy.
In Emergency Treatment in the Adult Horse, ] L Bertone (cd. ) .
W B Saunders, Philadelphia, 1 0:517-25.
Van Hoogmoed L and Snyder ] R ( 1 997). Adjunctive methods
in equine gastrointestinal surgery. In Surgical Management
of Colic, D E Freeman (ed. ) . W B Saunders, Philadelphia,
13:221-42.
Spasmodic colic
Edwards G B ( 1998 ) . Spasmodic colic. In Equine Medicine,
Surgery and Reproduction. T S Mair, S Love, ] Schumacher
and E D Watson (cds). W B Saunders, London, p. 29.
Foreman ] H ( 1 998) . Diseases of the small intestine. In Equine
Internal Medicine. S M Reed and W M Bayly (cds) . W B
Saunders, Philadelphia, pp. 627-636
Hillyer M H and Mair T S ( 1 997 ) . Recurrent colic in the
mature horse: a retrospective review of 58 cases. Equine
Vet. ]. 29:421-4
CLI NICAL EVALUATION OF THE COLIC CASE 9
Proudman C] ( 1 992) . A two year, prospective survey of
equine colic in general practice. Equine Vet. ]. 24 90-3
Rooney] R ( 1 970) Autopsy of the Horse. Williams and Wilkins,
Baltimore, pp. 69-96.
Acute colic - the decision to refer
Baxter G ( 1 992) . The steps in assessing a colicky horse. Vet.
Med. 87: 1 0 1 2-18.
Coffman ] R ( 1987 ) . Deciding when to refer the horse with
colic. In Current Therapy in Equine Medicine 2nd edn, N E
Robinson (ed. ) . W B Saunders, Philadelphia, pp. 30-2.
Edwards G B ( 1 998) . Gastroenterology 1. Colic. In Equine
Medicine, Surgery and Reproduction. Eds. T Mair, S Love,
].Schumacher and E.Watson. W.B.Saunders, London, pp.
20-54.
Mueller P O E and Moore ] N ( 1998) . Classification and
pathophysiology of colic. In Manual ofEquine Emergencies.
Eds. ] A Orsini and T] Divers. W B Saunders,
Philadelphia. pp 1 5 6-164
White N A ( 1 990 ) . Examination and diagnosis of the acute
abdomen. In The Equine Acute Abdomen. Lea and Febiger,
Philadelphia pp 102-142
Colic - decisions for surgery
Mueller P 0 and Moore] N ( 1 998 ) . Gastrointestinal
emergencies and other causes of colic. In Manual ofEquine
Emergencies Eds. ] A Orsini and T] Divers. W B Saunders,
Philadelphia pp 156-164
Ragle C A ( 1 999) The acute abdomen: diagnosis,
preoperative management, and surgical approaches. In
Equine Surgery. 2nd Edition. Eds. ] A Auer and] A Stick.
W B Saunders, Philadelphia, pp 224-232
White N A ( 1 990) . Examination and diagnosis of the acute
abdomen. In: The Equine Acute Abdomen Ed. N A White.
Lea and Febiger, Philadelphia pp 102-142
Preparation of the horse for referral
transport
Arden W A, Siocombe R F, Stick] A, et al. ( 1 990)
Morphologic and ultrastructural evaluation of effect of
ischemia and dimethyl sulfoxide on equine jejunum. Am.
]. Vet. Res. 5 1 : 1 784.
Durando M M, MacKay R], Linda S, et al. ( 1 994) Effects of
polymyxin B and Salmonella typhimurium antiserum on
horses given endotoxin intravenously. Am.]. Vet. Res.
55:92 1 .
Freeman D E ( 1 997) Surgery o f the small intestine. Surgical
management of colic. Vet. Clin. N. Am. 299.
Geor R], Weiss D], Burris S M ( 1 992) Effects of furosemide
and pentoxifYlline on blood flow properties in horses. Am.
]. Vet. Res. 53:2043,.
Hardy], Rakestraw P ( 1 999) Postoperative care and
complications associated with abdominal surgery: In, Auer
]A, Stick]A: Equine Surgery, 2nd edition. W B Saunders,
Philadelphia, 294-305.
MacAllister C G, Morgan S], Borne A T, et al. ( 1 993)
Comparison of adverse effects of phenylbutazone, flunixin
meglumine, and ketoprofen in horses. ]. Am. Vet. Med.
Assoc. 202:7 1 .
Mathews K A ( 1 998) The various types of parental fluids and
their indications. Advances in fluid and electrolyte
therapy. Vet. Clin. N. Am. 28:483-513.
Moon P F, Snyder] R , Haskins S C, et al. ( 1991 ) Effects of
1 43
9 COLIC
highly concentrated hypertonic saline-dextran volume
expander on cardiopulmonary function in anesthetized
normovolemic horses. Am. J Vet. Res. 52:1 61 1-18.
Moore R, Muir W, Bertone A, et al. ( 1995) Effect of dimethyl
sulfoxide, allopurinol, 2 1-aminosteroid U74006F, and
manganese chloride on large colon ischemia-reperfusion
injury in horses. Am. J Vet. Res. 56:67 1 .
Orsinij A , Kreuder K . ( 1 998) Intravenous catheter
placement: In Orsini j A, Divers T J: Manual ofEquine
Emergencies. Philadelphia, W B Saunders, 1 2-15.
Orsinij A, Kreuder K. ( 1 998) Nasogastric tube placement: In,
Orsini jA, Divers TJ: Manual ofEquine Emergencies.
Philadelphia, W B Saunders, 53-5.
Reeves M j, Vansteenhousej, Stashak T S, et aL ( 1990) Failure
to demonstrate reperfusion injury following ischemia of
the equine large colon using dimethyl sulfoxide. Equine
Vet.J 22: 126.
Semrad SD, Hardee GE, Hardee MM, et aL Low dose flunixin
meglumine: Effects on eicosanoid production and clinical
signs induced by experimental en do toxemia in horses.
Equine Vet. J 19:20 1 , 1987.
Spier Sj, Snyder j R, Murray MJ. ( 1996) Fluid and electrolyte
therapy for gastrointestinal disorders. In Large Animal
Internal Medicine. 2nd edition, B P Smith (ed. ) . Mosby, St
Louis, MO, pp. 775-83.
Van Hoogmoed L V, Snyder j R ( 1997) Acljunctive methods
in equine gastrointestinal surgery. Surgical management
of colic. Vet. Clin. N. Am. 231-234.
Intravenous catheterization and
complications
Bregenzer T, Conen D, Sakmann P, Widmer A F ( 1998) Is
routine replacement of peripheral intravenous catheters
necessary? Arch. Intern. Med. 158: 1 51-4.
1 44
Gardner S Y, Reef V B, Spencer P A ( 1991 ) Ultrasonographic
evaluation of horses with thrombophlebitis of the jugular
vein: 46 cases ( 1 985-1988 ) . J Am. Vet. Med. Assoc. 199:370-3.
Prognosis for acute abdominal pain
Freeman D E ( 1 997) Surgery of the small intestine. In Vet.
Clin. N. Am. Equine Pract. Surgical Management of Colic. W B
Saunders, Philadelphia, 1 3:299.
Furr M 0, Lessard P, White N A ( 1 995) Development of a
colic severity score for predicting the outcome of equine
colic. Vet. Surg. 24:97-101 .
MacDonald M H, Pascoe j R, Stover S M, et al. ( 1 989) Survival
after small intestinal resection and anastomosis in horses.
Vet. Surg. 1 8 : 4 1 5-423.
Moorej N, Owen R, Lumsdenj H ( 1976) Clinical evaluation
of blood lactate levels in equine colic. Equine Vet. J
8:49-54.
Orsini j A, Elser A H, Galligan D T , et al. ( 1 988) Prognostic
index for acute abdominal crisis (colic) in horses. Am. J
Vet. Res. 49:1 969-1972.
Parry B W ( 1994) Prognostic evaluation of equine colic cases.
In Abdominal disease in equine practice, jN Moore ( ed . ) .
Veterinary Learning Systems, Trenton, Nj, p p . 34-40.
Parry B W, Anderson G A, Gay C C ( 1 983) Prognosis in
equine colic: A study of individual variables used in case
assessment. Equine Vet. J 15:337-344.
Pascoe P j, Ducharme N G, Ducharme G R, et al. ( 1 990) A
computer-derived protocol using recursive partitioning to
aid in estimating prognosis of horses with abdominal pain
in referral hospitals. Can.J Vet. Res. 54:373-378.
Pelosoj G, Cohen N D , Taylor T S, et al. ( 1 996) When to send
a horse with signs of colic: Is it surgical, or is it referable?
A survey of opinions of 1 1 7 equine veterinary specialists.
Proc. Am. Assoc. EquinePrac. 42:250-3.
 10
Surgery for colic (including anesthesia)
Anesthesia for colic surgery
RD Gleed
Many gastrointestinal lesions in horses cause colic that
requires laparotomy for definitive diagnosis and treat­
ment. The ventral midline approach is favored for most
laparotomies because it permits direct observation and
exteriorization of the majority of the intestine; this
approach necessitates general anesthesia in dorsal
recumbency. Flank laparotomy, because it allows much
more limited access to the abdomen, is rarely indicated
but may be carried out either in lateral recumbency
under general anesthesia or standing with local anes­
thesia. Because standing flank laparotomy is rarely per­
formed, local anesthesia will not be discussed in this
chapter.
Some patients with signs of colic have surgical
lesions that cause minimal interference with other body
systems, for example horses with chronic intermittent
colic. Most horses with lesions requiring emergency
laparotomy have a range of ongoing, serious pathologi­
cal processes that interfere with anesthesia and substan­
tially increase the risks associated with anesthesia. Safe
anesthesia of horses with colic is one of the greatest
challenges in veterinary anesthetic practice.
Convention suggests that patients be stabilized prior
to induction of anesthesia. Many horses with colic have
pathology that is proceeding so rapidly that permanent
injury is imminent and it is difficult, or impossible, for
stabilizing measures to keep up with the rate of deterio­
ration in the cardiovascular, pulmonary, and metabolic
systems. Occasionally, intractable pain may necessitate
induction of general anesthesia on an emergency basis
before the horse 's behavioral response to abdominal
pain endangers both horse and handlers. Rapidly pro­
ceeding pathology and intractable pain often conspire
to reduce the time available for stabilizing the patient
and preparing facilities for anesthesia. This inevitably
increases the risks associated with anesthesia of patients
with colic. Centers that perform colic surgery should be
organized so that patients can be processed and anes­
thetized as efficiently as possible.
THE PULMONARY SYSTEM IN HORSES
WITH COLIC
Distention of abdominal contents is a common conse­
quence of colic. This distention impedes movement of
the diaphragm and decreases chest wall compliance. It
also pushes the resting (end-expiratory) position of the
diaphragm cranially, this may stretch the muscle fibers
of the diaphragm so that they are operating beyond the
optimal length for myofibril contraction. The end
result is that the work of breathing is increased and the
diaphragm becomes more susceptible to fatigue.
The cranial displacement of the diaphragm also
tends to reduce the functional residual capacity (FRC)
of the lung, i.e. the volume of gas left in the lung at the
end of tidal expiration is reduced. The latter process
increases the number of airways that are collapsed and
encourages alveolar collapse. In turn, alveolar collapse
increases venous admixture, the passage of blood
through the lungs without oxygenation, and, hence
reduces arterial oxygen content.
Endotoxins absorbed from the intestine during colic
damage pulmonary vascular endothelium. This, in
turn, may initiate loss of integrity of the pulmonary
145
10 COLIC
vascular endothelium, accumulation of water in the
pulmonary interstitium, and thus inhibit diffusive gas
exchange.
The conscious horse compensates for these prob­
lems by increasing ventilatory drive and redistributing
pulmonary perfusion away from collapsed lung tissue.
Unfortunately adoption of dorsal recumbency exacer­
bates most of the pathophysiological processes men­
tioned above and most anesthetic drugs reduce, or
obtund completely, the efficacy of the compensatory
mechanisms. The net effect is that hypercapnea and
hypoxia are common in horses anesthetized for colic
surgery. Equipment for augmenting inspired oxygen
and controlling ventilation is necessary for safe anesthe­
sia of most patients undergoing colic surgery. Centers
undertaking surgery on patients for the relief of colic
should have an anesthetic machine designed for horses
and equipped with a circle rebreathing system and a
mechanical ventilator. Such a machine should have
• 5 cm diameter hoses
• a large carbon dioxide absorber
• the ability to deliver a tidal volume of 20 liters ten
times per minute
• the ability to generate a peak inspiratory pressure of
40 cmH20.
THE CARDIOVASCULAR SYSTEM IN
HORSES WITH COLIC
Distention of the abdomen in horses with colic may be
sufficient to reduce venous return and hence reduce
cardiac output. Even simple intestinal obstruction,
unaccompanied by strangulation or thromboembolism,
induces secretion of a large volume of fluid into the
lumen of the gut. If ischemia is present in the intestine
then disruption of the intestinal mucous membrane
exacerbates this accumulation of intralumenal fluid
and also permits release of endotoxins into the peri­
toneum. These endotoxins attach to macrophages
that are responsible for release of proinflammatory
cytokines, mobilizing arachidonic acid and, hence, the
production of vasoactive substances such as throm­
boxane and prostacyclin. Thromboxane causes vaso­
constrIctIOn that occurs early in endotoxemia.
Vasoconstriction is soon superseded by persistent
vasodilation mediated by prostacyclin. The net result of
these processes is reduced total blood volume, pooling
of blood, and reduced perfusion pressure. The con­
scious horse may compensate for these processes by
increasing heart rate and vasoconstriction of non-essen­
tial vascular beds. Nevertheless, if the pathological
processes persist, reduced perfusion leads to an
146
increase in anaerobic metabolism, lactic acidosis, and
the classic signs of shock.
The cardiovascular compensatory mechanisms men­
tioned above tend to be attenuated by most of the drugs
used in anesthetic practice, hence animals with cardio­
vascular impairment before anesthesia are likely to
need intensive cardiovascular support during anesthe­
sia. Intraoperative events such as
• change in posture of the patient during hoisting to
and from the operating table or
• release of incarcerated ischemic bowel ( e.g.
internal hernia)
often produce hypotension and hypoperfusion because
the cardiovascular system is unable to compensate for
these sudden challenges.
PREPARATION OF THE PATIENT
Ideally, preparation of the patient for anesthesia should
involve a thorough physical examination. This may
involve all organ systems but should focus on assessing
the degree of pulmonary and cardiovascular impair­
ment. Cardiac rhythm should be ascertained prior to
induction of anesthesia; the presence of atrial fibrilla­
tion increases the likelihood of intraoperative hypo­
perfusion. Laboratory tests on venous blood should
include
• hematocrit
• total plasma protein
• base deficit of the extracellular fluid
• anion gap
• serum concentrations of sodium, potassium, and
ionized calcium.
A large bore catheter (� 14 gauge) should be placed in
a jugular vein so that intravenous fluids may be given
rapidly either by gravity or with a pump. In animals with
known fluid deficits, it is appropriate to place more
than one catheter to speed volume replacement.
Correcting pre-anesthetic volume and metabolic
and electrolyte abnormalities takes time. The extent to
which this is practical, or worthwhile, in the face of
ongoing disease processes and/or intractable pain,
requires the exercise of clinical j udgment. Horses with
colic often need to be anesthetized with cardio­
pulmonary and metabolic disruptions that are only
partially corrected or sometimes not corrected at all.
A distended stomach may rupture when the patient
goes to ground during induction of anesthesia.
Therefore, in all horses with colic, a nasogastric tube
should be placed prior to induction of anesthesia and
left in place until the end of anesthesia. This permits

decompression of the stomach and allows removal of
gastric fluid during surgery.
As mentioned above, damage to intestinal mucous
membrane releases endotoxins that initiate the produc­
tion of vasoactive arachidonic acid metabolites such as
thromboxane and prostacyclin. These can be inhibited
by non-steroidal anti-inflammatory drugs ( NSAIDs) . An
appropriate NSAID (e.g. flunixin meglumine 1 .0 mg/
kg Lv.) should be given as soon as damage to the intesti­
nal mucous membrane is suspected.
Both sodium or potassium penicillin and potenti­
ated sulfonamides cause cardiovascular depression that
may become important during anesthesia. Whenever
possible they should be given well in advance (> 30
min) of anesthesia. Drugs less likely to produce
hypotension should be chosen if practical.
Analgesia and chemical restraint of the horse with
colic is usually accomplished with drugs that act at
alpha2 adrenoceptors, Le. xylazine, detomidine, or
romifidine. Occasionally, these drugs are augmented by
opioid agonists such as butorphanol or meperidine.
The adverse side effects of these drugs are considerable
(see below) , nevertheless they are usually outweighed
by the necessity for pain relief and chemical restraint.
Immediately before induction of anesthesia the
mouth should be washed out with water from a 0.5 liter
dose syringe. This prevents food material being carried
into the trachea during orotracheal intubation.
INDUCTION OF ANESTHESIA
Induction of anesthesia should be accomplished with a
technique that puts the horse into recumbency gently
to minimize the possibility of rupture of distended
bowel. The walls and floor of the induction area should
be padded with a durable, washable surface, that is also
non-skid. It is usual to restrain both head and tail with
ropes or to use an induction gate/false wall or purpose­
built induction table with belly-bands. Immediately
after induction, an oro tracheal tube should be inserted
through a gag held between the incisors. Mechanically
controlled ventilation should be started promptly with
an oxygen-enriched mixture. The ventilator should be
set initially to deliver a tidal volume of 1 0- 1 5 ml/kg at a
rate of 6-10 breaths per minute. The volume in the
accessory cuff of the orotracheal tube should be
acljusted to just prevent escape of tidal gas during inspi­
ration.
The horse should then be placed on the operating
table where a system for supporting the horse, with even
distribution of its weight, is crucial to avoid compressive
muscle ischemia. Foam pads or mattresses filled with
air or water are used for this purpose. In dorsal recum-
SURGERY FOR COLIC (INCLUDING ANESTHESIA) 10
bency the head should be supported in a slightly flexed
position to optimize nasal venous drainage.
BRIEF REVIEW OF THE DRUGS USED IN
ANESTHESIA
The impaired pulmonary, cardiovascular, and meta­
bolic status of many patients with colic influences the
pharmacokinetics and pharmacodynamics of anesthetic
drugs. In general the conditions that cause surgical colic
also decrease the volume of distribution of injectable
drugs and increase the fraction of those drugs that are
in 'active' form. As a result most injectable anesthetic
drugs can be expected to have increased potency and
duration in these patients, although high sympathetic
tone may transiently counteract these processes early in
the course of an anesthetic. Decreased cardiac output
will also cause the depth of anesthesia to increase more
rapidly when inspired anesthetic concentration is
increased, hence changes in the depth of anesthesia of
a hypovolemic patient should be monitored carefully
during inhaled anesthesia.
Alpha2 adrenoceptor agonists
The dose-dependent sedation and analgesia that alpha2
adrenoceptor agonists produce has made them an
important part of the management of horses with colic.
Most horses that are presented for surgery at a sec­
ondary or tertiary care facility have already received one
or more doses of an alpha2 adrenoceptor agonist. The
ubiquitous use of these drugs in horses with colic
should not be allowed to distract from their adverse
side effects. Intravenous administration of alpha2-
adrenoreceptor agonists causes transient vasoconstric­
tion and an increase in blood pressure, but bradycardia,
often accompanied by second degree heart block,
ensues; cardiac output may be reduced to half its
normal value when conventional doses are used. This
hypoperfusion is usually characterized by prolonged
hypotension. Through muscle relaxation of upper air­
way musculature, the resistance of the upper airways is
increased and this increases the work of breathing.
Arterial oxygen tension decreases a little in response to
these drugs. Intestinal motility is reduced for several
hours after these drugs are given . Inadvertent overdose
with an alpha2 adrenoceptor agonist can be reversed
with an antagonist such as yohimbine (0.05 mg/kg i.v.)
or tolazoline ( 2-4 mg/kg i.v. ) .
When used as an adjunct to ketamine, the cardio­
vascular side effects of xylazine are attenuated to some
extent by the sympathetic effects of ketamine. The dose
of xylazine used as an adjunct to ketamine is minimized
147
10 COLIC
by the addition of diazepam and/or butorphanol to the
technique (Table 1 0 . 1 ) . Dosing with alpha2 adrenocep­
tor agonists to control pain before surgery can substan­
tially reduce the dose necessary during induction of
anesthesia.
Protocol 1
Premedication
xylazine 0.4 mg/kg Lv.
butorphanol 0.02 mg/kg Lv.
Induction
diazepam 0.1 mg/kg Lv.
ketam i ne 2.2 mg/kg
Protocol 2
Premedication
xylazine 0.4 mg/kg Lv.
butorphanol 0.02 mg/kg Lv.
Induction
1 l iter 5% guaifenesin + 2000 mg ketamine given
to effect
Acepromazine
Acepromazine is an unreliable tranquilizer in horses
experiencing colic pain. It antagonizes alpha) adreno­
ceptors and tends to produce systemic vasodilation and
hypotension. In animals with high sympathetic tone, for
example animals in pain, the inhibition of alpha) recep­
tors tends to prevent the vasoconstriction that ordinar­
ily occurs in the skin and splanchnic vascular beds with
endogenous catecholamines; it has little effect, how­
ever, on the beta receptor mediated vasodilation seen
in the muscle with endogenous catecholamines. The
net result is amplification of acepromazine's hypoten­
sive effects in patients that are excited or in pain.
Acepromazine can also produce permanent para­
phimosis or priapism that may disable a stallion. All of
these effects severely limit the use of acepromazine in
patients with colic.
Benzodiazepines
Diazepam and midazolam are classified as sedatives,
however when they are given as sole agents to horses
they tend to produce ataxia but little obvious sedation.
They are often used as adj uncts to ketamine when their
muscle relaxing properties aid induction of anesthesia
and orotracheal intubation. Although they have mini­
mal sedative properties, they reduce the dose require-
148
ment for other drugs that may have serious adverse side
effects, for example xylazine.
Opioids
Although some opioids tend to produce excitement in
horses when given alone, butorphanol, pentazocine,
meperidine, and morphine can all be given without
causing excitement. Butorphanol is probably the most
widely used opioid in horses and seems to act primarily
on kappa receptors. It provides good visceral analgesia
after 0.02 mg/kg i.v.
Ketamine
Ketamine is a dissociative anesthetic agent that is often
used to induce anesthesia in horses with colic. Although
its direct effect on the cardiovascular system is depres­
sant, this property is counteracted by a general increase
in sympathetic tone, so that its net effect is fairly neu­
tral. When used alone, it produces a poor quality of
induction of anesthesia, characterized by a short period
of ataxia and hypersensitivity. When given after an
alpha2 adrenoceptor agonist it produces a much
smoother induction. The quality of induction with keta­
mine is also improved by using other adjunct drugs
such as guaifenesin or diazepam (Table 1 0. 1 ) .
Guaifenesin (glyceryl guaiacolate ether, GG)
Guaifenesin (GG) is neither analgesic nor anesthetic, it
acts on interneurons in the spinal cord to produce mus­
cle relaxation. GG facilitates a smooth induction with
ketamine or thiopental and allows the dose of these
drugs to be reduced. It is usually administered as a 5%
solution in water or 5% dextrose. Concentrations of
1 0% or greater have been associated with phlebitis and
cause necrosis if inadvertently injected perivascularly.
The principal disadvantage of using 5% GG is that a
large volume must be infused over a short period
(0.5-1.0 liters in 2-4 minutes for most horses) . This is
difficult to accomplish if the drug is being given by
gravity through a 1 0 drop/ml infusion set and 1 4-gauge
catheter, however a pressure infusor may be used to
squeeze the bag of GG and expedite the process.
Thiopental or ketamine can be mixed with the GG or
may be given as a bolus when the GG starts to make the
horse sway (Table 1 0. 1 ) . Guaifenesin alone has minimal
effects on the cardiovascular or respiratory systems and
those effects that are seen are probably caused by the
effects of recumbency rather than the drug itself.
Thiopental
Thiopental is an ultrashort-acting barbiturate that
induces recumbency very soon after intravenous

administration. It causes profound cardiovascular
depression and transient apnea even when GG or other
adjunct medications reduce the dose. The cardio­
depressant properties of thiopental make it much less
popular than ketamine for induction of anesthesia in
patient� with colic.
Propofol
Propofol is used for induction of anesthesia in humans,
dogs, and cats. The dose required for induction of anes­
thesia in horses is very large and expensive even when it
is given with GG to reduce the dose. The quality of
induction of anesthesia is quite variable. Since it
appears to confer no important advantages over con­
ventional methods of inducing anesthesia, it is unlikely
that propofol will find favor for anesthetizing horses
with colic.
Telazol®
Telazol® is a proprietary combination of tiletamine,
a dissociative anesthetic, and zolazepam, a benzodi­
azepine. It has been used to induce anesthesia in horses
premedicated with xylazine or detomidine. Its effects
last longer than those of conventional xylazine-keta­
mine combinations and, hence, may give more time
after induction of anesthesia for inhaled anesthetics to
reach therapeutic levels. Use of tiletamine-zolazepam
(1.0 mg kg-I of the combination, IV) in horses with colic
is yet to be evaluated objectively, however this combina­
tion may find a place in anesthetic practice.
Inhaled anesthetics
Modern inhaled anesthetics are potent and usually
administered with oxygen as the carrier gas. Breathing
an oxygen-enriched gas mixture probably confers a
significant safety margin for patients with impaired gas
exchange and perfusion that are undergoing pro­
longed anesthesia. Because inhaled anesthetics do not
depend on metabolism for their elimination, it is rela­
tively easy to titrate the dose (inhaled concentration) to
accommodate changing surgical needs and physiologi­
cal status.
Halothane and isoflurane are the most commonly
used inhaled anesthetics in horses. Although isoflurane
is somewhat less potent than halothane (Table 10.2 ) , its
low solubility in blood makes it easier to acljust depth of
anesthesia with isoflurane than with halothane. In the­
ory, this should also lead to faster recovery from anes­
thesia with isoflurane; in practice the time taken to
stand is quite similar, however the quality of recovery is
usually better after isoflurane. Isoflurane may cause
more depression of ventilation than halothane,
SURGERY FOR COLIC (INCLUDING ANESTHESIA) 10
although this is a mute disadvantage in patients that are
mechanically ventilated. Both anesthetics reduce
cardiac output and systemic arterial blood pressure,
however, at equivalent doses cardiac output is likely to
be greater with isoflurane than with halothane suggest­
ing better tissue perfusion with isoflurane. The latter
attribute, along with easier control of anesthetic depth,
suggests that isoflurane is a better choice of anesthetic
for horses where the cardiovascular system is challenged
and unstable, as is often the case in horses with colic.
Infusion of 40 �g kg-I min-I of ketamine can be used
to reduce the inspired concentration of halothane or
isoflurane by approximately 25 per cent, this amelio­
rates the cardiovascular depression caused by anes­
thetic doses of these drugs. The latter technique,
although useful, is not without risk in patients with
altered pharmacokinetics and pharmacodynamics. It is
recommended that anesthetic depth is monitored care­
fully and that the infusion be stopped as soon as the
most intense surgical stimulation is over so that the dis­
sociative effects of ketamine have dissipated before the
horse starts to recover from anesthesia.
Sevoflurane is a relatively new addition to the veteri­
nary armamentarium; its blood solubility is even lower
that that of isoflurane, and hence depth of anesthesia
can be increased or decreased rapidly with sevoflurane.
The cardiodepressant effects of sevoflurane are
probably quite similar to those of isoflurane, however
horses recover more quickly and usually more smoothly
from anesthesia after sevoflurane. Although experience
with sevoflurane in horses is still accumulating, it
appears that the better quality of recovery after sevoflu­
rane is more noticeable after prolonged (> 2 h) anes­
thetics, often the case with colic surgery. Sevoflurane is,
as yet, substantially more expensive than the other
inhaled agents in the US. Whether or not the extra cost
is worthwhile is a matter of debate.
Desflurane is an even newer inhaled anesthetic. It is
less potent than the aforementioned inhaled agents,
requires a vaporizer that is heated, and has the potential
to permit even more rapid changes in depth of anes­
thesia and recovery. At present, its cost will probably pre­
clude its general use in veterinary medicine. Desflurane
has yet to be widely evaluated in horses with colic.
. malwalar;COfW8I'ItfiClon,,'"
"j1,,�lbhorsU> •. ;.
Halothane 0.9
Isoflurane 1.3
Sevoflurane 2.3
8.0
Desflurane
149
10 COLIC
Nitrous oxide is much less potent than any of the
inhaled drugs mentioned above. It is used in many non­
human species to enable the dose of other agents to be
reduced. Unfortunately, the volume of nitrous oxide
required in inspired gas (� 50%) reduces the inspired
oxygen fraction below that considered prudent in anes­
thetized horses. Nitrous oxide also tends to accumulate
in gas spaces, including the intestine where it may
exacerbate the ileus already present in many horses
with colic. Nitrous oxide has no place in anesthetizing
horses with colic.
Neuromuscular blockade
Neuromuscular blockade may be used to reduce the dose
of inhaled agents that is necessary to produce muscle
relaxation. In horses, the most commonly used of
these agents is atracurium. The usual initial dose is
0.1 mg kg-I Lv., subsequent doses are half of the initial
dose and are given when neuromuscular transmission
stars to reappear. Assessment of the extent of neuromus­
cular blockade is best accomplished with a peripheral
nerve stimulator, applied so that it causes contraction of
muscles served by the peroneal nerve or facial nerve. The
latter is more accessible in horses undergoing colic
surgery. Non-depolarizing muscle relaxants such as
atracurium should always be reversed (0.5 mg kg-I
edrophonium i.v. slowly) before recovery from anesthesia
in case persistent neuromuscular block causes weakness
that delays recovery. Because neuromuscular-blocking
agents have no effects in the central nervous system, ade­
quate depth of anesthesia should always be ensured while
they are being used. The depolarizing neuromuscular
blocker, succinyl choline, has been used in horses to expe­
dite induction of anesthesia, but it has no place in the
anesthesia of horses for colic surgery because it may cause
hyperkalemia and decrease blood pressure.
Parasympatholytics
Drugs such as atropine and glycopyrrolate decrease gas­
trointestinal motility for several hours and may exacer­
bate the postoperative ileus that is a component of
many colics. When used in conjunction with dopamine
or dobutamine, atropine and glycopyrrolate can cause
dangerous tachydysrhythmias. These drugs should be
used with great caution in patients with surgical colic.
MONITORING PATIENTS DURING
ANESTHESIA
Depth of anesthesia
Anesthetic requirement varies with changing levels of
surgical stimulation, duration of anesthesia, and
150
changing physiological status of the patient, among
other things. In order to avoid relative overdose of anes­
thetic drugs in horses with colic, it is essential to moni­
tor depth of anesthesia carefully because anesthetic
requirement may be much less than that extrapolated
from healthy animals and may vary considerably during
anesthesia.
A sluggish palpebral reflex is a sign of a light plane
of anesthesia that is usually just suitable for exploratory
laparotomy. Rotation of the eyeball, causing a small
amount of sclera to be visible, is likewise associated with
a surgical plane of anesthesia with inhaled anesthetics.
In very deep anesthesia the eyeball is central.
Occasional, slow nystagmus may also be seen in a light
surgical anesthetic plane, however this is sometimes
confused with variable small oscillations of the eye that
are seen in very deep anesthesia.
The precise dose of an inhaled anesthetic can be
measured using an anesthetic vapor analyzer that sam­
ples gas from the endotracheal tube. At the end of expi­
ration, the concentration in this location is known as
the end-tidal concentration and approximates the con­
centration in the alveolar gas and hence the 'dose' of
the inhaled agent being given. In healthy animals
undergoing surgery, the end-tidal concentration of
most potent anesthetics should be 1 .2-1 .6 MAC, where
MAC is the minimum alveolar concentration of the
anesthetic drug (see Table 1 0.2) that produces a lack of
response to surgical stimulation in 50 per cent of
patients. Unfortunately, the anesthetic requirement of
patients undergoing surgery for colic may be quite dif­
ferent ( usually less) than that of healthy patients and
may change during the course of anesthesia, hence the
use of a monitor of end-tidal anesthetic concentration
does not relieve the clinician of responsibility for con­
tinuously monitoring the depth of anesthesia.
Cardiovascular function
Palpation of the pulse and observation of the color of
the mucous membranes are important but insensitive
monitoring tools. The electrocardiogram is probably
the most commonly applied monitor because it is easy
to apply and allows detection of cardiac dysrhythmias,
however it gives little quantitative information about
pump function of the heart.
The mean systemic blood pressure is a sensitive indi­
cator of cardiovascular function. Under inhaled anes­
thesia, systemic hypotension is generally a characteristic
of low perfusion. Systemic blood pressure can be mea­
sured indirectly by a cuff device, encircling the tail or a
limb, that is inflated with air to a pressure exceeding the
systolic pressure, and hence sufficient to prevent flow
past the cuff. The cuff is then slowly deflated; the cuff

pressure at which intermittent flow is first detected
approximates systolic pressure and the cuff pressure at
which flow becomes continuous approximates diastolic
pressure. The method of detecting flow distal to the
cufI'may be based on phase shift of ultrasound (the
Doppler method) or on pressure oscillations in the air
cuff ( the oscillometric method ) . Although reasonably
reliable for measuring blood pressure in healthy horses,
these indirect methods often fail when blood pressure is
low or during peripheral vasoconstriction, therefore
they are of limited value in anesthetizing patients that
are undergoing surgery for relief of colic.
Systemic blood pressure is best measured directly
with a calibrated pressure transducer attached to
catheter in a peripheral artery, via a saline-filled, low
volume, low compliance tube. In horses in dorsal
recumbency, the transducer is usually zeroed at the
level of the shoulder joint, this approximates the right
atrial level. After sterile skin preparation, a 20-gauge
catheter is inserted into the facial artery, transverse
facial artery, or the great metatarsal artery; this catheter
should be flushed frequently with heparinized saline.
Many modern electrocardiographs come with a pres­
sure amplifier and channel for displaying both the pres­
sure waveform and numeric values for systolic, mean,
and diastolic pressures. An inexpensive alternative for
measuring mean blood pressure is to use an aneroid
manometer as the transducer. This must be separated
from the saline in the connecting tube by a column of
air; prior to connecting to the catheter the manometer
must be zeroed by locating the meniscus of the saline at
the level of the shoulder joint while the air space is open
to atmospheric pressure.
Mean arterial pressure should be maintained
around 80 mmHg and corrective action taken if pres­
sure drops below 70 mmHg.
Cardiac output is an important measure of cardio­
vascular function and has been measured in horses
using the thermodilution technique. This method is
technically difficult because it necessitates placing a
thermistor catheter into the pulmonary artery and gives
variable results because of oscillations in the baseline
temperature of blood in the pulmonary artery. It is
hoped that new technology, using indicators that can be
easily measured in the systemic circulation (e.g. lithium
or ultrasound velocity) , will be validated and find a
place in equine anesthetic practice.
Central venous pressure (CVP) can be measured
with a transducer or water manometer applied to a
catheter in, or near, the right atrium. For this purpose
in adult horses, a 70 cm ( 28 in) 1 . 1 mm internal diame­
ter catheter is often introduced via the jugular vein. In
dorsal recumbency CVP is usually 5-10 cmH20, but
because the central venous pressure is low, small incon-
SURGERY FOR COLIC (INCLUDING ANESTHESIA) 10
sistencies in determining the level for zero cause con­
siderable variability in this normal value. Nevertheless,
CVP is a valuable tool for measuring changing cardio­
vascular status. If the venous return to the heart is low,
as is the case in relative or absolute hypovolemia, then
CVP will be low. It will increase as the hypovolemia is
corrected.
Pulmonary function
Movement of the chest wall and the rebreathing bag or
bellows provides a rough indication of ventilatory func­
tion but gives little information about the efficiency of
gas exchange in the lungs. Modern capnographs con­
tinuously measure partial pressure of carbon dioxide in
the endotracheal tube; a capnograph is often incorpo­
rated in anesthetic agent monitors (see above) . End­
tidal carbon dioxide is usually 4-8 mmHg greater than
arterial carbon dioxide partial pressure but increases
and decreases with it. In horses with extensively col­
lapsed lung or severe spatial mismatch of pulmonary
perfusion and ventilation, the difference between end­
tidal and arterial carbon dioxide tensions may exceed
15 mmHg. In any case, when end-tidal carbon dioxide
exceeds 60 mmHg, an increase in alveolar ventilation
should be instituted. End-tidal carbon dioxide usually
forms a plateau that lasts until the next inspiration; tail­
ing off of this plateau is often caused by small leaks
around the accessory cuff or at a connector. Complete
disappearance of the carbon dioxide plateau is associ­
ated with disconnection from the breathing system or
indicates cessation of pulmonary perfusion (Le. cardiac
arrest) . If the capnograph does not approach zero dur­
ing inspiration, the most likely cause is increased
machine dead space either from exhausted carbon
dioxide absorber or a malfunctioning one-way valve.
Pulse oximeters use the relative light-absorbing
properties of hemoglobin and oxyhemoglobin to
measure arterial saturation with oxygen (Sp02) ' A light­
emitting diode and sensor are incorporated into a
spring-loaded clip that is usually applied to the tongue
margin so that light passes through the tongue. Because
the ability to detect a signal from the equine tongue
depends upon the design of the clip, it is advisable to
test a pulse oximeter before purchase. When S p02 is less
than 90 per cent, tissue oxygenation is seriously com­
promised and corrective measures should be instigated.
Although pulse oximetry is primarily designed to detect
inadequate oxygen exchange in the lung, it is also a very
useful indicator of perfusion. The audible or visual
signal that accompanies each pulse, is very reassuring
because it continuously confirms the presence of
peripheral blood flow. Difficulty in obtaining a signal
with a probe that ordinarily functions well on the horse
151
10 COLIC
tongue, may be associated with poor tissue perfusion
due to decreased overall perfusion (e.g. shock) or
vasoconstriction (e.g. after an alpha2 adrenoceptor
agonist) .
The partial pressures of oxygen (Pa0 2 ) and carbon
dioxide (PaC02 ) in arterial blood are probably the best
objective measure of pulmonary function (see below) .
Blood tests
The introduction of small, inexpensive, accurate equip­
ment for 'bedside' use has greatly increased the ability
of clinicians to detect and treat abnormalities during
anesthesia. These bedside monitors can be used to
intermittently measure such things as arterial pH,
PaC0 2 , Pa0 2, bicarbonate, base excess of the extracellu­
lar fluid, plasma sodium, potassium, ionized calcium,
creatinine, and glucose. To date, values for hematocrit
derived from these bedside monitors have been unreli­
able, probably because the machines are calibrated for
humans and the characteristics of equine red blood
cells are different from those of humans. From a practi­
cal point of view, hematocrit and plasma protein
concentration are probably best measured using
microhematocrit tubes, a centrifuge, and a refracto­
meter.
COMMON COMPLICATIONS OF
ANESTHESIA
Hypoxia and hypoventilation
Horses under inhaled anesthesia for colic surgery usu­
ally breath a mixture of gas that is more than 90 per
cent oxygen. Given a perfectly functioning lung, this
should produce a Pa0 2 of more than 500 mmHg. In
practice Pa02 values between 70 mmHg and 200 mmHg
are often encountered. Values in this range are usually
associated with more than 90 per cent hemoglobin sat­
uration with oxygen, hence they do not present an
immediate threat to oxygen delivery. They do, however,
suggest considerable pulmonary venous admixture that
warrants remedial action because oxygen delivery may
be threatened if inspired oxygen decreases (as is likely
during recovery from anesthesia) . When Pa0 2 is less
than 70 mmHg, there is significant hemoglobin desatu­
ration and remediation should be pursued urgently.
Normal PaC0 2 is 40 ± 4 mmHg. Collapsed lung,
restricted chest movement, and anesthetic drug­
induced inhibition of ventilatory drive conspire to
cause hypercapnea in anesthetized horses. A PaC02 of
less than 55 mmHg is generally considered acceptable,
however PaC0 2 in excess of this is likely to be associated
with an unacceptable respiratory acidemia.
152
Both hypoxia and hypercapnea occur in horses anes­
thetized for colic surgery despite the early initiation of
mechanically controlled ventilation with an oxygen
enriched mixture. Treatmen t of both usually revolves
around manipulation of the ventilatory pattern. A tidal
volume of 1 0-15 ml/kg and a respiratory rate of 6-1 0
breaths per minute are usually sufficient t o maintain
Pa0 2 and PaC0 2 within acceptable limits in anes­
thetized horses. In horses with distended abdomens it
may be necessary to increase tidal volume and/or
breathing rate to decrease PaC0 2• In order to reduce
the amount of the lung that is collapsed, peak inspira­
tory pressure should be increased. Application of more
than 40 cmH 20 pressure on the alveoli may cause them
to rupture, hence peak inspiratory pressure should not
be permitted to exceed this value. Collapse of lung tis­
sue between breaths can be minimized by application of
5-10 cmH2 0 positive end-expiratory pressure (PEEP) .
Unfortunately all of these maneuvers increase mean
intrathoracic pressure which increases pulmonary
vascular resistance, reduces venous return, and, in turn,
decreases cardiac output. These side effects often
predicate support for the cardiovascular system and
ultimately limit the extent to which ventilation can be
manipulated.
Many ventilators permit change in the ratio of inspi­
ratory time to expiratory time (I:E) . Assuming constant
breathing rate, increasing I:E prolongs the time avail­
able for ventilation of slowly filling parts of the lung.
Unfortunately, prolonging the inspiratory period
proportionately reduces the period available for lung
emptying and return of intrathoracic pressure to
atmospheric pressure. In any individual, the process of
determining the best I:E is necessarily empiric, however
optimal values are usually between 1 :2 and 1 :3.
Hypotension and hypovolemia
Hypovolemia in horses with colic is usually inferred
clinically from increased hematocrit, increased plasma
protein concentration, skin turgor, etc. Under anesthe­
sia, hypovolemia causes systemic hypotension, defined
as mean arterial blood pressure less than 70 mmHg.
During anesthesia hypotension is usually treated in
several ways. The inhaled dose of anesthetic should
be minimized immediately hypotension is detected.
Switching from halothane anesthesia to isoflurane or
sevoflurane will usually increase blood pressure.
Intravenous infusion of a balanced electrolyte solution
should commence. Large volumes of balanced ele­
crolyte solutions ( 20-30 liters) need to be given to
counteract hypovolemia because such fluids are not
confined to the blood but distribute throughout the
extracellular space. This may be an advantage because

in patients for colic surgery the hypotension/hypo­
volemia may be related to depletion of the entire
extracellular space. Quite often in the preoperative
period, and occasionally during anesthesia (e.g. after
an acute hemorrhagic episode ) , hypotension/hypov­
olemia may be so severe that there is insufficient time
for rehydration with a balanced electrolyte solution.
Under such circumstances infusion of 4 ml/kg hyper­
tonic (approximately 7.2% w/v) saline solution may be
used. This operates by drawing water into the blood
down an osmotic gradient from the interstitial fluid,
thus increasing blood volume. The beneficial effect of
this is short lived (approximately 30 min ) . Because it
tends to cause dehydration of the interstitial fluid
compartment, hypertonic saline should be followed
immediately by 30-40 ml/kg of an isotonic, balanced
electrolyte solution.
Large volumes of balanced electrolyte solutions,
coupled with ongoing protein loss from incontinent
bowel, may lead to a significant decrease in plasma pro­
tein and osmotic pressure. Because this may potentiate
hypovolemia and lead to edema, hypoproteinemia
should be addressed by infusing a fluid with high col­
loidal osmotic pressure, for example equine plasma,
hydroxyethyl starch, or dextran. Intraoperative hemor­
rhage and dilution by infused fluid may lead to
decreased hematocrit. Although a degree of hemodilu­
tion may be acceptable on the grounds that it reduces
peripheral vascular resistance, the hematocrit should
not be allowed to fall below 30 per cent as this may
threaten oxygen delivery during the increased oxygen
requirement seen in recovery from anesthesia. Whole
blood, packed cells, or polymerized bovine hemoglobin
(Oxyglobin®) may be used to replace red cells.
Sympathomimetics are commonly used to counter­
act the cardiovascular depression ordinarily seen
during inhaled anesthesia of equids. Cardiovascular
depression is likely to be even more pronounced in
horses with abdominal crisis, hence the use of sympath­
omimetics is almost universal. Dobutamine is a beta
adrenoceptor agonist that is infused intravenously at
1-5 flg kg-I min-I. Very shortly after starting infusion of
dobutamine, cardiac output and systemic arterial blood
pressure increase and there is splenic vasoconstriction
causing the hematocrit to increase. At higher doses
peripheral vascular resistance increases, heart rate
increases, and tachydysrhythmias may be seen. The
short plasma half-life of dobutamine makes it ideal for
infusion because overdose can be treated easily by
reducing the infusion rate. An alternative to dobuta­
mine is dopamine. At infusion rates of 1-5 flg kg-I min-I
the predominant effects are mediated through
dopamine receptors (increasing the splanchnic and
renal blood flow) and mixed betal- and beta2 adreno-
SURGERY FOR COLIC (INCLUDING ANESTHESIA) 10
ceptors (increasing cardiac contractility and rate) ; in
horses undergoing acute abdominal surgery these are
probably beneficial effects. At infusion rates over 5 flg
kg-I min-I, dopamine predominantly stimulates alpha
adrenoceptors and, hence, causes vasoconstriction; this
may lead to an unwanted increase in peripheral vascu­
lar resistance. Norepinephrine is an active metabolite
of dopamine that may accumulate after prolonged
dopamine administration, requiring reduction of the
infusion rate of dopamine. Tachydysrhythmias are very
common with overdose of dopamine. Ephedrine is a
mixed alpha and beta adrenoceptor agonist that can
increase cardiac output and systemic blood pressure. It
is usually given as a bolus of 0.03 mg/kg that is repeated
once, after an interval of 5 minutes, if insufficient effect
is seen. The effects of ephedrine last for approximately
20-30 minutes, thus making it less suitable for infusion
than dobutamine or dopamine. Metabolic acidosis and
endotoxemia may cause down regulation of adreno­
ceptors while hypovolemia may decrease the volume of
distribution of sympathomimetics, hence the dose of
any sympathomimetic must be titrated carefully in
patients undergoing surgery for relief of an abdominal
crisis.
Perfusion of the myocardium is largely dependent
on diastolic systemic blood pressure. When diastolic
blood pressure is less than 35 mmHg myocardial perfu­
sion is compromised and cardiotonics such as dobuta­
mine and dopamine are unlikely to be effective. A
specific alpha\ agonist such as phenylephrine (0.01
mg/kg i.v.) may be warranted under these circum­
stances, despite the fact that it will redistribute perfu­
sion away from the splanchnic circulation and increase
systemic vascular resistance. Phenylephrine is also used
as a treatment for renosplenic entrapment where its
constrictive effect on the splenic capsule decreases
splenic volume and discharges red cells into the
intravascular space.
Reperfusion of strangulated bowel may cause local
injury by releasing free radicals that contribute to the
death of the intestine hours to days after the end of
surgery. The decision on whether to excise potentially
viable bowel that has experienced ischemia is based on
clinical judgment and therefore prone to error. In such
circumstances the early infusion of a free radical
scavenger, for example dimethylsulfoxide (DMSO)
1 mg/kg i.v. in 5 liters 5% dextrose, may be warranted.
Clinical experience suggests that DMSO has no delete­
rious effect on the course of anesthesia.
Metabolic acidosis
Metabolic acidosis is a common complication of
acute abdominal crisis in horses, it is largely caused by
153
10 COLIC
anaerobic metabolism in poorly perfused tissues.
Moderate metabolic acidemia (pH 7.40-7.25, base
excess O.O-S.O mEq/l) usually resolves after rehydration
with balanced electrolyte solution. Severe acidemia has
multiple adverse effects including desensitization of
adrenoceptors that are important in treating hypoper­
fusion in anesthesia. Conventional therapy involves
sodium bicarbonate (S.4% w/v, 1 mEq/ml) given intra­
venously over 1 5-30 minutes at a dose sufficient to cor­
rect the base excess to -6 mEq/l, i.e.
sodium bicarbonate dose (mEq) =
base deficit difference from -6 (mEq/l) x
[0.3 x body weight]
where the volume of distribution of the sodium bicar­
bonate is represented by 0.3 of the body weight. Sodium
bicarbonate has fallen into disfavor because it causes an
increase in blood tonicity, hypernatremia and paradox­
ical respiratory acidosis of spaces that are accessible to
the carbon dioxide that is generated by buffering, for
example the intracellular space and CSF. Nevertheless,
judicious use of sodium bicarbonate is justifiable in
horses with colic; indeed, because sodium bicarbonate
(S.4% ) is hypertonic, it has similar effects to infusion of
hypertonic saline (see above) on blood volume (a bene­
ficial effect in most horses with colic) , plasma sodium,
and plasma tonicity. As with hypertonic saline, these
effects are transient and should be mitigated by infu­
sion of a balanced electrolyte solution. Paradoxical
acidosis is a problem with bicarbonate infusion but its
effects may be minimized if ventilation is adjusted to
maintain normocapnea.
Tromethamine (TRIS, THAM, 0.3 molar) is an alter­
native treatment for acidosis that distributes through­
out the extracellular and intracellular spaces. The dose
of tromethamine is usually calculated thus
tromethamine dose (ml of 0.3 molar solution) = cause of anesthetic morbidity and mortality, hence
base deficit difference from -6 x body weight (kg)
The solution of tromethamine does not contain sodium
nor is it substantially hypertonic, therefore it does not
cause a large increase in blood volume or dehydrate the
extracellular or intracellular spaces. Because it buffers
acid without generating carbon dioxide, it does not
cause paradoxical acidosis. It is used principally in those
patients where a period of hypernatremia and hyper­
tonicity are contraindicated.
Other abnormalities that are often encountered
include hypokalemia and hypocalcemia; both com­
pound the hypotension that is usual in these patients,
decrease gastrointestinal motility, contribute to delayed
recovery from anesthesia by causing muscle weakness,
154
and therefore warrant treatment. Potassium may be
given by augmenting balanced electrolyte solution
with 20 mEq/1 potassium chloride. Calcium gluconate
( 23%, 0.2-0.5 ml/kg) may be infused over 20 minutes
and then ionized calcium re-evaluated.
Movement
Because it is incumbent on the anesthetist to maintain a
minimal plane of anesthesia, occasionally horses move
during surgery. Increasing the inspired concentration
of anesthetic may take several minutes to take effect and
may lead to significant cardiovascular depression. Small
increments of ketamine (0. 1-0.2 mg/kg) or instituting
an infusion of ketamine (approximately 40 Ilg kg-I
min-I) may be sufficient to stop movement, however
when ketamine is given toward the end of anesthesia it
may cause disorientation and excitation during recov­
ery. Xylazine (0. 1 mg/kg) may be used but it has the
risk of substantial cardiovascular depression. Toward
the end of anesthesia butorphanol (0.02 mg/kg, i.v.)
may be the best choice.
RECOVERY FROM ANESTHESIA
Mter anesthesia, horses should be moved to a stall with
padded floor and walls. Ideally there should be no
right-angled corners in the recovery area. The stall
should be quiet and have lights with a dimmer so that
stimulation can be minimized if necessary. Pulse quality
and mucous membrane color should be observed care­
fully after change in posture to lateral recumbency as
this may initiate an hypotensive crisis that requires
intervention. A demand valve may be used to continue
controlled ventilation with oxygen until the horse has
partially recovered from anesthesia.
Post-anesthetic airway obstruction is recognized as a
maintenance of the airway is especially important dur­
ing the prolonged recovery that often accompanies
colic surgery. There is little objective evidence to favor
any particular strategy for maintaining a patent airway.
The author prefers to instill 6 ml of 0. 1 5% phenyl­
ephrine into each nostril 30 minutes prior to the end of
surgery, this reduces, but does not eliminate, the need
for mechanical airway dilation after extubation. Once
the horse reaches a light plane of anesthesia, the author
removes the orotracheal tube and subjectively assesses
the airway by feeling for air movement at the external
nares and listening for upper airway noise. Upper air­
way obstruction detected at this time can usually be
treated by inserting a tube into the nasopharynx and
taping it to the outside of the head to prevent aspira-

tion. (An old orotracheal tube is suitable for this pur­
pose. For adult horses it should be approximately
20 mm internal diameter and cut to about 45 cm long.)
An alternative method is to leave an orotracheal tube in
place until after the horse stands. This tube should be
taped securely to the outside of the head and observed
carefully for kinking when the horse starts to move.
Endotoxemia, hypoproteinemia, systemic vasocon­
striction, and inspiration against an occluded upper air­
way have all been implicated in causing pulmonary edema
in the recovery room. This potentially fatal condition
occurs infrequently, but any patient that starts to produce
stable white or pink tinged froth from the nares should
promptly be given the diuretic frusemide ( 1 mg/kg i.v. ) .
This should be repeated ifn o improvement has been seen
after 5-10 minutes. Although the diuresis may have
adverse effects on a dehydrated/hypovolemic patient, the
exigencies of pulmonary edema override the other con­
cerns. Additional therapy consisting of oral application
15 g of nitroglycerine 2% cream has been used empiri­
cally to reduce pulmonary hypertension.
Horses that have evidence of venous admixture dur­
ing anesthesia (Pa02 < 200 mmHg while breathing
>90% oxygen) should receive oxygen supplementation
during recovery by insuffiating 1 5 l/min oxygen into
the trachea. A stallion urinary catheter inserted via the
nose or oro tracheal tube and secured to prevent aspira­
tion, is suitable for this. In many horses this can be left
in place until after standing. If recovery is slow, assisting
the patient into sternal recumbency improves pul­
monary function.
Horses that are slow to stand may be physically
assisted by supporting the head and tail by pulling on
ropes threaded through appropriately placed rings in
the wall of the recovery stall. Very weak horses may
require hoisting using a purpose-built webbing harness
(like the Anderson Equine Sling) and a mechanical or
electric pulley (2000 kg capacity) secured to the ceiling
of the recovery space. The support for the pulley must
be engineered for the large forces that can be gener­
ated by a struggling horse.
Surgical approaches to the
abdomen
NG Ducharme
INTRODUCTION
A number of different surgical approaches to the
abdominal cavity of the horse are available to the
SURGERY FOR COLIC (INCLUDING ANESTHESIA) 10
surgeon. The site of the lesion (s) and anesthetic con­
siderations (e.g. possible impairment of venous return
for mares late in gestation) dictate the position of the
animal and the abdominal approach required. If there
is no financial constraint the decision on where to
make the abdominal incision must be based on which
approach gives the best access to the anticipated lesion,
and gives the least morbidity to the patient. Other fac­
tors, for example the facilities and equipment that are
available, must also be considered. Invasive surgical
approaches are described in this chapter, but in some
horses laparoscopy (although it allows only partial
abdominal exploration ) can be useful, albeit mainly as
a diagnostic procedure. This section describes the stan­
dard surgical approaches for horses with gastrointesti­
nal disease (see Chapter 3 for details on laparoscopic
approaches) .
PREOPERATIVE PREPARATION
There are two main approaches to the equine abdomen
(Figure 10.la, b)
1. ventral incisions such as midline or paramedian
2. left or right flank incisions made either through the
paralumbar fossa or by a 1 7th or 1 8th rib resection.
Surgical entry into the abdomen is made with the horse
under general anesthesia in dorsal or lateral recum­
bency, except for paralumbar fossa celiotomies that can
be done with the animal standing. The surgical area is
clipped, and a 5 cm linear band is shaved at the
intended incision site to allow better adhesion of the
adhesive impervious dressings applied as part of the
incisional draping in the operating room. In addition,
ventral abdominal approaches require, in males, sutur­
ing of the prepuce using a continuous pattern to pre­
vent intraoperative urine contamination of the surgical
incision. Following aseptic preparation of the surgical
site, impervious iodine-impregnated dressing is applied
to prolong suppression of microbial growth. After
proper draping, the incisions are made as described
below.
STANDARD SURGICAL APPROACHES
Ventral midline celiotomy (laparotomy)
A ventral midline celiotomy is performed with the horse
in dorsal recumbency. This is the preferred approach
for the vast majority of horses with abdominal surgical
disease. Its limitation is poor exposure of the structures
in the pelvic cavity and dorsal abdomen.
155
10 COLIC
1 7th rib
Resection
\
\
\
\
,:
�. �
The incision is made with a no. 22 Parker-Kerr
blade, starting at the umbilicus and extending proxi­
mally for 1 5-30 em (Figure 1 0. l a) . The length of the
incision is based on the size of the animal and whether
manipulation of the large intestine, requiring a larger
incision, is anticipated. Following cauterization of
cutaneous and subcutaneous arteries the incision is
extended through the subcutaneous tissue. A 2.5 em
incision is made into the linea alba with a no. 1 0
Parker-Kerr blade taking meticulous care since the
linea alba cannot be tented. It is useful to start the inci­
sion in the linea alba near the umbilicus as the linea
alba is wider at that location, minimizing the chance of
an unplanned paramedian incision. Once the linea alba
has been incised over 2-4 em, a long-handled Russian
forceps is placed into the abdomen (still outside the
peritoneum) and directed cranially while lifting the
linea alba. This serves as a guide and protects viscera
from inadvertent injury during the approach. The inci­
sion is then extended cranially taking care to stay on the
linea alba. If the rectus abdominus muscle is inadver­
tently incised, the midline ridge on the dorsal aspect of
the linea alba can be palpated, or a hemostat placed in
the rectus abdominus muscle on each side of the inci-
156
Flank
( Figure 1 0. 1 Schematic representation of
the location of a) ventral incisions (mid­
line or paramedian), b) flank incisions
made either through the paralumbar
fossa or by a 1 7th or 1 8th rib resection
sion to identify the direction of the correction needed
to return to the linea alba. The lateral movement of the
hemostat will be arrested by the linea alba on one side
of the incision while it is unimpeded through the rectus
abdominis muscle on the other side (Figure 10.2 ) . The
peritoneum is bluntly penetrated and separated along
the incision plane with the surgeon's fingers.
If an incision must be extended caudally to increase
access to structures near or in the pelvic cavity of males,
the midline skin and subcutaneous incision must be
extended laterally to the prepuce (left or right side
depending on the surgeon's preference) . By blunt dis­
section, the prepuce is reflected to the opposite side to
expose the linea alba. The linea alba incision can then
be extended toward the pubis bone as required.
Ventral paramedian celiotomy (laparotomy)
A ventral paramedian celiotomy is also performed with
the horse in dorsal recumbency. In horses without prior
ventral midline incisions, this approach has no real
advantage for structures accessed over the ventral mid­
line incision. Perhaps, when an incision needs to be
extended toward the pelvic inlet, the ventral parame-

Abdominal
inCISion
- correction needed to return to the
Abdomen
Inernal obloque
muscle
dian incision has a slight advantage. In these cases, the
prepuce does not need to be reflected as much prior to
entry into the abdomen. In the author's opinion, the
main use of the ventral paramedian incision is for
horses with excessive fibrosis from previous ventral mid­
line incisions or if prior use of mesh has minimized the
attractiveness of a ventral midline incision.
The skin incision is located 5-7 cm on either side of
the ventral midline, again starting at the level of the
umbilicus and extending cranially 1 5-30 cm (Figure
1 O . l a ) . After extension of the incision through the sub­
cutaneous tissue, the paramedian incision is sharply,
using a no. 10 Parker-Kerr blade, extended through
the external sheath of the rectus abdominis muscles.
Following this incision, the rectus abdominis muscle is
bluntly separated and the internal sheath sharply
opened using the same technique as described for the
linea alba in a ventral midline incision in order to pro­
tect abdominal viscera from iatrogenic injury. If the
incision needs to be extended beyond the prepuce, the
skin and subcutaneous incision is deviated laterally at
the level of the prepuce on the desired side. After inci­
sion of the skin and subcutaneous tissue, the prepuce is
reflected toward the midline and the incision through
the body wall is made in the same plane as the incision
proximal to the prepuce. In general, a paramedian
approach gives exposure similar to the ventral midline
incision but has a more complicated and longer abdom­
inal closure.
Paralumbar flank celiotomy {laparotomy}
A paralumbar flank celiotomy is made with the horse
either standing or anesthetized in lateral recumbency.
A left paralumbar celiotomy allows limited abdominal
exposure for correction of nephrosplenic entrapment,
SURGERY FOR COLIC (INCLUDING ANESTHESIA) 10
External obloque
muscle
Figure 1 0.2 If the rectus abdominus
muscle is inadvertently incised, a
hemostat can be placed i n the latter
muscle on each side of the incision
__ -=
-
to identify the direction of the
linea a l ba. Note that the lateral
movement of the hemostat will be
arrested by the linea alba on one
side of the incision while it is unim­
Transverse
peded through the rectus abdomi n is
muscle on the other side
closure of the nephrosplenic space, and exteriorization
of a section of the small intestine or small colon. A right
paralumbar celiotomy allows limited access to the base
of the cecum and the descending duodenum.
The skin incision is centered in the left or right
paralumbar fossa starting 5-7 cm below the transverse
process of the lumbar vertebrae and extending toward
(without invading it) the fold of the flank (Figure
1 0.lb) . After incision of the subcutaneous tissue, the
external abdominal muscle is sharply extended along
the plane of the skin incision. If only one arm is
needed for abdominal manipulation or for exterioriza­
tion of the small intestine or small colon, a modified
grid approach is preferable. In this case, the internal
oblique muscle is separated bluntly along its fiber ori­
entation, and the transverse abdominal muscle is
sharply incised along the plane of its muscle fibers
together with the peritoneum using curved Mayo
scissors. This combined incision of the transverse
abdominal muscle and peritoneum facilitates secure
closure of the peritoneum. A good closure of the peri­
toneum prevents air introduced into the abdomen
during standing surgery from escaping from the
abdomen into the subcutaneous tissue postoperatively.
If further exposure is required (e.g. for closure of the
renosplenic space) , instead of a modified grid
approach, the incision is opened as described above
except that the internal oblique muscle is sharply
incised in the same plane as the skin incision .
Flank celiotomy {laparotomy} through the
1 7th or 1 8th rib
Flank celiotomies through the 1 7th or 1 8th rib resec­
tion are done in horses anesthetized in lateral recum­
bency where access to the left or right dorsal quadrant
1 57
10 COLIC
is desired. This approach allows significantly greater
abdominal exposure of the left or right abdominal
viscera compared to the paralumbar fossa/flank
celiotomy. It is generally done on the right side for
procedures such as typhlectomy, resection of the right
dorsal colon, or improved access to the ileocecal valve
(Figure 10.3) . It is done on the left side for procedures
such as closure of the nephrosplenic space and correc­
tion of nephrosplenic entrapment. Either the 1 7th or
1 8th rib resection gives similar exposure. However, the
1 7th rib resection allows a more secure closure if a
stormy recovery is anticipated, since incorporating the
1 6th and 1 8th ribs on either side can bolster the
strength layer of this incision.
The skin incision is curvilinear along the lateral sur­
face of the selected rib. The most dorsal aspect of the
incision is extended sharply to the ribs, incising the
attachment of the external oblique muscle and the
insertion of the internal oblique muscle. The incision is
made on the rib, and the periosteum covering the rib is
reflected exposing the rib. Following elevation of the
periosteum at the dorsal aspect of the incision, a right­
angle forceps is used to encircle the exposed rib with a
Gigli wire. After transection of the rib with the Gigli
wire, the rib is elevated away from its periosteum until
its distal end is reached. At the distal end of the rib, the
periosteum cannot be easily elevated as it adheres to the
fibrocartilaginous aspect of the rib. The rib is freed from
the intercostal muscles by sharp dissection at its distal
end. A moist towel is placed on the remaining proximal
portion of the rib to prevent inadvertent damage to
viscera during exteriorization. The periosteum on the
medial aspect of the rib is incised and the peritoneum is
bluntly separated along the line of the incision.
Figure 10.3 Right 1 7th rib resection gives reasonable
access for typhlectomy, resection of right dorsal colon, and
transection at the i leocecal valve. In this horse the large
intestine, including the right dorsal colon, is exteriorized
158
Other approaches
A thorough knowledge of equine abdominal anatomy
allows the surgeon to perform many other incisions to
suit the particular gastrointestinal disease. For instance,
the author has used a transverse incision centered over
the umbilicus to allow better exposure of the pelvic cav­
ity. Likewise, specific access to a dorsal diaphragmatic
tear may be made through a thoracotomy; or to access
the dorsal and cranial aspect of the stomach the sur­
geon may need to perform a thoracotomy followed by
an incision into the diaphragm. In conclusion, the sur­
geon faced with an unusual lesion should feel free to
use an unusual approach that is directed to the sus­
pected lesion, and not be limited by a time-enforced
paradigm of a few selected incisions.
Surgica l exploration of the
abdomen
II
NG Ducharme
INTRODUCTION
Abdominal surgery in horses is now a routine proce­
dure conducted at many equine hospitals around the
world, primarily for the diagnosis and treatment of
acute colic. This procedure requires delicate and
thorough surgical manipulation to localize, identify,
and correct the particular abnormality. The surgical
approach into the abdomen and the site of the lesion
will determine which structures are seen first on entry
into the abdomen. This section describes the principles
one follows for complete exploration of the abdomen
and manipulation of the viscera.
ABDOMINAL EXPLORATION
Initial exploration
Proximal to any obstructive lesion, bacterial fermenta­
tion associated with intestinal stasis and continued
production of secretions lead to intestinal distension.
Such distension will often be immediately apparent on
opening the abdomen.
1 . In a small intestinal obstruction, the distended
small intestine often bulges out of the incision. The
surgeon proceeds to explore the abdomen while an
assistant keeps the intestine wall moist with sterile
isotonic solution.
 SURGERY FOR COLIC (INCLUDING ANESTHESIA) 10

2. In obstructive lesions affecting the small or large Detailed exploration

colon, the distended large colon may bulge out of
the incision on entry into the abdomen. Gas
accumulated in the large intestine must be
evacuated before the abdomen is explored to
ensure minimal serosal irritation of the viscera. This
can be done by placing a 1 4- or 1 6-gauge needle
(attached to a suction tube) into a tenial band, and
after tunneling the needle through the intestinal
wall the tip is inserted into the lumen. The author
prefers oversewing the puncture site with a pre­
placed simple interrupted absorbable
monofilament suture (size 00 or 000) in a cruciate
pattern. Suturing the decompression tract is
optional in the adult horse, but should be
considered in foals as they have thinner and more
likely to leak bowel walls. The author has observed
significant adhesions developing in young animals
at decompression sites that were not sutured.
3. To minimize serosal irritation during abdominal
exploration, one liter of lactated Ringer's solution or
1 % carboxymethylcellulose* can be instilled into the
peritoneal cavity. The surgeon dons an impervious
sleeve and proceeds with abdominal exploration.
*1 % carboxymethylcellulose is prepared by adding 10 g of
carboxymethylcellulose powder to 200 ml of boiling sterile
water and adding sufficient sterile water to form a 1 liter
solution. The preparation is then autoclaved at 1 2 1 °C for a
total of 20 minutes.
The abdominal cavity (divided into four quadrants)
and the pelvic cavity are explored briefly with the vis­
cera in situ. The objective is to identify the lesion(s) so
that appropriate equipment (i.e. surgical instruments
for anastomosis, colon table, etc.) can be requested. It is
neither crucial nor beneficial to spend a lot of time
looking for a precise diagnosis by palpation alone as
exteriorization will enable the surgeon to identify the
majority of intestinal problems. Therefore, abdominal
exploration is often completed after the distended
intestinal segment has been exteriorized and the lesion
identified and corrected.
The surgeon assesses each abdominal quadrant and
the pelvic cavity for
1 . normal abdominal viscera, including the urogenital
tract and ligamentous and vascular structures (i.e.
cranial mesenteric artery) , that should be present
2. abnormal findings, such as the presence and nature
(gas, firm ingesta, etc.) of intestinal distention,
intestinal wall thickness, tight bands, or abnormal
location of an intestinal segment.
Table 10.3 shows the structures that the surgeon should
evaluate in the four abdominal quadrants and the
pelvic cavity.
Figures 1 0.4-10.6 outline abdominal palpation of
selected structures that cannot be exteriorized.
Depending on the size of the animal and the target

·�_:�i����.;�e��{t(�·:��.�"���j.�i;.··
Structures to palpate

Left cranial quadrant Body and cra n ia l edge of the spleen; gastrosplenic ligament; fundus of the stomach;
omentum; left hemi-diaphragm; left lobe of l iver; small i ntestine; small colon as it joins
the transverse colon and duodenal-colic l igament between the d i stal aspect of the
duodenum and the most proximal aspect of the small colon; the left ventral and dorsal
colon medial to the spleen; the diaphragmatic and sternal flexures near the stomach.

Right cranial quadrant Right ventral and dorsal colon; right and quadrate lobe of the l iver; two or three d ucts
of the b i liary tree; proximal duodenum; epiploic foramen; pylorus and antrum of
stomach; right hemi-diaphragm; d iaphragmatic and sterna l flexures; right dorsal and
ventral colon; omentum; cranial mesenteric artery; right kidney; and, if enlarged, right
adrenal gland.

Right caudal quadrant Cecum; i leocecal valve; small i ntestine; right ureter if d istended; and, when a p propriate,
right inguinal ring or right ovary, uterine horn, and broad l igament.

Left caudal quadrant Left dorsal and ventral colon; pelvic flexure; body of spleen; nephrosplenic l igament; left
kidney; and, if enlarged, left adrenal gland and ureters; sma l l i ntestine; small colon; and,
when appropriate, left inguina l ring or left ovary, uterine horn, and broad ligament.

Pelvic cavity Bladder; descending colon and rectum; and, when appropriate, uterus and vas d eferens

159
10 COLIC
Mesentery Duodenum
organ, some of these structures can be seen by a combi­
nation of
• retraction of the abdominal incision
• placement of an intra-abdominal moist towel to
retract local abdominal viscera
• use of suction
• tilting of the operating table.
However, the surgical view is restricted and manipu­
lation is difficult at best.
Right cranial abdominal quadrant
Using the stomach as the reference point, the pylorus is
identified as a firm muscular structure from which the
160
Figure 1 0.4 Schema illustrating
identification of the epiploic
foramen. Lateral view of the right
cranial abdominal quadrant as
examined through a ventral mid­
line i ncision. The duodenum is
identified first, by applying trac­
tion on the duodenum with the
thumb and forefinger the surgeon
can use a finger to probe the duo­
denum's now tense mesentery in
a cranial-to-caudal direction until
the epiploic foramen is identified
Figure 1 0.5 Schema i l lustrating pal­
pation of the right dorsal colon and
transverse colon. Cranial view of the
right cranial abdominal quadrant as
examined through a ventral midline
incision
duodenum is found. By tensing the descending duode­
num, its mesentery becomes palpable, and the epiploic
foramen and medial surface of the liver can be identi­
fied (Figure 1 0.4) . The right dorsal colon can be pal­
pated axial to the duodenum as it joins the transverse
colon (Figure 10.5 ) .
Right caudal abdominal quadrant
By following the base of the cecum, the surgeon can pal­
pate the ascending duodenum as it traverses the
abdomen from right-to-Ieft around the cranial mesen­
teric artery (Figure 1 0.6) . The latter can be palpated as
an irregular firm structure with fremitus in cases of
thromboembolic colic associated with Strongylus vulgaris

------
Sloma(h Duodenum Cr.noal
mesent�nc Irtf!ty
larval migration. When present, the right ovary and
uterine horn can be palpated along the dorsal body wall
caudal to the right kidney.
Left caudal abdominal quadrant
By following the medial surface of the spleen dorsally,
one can identify the nephrosplenic ligament (the
ventral component of the suspensory ligament of the
spleen) between the dorsal-ventral surface of the spleen
and the left kidney (Figure 1 0.7) . When present, the
left ovary and uterine horn can be palpated along the
dorsal body wall caudal to the left kidney.
Left cranial abdominal quadrant
By following the medial surface of the spleen cranially,
one can identify the gastrosplenic ligament between the
SURGERY FOR COLIC (INCLUDING ANESTHESIA) 10
Figure 10.6 Schema illustrating
palpation of the ascending duo­
denum and cranial mesenteric
artery. Lateral view of the right
cranial abdominal quadrant as
examined through a ventral mid­
line incision
cranial-ventral surface of the spleen near the hilus and
left part of the greater curvature of the stomach (Figure
1 0.8) .
EXTERIORIZATION OF VISCERA
If not already present, the surgeon places an impervious
drape around the incision to receive the exteriorized
bowel. Prior to the manipulation of small intestine, 1
liter of a 1 % solution of carboxymethylcellulose can be
placed into the abdomen to prevent serosal irritation
during manipulation; this is recommended in foals but
optional for adults.
If the small intestine is distended, it is best to identify
the ileum and exteriorize the small intestines starting
Figure 10.7 Schema illustrating palpation of
the nephrosplenic ligament. View: left
caudal abdominal quadrant as examined
through a ventral midline incision. The sur­
geon can identify this l igament by following
the spleen dorsally and caudally
161
10 COLIC

Figure 10.8 Schema i l lustrating

palpation of the gastrosplenic
ligament. View: l eft cranial
abdominal quadrant as exam­
ined through a ventral midline
incision. The gastrosplenic l iga­
ment is found between the
medial surface of the spleen
and the left greater curvature
of the stomach, the left colon
Pelvic is medial to the surgeon's hand
flexure

distally until the lesion is found. The apex of the cecum

is exteriorized and pulled caudally exposing the dorsal
and lateral bands of cecum. Tracing the dorsal band
rostrally, the ileocecal fold is identified and followed
toward the base of the cecum until the ileum is found
and identified by its thicker wall and the antimesenteric
attachment of the ileocecal folds. While manipulating
the small intestine, the intestinal wall itself is grasped
while taking care not to pull on the mesentery, which is
especially friable in foals ( Figure 10.9) . The small intes­
tine is exteriorized until the obstruction is localized, or
the duodenum is reached. The goal is to exteriorize the
obstruction site to determine the best means of correct­
ing the problem. The following algorithm gives the sug­
gested steps to locate and exteriorize an intestinal
obstruction (Figure 10. 1 0) . If the obstructed site cannot
be exteriorized, one should attempt to reduce the
obstruction abdominally and then exteriorize the
involved intestinal segments. Figure 10.9 For exteriorization of the small intestine, the
If the large intestine is distended and is the site of surgeon handles the intestinal wall and avoids the fragile
intestinal lesions, the incision is lengthened appropri­ mesentery
ately to allow its safe exteriorization. Rupture of the
large intestine is a real possibility during manipulation
and exteriorization if it is distended. If the viability of
the large intestine wall is also compromised, the risk of decision must be made as to whether an enterotomy
rupture increases substantially. After a lengthened inci­ needs to be performed to empty the colon prior to
sion has been made and gas decompressed from the further manipulation.
cecum and large intestine, the surgeon places an arm The small colon is exteriorized by finding its charac­
underneath the left colon while an assistant lifts and teristic contents in the caudal abdomen and retracting
retracts the left side of the incision (Figure 10. 1 1 ) . The it out of the abdomen. Alternatively, the small colon
goal is to exteriorize the pelvic flexure first. If the colon may be identified by palpation of the duodenocolic
is markedly distended by fluid and solid materials, a ligament or the descending colon in the pelvic cavity.

162
 SURGERY FOR COLIC (INCLUDING ANESTHESIA) 10

Determine if an obstruction is present by intra-abdominal

exploration using an impervious sterile sleeve

I
Exploratory steps
Divide abdomen into four q uadrants and pelvic cavity
Perform in situ assessment based on Table 1 0.3
Assess for normal abdominal viscera
Assess for abnormal findings
Distention
Intestinal wall thickness
Abnormal location of intestinal segment

y 9
Is obstruction site
found?

Is the small
intestine
I Can obstruction be exteriorized?
I
distended?

EJ Yes

If the small intestine is involved
grasp and lift the site taking care
not to p u l l on the lesions or the
mesentery of the bowel i nvolved in
the lesion
Find the ileocecal junction and
begin exteriorizing the small
If the large intestine is involved it is usually gas
distended:
Relieve distention with gas suction.
Make sure the incision is long enough.
Place forearm under the left ventral and dorsal colon
and l ift the colon in a sl ightly rostral direction to
exteriorize the pelvic flexure.
Then lift and pull the colon in a caudal direction until
the sternal/diaphragmatic flexures are exteriorized.

I r-
intestine from d istal to proximal

�
until the lesion is found or the
lf lesion is not found
duodenum is reached

I
Starting in proximal jejunum, 'milk' small intestine content distally
Replace empty small intestine into abdomen simultaneously until i leocecal valve is reached

I
Place forearm under the left ventral and dorsal colon and lift the colon in a slightly rostral
direction to exteriorize the pelvic flexure, then lift and p u l l the colon in a caudal direction
until the sternal/diaphragmatic flexures are exteriorized.

I
Reach into the pelvic cavity and grasp the sma l l colon. Exteriorize the small colon from
distal to proximal unti l the lesion is found or the transverse colon is reached. If the sma l l
intestine h a s not been exteriorized, find the ileocecal junction a n d beg i n exteriorizing the -

smal l intestine from distal to proximal.

Figure 10.10 Algorithm summarizing the steps needed to identify and exteriorize various intestinal lesions

1 63
10 COLIC
Pelvic
flexure
CONCLUSION
The surgeon must remember that the goal is to correct
the cause of the intestinal obstruction or disease and
that multiple abnormalities can be present in the same
animal. For example. it is not uncommon to have a
large colon displacement. presumably because of
rolling. toge th e r with another disease process.
Therefore, complete but efficient intestinal examina­
tion is a sine qua non condition of proper abdominal
surgery.
Evaluation of gut viability
D E Freeman
In many cases the appell-ranee of strangulated bowel
leaves little doubt about the need for resection. but no
method can provide consist..e n t gllidance since the via­
bility of bowel that has incurred subtle changes is diffi­
cult to determine. The difference between the viability
of the small intestine and large colon of horses is clini­
cally important. but frequently overlooked. Criteria of
viability and the consequences of an incorrect decision
are different for the two segments (Figure 1 0 . 1 2) . In the
equine large colon. the term viable refers to the
affected segment's ability to recover fully without
undergoing further mucosal necrosis resulting in death
from endotoxemia and peritonitis. Although progres-
164
Figure 1 0. 1 1 Exteriorization
of the large intestine with a
ventral midline i ncision. The
surgeon is on the right side
of the horse while a n assis­
tant retracts the left side of
the incision. By placing the
left colon over the surgeon's
arm like a towel, the surgeon
can l ift the left colon while
attempting to exteriorize the
pelvic flexure first
sive necrosis is a concern in the small intestine, a seg­
ment judged viable because it clearly can survive and
repair the ischemic injury could be at great risk for
developing adhesions (Figure 1 0 . 1 2 ) . Adhesions are
less likely in the large colon. An important issue for
both segments is the expense of intestinal resection
(Figure 1 0. 1 2 ) . The added cost of a longer anesthesia
time, surgical expenses, and intensive aftercare could
be reasons for intraoperative euthanasia when there are
financial constraints. Increased duration of surgery for
resection could extend anesthesia time beyond safe
limits for draft breed horses.
SMALL INTESTINE
Only one study has compared different methods of
assessing viability in equine (pony) jejunum and it
found that all intestinal segments recovered from dif­
ferent types of ischemia without developing adhesions,
despite pessimistic predictions based on clinical judg­
ment (Figure 1 0 . 1 3) and fluorescein fluorescence.
However in another study, j ejunal segments subjected
to identical types and duration of ischemia were at
considerable risk of adhesion formation, even when the
bowel yielded a viable fluorescent pattern with fluores­
cein. Differences between the studies that could have
predisposed the animals to adhesions in the latter study
were
• strangulation of four segments versus one segment
per animal
 SURGERY FOR COLIC (INCLUDING ANESTHESIA) 10

SMALL INTESTINE
Questionable viability
I
I I
If viable If non-viable
I I
I I I
Incorrect decision Correct decision Correct decision Incorrect decision
Resection No resection Resection No resection
I I I I
Lon.g surgery Short surgery Long surgery Short surgery
Expensive treatment Inexpensive treatment Expensive treatment Inexpensive treatment
Anastomotic problems No anastomotic problems Anastomotic problems N o anastomotic problems
Risk of adhesions Less risk of adhesions Risk of adhesions Great risk of adhesions
I I I I
Good prognosis Excellent prognosis Good prognosis Poor prognosis

LARGE INTESTIN E
Questionable viability
I
I I
If viable If non-viable
I I
I I I I
Incorrect decision* Correct decision* Correct decision Incorrect decision
Resection No resection Resection No resection
I I I I
Long surgery Short surgery Long surgery Short surgery
Expensive treatment Inexpensive treatment Expensive treatment Expensive treatment
Anastomotic problems No anastomotic problems Anastomotic problems No a nastomotic problems
Endotoxemia Severe endotoxemia

I
Good prognosis Excellent prognosis Fair-good prognosis Poor prognosis
No risk of recurrence Risk of recurrence No risk of recurrence Risk of recurrence

Figure 10.12 Consequences of errors in assessing the viabi l ity of small and large intestine in random order. *The decision
to resect or not resect large colon after volvulus must consider the possibility of recurrence of the volvulus, a factor that
can justify resection of questionable colon in some cases

• more traumatic methods for inducing ischemia
• omission of antibiotics and flunixin meglumine in
the postoperative management.
Clinical criteria of viability are
• serosal color
• bowel wall thickness
• presence or absence of mesenteric arterial pulses
• spontaneous motility or motility evoked by
snapping a finger against the intestinal wall
• improvement in color after correction of the
strangulation.
Spontaneous or evoked motility will appear sluggish in
viable strangulated bowel because of 'splinting' of the
muscle wall by edema and hemorrhage. Edema and
hemorrhage in the intestinal wall is not unusual after
strangulation because occlusion of thin-walled veins
causes rapid mural congestion (Figure 10. 1 3 ) . Such
changes lead to high false-positive results (unnecessary
intestinal resections) because short intestinal segments
with these changes can survive without forming adhe­
sions (Figure 1 0 . 1 4) . Enterotomies are not recom­
mended for viability assessment in the small intestine
because of the risk of adhesions and because mucosal

165
10 COLIC
Figure 10.13 Appearance of a segment of 4 meters of small
intestine that was strangulated in the epiploic foramen
and was not resected. The horse recovered and did not
develop a known problem over a 2-year follow-up period
appearance is usually severe enough to lead to an
unnecessary resection. With long segments of question­
able viability, the risk of adhesions to bowel left in situ
must be balanced against the risk of adhesions with
resection and anastomosis (Figure 1 0 . 1 2) .
The advantages of fluorescein fluorescence (visual
or qualitative fluorescence) in equine small intestine
are that it allows rapid assessment of large areas of
bowel and is simple to use, safe, and inexpensive.
Fluorescein is given through the jugular catheter as a
10% solution at a dosage of 15 mg/kg of body weight,
and a portable ultraviolet lamp is used to demonstrate
fluorescence in the darkened room approximately 5
minutes after injection. Unfortunately interpretation of
equivocal fluorescein patterns is subjective and prone
to error, and patterns that have been regarded as non­
viable in the intestine of other species are viable in the
horse. Fortunately, non-viable bowel does not stain
from surface contact with the dye, and the hyperfluo­
rescent pattern caused by perivascular leakage in non­
viable bowel seems to be rare. In viable intestine
rendered hemorrhagic and edematous by venous occlu­
sion, intramural hemorrhage shields fluorescein in the
tissues from ultraviolet light, and a hypofluorescent or
'non-fluorescent pattern is produced. This accounted
for the high false-positive results, low overall accuracy,
and low overall specificity for fluorescein in one study
on ponyjejunum.
The Doppler pencil probe (9 mHz ) , calibrated to a
Doppler flowmeter, can be used to detect blood flow at
several points in the mesenteric vessels and in the
1 66
Figure 10.14 Segment of small intestine 1 5 m i n utes after
release from 3 hours of venous strangulation obstruction.
This segment did not cause postoperative complications,
and adhesions and other obstructive lesions were not
found at necropsy 45 days later. From Freeman et a/.
(1 988) Am. J. Vet. Res. 49:895-900, with permission
intestinal wall. The tip of the gas-sterilized probe is
coated with sterile, water-soluble gel to enhance con­
tact. It is held at a 45 degree angle to the tissue surface
and is pointed upstream in the direction of blood flow.
Doppler arterial signals are then judged as present
(viable) or absent (non-viable) . The Doppler technique
is most suitable for identifYing small areas of ischemia
and for selecting well-perfused margins for intestinal
anastomosis. However, it is impossible to scan large seg­
ments of ischemic bowel adequately, and as a result the
Doppler can miss foci of infarction.
In a study on pony jejunum, Doppler ultrasound was
found to be superior to fluorescein fluorescence and
clinical judgment in predicting an intestinal segment's
viability after it had been subjected to venous occlusion.
This is consistent with the results of similar studies in
dogs and cats. After combined arterial and venous
occlusion, fluorescein fluorescence is superior to clini­
cal judgment and Doppler ultrasound in viable loops.
However, the Doppler technique is inferior to fluores­
cein and clinical j udgment in detecting non-viable seg­
ments, regardless of the method of inducing ischemia.
The superiority of fluorescein has been attributed to its
ability to assess microvascular perfusion which corre­
lates closely with tissue viability, whereas the Doppler
device mainly detects blood flow in large vessels.
Other methods that could be applied to viability
assessment in equine small intestine are surface
oximetry and measurement of surface temperature.
The perfusion fluorometer (quantitative fluorescence ) ,
laser-Doppler flow meter, and tetrazolium analysis of

the mucosa, have some potential but are cumbersome
and require special equipment. In clinical cases, a mean
intralumenal hydrostatic pressure of 15 cmH20 in intes­
tine proximal to an obstruction was significantly associ­
ated with low survival; however, this may be more useful
as an indicator of prognosis than intestinal viability.
The author has modified clinical criteria, based on
the findings of one report, and tends to leave intestine
in place that has scattered ecchymoses, dark pink to
light red discoloration, and mural edema as the pre­
dominant changes (Figures 1 0 . 1 3 and 10. 14) . In a
recent clinical study where this approach was used, long
and short-term outcomes were better when such
segments were left in place rather than resecting the
intestine. Although intestinal damage was considerably
more severe in the resected groups, the results would
suggest that a more optimistic approach can be applied
to leaving questionable small intestine in place. The risk
of adhesions exists, especially in the more severely com­
promised segments, but might not be worse than after
anastomosis. In addition, it is not unusual for distended
intestine to develop edema and serosal hemorrhages,
and yet be sufficiently viable to heal an anastomosis
(Figure 1 0. 1 5) .
In conclusion, fluorescein fluorescence offers little
improvement over clinical judgment, although it is
accurate when it produces a viable fluorescent pattern.
A viable fluorescent pattern in a questionable segment
therefore means that the segment could be left in place,
but a non-viable pattern is an indeterminate finding. In
the author's experience, the most unpredictable out-
Figure 10.15 End-to-end anastomosis made in hemor­
rhagic and edematous small intestine to avoid resection of
too much bowel. At a repeat celiotomy 5 days later, a
small adhesion was broken down proximal to the anasto­
mosis and the horse did not develop any complications
over a 3-year follow-up period
SURGERY FOR COLIC (INCLU DING ANESTHESIA) 10
come arises with the rare small intestinal segment that
appears normal at surgery after release of strangulation,
but deteriorates subsequently because of undetected
vascular thrombosis or possibly reperfusion injury.
Another important issue is the amount of bowel that
can be removed, and recent evidence suggests that
removal of 60-70 per cent is close to the limit.
LARGE INTESTINE
The large intestinal disease that is most likely to cause
difficulty with viability assessment is large colon volvu­
lus, and the decision to resect is further complicated by
poor access to viable margins, the risk of recurrence
(Figure 1 0. 1 2 ) , and selection of a method for prevent­
ing recurrence. A segment that appears viable based
on serosal appearance can have irreversible mucosal
changes and microvascular thromboses. A pelvic flex­
ure colotomy can be very useful in such cases, as it
allows evacuation of the bowel and assessment of bleed­
ing from the cut edges. If the mucosa is dark red, the
prognosis is better than if it is black, but dark discol­
oration of the mucosa can be associated with viability.
Visual assessment of motility in the large intestine is not
as reliable as in the small intestine, because large intesti­
nal motility normally appears sluggish.
Evaluation of histologic changes from frozen biop­
sies has been used to assess the degree of epithelial
injury to the equine large colon. A full thickness intesti­
nal biopsy is cooled to - 1 50°C to - 1 60°C in 2-methyl­
butane immersed in liquid nitrogen until the solution
almost reaches its freezing point (approximately 5-10
minutes) and is processed for immediate evaluation.
The prediction of viability is based on assessment of
hemorrhage and edema in the mucosa and submucosa,
the extent of epithelial cell damage, and the intersti­
tium to crypt ratio (normal I:C < 1 ) . Intestine is less
likely to survive with a greater than 50 per cent loss of
the crypt epithelium, and an I:C ratio greater than 3.
Formalin-fixed sections can be used for delayed viability
assessment and to help decide between the need for
further treatment, surgery, or euthanasia, if the clinical
course deteriorates after surgery.
Combined evaluation of tissue blood flow (surface
oximetry or laser Doppler) and histologic injury
(frozen tissue sections) has been recommended to
assess large colon ischemia. Surface oximetry is a mea­
sure of the partial pressure of oxygen on the tissue sur­
face (PsO) and is determined by oxygen content in
blood beneath the probe, the diffusion distance from
the vessels to the surface, the local tissue oxygen
consumption, and blood flow. A good outcome is asso­
ciated with a Ps02 > 20 mmHg. The disadvantages are
167
10 COLIC
that the equipment is expensive, only small areas of tis­
sue can be evaluated, and contact between probe and
tissue should be constant. Pulse oximetry can be used to
assess oxygen saturation, but it has not been evaluated
in the horse and it may not be as sensitive to decreases
in local tissue blood flow as surface oximetry.
Fluorescein fluorescence might be more suitable for
assessing large intestine than for small intestine because
the large intestine has a lower risk of adhesions in seg­
ment� that produce a viable pattern. The fiberoptic per­
fusion fluorometer has the advantage over qualitative
fluorescence of providing quantitative information and,
therefore, is an objective measure of perfusion. Results
were inconclusive in one study on experimental
ischemia in equine small and large intestine, although
it did identify the ventral colon as more susceptible to
ischemia than the dorsal colon. In horses with large
colon obstruction, an intralumenal hydrostatic pressure
greater than 38 cmH20 had a high sensitivity, speci­
ficity, and positive and negative predictive values for
predicting low survival.
Viability assessment of the small colon has not been
studied to the same extent as it has for the large colon
and small intestine, but this segment has some unique
ischemic lesions that can be difficult to evaluate. The
small colon seems very sensitive to pressure necrosis at
the site of a focal impaction, and resection is indicated
for segments with black and green discoloration. Also,
the entire small colon proximal to an obstruction
should be examined because it is not unusual for an
impaction to move distally and reimpact at several sites,
causing scattered areas of mural necrosis.
Enterotomy, resection, and
anastomosis techniques
NG Ducharme
INTRODUCTION
Enterotomy, resection, and anastomosis are basic pro­
cedures used to surgically treat horses with a variety of
gastrointestinal diseases. The indications for the use of
these procedures will be covered in the following chap­
" ters where specific disease entities are discussed.
In the last 20 years many studies have provided
equine surgeons with significant information, thereby
increasing the success of abdomin al surgery.
Information is now available on the preferred location
of intestinal incisions, some factors associated with the
occurrence of obstructive intra-abdominal adhesions,
1 68
and measurable effects of various suture patterns and
materials. The introduction of new synthetic suture
materials, development of stapling instruments, and
institution of early surgical intervention have paralleled
these studies. All these factors have contributed to the
reduced morbidity and mortality of horses with 'surgi­
cal colic'. Yet, in many of the decisions to be made at
surgery, there remain considerable preferen.ces of the
surgeon, both in the interpretation of the available data
and in the techniques to use. Whenever possible, this
chapter will focus on the techniques that are supported
by facts, and it will limit itself to a few of the more com­
mon alternatives. The introduction of laparoscopic
techniques has forced some changes in surgical proce­
dures, and will likely transform these procedures in
years to come.
SUTURE MATERIALS
A variety of suture materials can be used and to some
extent the choice of which material to use is based on
the surgeon' s preference. Intuitively monofilament
suture materials are superior to multifilament materials
because they have less likelihood of capillary action that
might wick intestinal contents to the serosal surface. In
addition some suture materials such as chromic catgut
have been shown to be more inflammatory and increase
the risk of adhesion formation.
Non-absorbable suture materials are only used in
animals where delayed healing is expected because of
the nutritional status of the patient. A continuous pat­
tern of these non-absorbable sutures is avoided in
young animals for fear the anastomosis site will not
enlarge as the animal grows and, therefore, will result in
a delayed stricture.
Exposure of suture materials at the serosal surface
increases the risk of adhesions at the anastomosis/
enterotomy site, and therefore small suture materials
are preferred (no. 00 or no. 000; 3 or 2 metric) .
The ideal suture material has not been conclusively
studied, but synthetic absorbable materials such as
polyglycolide, polyglactin 9 1 0, poly-p-dioxanone, poly­
glyconate, and polyglecaprone 25 are recommended at
this time in procedures where staples are not used.
SUTURE PATTERNS
The various suture patterns used for an intestinal anas­
tomosis and enterotomy are shown in Figure 1 O . 16a-h.
The effects of the suture pattern on an intestinal
enterotomy/anastomosis should be considered in the
 SURG E RY FOR COLIC (INCLUDING ANESTHESIA) 10

light of several parameters, all of which have been a

reviewed in many studies

• the diameter of the intestinal segment at the site

• its bursting strength
• alignment of intestinal layers
• the likelihood of inducing adhesions.

For optimal bursting strength two-layered anastomoses

are used.
In horses, exposed mucosa and seromuscular raw
edges have been associated with an increased risk of

I
Figure 10.16 Suture patterns used in equine i ntestinal
procedures, a) simple interrupted, b) simple continuous,
c) Gambee - continued

1 69
10 COLIC
Figure 10.16 Suture patterns used in equine intestinal procedures continued
(interrupted or continuous), e) Cushing - continued
adhesion at the enterotomy/anastomosis site (Figure
1 0. 1 7 ) . Simple interrupted patterns, even the Gambee
technique, can result in such exposure. Therefore,
when apposing patterns are used, they are often over­
sewn with an inverting pattern.
Exposed suture material also increases the risk of
adhesion at the enterotomy/anastomosis site. There­
fore, inverting suture patterns in the seromuscular layer
result in less adhesions than interrupted patterns.
Small-sized suture material (no. 000 or 00; 2 or 3
metric) and less reactive material (avoid chromic
catgut) should be targeted.
Many surgeons feel that a simple continuous pat­
tern results in more reduction of an anastomosis
diameter than a simple interrupted pattern. One
equine study found this to be untrue. However, if the
surgeon over-tightens the suture material in an effort
to obtain a leak-proof anastomosis, there is the poten-
170
\ -.
"
"' .;;,, �, ... "
,
- the inverting patterns of d) Lembert
tial for a purse-string anastomosis. Therefore, if a
simple continuous pattern is used it should cover only
one half of the anastomosis before being tied, and a
second continuous pattern should be used on the
remaining half.
Because maintenance of proper lumen diameter at
the enterotomy or anastomosis site is critical (especially
in the small intestine, pelvic flexure, and small colon) , a
double-inverting pattern or three-layered anastomosis
should be avoided.
In conclusion, to decrease the morbidity of entero­
tomy/anastomosis procedures, the standard procedure
for hand-sewn anastomosis is a two-layer closure with
the first layer closed with a simple continuous pattern.
Some surgeons prefer this layer to be in the mucosa­
submucosal layer while others also include the sero­
muscular layer in the intestinal layer. A second
inverting pattern is placed in the seromuscular layer.
 SURGERY FOR COLIC (INCLU DING ANESTHESIA) 10

------ -------

Figure 10.16 Suture patterns used in equ i ne intestinal pro­

cedures - continued: the inverting patterns of f) Connell,
g) Schmeiden, h) Marshall U

171
10 COLIC

If the enterotomy must be made near or into the

abdomen (i.e. right ventral colon enterotomy) , an
impervious drape is sutured to the bowel around the
intended intestinal incision site using a simple continu­
ous pattern.

ENTEROTOMIES

The enterotomy site is determined by the site and type

of lesion. The purpose of the enterotomy is to evacuate
the contents of a section of bowel or to allow entry of an
instrument, lavage device, or the surgeon's fingers or
hand into the intestinal lumen to remove an obstructive
Figure 10.17 Adhesions at the site of an end-to-end
lesion such as an enterolith, foreign body, or impaction.
anastomosis performed with a suture pattern resulting in
More rarely, an enterotomy is made to help assess the
exposed mucosa. Dr Rick Hackett, with permission
viability of an intestinal segment by inspection of the
mucosa or to allow biopsy of a mural anomaly.
Many investigators have studied the ideal location
within each intestinal segment for an enterotomy. In
STAPLES AND STAPLING EQUIPMENT the large intestine, antimesenteric band enterotomies
; JlNi\i'···''�N;:''1'>,,,
""""m;'"'"'_';V;"*"';"f\;V'';>''''_'''""'N''#.(;i'i:'''�"''©>''''':''=;'''''"'''''';1"11�1'>'@1"""""'''":''''''' ,�,,,,"'''"":I@�%;"",II�U"W<18''"''''''''"'1%,9·.·.'"'

are quicker to heal, have less inflammation, and result

When using staples, at least in adults, 4.8 mm staples are in more accurately apposed intestinal layers with a
preferable to 3.8 mm staples because the closing height higher burstin g strength than enterotomies through
in the former staples (2 mm versus 1 .5 mm) is preferable the sacculations. Equally important, enterotomies adja­
given the thickness of a normal equine intestinal wall. cent to tenia bands result in a narrower lumen and a
predisposition to postoperative obstruction at the anas­
tomosis site. Because of the thickness and line of ten­
INTESTINAL PREPARATION FOR sion of the longitudinal muscle fibers forming the tenia
ENTEROTOMIES AND ANASTOMOSIS bands, transverse closure of an enterotomy made on the
tenia is likely to result in an unwanted increased tension
Following exteriorization, the intended enterotomy/ at the suture line. Table 10.4 summarizes the current
anastomosis site must be properly prepared to prevent recommendations regarding enterotomies in horses.
abdominal contamination by intestinal contents.
Barrier drapes are placed surrounding the abdominal
incision as part of the normal surgical incision draping
ANASTOMOSIS
in order to prevent the fluids that are being used to
keep the exteriorized intestine moist, from soaking
General considerations
through the drapes into non-sterile areas. Therefore,
after the intestinal segment that requires incision or The length of intestine that can be resected without
resection has been exteriorized, the remaining bowel is special dietary modification is still a matter of conjec­
replaced in the abdomen. The surgeon should leave ture. The concern is that extensive intestinal resection
sufficient bowel exteriorized away from the incision to can result in 'short bowel syndrome' where a decrease
prevent abdominal contamination from spillage of in absorptive surface leads to carbohydrate, lipid, and
intestinal content. A moist towel is placed under the mineral malabsorption. resulting in weight loss and
intended enterotomy/resection site and used to isolate poor performance. It has been shown that resection of
it from the normal exteriorized bowel and the sterile 60 per cent of the small intestine in a normal pony can
surgical field. result in malabsorption syndrome. However, the length
If significant splatter of intestinal content is of a strangulated small intestine can increase up to 25
expected during the enterotomy/resection procedure, per cent, making the true length of small intestine
an impervious drape should be used to prevent abdom­ resected less clear. Clinical experience has revealed that
inal contamination; and the exposed bowel should be resection of up to 50 per cent of the small intestine
irrigated frequently to prevent adherence of intestinal does not interfere with normal intestinal function.
contents to the serosa. Furthermore, there are anecdotal reports suggesting

172
 SURGERY FOR COLIC (INCLU DING ANESTHESIA) 10

Intestinal Location of enterotomy Diredion of closure

segment

Small intestine Along the long axis opposite the Transverse closure to
mesenteric attachment m i n imize stricture

Cecum At the a pex on either side of the Longitudinal closure

dorsal bands to prevent postoperative
contact between enterotomy and
incision site

Large colon Along the long axis opposite the Longitudinal closure
mesenteric attachment and on the
anti-mesenteric band when possible,
avoid pelvic flexure to m i n i m ize
lumenal stricture

Small colon On the anti mesenteric band Longitudinal closure

that possibly up to 70 per cent of the small intestine The surgeon should target 30-50 cm of normal intes­
length can be resected with enough residual small intes­ tine on either side of the non-viable intestinal segment.
tine to adapt sufficiently to maintain appropriate diges­ The mesentery segment is transected by starting the
tive function. The ventral and dorsal colon can be intended line slightly distal to the first vascular pedicle
resected up to the level of the cranial aspect of the (Figure I D. 1 8 ) . One should be careful to leave 1-2 cm
cecocolic ligament, the colon adapts by increasing the of normal mesentery beyond the remaining vessels to
absorptive (inter-crypt) area of its remaining length, prevent their inadvertent puncture during closure of
allowing normal colonic function. It is unclear how the mesentery (Figure I D . 1 8 ) . This is especially impor­
much small colon can be resected, but clinical experi­ tant in the small colon mesentery where fatty tissue
ence suggests that the small colon resection limit has interferes with identification of mesenteric vessels. The
not been identified yet. goal is to resect as much compromised mesentery as
If significant fluid and gas is present in the intestines possible while allowing complete closure of the mesen­
proximal to the intended anastomosis site, the intesti­ teric defect. Each mesenteric vessel is either double
nal content should be evacuated through an entero­
tomy in the section of intestine to be resected. To avoid
tearing the mesentery during the milking of intestinal
content, the mesentery of the affected bowel is not
transected until the evacuation is complete. This is not
always possible since the mesentery of the affected
bowel may need to be transected so the intestine can be
moved away from the incision. Evacuation of intestinal
content has three objectives

I . to help identity the margin of resection needed

2. to minimize contamination of the surgical site and
abdomen during transection and anastomosis of
the intestine.
3. mimimize postoperative ileus

The section of intestine to be resected must have clear

viable margins and be near an intact blood supply. The
section to resect is chosen based on
1 . viable margin in the small intestine or small colon
2. proximity of the next vascular arcade.
Figure 10.18 Mesenteric resection in preparation for
intestinal anastomosis. Note that 1 -2 em of normal mesen­
tery is left beyond the remaining vessels to prevent their
i nadvertent puncture during closure of the mesentery

1 73
10 COLIC
ligated with no. 00 (3 metric) synthetic absorbable
suture material or stapled with an appropriate stapling
device. If the vessel ligation must be placed in thick­
ened, edematous mesentery, larger suture materials
should be used and the stapling device avoided. When a
long section of mesentery must be resected, it is possi­
ble to lose proper alignment of the intestinal segment.
This can lead to an inadvertent 1 80 degree rotation of
the anastomosis. To prevent such an occurrence either
of the following two techniques can be used.
1 . During ligation of the first mesenteric vessel, one
suture end is left long, clamped by a hemostat, and
placed in an Allis tissue forceps (Figure 1 0 . 1 9 ) . The
following mesenteric vessel ligation sutures are
treated similarly until all are incorporated
successfully into the Allis tissue forceps.
2. The defect in the mesentery is closed first. The
mesentery is closed leaving approximately 15 cm of
unsutured mesentery to allow appropriate access
during the anastomosis procedure. Two methods
Ligature
Long suture
grasped by
hemostats
174
can be used to close the mesentery using no. 00 or
no. 000 (3 or 2 metric) synthetic absorbable suture
material
• In most cases, the surgeon can start in the middle
of the mesenteric defect and close the defect
toward the intestine using a simple continuous
pattern (Figure 1 0.20)
• In extensive small intestinal resection where large
mesenteric defects are created, the surgeon can
start at one end of the mesenteric defect and
gather the mesentery in an 'accordion-like'
fashion toward the other side of the mesenteric
defect (Figure 10.21 ) .
After the anastomosis is completed, the remammg
mesenteric defect is closed with a simple continuous
pattern using an absorbable suture material.
Following evacuation of the intestine or the move­
ment of fluid and gas content, the flow of ingesta, oral
and aboral ( 20-25 cm) from the intended line of
intestine transection, is blocked by the placement of
Figure 10.19 One end of the suture
used for mesenteric vessel ligation is
clamped with a hemostat and incor­
porated i nto an Allis tissue forceps.
Subsequent sutures are incorpo­
rated in order, preserving the order
of mesenteric vessel ligation
 SURG E RY FOR COLIC (INCLUDING ANESTHESIA) 10

Cut end of intestinal clamps (e.g. Doyen or Glassman) or encir­

small intestine
cling Penrose drains (Figure 1 0.22) . All instruments
capable of serosal damage can induce adhesions and
the author prefers Penrose drains because they are the
least traumatic. The intestinal clamp or the Penrose
drains should be removed as soon as the anastomosis
appears leak-proof, this is usually after the first layer of
anastomosis is completed.
The surgeon must decide which anastomotic proce­
dure to perform. Although much information has been
published on equine intestinal anastomosis, the ideal
technique has not been identified, probably because
many techniques are successful and the type of anasto­
mosis has no effect on survival rate according to at least
one study.

Figure 10.20 The mesenteric defect is closed toward the
intestine using a simple continuous pattern. A 10-1 5 cm
section of i ntestine is left unsutured to facil itate the
anastomosis
Hand-sewn anastomoses
One advantage of hand-sewn techniques is the ability to
perform an end-to-end anastomosis that physiologically
approximates normal intestinal transit most closely. In
addition, a hand-sewn anastomosis is readily adaptable
to various thicknesses of intestinal wall, leading to a
secure anastomosis in most conditions. The disadvan­
tages are associated with an inherent increase in conta­
mination associated with open bowel procedures that
require more manipulation of the intestines and result
in more foreign bodies at the anastomosis.

Figure 10.21 The mesentery is sutured in an

accordion-l ike pattern to prevent formation of
Mesentery
a mesenteric defect

Figure 10.22 The flow of i ngesta in the proximal and distal

intestine is arrested using Penrose drains 20-25 cm away
from the intended l ine of transection to prevent inadver­
tent contamination during e nterotomy or a nastomosis
procedures

175
10 COLIC

In all small intestine and small colon procedures,

-
____ ----------�
7----

�---- /
----
end-to-end or functional end-to-end anastomoses are
preferred. End-to-side procedures are sometimes used
for jejunocecal anastomosis. Side-to-side anastomosis
are more commonly used for jejunocecal, colocolonic
anastomosis and for jejunocolic anastomosis (in cecal
bypass procedures) .

Figure 1 0.23 The intestine is transected at a s light angle to
ensure that the anti-mesenteric intestinal wall retains ade­
quate perfusion since it is the intestinal section furthest
from its blood supply
Once it has been decided to use a hand-sewn anasto­
mosis, the intestine is transected at a slight angle so the
antimesenteric side is shorter than the mesenteric side
(Figure 1 0.23) . This ensures adequate blood flow to the
area of intestinal wall most distant from the blood sup­
ply. The open end of the intestine is covered by moist
gauze until the next transection is done.
Stapled anastomosis
The major advantage of the stapling technique is asso­
ciated with the closed nature of the anastomosis that
limits potential contamination. In addition, the B­
shaped configuration of the staple closure yields better
tissue blood flow. Speed of technique and decreased tis­
sue handling have often been mentioned as advantages
of the stapling technique, but these advantages are
negated if the stapled line is oversewn. The main disad­
vantages of the stapling technique are the cost and the
need for familiarity with the use and pitfalls of the
equipment, and the inability to create end-to-end
anastomosis.
End-to-end anastomosis
This procedure can only be done at the time of writing
using a hand-sewn technique unless the end-to-end
anastomosis stapling instrument is used. Staple anasto­
mosis is not recommended because of the resulting
small-diameter anastomosis with the current stapling
instrument (EEA) .
The anastomosis is started at the mesenteric side.
The site is critical because bleeding and swelling asso­
ciated with the transected mesentery can make it diffi­
cult to identify the intestinal layers at this site . After
the knot is tied at the mesenteric site, one end of the
suture is left long and clamped with a hemostat. A stay
suture is placed at the antimesenteric side joining
both ends of the transected intestinal segments. This
divides the intestine into two equal halves. Using the
needle end of the suture placed at the mesenteric
attachment, the near side is closed using the surgeon's
preferred apposing pattern, usually a simple continu­
ous pattern through all layers. The suture is tied when
the antimesenteric stay suture is reached. The intes­
tine is rotated and a second strand of suture material
is used to finish the first layer using the same pattern
(Figure 1 0.24) .

Standard types of anastomosis

Anastomosis at specific sites, such as jejunocecal or
jejunocolic anastomoses, is discussed in the respective
chapters covering diseases of these sites. The following
section focuses on the general principles used in equine
intestinal anastomosis.
There are three main types of anastomosis
Figure 1 0.24 After the first half of the a nastomosis is com­
• end-to-end pleted, the intestine is rotated and a second strand of
• end-to-side suture material is used to finish the first layer using the
• side-to-side. same pattern

1 76
 SURGERY FOR COLIC (INCLUDING ANESTHESIA) 10

End-to-side anastomosis incision is made midway between the mesenteric and

antimesenteric side (Figure 1 0.26 ) . These anastomoses
This procedure is done using a hand-sewn technique.
are started at the mesenteric side of the proximal
Occlusion of the flow of ingesta can be done with a
intestinal segment; again. after the first knot is tied, one
Penrose drain for the small intestinal segment but must
end of the suture is left long and clamped with a hemo­
be made with an intestinal clamp for the large intestinal
stat. A stay suture is placed at the antimesenteric side
segment (Figure 1 0.25) . If the proximal intestinal seg­
joining both ends of the transected intestinal segments
ment needs to have its lumen enlarged. a longitudinal
to divide the anastomosis into two equal halves. Closure
is performed as described above. To minimize distrac­
tion force on the anastomosis, an additional Marshall
'u' suture is placed I cm caudal to the anastomosis site
where the anticipated line of tension is expected
(Figure 1 0.30) .

Side-to-side anastomosis
Hand-sewn anastomosis
After transection of the intestine the open ends are
sutured as described in enterotomies. The bowel ends
are laid alongside each other (in the proper direction
to create, wherever possible. an isoperistaltic anastomo­
sis. Figure 1 0.28) . and a stay suture is placed at one end
of the intended incisional line. Another suture is placed
at the other end of the intended incision line, and a
simple continuous pattern is used to appose the sero­
muscular layer of each intestinal segment. Once this
layer is completed, both intestinal segments are incised
parallel to this suture line, and the far layer of the anas­
tomosis is closed with a simple continuous pattern
taking care not to over-tighten the suture creating a
Figure 10.25 End-to-side anastomosis, occlusion of the
flow of ingesta may require the use of an intestinal clamp
if it is performed between the small and large intestine

Cecum Cecum

Incision in cecum for Marshall · U · sutures

anastomosis Anastomisis
I leocecal Cecocolic
fold fold

Small
intestine

Figure 10.26 End-to-side anastomosis - a longitudinal inci­ Figure 10.27 Side-to-side hand-sewn jejunocecal a nasto­
sion is made at the anti mesenteric side of the proximal mosis - 1 cm caudal to the anastomosis side where the
i ntestinal segment to enlarge its lumen for a sufficient anticipated line of tension is expected, an additional cruci­
length anastomosis ate suture is placed

177
10 COLIC

Figure 1 0.29 Side-to-side hand-sewn intestinal a nastomo­

sis - after seromuscular apposition of the far side of the
anastomosis is completed, both intestinal segments are
incised parallel to this suture line and the far layer of the
Figure 10.28 Side-to-side hand-sewn intestinal anastomo­ anastomosis is closed with a simple continuous pattern
sis - the intestinal segments are overlapped and when pos­
sible are placed in such a way as to create an isoperistaltic
anastomosis

purse-string effect (Figure 10.29 ) . At each end of the

first layer, a Marshal 'u' suture is placed to reinforce the
corner of the anastomosis, and the near side of the
anastomosis is closed using a simple continuous pattern
oversewn by an inverting seromuscular pattern (Figure
10.30) .

Stapled anastomosis
Since the bowel has been previously transected with sta­
ples using the gastrointestinal anastomosis or tissue
anastomosis instruments, the bowel end does not need
to be closed, and the potential for contamination is Figure 1 0.30 Side-to-side hand-sewn smal l intestinal anas­
avoided. The stapled intestinal end has exposed tomosis - the near side of the anastomosis is c losed using
mucosa and seromuscular layers and should be over­ a simple interrupted pattern oversewn by an inverting
sewn with an inverting pattern. A stay suture is placed in seromuscular pattern
the middle of the intended anastomosis site to lift that
section of intestine. Using a no. 10 Parker-Kerr blade, a
stab incision is made at the antimesenteric side into
each intestinal segment to be anastomosed (Figure
1 0.3 1 ) . Each arm of the GIA is inserted into the lumen
and directed toward one end of the intended anasto­ integrity. The defect where the instrument was inserted
mosis site (Figure 10.32 ) . After the instrument is fired, is usually sutured closed as for an enterotomy, but a line
it is withdrawn, loaded with another cartridge, and rein­ of TA staples can be used to close this defect as well.
serted in the opposite direction. It is critical that the The staple lines are inspected for integrity and are over­
instrument be fired across the previous staple line on sewn if deemed necessary. As in a hand-sewn anastomo­
the far side of the anastomosis (Figure 1 0. 33) . If this lat­ sis, to minimize distraction force on the anastomosis, a
ter procedure is not done, a leakage will occur at the Marshal 'u' suture is placed 1 em caudal to the anasto­
intersection of the two staple lines. The instrument is mosis side where the anticipated line of tension is
withdrawn and the anastomosis line is inspected for expected.

1 78

Mesentery
Figure 1 0.31 Side-to-side stapled anastomosis - using a no. 1 0 Parker-Kerr blade, a stab incision is made into each i ntesti­
nal segment to be anastomosed
Figure 10.32 Side-to-side stapled anastomosis - each arm
of the GIA stapling instrument is inserted into the lumen
and directed toward one end of the intended anastomosis
site
SURGERY FOR COLIC (INCLUDING ANESTHESIA) 10
Figure 10.33 Side-to-side stapled anastomosis - the
stapling instrument (GIA multifi re) is appl ied in the oppo­
site direction making sure that the instrument is fired
across the previous staple l i ne on the far side of the
anastomosis
179
10 COLIC
Functional end-to-end anastomosis
This procedure is done with stapling techniques only. It
has been termed a functional end-to-end because of its
gross appearance as the anastomosis matures (Figure
1 0.34) . However, motility following functional end-to­
end anastomosis is akin to that of a side-to-side anasto­
mosis and the motility pattern is inferior to an
end-to-end anastomosis. The author prefers this type of
anastomosis because it is closed and the result is a larger
lumen, which is associated with less postoperative ileus
than sutured end-to-end anastomosis.
Figure 10.34 Functional end-to-end anastomosis in the
small colon 3 weeks postoperatively. Note the end-to-end
appearance of the small colon at this early time postoper­
atively. The horse was euthanized for unrelated reasons
180
A 1 cm section of the antimesenteric corner is cut
with straight Mayo scissors and each arm of the CIA sta­
ple introduced into each intestinal segment, being care­
ful to direct the anastomosis toward the mesentery
(Figure 10.35) . After the instrument is fired, another
cartridge is loaded and the instrument is fired again to
create a stoma approximately 1 .5-2 times the diameter
of the intestinal segment (Figure 10.36) . The introduc­
tion site of the stapling instrument is closed with a line
of staples or hand sewn. In earlier descriptions of this
technique, veterinary surgeons would oversew this seg­
ment, but it was found that this inversion can lead to an
intussusception. Instead, the author recommends
covering the exposed mucosal edge with a fold of
mesentery (Figure 10.37) .
CONCLUSION
Because of the time period required for enterotomies
and anastomoses of the large colon, the speed associ­
ated with a stapling instrument is a significant factor.
However, edema present in many disease processes
affecting the large colon may prevent the use of staples
where time may be most important. When an intestinal
procedure is performed in horses, a two-layer closure is
standard with the second layer sutured in an inverting
pattern. Most incisions are made on the antimesenteric
side, and when applicable, centered on the tenia bands.
Since the performance of an enterotomy or anastomo­
sis increases the risk of intra-abdominal adhesions, the
surgeon should consider coating the anastomosis site
Figure 1 0.35 Functional end-to-end a nastomo­
sis - the arm of the GIA stapling instrument is
i ntroduced into the anti mesenteric opening
created i n each i ntestinal segment. Care must
be taken to direct the anastomosis toward the
mesentery
 SURGERY FOR COLIC (INCLUDING ANESTHESIA) 10

Figure 1 0.36 Functional end-to-end anastomosis ­

the arm of the GIA sta pling instrument is re-intro­
duced into the intestine to i ncrease the length of
the anastomosis

Line of
mesenteric apposision

Figure 10.37 Functional end-to-end anastomosis - after

the anastomosis is completed. the mesentery is closed
with a simple continuous pattern using an absorbable
suture materia l (no. 000; 2 metric). Care is taken to cover
the exposed i ntestinal edges with a fold of mesentery
during mesenteric closure.

with carboxymethylcellulose or an absorbable adhesian prevent incisional seromas/hematomas and contamina­

barrier (Interceed, Ethicon, Inc, USA) (see Surgical tion, so that primary closure occurs unimpeded. Factors
exploration of the abdomen) . that influence healing of such incisions can be divided
into

• physiological status of the patient

Closure of the a bdomen (hypoproteinemia, old age, etc.)
• status of the wound (degree of contamination,
repeat incisions, suture considerations (i.e. type,
NG Ducharme
pattern) ) .

INTRODUCTION Although the surgeon has little influence on patient

factors, he/she can influence wound factors that
The goals of abdominal closure are to obtain a secure affect the prevalence of some incisional complications.
apposition of the strength layer of the incision, and to Complications of incisional closures include

181
10 COLIC

• dehiscence
• infection
• drainage
• hernia. Incisions Strength layer

For example, incisional dehiscence can occur because Ventral midline Linea alba
the sutures break or cut through tissue, knots slip, or
there is premature degradation of the suture material. Ventral paramedian External sheath of rectus
The surgeon can influence the prevalence of incisional abdominis muscle
dehiscence, as well as other incisional complications, by
Paralumbarlflank External oblique abdominis
selecting an appropriate suture material and pattern for
m uscle and its aponeurosis
abdominal closure, based on the incision status, and the
size and physiological status of the animal. Since an 1 7th or 1 8th rib Externi and i nterni
incisional infection increases the risk of hernia from resection i ntercostales muscles and
6-1 7 times, it is worth making every effort to prevent external oblique muscle.
incisional contamination. Incisional infection rates The adjacent ribs can be
increase with open bowel procedures, probably because i ncorporated in the closure.

of inadequate prevention of incisional contamination.

Prior to closing the abdomen, contaminated instru­
ments must be discarded and the surgeon must don a
increased. Since infected non-absorbable suture materi­
new gown and/or gloves if they are contaminated. All
als create permanent suture sinuses, non-absorbable
overlaid small, contaminated drapes around the inci­
suture material should be avoided. Although suture
sion should be removed. If contaminated drapes are
sinuses have a low morbidity, their removal is generally
well secured, their removal could result in incisional
required to resolve a draining tract. Furthermore, a sur­
and abdominal contamination. Therefore, well-secured
gical revision may require mesh placement to manage
contaminated drapes should be covered by new sterile
an incisional hernia, and a suture sinus can force a
impervious drapes. Any incisional contamination
delay or an additional surgical/anesthetic procedure to
should be lavaged with sterile physiologic solution con­
resolve the infection process. Absorbable sutures are
taining appropriate broad-spectrum antibiotics.
therefore preferred, and no. 2 polyglycolic acid and no.
Aside from the obvious consequences of incisional
3 polyglactin 9 1 0 are the next strongest sutures to use.
dehiscence and hernia, incisional drainage and infec­
tion increase hospitalization time and are associated
with increased costs. The purpose of this chapter is to
review the surgical factors for incision closure that influ­
ence the prevalence of incision complication rates.

Suture material Breaking strength

mean 'SEM'
SUTURE MATERIALS (Newtons)

5 Polyester multifilament braided 270.5 ± 7.3

The goal is to re-appose the strength layer of each inci­
sion with suture material at least as strong as the linea 2 Polyglycolic acid multifilament 2 1 3. 5 ± 2.8
alba (Table 1 0.5) . braided
However, currently there is no known suture mater­
ial as strong as the linea alba. The suture materials' 3 Polyglactin 910 multifilament 209.1 ± 7.8
braided
strengths are shown in descending order in Table 1 0.6.
Chromic catgut should be avoided in incision closures 2 Polydioxanone monofilament 1 57.8 ± 6.1
because the material's rapid loss of strength leads to an
unacceptable complication rate. 2 Polypropylene monofilament 1 37.2 ± 3.2
Given the strength of polyester suture material and
1 Polyglycolate monofilament 1 46 . 1 ± 3.7
the significant tension on equine incisions, these non­
absorbable sutures were commonly used in the past. 2 Nylon monofilament 1 13.0 ± 7.0
However, many equine abdominal surgeries are clean­
Means with different superscripts are significantly different
contaminated or contaminated procedures where the
from one another (P < 0.05)
risk of incisional contamination or infection is

182
 SURGERY FOR COLIC (INCLUDING ANESTHESIA) 10

As well as the in-vitro data reported in Table 1 0.6, there
is ample clinical experience to indicate that the
strength of these synthetic suture materials (no. 2 poly­
glycolic acid and no. 3 polyglactin 910) are sufficient for
secure abdominal closure. Their multifilament nature
increases the risk of suture sinus formation, but when
the suture material degrades the infection resolves. The
monofilament sutures are weaker and have a higher
rate of knot slippage because of their lower coefficient
of friction, but the absorbable monofilament sutures
may be acceptable in situations such as infected or con­
taminated wounds in lighter weight animals. The non­
absorbable monofilament suture material in horses, as
in humans, is less than ideal. Nylon is weaker and
polypropylene has been associated with suture sinuses,
although its strength is similar to polyglyconate and
polydioxan suture materials.
Absorbable mono- or multifilament sutures are also
generally used to close the other layers (no. 2 for mus­
cular and no. 0 for subcutaneous tissues) . Skin incisions
are usually closed with staples for increased speed. Two
exceptions to the use of skin staples occur when
• the incision is compromised to a degree that
evisceration during recovery is possible
• a flank incision through the 1 8th rib resection has
been done.
These incisions are intrinsically weaker and are associ­
ated with a higher complication rate than others. In
these situations the author recommends closure of the
skin incision with monofilament sutures (no. 1 or no. 2)
in a continuous pattern protected with an oversewn
stent bandage.
and subcutaneous) are also generally closed with a
simple continuous pattern.
Perhaps more important than the suture pattern is
the bite size. The optimal bite size for closure of the
strength layer of an adult equine incision is 1 5 mm from
the incisional edge.
INCISIONAl PROTECTION DURING
RECOVERY
A critical postoperative time for the surgical incision is
immediate recovery, since the incision is not yet pro­
tected by a fibrin seal and is, therefore, exposed to con­
tamination because of its proximity to the floor and the
likelihood of urine and other recovery stall contami­
nants. For this reason, the author suggests placing a
sterile stent bandage, secured with non-absorbable
sutures placed in a simple continuous pattern, over the
incision. The stent and skin are then covered by an
adhesive, impervious drape extending at least 10 em on
all sides of the incision (Figure 1 0.38) .
Since the stent increases the risk of incisional infec­
tion by harboring blood and incisional drainage mater­
ial in a milieu adjacent to the incision, it should be
removed immediately if it becomes wet or contami­
nated, and within 24 hours in almost all other cases.
The flank/rib resection incisions are the exception

SUTURE PATTERN

The peritoneum is only closed in standing laparotomy

to minimize the possibility of air escaping the abdomen
postoperatively and reaching the subcutaneous tissue.
The incision strength layer (Table 1 0.5) can be closed
by selecting one of many suture patterns: simple
interrupted, cruciate, and simple continuous. Bio­
mechanically, the continuous suture patterns are
stronger than simple interrupted patterns, but the
cruciate and near-far-far-near patterns have not been
critically evaluated in horses. Although biomechanical
studies identifying the strongest abdominal closure in
horses are incomplete, clinical studies i ndicate that
near-far-far-near suture patterns should be avoided,
because they are associated with an increased risk of Figure 10.38 Ventral abdominal incision immediately post­
incisional drainage and infection. The author prefers to operative. Note the stent bandage suture over the incision
close an incision in two or three sections of simple con­ for tension rel ief and i m pervious iodine-impregnated
tinuous pattern. The other layers (fascial, muscular, drape applied over the incision site

1 83
10 COLIC
where a stent can be kept for 5-7 days if changed daily,
because the incision tension increases the risk of
incisional seroma/hematomas.
CONCLUSION
Adherence to aseptic techniques and incisional closure
based on the biology of healing will influence the
suture material and pattern used. This should signifi­
cantly impact and lower the prevalence of incisional
complications, which can be as high as 37 per cent of all
abdominal incisions.
Repeat laparotomy
NG Ducharme
INTRODUCTION
Repeat laparotomy is required in up to 10 per cent of
horses undergoing surgery for acute abdominal pain.
An acute need for a repeat laparotomy is generally
based on
• the persistence of ileus
• a return of abdominal pain
• a deterioration in cardiovascular status.
Indications for a delayed repeat laparotomy are usually
related to recurrence of the initial problem or associ­
ated with the formation of obstructive intra-abdominal
adhesions. Evaluation similar to that made prior to the
initial emergency laparotomy, such as a thorough phys­
ical examination and the assistance of judicious ancil­
lary testing, are useful for the decision to re-operate.
Confounding variables associated with the previous
surgery and intensive supportive care complicate the
interpretation of the clinical and clinicopathological
data. For example
• the acid-base status is usually more controlled
postoperatively because of intravenous fluid and
electrolyte therapy
• pain may be attenuated by analgesics
• cardiovascular status is better stabilized by various
medications that combat endotoxic shock.
However, rectal palpation of mild to moderately dis­
tended loops of small intestine can be tolerable because
of the ileus, and cytological examination of the peri­
toneal fluid is always abnormal perioperatively. Aside
from the financial implications that the attending vet­
erinarian must balance in deciding whether or not to
184
re-operate, the knowledge that the incidence of many
complications, such as incisional infections, increases
while the long-term prognosis for survival declines in
horses subjected to repeat laparotomy must also be
taken into consideration.
HOW TO MAKE THE DECISION
Deviation from a normal postoperative recovery is an
important sign indicating the need to assess whether or
not a problem is present; appropriate measures may
then be undertaken in a timely fashion. Of course,
there is a significant range for 'normal' postoperative
recovery. Horses with necrotic bowel at the initial
surgery may take 2-3 days for their cardiovascular
system to return to normal, and older horses (> 15 years
of age) have a more prolonged persistence of elevated
heart rate (>60 bpm) postoperatively (> 3 days ) .
Abnormalities that are causes for concern are summa­
rized in Table 1 0.7.
The main indications for a repeat laparotomy are to
remove necrotic intestine or revise an unacceptable
anastomosis. Since the goal of perioperative intra­
venous fluid therapy is to restore extracellular fluid
volume and normal acid-base balance, persistence of
anomalies may indicate a serious intra-abdominal prob­
lem. For example, the packed cell volume should be
normal within 24 hours. Persistence of a significant
elevation in packed cell volume (> 50%) may be an indi­
cation of significant endotoxemia, and the clinician
must be concerned that bowel necrosis and peritonitis
may be the source. Mural necrosis, associated with post-
Persistence of e levated hematocrit > 50% after 24 h
Heart rate elevation greater than 80 bpm for > 48 h
Clinical signs of persistent or deteriorating
endotoxemla for > 48 h
Divergence in the changes i n hematocrit (increasing)
and total plasma protei n concentration
(decreasing)
Elevation i n rectal temperature
DepreSSion for more than 48 h
Abdominal d istention
Severe abdominal pain
Persistent ileus (nasogastric reflux) after 72 h
Hematological changes consistent with degenerative
left shift
Appearance of mixed bacterial contamination in
previously 'aseptic' peritoneal fluid

ischemic degeneration or reperfusion injury, and anas­
tomosis leakage both lead to intra-peritoneal migration
of intestinal contents and gram-negative organisms.
This leads to overwhelming absorption of bacteria and
endotoxins resulting in persistent endotoxemic shock.
In addition, the septic peritonitis resulting from the
abdominal contamination leads to a tremendous
amount of intravascular fluid and fibrin shift into the
abdominal cavity so dehydration and hypoproteinemia
occur. Therefore, any clinical or clinicopathological
evidence of persistent endotoxic shock warrants further
investigation. Ileus is a feature of abdominal surgery in
any species. However, persistent signs of ileus, such as
nasogastric regurgitation and abdominal distention, are
abnormal if the primary problem was minor or treated
early. and should always be evaluated if they persist
more than 72 hours. This is because ileus and abdomi­
nal distention can be signs of intestinal necrosis, anas­
tomosis complications, and improper electrolyte
balance. Therefore, any one or more of the abnormali­
ties described in Table 10.7 warrant further investiga­
tion. The clinician must look for a reasonable
explanation for the abnormal postoperative course.
The clinician has an advantage in knowing the risk
factors in the postoperative period requiring revision
surgery (Table 10.8) .
Any prior abdominal surgery may lead to obstructive
adhesions.
Judging intestinal viability is still very much an
imperfect science. Given the morbidity of intestinal
anastomosis, each surgeon must make a decision based
on apparent viability at a point in time, with the goal of
resecting only bowel that has vascular damage that will
proceed to necrosis or enough serosal inflammation to
result in abdominal adhesions. Sometimes the decision
T" 10.. ." � from tlte primary celIotoMY
kI'lOM te lncte.A:;tl!ie MH fOf a repeat celiotomy
�:
Compromised bowel not resected
Ileal stump not resected in h orses with i leocecal
intussuception
Enterotomy and anastomosis in compromised bowel
Ileocecal anastomosis
Small colon impaction treated without evacuation
of the large intestine
Incomplete abdominal exploration
Delayed:
Primary conditions: nephrosplenic entrapment
large colon volvulus
cecal i mpaction/dysfunction
SURGERY FOR COLIC (INCLUDING ANESTHESIA) 10
is so difficult at the initial surgery that a 'second-look
laparotomy' is planned. Usually the decision is made
early in the postoperative period based on one or more
of the abnormal signs listed in Table 1 0.7. Laparoscopy
can sometimes be used for these purposes, but it is not
commonly done because of
• incomplete abdominal exploration with
laparoscopy
• frequent abdominal distention in postoperative
colic which interferes with laparoscopic observation
• concerns with the effect of abdominal insufflation
on a ventral abdominal incision.
SURGICAL PROCEDURE AND
REVISIONS
Acute repeat laparotomy
Preparations for a repeat laparotomy are the same as
for emergency laparotomy except
• there is a more frequent need for a plasma
transfusion to combat hypoproteinemia
• there is an increased rate of incisional
complications requiring special consideration
• there is more frequent consideration for parenteral
nutrition because of the inherently longer feed
deprivation in these horses.
Usually the same incision is used. After appropriate
aseptic preparation, the skin sutures/staples are
removed using a separate instrument package. The
incision is cleaned with sterile physiological saline solu­
tion and the surgeon dons a new glove. The subcuta­
neous and fascia lata sutures are removed.
Exploration of the abdomen is targeted toward the
suspected area. The surgeon must be very careful not to
pull on any anastomoses as they may have been weak­
ened by postoperative swelling. Instead, the bowel on
either side of the anastomosis is grasped and exterior­
ized taking care not to apply any tension on the anasto­
mosis. If an anastomosis is leaking, it is isolated
immediately by placing a sterile moist towel around the
site, and placing the area over an impervious drape.
The surgeon must then identity the cause of the anasto­
motic failure. If it is associated with necrotic bowel, fur­
ther resection is required. When no intestinal necrosis
is present, it is possible that only one or more sutures
are required to correct the leakage. However, primary
anastomosis failure is rare. Therefore, if necrotic bowel
did not cause the failure, it is important to carefully ver­
ity that there is no kink or abnormal tension on the
anastomosis because of its placement or orientation.
This is more often the case in ileocecal and jejunocecal
1 85
10 COLIC
anastomoses. Alternatively, there may be a more distal
obstruction present.
Another type of anastomosis complication is
impaction at the site. This is seen when
• the lumen of the anastomosis is small and is further
reduced by postoperative swelling
• a small colon enterotomy or anastomosis was
performed yet the large intestine was not evacuated.
In the former case the surgeon must decide if the
anastomosis should be enlarged or if removal of the
impaction by digital manipulation is sufficient.
Enlargement of the anastomosis can only be done by
incising between two simple interrupted sutures or
between the end and start of two continuous patterns,
as an incision between two points on a continuous anas­
tomotic suture would be catastrophic (Figure 10.39) .
One area prone to complication is the distal stump
of the ileum where viability may deteriorate because of
an associated transection of the ileal artery as part of a
distal jejunal resection (Figure 10.40) . This is especially
true during treatment of ileocecal intussusception,
because the distal blood flow is often compromised in
these cases - mural blood flow from the ileocecal area
and the blood supply from the ileal artery branch of the
ileocecocolic artery.
Other obstruction sites encountered include an
internal rent as with incomplete closure of the ileocecal
fold or when a mesenteric rent extends dorsally near
Cecum
InciSion to enlarge
anastomosIs
Anastomosis
Figure 10.39 Enlargement of the jejunocecal end-to-side
anastomosis can only be done by incising between two
simple interrupted sutures or between the end and the
start of two continuous patterns
1 86
Cecum
Medial
cecal artery
artery
J eJuno Ileum
Right
colle artery
Figure 10.40 Schematic drawing showing vascular supply to
distal jejunum and ileum. A technical error that may result in
postoperative devitalization of the ileal stump is transection
of the ileal artery during the jejunal resection. This is espe­
cially true during treatment of ileocecal i ntussusception
the root of the mesentery. Although a dorsally extend­
ing rent can be repaired, the procedure is difficult. One
needs to identify the two segments of bowel and apply
sufficient traction to tense the mesentery. Moist towels
must be placed into the abdomen to prevent acljacent
bowel from obstructing the view of the surgeon. The
surgeon must place one hand on the backside of the
mesenteric defect to prevent inadvertent suturing of
adjacent structures. Using the aid of assistants and long
instruments, after retraction of the body wall, the sur­
geon suctions peritoneal fluid, and sutures the defect
from dorsal to ventral. An assistant with a long-handled
needle holder is often needed to grasp the tip of the
needle, because the surgeon's one hand is unavailable
for any manipulation other than protecting the far side
of the mesentery. The size of the vessels near the cranial
mesenteric artery is significant, and extreme care is
needed to avoid them while closing the defect.
Delayed repeat laparotomy
Horses that are re-operated months after their emer­
gency procedure usually have a different type of abnor­
mality. The surgeon can use the surgical approach
of preference; the author prefers re-entering the
abdomen at the previous site unless a mesh is present,
when a mesh is present a parallel incision lateral to the
mesh is used.
Entry into the abdomen is more problematic
because adhesions to the previous incision may be
present. With a ventral incision, it is not uncommon to

find the apex of the cecum adhered to the incision.
Care must be taken to avoid entering the adhered viscus
during dissection to allow uncontaminated abdominal
exploration.
Problems encountered are usually related to the
presence of adhesions or a mesenteric rent defect and
are treated as described in Chapter 13. If recurrence of
the initial condition is seen (e.g. nephrosplenic entrap­
ment, large colon volvulus, cecal impaction) , strong
consideration should be given to undertaking a more
permanent treatment, such as obliteration of nephro­
splenic space, colopexy, and complete cecal bypass.
ABDOMINAL CLOSURE AND
POSTOPERATIVE CARE
Abdominal closure is similar to that for an emergency
laparotomy but requires care to avoid the frayed inci­
sional edge. Sutures may need to be placed at a greater
distance from the incision edge for that reason. It is
unclear what is the ideal pattern and suture material
required for a repeat laparotomy closure. The author
prefers a simple continuous pattern (with absorbable
material) . Multifilament sutures should be avoided
because the condition of the body wall weakens the inci­
sion, not because the suture materials fail. In addition,
given that the incidence of incisional infection may
be as high as 88 per cent in a repeat laparotomy, the
use of non-absorbable multifilament suture materials
becomes almost contraindicated.
Postoperatively, the author prefers to apply an
abdominal support bandage for these horses because of
the suture incision weakness.
BIBLIOGRAPHY
Anesthesia for colic surgery
Bottoms G D, Fessler] F, Roesel 0 F, Moore A B ,
Frauenfelder H C ( 1 98 1 ) Endotoxin-induced
hemodynamic changes in ponies: effects of flunixin
meglumine. Am.]. Vet. Res. 42: 1 5 1 4-18.
Hardy], Bednarski R M, Biller D S ( 1 994) Effect of
phenylephrine on hemodynamics and splenic dimensions
in horses. Am. ]. Vet. Res. 55:1 570-8.
Lukasik V, Gleed R D, Scarlett] M, et al. ( 1 997) Intranasal
phenylephrine reduces post anesthetic upper airway
obstruction in horses. Equine Vet. ]. 29:236--8 .
Moore] N, Garner H E, Shapland] E, Hatfield D G ( 1981 )
Prevention of endotoxin-induced arterial hypoxemia and
lactic acidosis with flunixin meglumine in the conscious
pony. Equine Vet.]. 1 3:95-8.
Muir W W, Sams R ( 1992) Effect� of ketamine infusion on
halothane minimum alveolar concentration in horses. Am.
I Vet. Res. 53: 1 802-6.
SURGERY FOR COLIC (INCLUDING ANESTHESIA) 10
Pedrick T P, Moon P F, Ludders] W, Erb H N, Gleed R D
( 1998) The effects of equivalent doses of tromethamine or
sodium bicarbonate in healthy horses. Vet. Surg.
27:284-9 1 .
Surgical exploration o f the abdomen
Hay W ( 1 999) Abdominal adhesion prevention in horses.
Proceedings of the 9th A merican College of Veterinary Surgery
Symposium, San Francisco, pp. 1 1 6-- 1 7.
Southwood L L, Baxter G M ( 1997) Current concepts in
management of abdominal adhesions. Vet. Clin. N. Am.
Equine Pract. 1 3:415-35.
Evaluation of gut viability
Allen D, White N A, Tyler D E ( 1 986) Factors for prognostic
use in equine obstructive small intestinal disease. ]. Am.
Vet. Med. Assoc. 189:777-80.
Brusie R W, Sullins K E, Silverman D G, Rosenberger] L
( 1 989) Fluorometric evaluation of large and small
intestinal ischemia in the horse. Equine Vet. ]. 2 1 :358-63.
Bulkley G B, Zuidema G D, Hamilton S R, et al. ( 1 98 1 )
Intraoperative determination o f small intestinal viability
following ischemic injury: a prospective controlled trial of
two adjuvant methods (Doppler and fluorescein)
compared with standard clinical judgement. Ann. Surg.
1 1 93:628-37.
Freeman D E, Gentile D G, Richardson D W, et al. ( 1988)
Comparison of clinical judgement, Doppler ultrasound,
and fluorescein fluorescence as methods for predicting
intestinal viability in the pony. Am. ]. Vet. Res. 49:895-900.
Freeman D E, Hammock P, Baker G], et al. ( 1 999) Short-term
and long-term survival and prevalence of postoperative
ileus after small intestinal surgery in the horse. Submitted
to Equine Vet. ].
Hughes F E, Slone D E ( 1 997) Large colon resection. Vet.
Clin. N. Am. Equine Pract. 1 3:341-50.
Moore R M, Hance S R, Hardy] , et al. ( 1 996) Colonic luminal
pressure in horses with strangulating and
nonstrangulating obstruction of the large colon. Vet. Surg.
25: 1 34-4 1 .
Purohit R C, Hammond L S, Rossi A , et al. ( 1 982) Use of
thermography to determine intestinal viability. Pmc.
Equine Colic Res. Symp. 1 7-18.
Sullins K E, Stashak T S, Mero K N ( 1 985) Evaluation of
fluorescein dye as an indicator of small intestinal viability
in the horse.]. Am. Vet. Med. Assoc. 186:257-6 1 .
Sullins K E, Stashak T S, Mero K N, McChesney A E ( 1986)
Intravenous fluorescein dye as an indicator of small and
large intestinal viability in the horse. Proc. Equine Colic Res.
Symp. pp 280-8.
Van Hoogmoed L, Snyder] R ( 1 998) Intestinal viability. In
Current Techniques in Equine Surgery and Lameness 2nd edn,
N A White and] N Moore (eds) . W B Saunders,
Philadelphia, pp. 273-9.
Enterotomy, resection, and anastomosis
techniques
Archer R M, Parsons] C, Lindsay W A, Wilson] W, Smith D F
( 1 988) A comparison of enterotomies through the
antimesenteric band and the sacculation of the small
(descending) colon of ponies. Equine Vet. ]. 20:402-13.
1 87
10 COLIC
Baxter G M, Hunt R], Tyler D E, Parks A H, ]ackman B R
( 1 992) Stapled side to side versus end to end jejunal
anastomosis in the horse. Vet. Surg. 1992;21 :47-55.
Beard W L, Robertson] T, Getzy D M ( 1 989) Enterotomy
technique in the descending colon of the horse. Effect of
location and suture pattern Vet. Surg. 1 8 : 1 35-40
Dean P W, Robertson] T ( 1 985) Comparison of three suture
techniques of the small intestine on the horses. Am. ]. Vet.
Res. 46: 1 282-6.
Dean P W, Robertson ] T, ]acobs R M ( 1 985) Comparison of
suture materials and suture pattern for inverting intestinal
anastomosis of the jejunum in the horse Am. ]. Vet. Res.
46:2027-77.
Frankeny R L, Wilson D A, Messer N T 4th, Campbell-Beggs C
( 1 995) Jejunal intussusception: Complications of
functional end-to-end stapled anastomosis in two ponies.
Vet. Surg. 1995;24:515-17.
Freeman D E ( 1997) Surgery of the small intestine. Vet. Clin.
N Am. 1 3:261-30 1 .
Hanson R R , Nixon A], Calderwood-Mays M, Gronwall R,
Pendergast] F ( 1988) Comparison of staple and suture
technique for end-to-end anastomosis of the small colon
in the horse. Am. ]. Vet. Res. 49: 1 62 1-8.
Hocking M P, Carlson R G, Courrington K R ( 1 990) Altered
motility and bacterial flora after functional end-to-end
anastomosis. Surgery 108:384-9 1 .
Latimer F G, Blackford ] T , Walk N ( 1996) Closed one stage
end-to-endjejunojenunostomy in horses utilizing linear
stapling instrumentation. 25:25-432.
MacDonald M H, Pascoe] R, Stover S M, Meagher D M
( 1 989) Vet. Surg. 18:415-23
Mackey V S, Pascoe] R, Peterson P R ( 1 987) A potential
technique error in stapled side-to-side anastomosis of the
small intestine in the horse. Vet. Surg. 16: 1 89-92.
Phillips T], Wamsley] P ( 1 993) Retrospective analysis of the
results of 1 5 1 exploratories in horses with gastrointestinal
disease. Equine Vet. ]. 25:427-3 1 .
Ross M W, Stephens P R, Reimer] M ( 1 988) Small colon
intussusception in a broodmare. ]. Am. Vet. Med. Assoc.
192:372-4.
Sullins K E, Stashak T S ( 1 989) Evaluation of two techniques
for large intestinal resection and anastomosis in the horse
J Invest. Surg. 2 : 1 1 5-24.
1 88
Young R L, Snyder] R, Pascoe] R, Olander H ], Hinds D M.
( 1 99 1 ) A comparison of three techniques of pelvic flexure
enterotomies in normal equine colon. Vet. Surg. 20: 1 85-9.
Closure of the abdomen
Gibson K T, Curtis C R, Tuner A S et al. ( 1 989) Incisional
hernias in the horse: incidences and predisposing factors.
Vet. Surg. 18:360-6.
Honnas C M and Cohen N D ( 1 997) Risk factors for wound
infection following celiotomy in horses. ]. Am. Vet. Med.
Assoc. 2 10:78-8 1 .
Ingle-Fehr] E, Baxter G M, Howard R D, Trotter G W and
Stashak T S ( 1 997) Bacterial culturing of ventral median
celiotomies for prediction of postoperative incisional
complications in horses. Vet. Surg. 26:7-13.
Kobluk C N, Ducharme N G, Lumsden] H et al. ( 1 989)
Factors affecting incisional complication rates associated
with colic surgery in horses: 78 cases ( 1 983-1985 ) . ]. Am.
Vet. Med. Assoc. 195:639-42.
Trostle S S and Hendrickson D A ( 1 995) Suture sinus
formation following closure of ventral midline incisions in
three horses.]. Am. Vet. Med. Assoc. 207;742-4.
Trostle S S, Wilson D G, Stone W C and Markel M D ( 1 994) A
study of biomechanical properties of the adult equine
linea alba: Relationship of tissue bite size and suture
material breaking strength. Vet. Surg. 23:435-441 .
Wilson D A, Baker G ] & Boero M J . Complications of
celiotomy incisions in horses. Vet. Surg. 24:506-14.
Repeat laparotomy
H uskamp B, Bonfig H ( 1 986) Relaparotomy as a single
therapeutic principle in postoperative complications of
horses with colic. Proceedings oj the 2nd Symposium on Equine
Colic Research 2 : 3 1 7-21 .
Ingle-Fehr] E, Baxter G M, Howard R D, Trotter G W,
Stashak T S ( 1 997) Bacterial culturing of ventral median
celiotomies for prediction of postoperative incisional
complications in horses. Vet. Surg. 26:7-1 3.
Parker] E, Fubini S L, Todhunter R] ( 1 989) Retrospective
evaluation of repeat celiotomy in 53 horses with acute
gastrointestinal disease. Vet. Surg. 1 8:424-3 1 .
 11
Postoperative treatment and
complications

thrombophlebitis
Postoperative monitoring •

NG Ducharme
INTRODUCTION
Correct postoperative care after intestinal surge!)' is
crucial to ensure the comfort of the equine patient.
Early recognition of clinical signs is essential for suc­
cessful management of postoperative complications.
Th", intensive Cilrc discussed in this section is also rele­
vant to horses under observation as possible surgical
candidates or under intensive medical care.
The important goals of postoperative care are
• to return or maintain the cardiovascular status
• to identify and manage ileus
• to recognize promptly various postoperative
complications.
Th<� various abdominal postoperative complications are
• pam
• ileus
• peritonitis
• anastomosis and enterOlOmy obstructions or failure
• anterior enteritis
• incisional problems
• diarrhea.
Non-abdominal complications include
• shock
• hypoproteinemia
• dehydration
• laminitis
• lal)'ngospasm
• laryngeal paralysis
• h}poxic cerebral injul)'
• wounds sustained during a colic episode
• myopathy.
Immediately upon recovery, the cardiovascular status
must be maintained with appropriate intravenous fluid
and plasma therapy. Csing acid-base and electrolyte
status combined \\ith packed cell volume and total pro­
tein concentration, the type of intravenous fluid and its
administration rate is chosen (see Chapter 9)
Another significant consideration is postoperative
ileus. In horses this primarily small intestinal disease is
characteri�_ed by reflux of intestinal secretions into the
stomach causing abdominal pain, this may result in
gastric rupture if left untreated. Ileus is commonly
seen after treatment of small intestinal diseases associ­
ated with intestinal ischemia or severe inflammation
(Le. 'high risk' patients). It may also be seen after sur­
gical treatment of large bowel disease. Postoperatively,
for prevention of ileus, the electrolyte status (including
calcium, potassium, and chloride) must be maintained
in phYSiological balance. The author does not rou­
tindy feed horses (at 'high risk' for ileus), recovering
from imestinal surgery until the third day postopera­
tively. It is important, on recovel)', to place a naso­
gastric tube in these 'high risk' patients to evaluate the
presence of gastrointestinal reflux every 2 hours for
the first 24-hour postoperative period. Fluid is not
offered until na�ogastric reflux ha� c,eased. A �mall
amount of water (1-2 liters) is then offered every 2
hours for the next 12-24 hours. If the horse can cope
with oral water for that period, solid food is slowly

189
11 COLIC

reintroduced. It is reasonable to return to water and
feed intake as carly as possible within the first 24-hour
postoperative period in patients at 'low risk' for ileus.
For early return to feed, water is olrered firs! as
described above, followed by a mouthful of grass or
handful of soft hay after a few hours. Patients must be
monitored for ileus - elevation of heart rate and/of
return of abdominal pain are good indicators of the
need for nasogastrk intubation. Note that ileus may
not be obvious for up to 48 hours in the postoperAtive
period.
PROTOCOLS FOR MONITORING
PATIENTS
For appropriate intensive care, a rational plan must be
made to ensure an appropriate nature and frequency of
checks. The two monitoring protocols described in the
following paragraphs are used at the author's hospital.
Both protocols should be kept at the patient's side
(attached to the stall door) for frequent consultation,
The use of protocols such as these allows the care givers
to provide the best quality intensive care for the patient.
The primary protocol refkcL� the postoperative
treatment plan. This is outlined in Table 11.1, it
includes 'red flag' indicators that should trigger an
immediate veterinary evaluation and decision.
The actual lime of each evaluation, treatment, or
check ordered in the primary protocol (Table 11.1) is
recorded on the secondary colic protocol (Table 11.2).
The purpose of this protocol is to characterize the spe­
cific orders in the primary protocol (for example, time
medication i� ;uimini�terer:l, lime of na.�ogaslric reflux
checks, etc.). Furthermore, it allows a rapid evaluation
of the progression of the patient's condition. A com­
mon error in any protocol is to record a decimal alone
(for example . 9 mg/kginstead of O. 9 mg/kg). The former
should never be tolerated as it can be misinterpreted as
9 mg/kg if the decimal point is not seen. Finally, for
increased safety, it is best to indicate both the dose and
volume of medications to be administered.

1. Colic evaluations made every ___ hours

2. Medications
.) intravenous fluids type__ rate
b) non-steroidal anti-inflammatory agents dose time route
<) antIbiotics·
gram positive dose time route
gram negative dose time route
anaerobes dose time route
d) others (I.e. vasodilators) dose time route
e) motillty modifiers
3. Packed cel! volumeltotal protein concentration every ___hours
4. laboratory tests {other than PCV} every ___hours
5. Suction nasogastric tube or check tor reflux every ___hours
6. Other instructions ______________
7. Contact the attending veterinarian if any of the following occurs
a) severe pain
b) heart rate greater than _
c) respiratory rate greater than_
d) packed cell volume greater than _or len than _
e) total protein concentration greater than _or less than _
f) temperature greater than_
g) intravenous fluids cannot be administered at prescr ibed rate
h) nasogastrk tube is removed by horse or tube becomes obstructed
i) other

-Antibiotks with activity ilgalnst the following organisms �hould be considered

190
 POSTOPERATIVE TREATMENT AND COMPLICATIONS 11

Table 11.2 Standard colic evaluatiOn

case number: Name: I Owner: I Clinician:

Date

Time

Rectal temperature

Respiration rate

Heart rate and character

Color of mucous membrane

Capillary refill time

Packed cell volume and total protein

Attitude/degree of pain

Gut motility (all four quadrants)

Feces and urine (charactertvolume)

Digital pulse (quality)

Medication

Fluid therapy

Flush catheter

Feed and water consumption

Gastric reflu)(

Other comments

Systemically, endotoxin activates numerous host­

Treatment of endotoxemia defense mechanisms, leading to the formation or
release of free radicals, lipid mediators (eicosanoids,
DM Ainsworth leukotrienes, platelet-activating factor), '-")'tokines
(tumor necrosis factor alpha (TNF.) , interleukin-l and
PATHOPHYSIOLOGY 6 (IL-I, IL-6», and fac.tors involved in coagulation (tis­
sue thromboplastin, plasminogen activator inhibitor
Endotoxin is a complex molecule comprised of (PAl), tissue plasminogen activator (tPA), factor XII).
This endotoxin response, calied the systemic inflamma­
• a lipid moiety (lipid A)
tory response syndrome (SIRS), is a sell�perpetuating
• a core polysaccharide
response which prim arily targets the structural and
• repetitive units of O-specific polysaccharide.
functional integrity of the endothelial ce!Is.
As an integral component of the cell wall of gram-nega­ Manifestations of the SIRS include
tive bacteria, concentrations of endotoxin increase in
• fever
the surrounding milieu whenever bacteria undergo
• tachypnea
periods of rapid growth or death. Systemic manifesta­
• tachycardia
tiOllS of endotoxemia occur when the intestinal
• pulmonary hypertension
mucosal harrier is compromised, allowing endotoxin to
• systemic hypotension
access the peritoneal ca,ity or systemic circulation. In
• cardioV".!scular collapse.
addition to enteric di�ea3e, horse� with hepatic disca.se,
retained placcntas or metritis, hemorrhagic or hypo­ Imbalances in coagulation path\\'ays may cause
volemic shock, pneumonia, severe trauma, and sep­ microvascular thrombi formation, tissue hypoxia, and
tiu'mia are at risk for the development of endotoxemia. muhi-organ dysfunction or failure. Horses with endo-

191
 11 COLIC

lm.,:cmia and SIRS are ;\1 increlUc d risk for the dc\"C\op­ Non..steroldal antl·infJammatory drugs (NSAlDs)
Im:m of laminitis. g,mroimcnina[ ilells and diarrhea,
Ouring cllciowxcmia. nll'mhr.ne-bound phospholipltSC
jugular I'eln thromlx)Sis. disseminated intr.wascular
coagubuiou (DIC), <lnd renal fail ure. 1\ is acti\'lIICd, rdt:4.�inK arachidonic acid which I.�

t bolized
me a by either

• cyd,x)xYf:cnase (COX) to form prostaglandins

TREATMENT PRINCIPLES (PCE�, p(;F2,., I>Gly) and thromboxane (TXA.,), nc

• lip ox�cnase (LOX), to Jorm Icukotrienes (I:rn.,
ITt:" LTD,. and LTE,).
Tlu: trc,Hment optio05 fllr c:ndoloxcmia iln:

The� lip id mcdiatnrs !;:xen potenl dkci.S on ,"a.<;(:ul'll"

• intravenous fluids
and hronchial smooth muscle, on micro\"aS(:ul.lr I)('r­
• llon-steroidal anti-inflammillory drugs (NSAIDs)
meahility, and on platelet an d granulocyte function and
• biological prodtlcl� and drugs which ncutrali7c
integrity. DurinK endotoxemia. increases in plasma
endnt/)xin
TXJ\ and PGI� corrdate with the developmcnt of pul­
• KlunKorti(:()id�
monary hypertension and systemic hypotension, respec­
• agent!; dircctt:d a!f.lin�t central inflammatolT
tively. Increasc� in plasma PGF1� are also associated with
mediators
decrea�t:� in lu ng function. the development of pul­
• free radical s(:av\:nKcr.�
monary hypertension and hypoxemia. ;o..!on-steroidal
• a�illnctj\'t: therapies.
anti-infi ammatol)' drugs (NSAIDs) are uscd to inhibit
or attl�nuatc COX pathways lI.Ild thus ameliorate the
Intravenous fluids eITects of endoLOxemia. Basc:rl upon experimcntal

The prima ry Irc;tuneOI idelllifr and alleviate trials, !lunixin mcg!umine (0.2::0-0.5 mg/kg i.\'. two OJ"
goal is 10
three times daily) is more efl"ectivc in antagonizing tht:'"
(ifplKSihld the primllry inching eveol. Thereafter, sup­
drecl.� of endotoxin-induc.ed eicosanoid produ ction
punil'l:! nlC'lt.�lIrcs designed to ('nmbat or prevent the
dC'idopmt:nI of shock and cosun- tissue perfusion arc than OIher NSAlDs suc.h as phen),lbulal:olle, dip)'ruue,

impiclllcllwd_ Agj.,'Tt-..s.\ivC in!r.t\1:nous f1uid-lherapy to

and ibuprolen. (In conu
...
.!s t. phenylbutaHme, Uillike

T(-SlOre pla.,ma volume and COntTt acid---base imbal- fiunixin megl umine, does nut mask the C'drciio\<tscuiar
alterations that might otherwise prolong a dr;:cisioll for
3nC(1) is imti{utt:11 immcdiatd)-_ Depending on the
degree of cndotoxemia, imrnwllOlIs cl)o'8t<1l1oill thl�rapy surgk"al intervention.) Eltel1ac (0.5 IIIg/kg) i.s anllther

at r.Hd 01 !")-8 mllkg for the fir» flOW hours may initiall y �SAID whic.h will all�'iate some of Ih� clinical allolab·

be Ilcc�S$ary. III shocked hor��_ hypertonic saline wlll­ oratory filldin� of c(luinc encioloxemia. Limited

tinns (i.5%) given intran:nousl)· (4 ml/kgJ over a experimental and dinica! data on kCloprofen , touted a�

1:>--20 minute period_ are hcndidal but should be fol­ both a COX and LOX i nhibitor , 5uggcst thal it i� as clll­

lowed by intr,,j\'enous isotonic cIJ'l'talloid solutions sup­ ca!:inliS as fiunixin meglumine in inhibiting increases in

plemented with puta.'i.�illm chloride (20 mEq/I). If prostagI3ndiu�. mmor necrosis fact.or, and leukotrienes

!H:m(ldynamic: renal failure dcvclop s, intraveIlous when ketoprofen is giv!;:n al a dosage of 0.25-0.5 mg/kg

furosemide (0.5 mg/kg i.v., one or twice) and/or i.v. b.i.d. nr t.i.d. While ketoprofen has the touted

dopamine infusiollS (2-5 p.g/kg/min) are started. A� added benefit of inhihit.ing LOX, the relative impor­

cndotoxcmic horses are often hypoproteinemic, over­ tance of the leuko!riencs in the pathophysiology of

aggressive fluid the rapy may decrease plasma ollcotic enciotoxelllia has not heen determined in the eq;line

pressure, promoting Ihe development of wInnie and species. Bast-d on porcine studies, these ararhidonir

peripheral ('clema. WI)('I) tOtal serum protein levels are acid metabolites playa minor role. Toxicit}' studies sug­

le!i..\ than 4f) gil (4.0g/dl: albumin < 199/l or 1.9 g/dl), gest that kctnpmkn i� less ukcrogcnic: than phenylbu­

fn·.�h or li·ol.en plasma or serum (sec below) should be tazonc or flunixin megtuminc . When I\SAIDs arc

adcninistert':d \\11h the r�·ali1.ation that the amount of administered In endOlox�mic foals, anti-ukel· medica­

pla.�ma required 10 incrC:3SC p rolein k-wIs hy I gldl may tiuns sucll a.� famutidine (1 mg/kg p.o. s.i.d.) , sucr ...lf,uc

exceed 10 liters. Howt....-er. 1-3 liu�fli of fresh or froM-II (1-2 g p.o. t.i.d.) or ()mepral.Olc (Illig/kg p.o_ s.i.d_)
plasma lIlay be beneficia l in supphing hOlh antithrom
.. should he given ("(lIlcucrently.
hin III and fihronectin and in II�u:.rrillg the de\o"C!op­
nWn! Hf C"o:tgulopalhies (sec belo",). Dextran 40 Biological products and drugs that neutralize
( 10-15 ml/kj( i.,·. m·er 30 min) or lIetasta.·ch JO ml/kg
endotoxin
arc also beneficial in increasing plasma 11I1cotic pres­ It might be expt�cted lhat administl<ttioll of
.mre in (�ndoloxt':mic horses. immunoglohulins l!irec.tcd against endo\Oxin would

192

either confer protection against the development of, or
Illitigate the existing signs of endotoxemia. Antibodies
formed against the conserved regions of endotoxin
(core of lipopolysaccharide) are produced llsing bacte­
ria with mutations in the outer 0 polysaccharide region
which exposes the core region.Thus(;ommercial prepa­
rations of hyperimmune serum or plasma containing
antibodies against mutant Elrherirhia I:oli 05)
Salmondfa typhimuriwn (Re mutant) haw been utilized.
Cnfortunatdy, data from equine trials have both sup­
ported and refuted the therapeutic benefit of anti-cndo­
toxin antibodies. In one double blind clinical study,
administration of 1-2 liters of plasma containing.J5 anti­
hodies 10 horses \"ilh clinical signs of endotoxemia \,'as
associated with an increased sUD.'ival rate (87% versus
!)�(Y,. in controls), an improvement in clinical appear­
ance, and a shorter duration of hospitalization when
compared with horses treated with pre-immun(� plasma.
Yet, in experimental studies of sub-lethal endotoxemia,
treatment of foals with antij5 .If'rum either
• phospholipase � (and thus arachidonic acid
failed to improve clinical or dinicopathologic
parameters, or
• was <lss(){:iated with a deterioration in the clinical
signs and rytokine response.
While it is difficult to compare these SlIIdies one for
one, differences in outcome may be at!ributcd to
• differences in the volume and/or anti-endotoxin
titer
• the nature of antibody developed and its <lvidity for
the inner core regions of native endotoxin
• the IgG isorype produced (e.g. I gGa, IgGb, IgGc, or
Iget).
In addition, tbe presence of other products included in
lhe plasma - fibron(�ctin, coagulation factors, and
antithrombin III - not present in the serum, may also
have contributed to the differt�nces between the clinical
and experimental trials.
Another therapeutic approach to endotoxin inacti­
\·ar.ion, utilized in experimental trials and on a limited
clinical basis, entails the use of polymyxin B sulfate.
This cationic polypeptide antibiotic is purported to
bind to and neutralize lipid A. When polymyxin B is
given at a dosage of 6 000 It] /kg of body weight prior to
{�ndotoxin challenge, there is <l reduction in the severity
of clinical signs of endOloxemia and in the magnitude
of the TNF" and 11.-6 response. Interestingly, in an
experimental endotoxin trial, foals pre-treated with
]xllymyxin B fared better than those pre-treated with
Salmonella typhimurium hyperimmune sera. However the
use of Polymyxin B can be associated with the develop­
ment of adverse eflects. Its binding a�idiry to anioni{:
phospholipids of cell membranes makes it nephro-, oto,
POSTOPERATIVE TREATMENT AND COMPLICATIONS 11
and neurotoxic. Caution should be exercised with iL'i
use in endotoxemic horses at risk for the development
of hemodynamic renal failure. In an effort to minimize
drug toxicities (this require extravasation of the drug),
polymyxin B has been conjugated (0 dextran 70. When
this combination is given intravenously (4 g polymyxin
B-dextran conjugate/kg body wt) prior to endotoxin
or challenge, clinical alterations and elevations in
eicosanoids and cytokines are prevented. The poten­
tially promising results of this study remain to be exam­
ined in clinical cases with fulminant endotoxemia.
Glucocorticoids
Known for their membrane-stabilizing properties, the
administration of (orti(osteroids should reduce the
clinical signs of cndotoxemia given that these agents
• prevent aggregation, adhesion, and degranulation
of neutrophils
• stimulate liptXortin synthesis, an inhibitor of
metabolism)
• block complement acth�J.tion
• attenuate cytokine secretion
• inhibit inducible nitric oxide synthase
• exhibit antioxidant effects.
Such effects should decrease capillary leakage and
prevent hypovolemia and t.he formation of interstitial
edema. However, in an experimental model of endo­
toxic shock in anesthetized ponies, dexamethasone
(2 mg/kg) or prednisolone (IO mg/kg) administered
after intravenous endotoxin were inferior to flunixin
meglumine in preventing eicosanoid synthesis and the
accompanying hemodyn<lmic changes that occur dur­
ing the first 2 hours of endotoxin challenge. In
addition, their immunosuppressive effects and their
potential for precipitating laminitis makes glucocorti­
coid usc less routine during endotoxin therapy.
Agents directed against central inflammatory
mediators
Several lines of evidence support the role of TNFa as a
central mediator of endotoxin. These include the find­
ings that
1. T�F� is detected early in the circulation of horses
or foals following administration of
lipopolysaccharide
2. infusion ofT:-.IFa causes physiologic and pathologic
changes indisl.inguishable from those observed in
animals with endotoxemia
3. in mice and baboons, passive immunil.ation with
antibodies to TKFa confers protection <lgainst the
193
11 COLIC
lelhal dft:Cl� of endotoxin and intravascular
F,srh"rirllia coli administr-uion
4. ill hUn];!n p<lljt:nL� Wilh mcningocuccal septicemia,
serum TNF" ilcli\11), i� a useful prcdictoroffillaI
olltcome.
11ms, dru�s or b iological prod ucLS that either reduc e
the formation ofTNF" or 'nculr.lli�.c· drculaLing levels
of this cytokillC, have bt.'en SLUdicd.
"cnwxifylli n<.' is a melhylxamhinc dcrivaliw that, in
addition to phosphodiester� inhibition, reduces
lJilm production I)f T�F" by macrophage;; exposed to
('nciotoxin. It <llso reduces neutrophil adhesion and
dcgr;lllul;ttion. decrt:asc� superoxide rddical format.ion,
mpJlresse� philR()(:ytusiM, and inhibits the production of
illlt:rft:rnn �amma, 1l�J, HAl, and tissue thrombo­
phlstin. Pl: ntoxifyllinc also impro\'cs dcformability of
nythmcytcs (rhco!ogic properties). In clinical cases of
cndntoxcmia, pcmoxifyIIinc is administered (7.5 mg/
k� p.o. b,i.d.) not only for il.� ami-TNF" effects, but aim
in an effort 10 improve the perfusion of the hoof
bminae (rheologic propenies). In experimental endn­
IOl(('mia models, pentoxifylline admininercd W
ures arwr endotoxin ch..l!enKc aU.enuateci endotoxin·
iuducc.."(\ tempc'r.lture and r"f:Spi ral ory rate cle';tdtiolls
hut 11;1(1 IW dTect (m ht'mawlogicaI parameters or on
cicO'!;!lloid and c}'tokine (i ncl uding TNFQ) production.
Clinic;!1 trillL, examining the cflicacy of penioxilYllinc
in pre\i(�nlinK laminitis have nOi been conducted at the
l im e f)f�'riting.
t',xpcrimcntal trials have also examined the eflk<lc),
of Old m inistering antihodies directed against TNFa in
equine endotuxemil: mndd�. In Miniature Horw.�, if
anti-TNFg antih()(lie� (2 mg/kg of murine monoclonal
antibodies d irec ted :lK""inst recombinant equine TNFg)
are given prior f.<) enommdn Challenge. an appreciable
amelioration of th�: clinical and hcmatologic re�pomc
i� found. Ho....·el·er, i f ami-TNFg antibodics (O.l mg/kg
of rahhit. PQIyc10naI antibodies directed against recom·
binant human T�Fg ) arc aoministercd 15 minutes after
the start of endotoxin challenge, a beneficial effect is
lIot ollserveo. With additional experimental and dini­
(:<11 trials anti-TNF� lIlay prove useful during certain
siages or cndoloxemia in clinical case�.
Free radical scavengers
J)urinll: (�ndOlOxemia. reacti�'(' oxygen speci� (ROS)
arc Keller,lIed by (lCliVdted phagoc)'lcs and by the imra­
cellular xant hine oxidase !>yslcrn hich is activated
.....
(lurinK i�chcmic reperfur.ion i njury. ROS can attack
\inlt<1l1y all biochemical cell COmponents hill polyunsat­
urated rallY acids. located within the phospholipid
mcmhr<1IlC stnl(·ture of the cell and cellular organell�,
an· mOM su scepti ble to their effects. ROS also
194
enl.yme inactivation, d�p()lymerization of nucleic acids
and po lrsaccharides, and increases in capillary penne­
ability and prostaglandin product ion.
The lazaroids are 21·aminosleroid compounds with
structural s imila rities to cortieoslCroids. They lack glu­
cocorticoid or mineralocorti c oid enects. It is believed
thallhe lal';aroids insert them�lves preferentially within
the mcmbnlllc of the \".lsc..'Ular endOthelium and inhibit
lipid pernxidation, allenuate cy tok ine production, sup­
pre!l.� the exprel'Sion of adhellion molecules, and inhibit
ill
trdnSClldothelial neutrophil migration and activation.
Although cl i n ica l trials in endotoxemic horses arc lack·
ing, trcatmCllt of neonatal calves with tirilazad mesylate
(1.5 mg/kg i.v.), either pri or to or following endotoxin
challenge attenuated tbe dinical signs of endotoxemia
and suppressed tbe generation of TN Fa'
DimethyI$ulfoxidc (DMSO) is also classified as a free
radical scavenger and its use ha.� been advocated in
numerous equine in flammatory conditions. Dosage
recommendations are variable ranging from 20 mg/kg
i.v. b.Ld. to 1 g/kg Lv. �.i.d. administered as a 10% solu·
tion. Rigorous dinica! or experimental trials reg-J.rding
min·
its efficacy in equine endotoxcmia arc lacking. In an
experiment al stud r of neonatal calves challenged with
endotoxin, DMSO failed to suppress eicosanoid pro­
d uctio n or exert any prOlective effeeLS against endo­
toxema
i . I n deed , (;ah'cs exhibite d a prolongation of
clinical compromise, hypotension, and hypoglycemia as
compared to the c ontrols. In <III experimental �tlldy of
reperfusion injury, DMSC) (1 g/kg i.v. as a 10% solu­
tion) was ineffective in providing a mucosal protective
df{'.ct tl) the equine jejunum.
Two other agents that arc t hought til protec.t againsl
free n\dical i�jl!ry include
1. allopurinol. an inhibitor of xanthine oxidase that
catal)'�es the formation of superoxide anion from
uric acid
2. :\·acetylcysteine, an &gent that replenishcs
glutathione, a major intracellular antioxidant.
Although allopurinol administration (50 rng/kg i.v.)
failed to prevent mucosal injury in anesthetized horses
with expcrimemally.indu(;ed i.'iChemic bowe! injury, in a
different study, the pre-treatment of horses (50 mg/kg
i.v.) significantly reduced endotoxin-induced increases
in xamnine oxidase aClhiry. Clinical trials documenting
ic..\ efficac y in endolm:('mia are currently lacking.
:-.10 information is avai l a ble rCb'ilrding the effir
....cy of
N-acel}'lcyslt'inc (:>:AC) in the horse. In sUIne spt'cic..>s
with endmoxemia. NAC decreases ne utrophil or
platelet·aggregating acti�ily, markedly reduces p ul.
monary hypertension, and aUenu;l.tes vascular perme­
ability changes. In dogs, pretreatment with �AC
(""USC (150 mg/kg i.v. followt!d by a 20 mg kg -I h-I infnsion)

increases glutathione peroxidase adivity, improve�
myocardial function and tissue oxygen extraction, and
decreases T;\Fa production.
Adjunctive therapies
Antibiotics
In many endotoxemic horses, a compromised intestinal
murosa enhances systemic absorption of endotoxin and
baCleria. This situation, as well as intravenous catheter
placement and fluid administration, provides portals
of entry for infectious organisms suggesting that
r-ndotoxic horses should receive antimicrobials.
Nevertheless, arguments both for ,lIld against anti­
microbial use can be made. The advantages of using a
broad spectrum antibiotic include prevention
secondary complications snch as scpticemia, septic
phlt'bitis, and septic pulmonary, rcnal and hepatic
emboli. The major disadvantages to their usc include
exacerbation of dinical signs by increasing circu!at.ing
endotoxins, nephrotoxicosis, and alterations in gastro­
intestinal flora producing diarrhea or secondary Ii.mgal
infections.
Depending on microbial sensitivity patterns for spe­
cillL hospital or practice settinbS
' , third generation
cephalosporins like ceftiofur (2.2-3.3 mg/kg i.v. b.i.d.)
alolle or in combination with sodium or potassium
penicillin (22 DOO Ill/kg i.v. q.i.d.) can be used initiaHy.
The aminoglycosides in combination with penicillin
can he used if renal function is not compromised (gen­
tamicin 6.6 mg/kg i.v. s.i.d., amikacin 12-15 mg/kg i.v.
s.i.d.). Oxytetracycline (6.6 mg/kg in I liter of saline
administered slowly i.v. s.i.d.) is the treatment of choice
in endotoxemic horses with Ehrlichia rislicci infections
(Potomac horse fever), but it has also heen associated
with toxic nephropathies. Metronidazole (15-25 mg/kg
p.o. h.i.d. to t.i.d.) is included in the therapeutic
n-gimen if anaerobic org-,misms are involved.
Therapies targeting gastrointestinal tract
function
Nasogastric intubation in horses with obstructive,
inflammatory, or strangulating bowel disorders
removes ingesta and prevents !f<lstric rupture. In adult
horses (450-!'>OO kg) with colitis, activated charcoal
(\-2 kg in several liters of water) ....;Ih or without the
addition of bismuth subsalicylate 0-2 liters) \;a na.�o­
gaslri( tube is used to decrease endotoxin absorption
and to inhibit inflammatory mediator production
within the intestinal tract.
In endotoxemia, ileus develops from electrolyte
alterations and from the generation of inflammatory
mediators. Thus, intravenous fluids should be supple-
POSTOPERATIVE TREATMENT AND COMPLICATIONS 11
mented with potassium chloride (15-20 mEq/l)
and/or calcium borogluconate (200 milS liters of
fluids) to correct potential electrolyte imbalances
contributing to gastrointestinal stasis. Intravenous
lidocaine bolus (1.3mg/kg) toHowed by a 24 hour lido­
caine drip (0.05 mg kg-I min-I) significantly decreases
reflux volume in horses with ileus. However, side effects
of lidocaine administration include muscle fascicula­
tions, ataxia, and delayed detection of laminitic pain.
Therapies preventing laminitis secondary to
endotoxemia
Although experimental studies fail to demonstrate a
definitivc association between endotoxemia and the
development of laminitis, it is well recognized clinically
of
that such horses are at risk. As it has been shown exper­
imentally that endotoxin chalknge alters nitric oxide
(vasodilatory) pathways in equine digital vessels, it is
likely that lipopolysaccharide contributes to the vascu­
lar alterations observed in laminitis. I lorses with endo­
toxemia are treated prophylactically against laminitis by
• housing them in well-bedded stalls
• providing frog support by taping lily pads to the
soles
• applying a half-inch (I.3cm) band (IO-20 mg) of
2% glyceryl trinitrate paste over the digital arteries
daily
• limiting carbohydrate intake.
Additional therapies include the administration of pen­
toxifylline (7.5 mg/kg p.o. b.i.d., see above) and flu­
nixin meglumine (0.25 mg/kg i.v. t.i.d.). Horses with
acute-onset laminitis benefit from the addition of anal­
gesics (2.2-4.4 mg/kg phenylbutawne i.v. or p.o. s.i.d.)
and possibly by the addition of a ROS scavenger
(DMSO 0.1-1 g/kg, diluted as a 10% solution i.v. s.i.d
or b.i.d.) to their therapeutic regimen. Corrective trim­
ming to shorten the toe is advocated in acute cases.
Therapies for horses with disseminated
intravascular coagulation (DIC)
in healt.h, the cndothelial cell surface provides a
thrombo-resistant surface because of its synthesis and
secretion of prostacyclin, {PA, protein S and the expres­
sion of thrombomodulin. In elldotoxemia, this
tbrombo-resistance is impaired by
• the expression of procoagulant substances such as
tissue thromboplastin and phospholipids
• direct activation of the intrinsic ,md extrinsic
coagulation pathways
• act.ivation and aggregation of platelets (platelet
activating factor)
195
11 COLIC
• increases in factors that inhibit fibrinolysis (PAl)
• decreases in factors that either potentiate
fibrinolysis (tPA and protein C) or that inhibit
thrombin formation (anti-thrombin Ill).
The net effect is that during endotoxemia, a hyper­
coagulable and hypofibrinolytic state develops causing
mkrothrombi formation, perfusion abnormalities and
multi-organ failure. Hemorrhagic diathesis, a less com­
mon clinical manifestation afOle, mayaIso be observed.
To date, no controlled studies of the prevention or
treatment of DIC in the horse have been reponed.
Intuitively, intravenous fluid therapy, a mainstay in any
horse with endotoxemia, is initiated to deter multi­
organ failure. Although controversial, the administra­
tion of subcutaneous heparin has been recommended
[0 reduce thrombin formation. Its efficacy, however, is
dependent on complexing with antithrombin III, which
may become deficient in coagulopathies. In general,
when antithrombin III activity is less than 60 per cent,
or when life-threatening hemorrhage is occurring,
fresh heparinized plasma (I5-30 mg/kg) should be
provided intravenously. The dosage for heparin admin­
istration mnges from 12.">-150 IU/kg b.i.d. s.c., for 2-3
days, but secondary complications such as thrombocyto­
penia, anemia, and hemorrhage may occur. Heparin
use has not been recommended in laminitic horses
since heparin induces red cell aggregates which may
make lamina! perfusion worse.
CONCLUSIONS
In summary endotoxemia is a complex multi-systemic
inflammatory response involving numerous mediators.
At the time of writing, there remains no single best
therapeutic agent to treat endotoxemia. A number of
different drugs and approaches show promise in exper­
imental trials, but appear most useful if given prior to
endotoxin challenge. In general, intravenous fluids
coupled with flunixin meglumine administration has
proved to be the mainstay of therapy.
Nutritional support after
alimentary tract surgery
Sl Ralston
INTRODUCTION
While many horses recover from abdominal surgery
without special nutritional management, careful atten-
196
tion to feeding horses following abdominal surgery (".an
dramatically affect the outcome of a case. Immediate
postoperative care is critical to ensure proper wound
healing and reduce the risk of adhesions and infection.
Prolonged fasting (> 3 days in adults, less in foals and
neonates) will result in atrophy of the intestinal
mucosa, reduced wound healing, increased susceptibil­
ity to infection, and increased risk of adhesions and
diarrhea. Enteral alimentation is critical to the mainte­
nance of gastrointestinal mucosa. The primary energy
source utilized by enterocytes is glutamine obtained
from the lumen, not the blood. Lack of enteral alimen­
tation for as little as 3 days causes mucosal atrophy in
dogs. Clinically normal horses fasted for only 5 days
have reduced immune competence. In other species it
has been demonstrated that malnutrition adversely
affects wound healing. Even the anticipation of eating
will stimulate gastrointestinal motility, this may help
reduce adhesions, and will also enhance metabolic
responses to the nutrients ingested. Failure to provide
adequate nutritional support in the immediate postop­
erative phase will potentially jeopardize the chances of
survival, especially in complicated cases where dehis­
cence of suture lines, ileus, and gasuic reflux are prob­
lems. Long term management becomes critical in cases
where large portions of either large or small intestine
are resected.
IMMEDIATE POSTOPERATIVE CARE
Non-complicated cases
Reintroduce feed as soon after surgery as possible. The
need for energy, protein, B vitamins, and perhaps
vitamin C are increased in the immediate postoperative
phase. If dehiscence or gastric reflux is not a concern,
the horse should be offered small amounts
(0.25-0.5 g/kg) of good quality alfalfa or alfalfa/grass
mix hay every 1-2 hours after recovery from anesthesia.
If the horse has a history of allergy or intolerance to
alfalfa, grass hay can be used. If this regimen is toler­
ated, hay can be offered freely and concentrates can be
re-introduced within 24 hours. A 14-16% protein con­
centrate should be used for the first 1-2 weeks after
surgery with B vitamins (10-20 m! of B-complex solu­
tion/day) and perhaps vitamin C (0.02 gm/kg bj.d.)
added to the feed during the first 4-5 days. Bnm mashes
are commonly used, but are not necessary. Bran is not
laxative but is a good source of fiber and contains 16%
protein and over 1% phosphorus. Prolonged (> 1-2
weeks) daily administration of bran or bran ma�hes is
contraindicated, especially if the horse is not fed a
legume-based forage with sufficient calcium to counter
 POSTOPERATIVE TREATMENT AND COMPLICATIONS 11

the high phosphorus content. The horse's body condi­ placed using proper sterile technique and dedicated
tion and previous ration will dictate the amount of con­ only to the delivery of nutrients. Drugs should never be
centrate offered. added to the parenteral nutrient solutions, nor should
blood samples be drawn from the catheters.
Inappetance Intravenous administration of as little as 0.20 per cent
of the horse's estimated caloric and protein needs is
Inappetant horses should be allowed to grdle as soon
better than total starvation.
and as frequently as possible or have freshly cut grass
(not lawn clippings) brought to them if available. Any
horse that refuses to try to graze when given access to
LONG TERM CARE
fresh grass is a good candidate for extra-Dral alimenta­
tion. Carrots, apples, and sweet feed (grain mixes with
Celiotomy, cecal resection, and minor
molas.�es) also can be used to stimulate intake.
resection
Dehiscence concerns There are no special requirements once the horse has
recovered from surgery if only the cecum or less than 50
In cases where dehiscence of suture lines after an
per cent of the duodenum orjejunum were removed or
intestinal resection is ofconcern, hay runes or complete
if resection was not necessary. The horse can be
pclkted feed (balanced feeds designed to be fed with­
returned to a normal, well-balanced ration appropriate
out hay, 0.25-0.5 gm kg-I feeding-I) (:an be soaked to
for its age and activity within 2-3weeks of surgery.
make a slurry. The slurry can be offered orally every 2-3
hours or delivered via nasogastric tube. Liquid diets,
Major large colon resection
such as Ensure HN (it wi!! need to be diluted with water
to prevent hyperosmolar problems), Osmolile or Ifboth the left and right colons are removed, the horse
EquiCare (0.1-0.25 ml ktf l feeding-· I) ran also be used will require higher than maintenance protein and phos­
if the larger particle diets arc not wlerated. phorus, decreased fiber, and possibly inrreased B vita­
mins. Alfalfa, excellent quality legume/grass mix hay
Ileus and/or pasture are the forages of choice. Concentrates
may be needed to maintain weight hut no more than
Voluntary oral intake of even small amounts of nutrient
0.4 g/kg should be offered per meal. Pclleted,
slurries should be encouraged if at all possible. Horses
extruded, or textured grains can be used. Fats or edible
with ileus may benefit from having very small amounts
oils (S 1.0 ml/kg) may be added to further increase
(10- -20 ml) of nutrient solutions such as the liquid diets
caloric intake, but they fIlust be introdured slowly. If
or slurries flushed into their mouths. If the ileus persists
only grass hay is fed, protein supplementation will be
for more than a day or two, consider parenteral nutri­
necessary.
tion (see below).

Major small intestinal resection

Gastric reflux
If more than 60 per cent of the small intestine is
11 gastric reflux or other concerns prt'"vent feed intake
removed it is best to avoid large amount.� of grain or
for more than 48 hours, parenteral nutrition should be
concentrates. No more than 0.2 g/kg should be offered
considered. Intravenous administration of only 5% dex­
per feeding to avoid overwhelming the residual small
trost'" is not recommended, however. It will not provide
intestinal digestive and absorptive capacity. Beet pulp­
significant amounts of calories and will stimulate
based 'complete' fr-ceds arc recommended. Ideally 50
insulin release which will inhibit lipolvsis, thereby pro­
per cent or more of the ration should be high quality
moting catabolism. Fifty per cent dextrose, amino acid
legume hay or pasture. If the ileum is intact, edible veg­
and lipid solutions are available for intravenous admin­
etable oils may be llsed to incrca.5c calOlic intake (up to
istration and should he employed when oral or intra­
1.0 ml ktfl day-I).
gastric alimentation is impossible. If the clinicians
and/or their technicians arc unfamiliar ".,�th com­
Ileal bypass or resection
pounding such solutions, human hospitals will fre­
quelltly be willing to assist in the fonnulation and Removal of the ilcum will increase the necd for fat­
preparation of the bags. B-complex vitamin solutions soluble vitamins A and E. Ddkiency signs however may
(10-20 mI!day) should be added to the nutrient solu­ appear only 1-2 years after surgery. It is not known if
tions. The solutions should only be delivered tbrough a oral supplementation of increased amount� of these
venous catheter (preferahly a centml venous catheter) two vitamins (60000 IV retinyl palmitate, 1000 IU alpha

197
11 COLIC
tocopherol/clay) will be prcventative. Parenteral
adminiSlr31ion may be necc:s$lry if dinical signs of ddi­
ciCEK}' appear. Ther� also may � an increased need for
C'
d kium and a reduced tolcrdncc for fals. The rdrion
should contain at least 0.8 per cent calcium and edible
oit.� shnuld not he ll� a.� liupplemenlS.
P os toperativ e sh ock and
organ failu re
LR Goodrich
INTRODUCTION
In 1895, James Collins Warrell referred LO shock as 'a
momentary pau�e in the act of death'. More recent def­
definr-d it a.� a 'gcncra!il.cd inadequacy of
initi()n� have
blood fl(lw tn tissues rdative to their metabolic
demand� !t'ading to widespread cdlular hypoxia and
vi[<l1 organ dy!lfunclion'. Depending on the context of
prt!'senl'Hion, shock varies in its description between its
ph�siol()giC<l' and iL� dinical p,Ir<lmetcu;, For clinicians
a more approp rilue definition may he 'the state in
which profound and widespread reduclion in efTecth-e
tissue perfu$ion leads to re\·Cl"5ibk, and then, if pro­
longed, irre\"t)r�ible cellular injury'.
Despite recent ad.....mCe5 in diagnostics and cardio­
\'ascular treatment, shock remains an important came
ofcomplinttion� and dc:ath in b()(h humans and domc�­
lie animals. A survey of 259 surgical colic cases revealed
that over 50 per cc:m of falalities occurred in the post­
operative period, and 70 per cellt of these were due to
shock as weI! as pOSlopcrauve ileus. In the light of these
findings i t becomes apparent that a fundamental
understanding of the procem:s leading to circulatory
inadequacy is an essential element in successful man­
agement of Ihis morhid �yndromc.
CLASSIFICATION
Se\"e!'"...1 da.��ificalion s�"Slems exi" that describe the dif­
ferent types of shock.. TIle most common s),s[("m uses
insults of variolls etiologi es according to the character
of the pre......ili ng drculalOr}, disrupt
ion. The four
primary C".Hegori<.'S are
• ("anii(lg�nk shMk
• obstructh·e shock
• hypo\"olemic shock
• distributive shock.
19B
Cn.rdiogtnir and ooslrurliw ShfXk
These condition.� ndate I() an inability of the heart to
pump blood, and I() a restriction of cardiac ejection.
resp«ti\dy. Since these Slates of shock are nOl gener­
i
ued ",;th
ally associl J>OSlOperatve complications follow­
ing gastrointestinal surgery they will not be discu.�
funner. The other two classifications Ihat are more
commonly seen following gasuointestinal surgery arc
hypovolemic and distribllli\"c shock.
HyJmwlnnic (JI(1Twrrlwgk) lhodt
This refers to the It)$S of whole hllx)(i, u�ually because of
llt:morrhage, resulting in !os� of intTavascular \·olume.
Oth�r causes include loss of plasma (exudation into
lumem of hol1o..... organs or body cavities), or loss ofIm'-'
protein fluid (as in diarrhea). Tht: !ac.k of int.ravascular
volume results in pcwr \';ls!;ular flJling volume, leading
to decreased cardiac return and hence, decreased
cardiac output, arterial flow, and pressure.
Di.liri!mtiVlr .11iock (.�(ir and tndolo.xnnic)
This occurs as a fesuh of expansion or the iml'"dv'dscu­
Jar space by localiled or gener.t1ized loss of vascular
resistance. This is the 1Il000t common form of shock
that gastrointestinal surgeons deal ",;th, it is often
ated hy sertic�mia and/or e.ndoLOltemia. Other
initi
causes can he neurogenic in origin such as anesthetic
mUihaps, spinal cord injury, or anaphylaxis.The result
uf Ihc:$(' cauSC$ is similar to hypo\'oiemic shock in that
.
....,,$Cular filling volum�. and cardiac return and output
arc all reduced. In addition there a lo� of loc.ll con­
[TIll mechl\ni.\m� rhlH J+ft' rf'_�ponsible for matching
capillary blonc! flow with tissue needs. This point
become� important in that, although cardiac output
may be increased in the early stages of St:pticlender­
toxic �hod., Ihe bJ()od flow to local parenchymal tissue
may be decreased resulting in tis.,ue hypoxia and
dysfunction.
The classification s)'Sterns indica.te that shock is
neatly separated into specific catcgories, however vari­
ous clinical events may initiate two Of more forms of
shock.. For instance, horses with strangulated inte�t.in('
may have hypovolemic components due to los
ses of
intralumcnal fluid u welt as losses of fluid due to 5Cvere
dehydration from sweating. In addition to lhi� ongoing
hypo\'olemic shock, loss of control mechanisms (dis­
trihutive shock) because of conCUfTent scps
i� rna}' add
to the stale of prograsivc shock. Con�-el"M!ly. horses in
....hich sepsis is the initialing factor may not only have
poor regulation of\"3scular wnc but also abnonnal cap­
illary and venou� pemll_'abilil)· lhat leads 10 fluid 10M
and hypovolemia. Therefore calegOlizations ;lre lI!ioCflll
in understanding th<.' pathophysiologic origins of each
inilb!.l insult. Nevertheless, if effecth·e tht"Tdpy i5 not
 POSTOPERATIVE TREATMENT AND COMPLICATIONS
instituted early in any category of shock, the end result
is olien similar for all c_ategories.
PATHOPHYSIOLOGY
Hypovolemic shock
Hypovolemic shock in the postoper<ttive period most
commonly occurs because of mesenteric- vessel bleeds
from the small intestine, small colon, or occasionally
from the {:olonic vessels in cases of large colon resec­
tion. Circulating blaac! \'nhnne constitutes <tpproxi­
mately 8 per cent. of IXJdy weight. Adult animals can lose
up to one-third of this volume and survive with a rea­
sonably good prognosis. How(�ver when the volume loss
is greater than this there exists an obligatory need for
resuscitation.
For horses in hypovolemic shock due to hemor­
rhage, it is helpful to understand events occurring at
the vessel wall. Discontinuity of the vessel wall occurs
and platelets become activated because of changes in
laminar blood flow. This exposes receptors on the
platelet surface and allows exposure of the platelet to
collagen on the damaged vessel wall. Platelel� then
extrude their contents, including thromboxane, sero­
tonin, and bradykinin which causes vasoconstriction,
and platelet factor 4. Additional plate\el� then adhere
to the vessel wall, adding to the growing clump at the
site of vascular disruption.
Fibrin formation occur� within minutes as protein­
dOlling factors in the plasma undergo a cascade of
activation. The fibrin strand stabilizes the platelet
dump as it forms. If the defect in the vessel wall is
small and pressure is low the platelet-fihrin aggregate
will fill the detect and blood wi\! cease to exit th(�
vessel. Often the hlood that has leaked out of the
vessel into thc surrounding tissue will also form a
platelet-fibrin clot and contribute to the cessation 01
bleeding. Adequate hemostasis does not always occur
especially when the injured vessel is large and the pres­
sure is low. The platelet-fibrin clot may not be large
enough to occlude the defects and bridge the cut sur­
j�l.{.es. In this case, the surrounding dot joins with the
clot inside the vessel to bridge the defects. Each pulse
forces more blood through the hole into the surround­
ing clot. in arteries that are large and under high pres­
sure, but the pressure from the surrounding clot may
never reach a point where it is equal to the pressure
inside the artery. Tn arteries, muscle spasm reduces the
diamCln of the vessel defect which the dot must span
ill order to seal the hole, but constant pulsatile pres-­
sure may reduce effective occlusion of the defect in the
vascular wall. If pressure in the clot surrounding the
11
injured artery does not reach the pressure present
",ithin the artery bleeding into the interstitium or
abdominal cavity, then hemorrhage will continue until
adequate surgical intervention has taken place or sys­
temic hypotension develops. At that point, pressure in
the artery drops to the level of the surrounding tissue
clot. If systemic arterial pressure reaches 50 mmHg or
lower, the platelet-fibrin plug may seal the defects.
Often, before this time, it is likely that over 30 per cent
of circulating blood volume wi\! have been lost. It is
important to consider that dilution and reduction of
blood visco�ity resulting from volume expansion with
large volumes of cry'ita\!oid fluids, may further chal­
lenge the clot-hypotension relationship.
The compensatory mechanisms activated during
this described attempt to control hemorrhage include
baroreceptor reOexes and the sympathoadrenal
systems. Receptors are present in the walls of the great
vessels and arc sensitive to reduced hydrostatic pres­
Sllres. Most important are the receptors in the carotid
sinuses and aortic arch, that detect decreased pressures
within the hrain and general circulation. These recep­
tors are responsible for initiating elevation in heart r.lte,
vasoconstriction, and increases in arterial blood pres-­
sure, via sympathetic nelVe activity. Sympathetic activa­
tions induce an increase in venous tone and the blood
is not allo\\'ed to pool in veins. This in turn increases the
pre-load on the heart.
Arterial constriction during hemorrhagic shock is
not, over<lll, unibrm. Peripheral vasoconstriction is
most severe at the splanchnic, cutaneous, and skeletal
tissue areas. Areas such as the brain and heart are
spared however, so that when a systemic drop in blood
pressure occurs blood is preferentially shunted to these
organs that are ...ital in the most immediate sense. The
skeletal muscle vascular beds maintain fairly adequate
perfusion because of reflex vasodilation in response to
the autocoidal efrects of cellular metabolic products.
The reflex sympathetic activity initiates pacemaker cells
through beta, receptors, increasing heart rate. Other
sympathetic nelVe fibers innelVate the adrenal medulla
and cause catecholamine release.
A renal contribution to homeostasis is of major
importance in animals sUlviving this acute phasr"C of
hemorrhage. In response to decreased renal perfusion,
specialized cells next to each glomerulus produce ren­
nin and secrete it into dferent arterioles. This induces
angiotensin I formation from angiotensinogen. The
renin-angiotensin system is responsible for the release
of aldosterone which increases sodium and water
resorption and antidiuretic horrnom� (ADH), whid,
increases permeability of pores in the collecting ducts
of the kidney so that water can pass back into the renal
interstitium and thr"Cn into the vascular space instead of
199
11 COLIC
being excreted as urine. This reflex is <In important fac­
lor ill maintaining adequate bloori pressure 6-12 hours
following blood loss.
The reflexes described above are the body's altempt
to maintain blood pressure. These events occur at the
same time that activation of the clotting cascad", is fUlle­
lionillg to stop profuse hemorrhage. In horses suffering
from hypovolemic shock due to diarrhea or inadequate
oral fluid the same reflexes (increased cardiac output,
vasocooslTiction, ;md W'dler retention to maintain blood
pressure) occur.
Distributive shock
Although hypovolemic shock is occasionally seen in the
perioperativc period of gastrointestinal surgery, by far
the most common type of shock seen in the horse is
distributive shock caused by sepsis, endotoxemia, or
splanchnic ischemia associated \\�th acute strangulating
and non"strangulating intestinal infarction. Often alt
three conditions can cuntribute to shock. Several inves­
tigawrs have determined that up to 40 per cent of
horses with colic presented to a veterina!)' college are
endolOxemic, and most endotoxemic horses have
intestinal strangulation obstruction or severe inllamma­
lory int�stinal diseases. Furthermore, the prognosis for
sUlvival is inversely correlated with the presence of
lipopolysaccharide in the circulation. In some cases all
three causes may be contributing to distributive shock.
Early and late phase pathologic events usually char­
acterizc distributive shock caused by sepsis or endotox­
cmia. In the early phase, increased cardiac output occurs
along with reduced peripher.l! vascular resistance, nor­
mal to slightly decreased mean arterial pressure and
fever with warm extremities. It is in this phase that the
lipopolYS<lccharide components of the outer membranc
of enteric hacteria initiate the host's mononuclear
phagocytes n:sulting in symhesis of proinflammatory
mediators. The most widely recognized mediators
include the C)'tokines, lipid-derived mediators, and coag­
ulation/fibrinolytic factors. Cytokim�s most commonly
involved include tumor necrosis factor, interleukins,
and interferons. Lipid-derived mediators include throm­
boxane (TXA..,) and prostaglandins (PGS, PGF2a, and
PGJ"). Release offibrinolytic factors in this stage ofshock
resulL� in decreases in plasma antithrombin III activity,
protein C, and plasminogen anivity. This also results in
coagulation times indicative of the presence of a hyper­
coagulable state in endotoxemic horses with colic. It
should be mentioned that during the early stage ofsep­
tic/endotoxcmic shock in which the above mentioned
mediators arc bcing relcased, a syndrome named the sys­
telTJic inflammatory response syndrome (SIRS) has been
used to describe the sequence of evenL, and the (:on-
200
current clinical events. This term refers to an exagger­
ated systemic response to an inju!)'. V,'bile not only used
to describe the events of shock, it is commonly used ill
humans to describe various states of shock. Briefly, SIR-\)
develops when the local response to iI�Ury or to an
initiating stimulus becomes amplified. If homeostasis is
not re-established, the multipk inflammatory cascades
result in loss of microcirculatory function and subse­
quent damage to other organs. This leads into the
second stage of distributive shock caused by
sepsis/endotoxemia.
The late phase of septic and cndotoxic shock is char­
acterized by decreased myocardial and peripheral vas­
cular tone, incn�ased microvascular permeability,
increased intravascular coagUlation, and leukocyte
adherence. Progression of the inflammatory cascades
initiated in SIRS ensues and vascular hyporeactivity pre­
vails as the one distinct and important <Ibnormality. The
prevailing opinion is that lipopolysaccharides and select
cytokines induce the calcium-insen�itive form of the
nitric oxide �ynthasc molecule within the VAscular wall.
Over-production of nitric oxide leads indirectly to sup­
pression of calcium mobilizatioJl and a decreascd
contractile function. In many cases the progression of
SIRS results in multiple organ dysfunction syndrome
(MODS). In human medicine there exist various scor­
ing systems eval u<lting v.arious serologic parameters such
as creatinine, bilirubin, and platelet count. As the scores
incre;!.�e, the incidence of mortality also increases. For
example four body systems suffering from dysfullction
resuits in 80 per cent mortalit.ics. In the horse MODS is
most commonly as.'!ociated with the gastrointestinal
tract. The gut h;!.� been termed the 'motor of failure' in
its capability of generating the demise of ot.her organ
systems. Reperfusion of the gut can be responsible for
• activation of calcium influx with oxygen radicals
adding to mucosal if!jury
• bacterial translocation with heightened
endotoxemia
• the release of cytokines resulting in wsodilation
and vascular leakage.
The combination of these three factors increases the
predisposition to MODS. Other organs that can com­
monly be secondarily affected are the kidney, liver, and
lungs.
CLINICAL FINDINGS
Hypovolemic shock
Horses experiencing hypovolemic shock due to helllOr­
rhage commonly have elevated heart rates, pale mUCOllS
 POSTOPERATIVE TREATMENT AND COMPLICATIONS
membranes, a thready rapid pulse, prolonged capillary
refill time, and cool extremities. Often they are sweat­
ing and agitated. If hemorrhage continues unmiti!f<l.ted,
eventual collapse ensues. Rectal temperature may be
normal or decre-d-�. If shock is protracted the horse
may he oIiguric. As circulatory and respiratory function
deterior.tte, the gums may take on a gray-blue color.
If bleeding is not controlled acute death occurs.
Laboratory eVMuation is frequently not helpful in the
acute phases but may reveal metabolic acidosis,
increases in lactic acid, and increases in blood urea
nitrogen. Hematocrit often stays unchanged in the
acute phase of hemorrhagic shock but evcntually
decreases during the later phases especially if large
doses of crystalioid fluid therapy are instituted. Plasma
protein usually parallels this. It is important to remem­
ber that the various components of blood are being lost
equa!Iy, and the relative proportions of red cell mass
and plasma will remain unchanged. Ultrasonography
is the diagnostic modality of choice in cases where
hemorrhage into the abdominal cavity is suspected.
Hemoperitoneum is easily evaluated with ultrasound
using a 5.0 MHz probe transabdominally. Blood
appears hypoechoic with swirling of the cellular ele­
ments. Questionable aooominal bleeding can be more
accurately confirmed by paracentesis. Although analysis
of peritoneal fluid is not always straightforward in mak­
ing Ihis determination, a helpful rule of thumb is that a
packed cell volume of 5 per cent or greater, and a total
protein of 3.5 gldl or greater support the presence of
frank hemorrhage.
The clinical findings among horses experiencing
hypovolemic shock resulting from vascular fluid loss
dm' to acute diarrhea or inflammatory bowel condi­
tions, can look similar to those horses with acute hem­
orrhage. Labor,ltory evaluation however may reveal
relatively early declines in plasma protein concentra­
tion and electrolyte abnormalities as well as a marked
metabolic acidosis. However, because infection may
also be occurring in these horses the findings can often
be similar to those in horses with distributive shock due
to sepsis.
Distributive shock
Horses in the initial stages of distributive shock due to
sepsis or endotoxemia have clinical signs consistent
with the 'early' phase. These signs include fever with
warm extremities, depression, tachycardia, increased
respiratory rate, injected mucous membranes (Plate
11.1), hypocapnea and leukopenia or leukocytosis.
Hemodynamically, horses have decreased arteria! pres­
sure, elevated cardiac output, and low peripheral vascu­
lar resistance. As distributive shock progresses, cardiac
11
output begins to fall along with arterial pressure.
Horses in acute abdominal crisis, and in particular with
splanchnic ischemia, exhibit sweating, tachycardia,
weak pulses, and cyanotic mucous membranes (Plate
11.2). laboratory evaluation may reveal hemoconcen­
tration, leukopenia, coagulation abnormalities, meta­
bolic acidosis, and elevation of blood urea and
creatinine levels. This stage is often referred to as the
'late', 'cold', or 'hypodynamic' stage of shock. Gross
hypoperfusion is occurring resulting in multiple organ
dysfunction syndrome.
TREATMENT
-.
---.--------
Hypovolemic shock
Initial goals in the treatment of hypovolemic shock
include partial restoration of circulating blood volume,
maintenance of oxygen delivery to tissues, and support
of coagulation and thrombus formation when hypo­
volemic shock is due to hemorrhage. It is important to
remember that supportive therapy in hypovolemic
shock due to hemorrhage does not end when the bleed­
ing is controlled. Many pathologic processes continue
following control of hemorrhage and, if allowed to
progress, these processes result in damage to other
organ systems such as the gastrointestinal tract and the
pulmonary system. Failure of these systems can be rec­
ognized as ischemia-reperfusion injury and pulmonary
edema, respectively,
To restore partial circulating blood volume rapidly,
a large bore catheter should be placed and crystalloid
fluids given in appropriate dosages. Options for crystal­
loid fluids include saline, lactated Ringer's solution,
plasmalyte, and hypertonic saline. Replacement volume
should be calculated according to total loss as well as
maintenance volume required. Crystalloid fluids move
freely from the intravascular to the interstitial space and
approximately 20 per cent remain in the intravascular
space. Lactated Ringer's solution consists of sodium
and chloride with added calcium, potassium, and lac­
tate (buffer solution). Plasmalyte and normasol include
other buffers as well as magnesium. Lactated Ringer's is
inferior to normasol and plasmalyte when blood is
being transfused since the calcium added to these solu­
tions can interact with citrate antic()agulant� in col­
lected blood. Hypertonic saline is advantageous in
hypovolemic shock for many reasons. Initially this solu­
tion can rapidly expand intravascular fluid volume.
Additionally, there is evidence that other beneficial
cffect� include modulation of neutrophil activity
thereby potentially decreasing the incidence of
ischemia-reperfusion injury and bacterial translocation.
201
11 COLIC
It is important to rememocr however that unless bleed­
ing in the patient with hypovolemic shock is controlled,
hypertonic saline should not be used because of the
rapid volume expansion and the resulting effects of dis­
lodging a tenuous clot formation. Alternatively, colloid
fluids may be considered for volume expansion. These
include hetastarch, plasma, dextrans, and 5% albumin.
Colloids contain large molecules, which prevent egress
of fluid out of the intrav<lscular space allowing both an
expansion of plasma volume and an associated increase
in cardiac output. The volume of crystalloid fluids
infused would have to be three times that of colloids for
an cfJllivalt>n! improvement in cardiac peIfonnance.
Hetastarch should be administered at 6 ml/kg in place
of hypertonic saline. Similar to hypertonic saline,
concerns regarding initiation of bleeding exist for
hetastarch as well.
To increase the oxygen-carrying capabilities for the
horse in hypovolemic shock due to hemorrhage, whole
blood should be administered. The blood volume
needed should be estimated according to the horse's
weight, suspected volume of blood lost, and present
packed cell volume and total protein. Packed cell vol­
umes of less than 20 per cent and total protein values of
less than 3.5 gldl should be treated with the adminis­
tnuion of whole blood. For an adult horse, blood vol­
ume is approximately 8 per cent of body weight or 40
liters. If the packed cell volume drops from 36 to 12 per
cent a loss of erythrocytes is at least 27 liters of blood.
Generally, replacing 20-40 per cent of the deficit is ade­
quate therefore 7-10 liters of blood should maintain
the oxygen-carrying capacity of blood. Up to 25 per
cent of the donor's blood volume can be removed at
one collection (10 liters in a 500 kg horse). This may be
repeated every 30 days. Cross matching should be per­
formed prior to administration, or transfusion should
be performed from a universal donor. Alternatively,
blood substitutes such as Oxyglobin (Biopure,
Cambridge, MA) can be administered, however cur­
rently, for an adult hor�e, these prOdUCL� are prohibi­
tivelyexpensive.
If cessation of bleeding relies on a tenuous clot for­
mation, antifibrinolytic drugs should be considered.
Options include aminocaproic acid, transexamic acid,
and conjugated estrogens. Of these choices amino­
caproic acid has been used most often in horses, given
intravenously in doses of 20 g in 500 ml saline per
450 kg horse (loading dose), and then 1 0 g twice to
three times daily. There have been no proven efficacy
trials in horses at the time of writing.
The 'low' doses offlunixin meglumine (0.25 mg/kg
i.v. t.i.d.) should be administered as an adjunct in an
attempt to minimize the inflammatOI), cascades initi­
ated by ischemia resulting from compromised
202
blood-bowel layer, hypoxic cellular injury, and any
potential foreign leukocytes from blood transfusions.
Broad spectrum antimicrobial therapy should also
be used in cases where translocation of bacteria due to
splanchnic ischemia is suspected. It should be consid­
ered, however, that the toxic potential of these druw; is
enhanced by dehydration or volume contraction.
Distributive shock
Distributive shock postoperatively is commonly associ­
ated with acute and extensive disruption of the gastro­
intestinal mucosa. This is one of the most commonly
treated syndromes in the horse postoperatively as well
as the second most common reason for postoperative
mortality. If not treated in its early stages, progression
to the late stages results in a decreased prognosis and
complications such as multiple organ failure. Horses
with septic and splanchnic ischemia should recdve ade­
quate replacement of intravascular volume with the iso­
tonic crystalloid fluids mentioned above. Much like the
treatment of hypovolemic shock, the most import.ant
goal of distributive shock treatment is volume replace­
ment. Monitoring of clinical signs during treatment wi!!
be an adequate representation of therapeutic suffi­
ciency. When replacing volume in the treatment of dis­
tributive shock however, the clinician should be less
hesitant in the usc of hypertonic saline since the com­
mencement of hemorrhage is not an issue. Hypertonic
saline along with hyperoncotic fluids allow the tempo­
rary shift of interstitial and extravascular fluid to the
intravascular space causing increased myocardial con­
tractility because of temporary increased sodium and
potassium ions "'-lthin the V'dscu!ar space. This rapid
method of volume expansion, though, should be fol­
lowed immediately with isotonic crystalloid solution.
Additional benefits of administrdtion of hypertonic
saline in the septic/endotoxemic horse relate to its
effects on neutrophils. Hypertonicity has been associ­
ated with eliminating the receptors on leukocytes that
respond to lipopolysaccharides thereby attenuating
endothelial damage. Furthermore, resuscitation with
hypertonic saline and lactated Ringer's solution appar­
ently resulted in a reduced rate of early bacterial
translocation to mesenteric lymph nodes in one study.
Acid-base normalization is also very important in
the treatment regimen of distributive shock. In the
early stages of sepsis, a respiratory alkalosis may be evi­
dent. However, as shock progresses a metabolic acidosis
is the primary acid-ba�e abnormallty caused by an
anaerobic metabolism in the tissues as well as renal
hypoperfusion. Often mild cases of metabolic acidosis
will resolve without administration of bicarbonate when
a sufficient amount of volume replacement is adminis-

teredo This of course is the most physiologic route in the
treatment of acid-base abnormalities. When metabolic
acidosis is severe (pH < 7 . 1 ) or fluid replacement does
not correct the abnormality then administration of
bicarbonate is necessary. The following formula may be
followed as a guide to estimate the dose of bicarbonate
to he administered.
:-';aHCO� replacement (mEg) = 0.3 x body weight (kg)
x base deficit
Periodic monitoring of blood gas will allow proper
adjustment in dosing.
Antibiotic therapy is indicalf'o in riislrihwivf' �h()rk
cau�ed by sepsis. Often in cases of eXlensive bowel com­
promise and resection many different bacterial isolates
are possible, however, isolation of these organisms is
rare. Therefore combinations of high doses of peni­
cillin G and an aminoglycoside are commonly used
because of their broad spectrum ofbactericidal activity.
This combination of antibiotics should be continued
paM the arute phase of distributive shock because of lhe
possibility of sepsis and/or splanchnic-ischemia.
Anti-inflammatory therapy is extremely important in
horses with distributive shock due to sepsis/endotox­
emia. The use of flunixin meglumine has become stan­
dard in the treatment of distributive shock. This drug
acts by inhibiting cydooxygenase and will prevent or
attenuate the early hemodynamic responses to endo­
toxin. Various studies have found that flunixin meglu­
mine significantly reduces endotoxin-induced increases
in plasma concentrations of thromboxane
prostaglandins. The 'low dose' commonly used in clini­
cal situations is 0.25 mg/kg i.v. Li.d. This dose will
rewin the ability to prevent generation of cyclooxyge­
na.�{'-derived products and has minimal toxic side
effects. Following surgery however, it is important to
keep in mind that postoperative pain resulting from
intestinal manipulation may require initial higher doses
(0.5 mg/kg) and slow decreasing of the dose over a
period of 3--4 days. It should be mentioned that
although some debate still exists regarding the use of
steroid therapy in distributive shock, extensive clinical
trials in the human population reveal no beneficial
effects and occasional adverse effects when used.
Therefore, although exact extrapolations cannot be
made to the equine population, steroids are not recom­
mended.
Polymyxin B is a recent addition to the treatment
armamentarium for distributive shock due
sepsis/endotoxcmia. This antibiotic is reported to bind
and remove endotoxin from the circulation by binding
the lipid A region of endotoxin. Studies in foals pre­
lTeated with polymyxin B that underwent induced
experimental endoloxemia had reduced signs of
POSTOPERATIVE TREATMENT AND COMPLICATIONS 11
endotoxemia, absence of leukopenia and lower than
expected tumor necrosis factor levels in serum.
Recommended doses are 1000-3000 Ie/kg given intra­
venously twice daily. While these doses are sub­
therapeutic antibiotic doses, polymyxin B can be
nephrotoxic and dose monitoring of creatinine and
blood urea nitrogen should be performed.
Plasma products are available with antibodies
directed against the core oligosaccharide and lipid A
regions of endotoxins from mutant gram-negative
bacleria. Vo.'hile many referral centers administer these
product�, their efficacy still remains in question.
Hyperimmune plasma products may however provide
the septic/endotoxemic horse with levels of antithrom­
bin III that appear to be deficient in horses with colic.
Heparin injected into the plasma before transfusion
may improve the efficacy by activating antithrombin III
prior to administration.
PentoxifyIIine (6.6-8.0 mg/kg p.o. hj.d.) is another
drug used to treat horses for endoloxemia. In both
in vitru and ex vivo studies in horses, pentoxifylIine
reduced endotoxin-induced production of cytokines,
thromboxane, and tissue factors. Clinical trials have
revealed that when used alone its beneficial cllects may
be minimal but when combined with flunixin meglu­
mine, hemodynamic responses to endotoxin may be
reduced more effectively than with either drug alone.
Supplemental oxygen therapy is not usually neces­
sary for horses in which arterial oxygenation tensions
are normal (PaO� 100 mmHg) or dose to normaL In
and these cases hemoglobin is fully saturated and further
supplemental oxygen therapy will he of little benefit.
However, when arterial oxygen tensions fall below
85 mmHg hemoglobin desaturation IIlay occur and
supplemental oxygen can be delivered in the standing
horse through nasal or transtracheal catheter place­
ment. F10ws of 15 l/min should be administered with
adjustmenL� made according to blood gas measure-­
ml':nts.
PERIOPERATlVE MONITORING
....i.'h re this chapter is dedicated to postoperative assess­
ment and treatment of shock, treatment will be more
effective if instituted to patients preoperatively.
Treatment should begin prior to induction for generAl
anesthesia in patients when large amounts of intestinal
to compromise are suspected. Although there are situa­
tiOIlS in which patient� can not be volume expanded
adequately preoperatively, every effort should he made
to promote proper treatment as soon as possible. Care
may be expedited by placement of two large-bore
catheters and fluids administered under pressure.
203
11 COLIC
Adequat� supplies of necessary treaunem modalities
should be available along 'Hilh the equipment to ade­
quately monitor treatment. Prior planning for critical
care for patients in shock is important in situations
where there are small time frames. Proper anesthetic
monitoring is also crucial (see Chapter 10). Often dfec­
tive treatment and monitoring during anesthesia of the
colic patient has a direct outcome in the postoperative
period.
THE FUTURE
The field of shock has become an intensely studied area
with new advances being made frequently. As new
developments occur in both the monitoring and treat­
ment of shock clinicians will become more effective in
its early diagnosis, monitoring, and treannent. This
chapter has covered most current monitoring and treat­
ment techniques that have been clinically evaluated in
the equine patient. As sound clinical trials reveal new
techniques it is the responsibility of clinicians to judi­
ciously use the new methods to benefit the equine
patients.
P os toperative pain
um
LR Goodrich
INTRODUCTION
===:.:.:.... __ .
. .._._.. _._. _ ..
Postoperative pain is a complication that gastrointesti­
nal surgeons deal with frequent.Iy. Abdominal pain,
otherwise called colic, is defined as 'an unplea�ant
experience that is commonly associated with tissue
injury'. Various physiologic sources of pain include
• the type of stimuli
• the various receptors that are stimulated
• the neuroanatomic pathways transporting the pain
stimulus from the site of injury to the central
nervous system
• the various reactions in response to pain.
Thus postopemtive pain, induced by gastrointestinal
surgical procedures, induces a series of behavioral,
neurophysiological, endocrine, metabolic, and cellular
responses (the stress response) that initiate, maintain,
and intensify the release of pain and inflammatory
mediators. I tshould be stated that pain is a complex sen­
sation that can manifest differently in horses affected by
similar abdominal problems. It is the surgeon's respon-
204
sibility to interpret clinical signs exhibited by their
patients and judiciously manage pain based on a com­
plete understanding of the facton; involved.
NEUROANATOMY AND
PATHOPHYSIOLOGY
Sensory neuroreceptors arc located in the mu(:{).')a and
muscularis of hollow viscera, within serosal structures
such as the peritoneum, and within the mesentery. i:l
addition to nociception (the perception of noxious
stimuli), [hf' �ensory nellror('cep!or.� arf' rf'spnnsiblc for
regulation of motility, secretion, and blood flow to the
gastrointestinal tract�.
Neuroreceptors responsible for the p<Tception of
pain are separated into two distinct types of afferent
nerve fibers
L myelinated A-delta fibers
2. unmyelinated C fibers.
A-deita fibers are responsible for mediating sharp,
well-localized pain associated with an acute injury.
These fibers transmit somatoparietal pain �ia spinal
nerves. C fibers are found in viscera, peritoneum, and
mesentery, as well as in muscle and periosteum. C fibers
convey nociception from abdominal viscera and this
pain tends to be dull, burning, diffuse, and of a more
gradual nature in onset. C fibers utilize substance P and
calcitonin gene-related peptide as neurotransmitters.
Local regulatory reflexes within the gut are activated
when C fibers are stimulated.
Three pathways mediate abdominal pain
I . first-order neurons, that innervate the viscera, carry
information to the thoracolumbar sympathetic
nervous system, and then synapse in the dorsal
horn of the spinal cord
2. second-order neurons, which ascend from the
dorsal horn via the spinothalamic and
spinoreticular tracts to synapse with the thalamus
and reticular formation
3. third-order neurons, which progress from the
spinothalamic system to the somatosensory cortex
and from the spinoreticular system to the limbic
system and frontal lobe of the cortex.
These multiple inputs of nociception in the eNS clabo..
rate the variability of pain.
Abdominal visceral nociceptors respond to mechan­
ical and chemical stimuli. The primary mechanical sig­
nal to which visceI'".ti nociceptors arc sensitive i.� stretch.
This differs to somatoparietal nociceptors in that cut­
ting, tearing, or crushing of viscera does not elicit pain.
The visceral stretch receptors are located in the muscu-
 POSTOPERATIVE TREATMENT AND COMPLICATIONS 11

lar layers of the ho!low viscem, between the muscularis input to the spinal cord and eNS. Conversely, recurrent
lllucosa and submucosa, also in the serosa of solid gastrointestinal pain (e.g. with re-laparotomy) may sen­
or!fans as well as in the mesentery. Mechanoreceptor sitize intestinal receptors making perception of baseline
stimulat.ion can result from rapid distention of a viscus afferent activity more painful.
(small intestinal strangulating obstruction), torsion of
thtO mesentery (large colon volvulus), or tension on the
CLINICAL SIGNS
mesente!l' (small intestinal adhesions).
Chemical nociceptors are located primarily within
Postoperative pain is usually less intense than the pain
the lIlucosa and submucosa of the hollow viscer<l. These
exp�ri�nced preoperatively unless
rtOceptors are directly stimulated by mediators of pain
and inflammation. Such chemicals include histamine, • postoperative ileus results in similar distention
serotonin, bmdykinin, leukotrienes, prostaglandin E�, • there is ongoing tissue ischemia
illtnleukins (IL-l, IL-6), neutrophil-chemotactic pep­ • there is recurrence of the original lesion or the
tides, nen'e growth factor (:-.JGF) and neuropeptides original lesion was not corrected surgically
including substance P and calcitonin gene-related pep­ • a new lesion has developed .
tide. Collectively, these mediators have been referred to
Abdominal pain can be sepamted into three distinct
as the 'sensitizing soup' because their accumulation is
calegories
thought to result in visceral sensitization.
This visceral sensitization has been describtOd as • visceral
resulting from the recruitment of certain (silent) affer­ • somatoparietal
ent receptors. With prolonged or recurrent peripheral • referred.
stimulation because of distention or stretching of the
Visceral pain is caused by nox:ious stimuli triggering vis­
mesentery, the excitability of the second-order neurons
ceral nociceptors. Somatoparietal pain is initiated by
is enhanced and outlasts the duration of increased
stimulation of the parietal peritoneum, and referred
periphtT<l1 stimulation. This has betOn referred to as
pain is pain perceived in areas remote to the diseased
central nervous system 'wind-up' and results in hyper­
organ. In the equine patient it is difficult to differenti­
algt"sia. After the peripheral stimulation subsides, sensi­
ate t.hese various types of pain.
til.t"d second-order neurons continue to fire and
In a�sessing pain the general attitude of the patient
sub-threshold stimull that are oth�lWise non-painful are
should first be noted. It is helpful to assess the horse's
still perceived as painful.
attitude from outside the stall since the tendency to lie
The biochemical resuit of hyperalgesia can be
down can be inhibited when a person is in the stall with
cxplaincd by the accumulation of Lhemical mediators
the patient. Signs are varied and include pawing, turn­
which enhance neural sensitivity and intensify the pain
ing the head toward the flank, kicking with the hind
n�sponse. Once transduced the electrical impulses are
feet at the abdomen, crouching in attempt to lie down,
transmitted to (:;"fiber terminals in the dorsal horn (sec­
stretching and appearing to attempt to urinate, grind­
olld-order neurons) where the excitatory neuropep­
ing the teeth, dropping to and rolling on the ground,
tides such as tachykinins, neurokinins, and amino acid
sweat.ing, and quivering of the upper lip.
glutamate arc released and cause an increase in mem­
The severity of pain can vary from mild (occasional
brane excitability and activate postsynaptic recepLOrs,
pawing) to severe (dropping to the ground and rolling
primarily :'\i-methyl-D-aspartate (NMDA).
violently). Postoperatively most horses are administered
The phenomenon ofvjsc�ral sensitization has not yet
analgesic doses of NSAlDs, the severity of pain must
heen demonstrated in horses. However in humans it has
therefore be considered in this light, i.e. the pain exhib­
been supported by experiments in which repeated series
ited would most likely be worse without the analgesics.
of balloon inflations in the colon led to an increase in
� a rule, the more severe the aooominal lesion, the
pain intensity and a 228 per (ent increase in the size of
greater the pain. However, difterent horses manifest
the area where pain is experienced. It is highly probable
pain in a variety ofways and some horses have a greater
that the equine patient has similar decreases in pain
tolerance to pain than others.
t.hreshold with ongoing pain. Furthermore, it has been
The external appearance of the animal can be help­
demonstrated in the equine patient as well as the human
ful in assessing the disease
patient that preoperative treatment with local or
regional anesthesia or non-steroidal anti-inflammatory • bloating indicates distention of the cecum and/or
drugs (NSAlDs) results in reduced severity of postoper­ large colon
ative pain. This implies that CNS response to peripheral • splinting of the abdomen usually indicates
injury can be mediated by prior reduction of afferent somatoparietal pain from the peritoneum or pleura

205
11 coue
• sweat.ing also indicates severe pain and potential
response to endotoxic shock.
DIAGNOSIS
Together with the clinical signs, temperature, pulse,
and respiratory rates should be monitored postopera­
tively, these are commonly elevated in horses exhibiting
pain. Auscultation should be performed over the left
and right paralumbar regions and propulsive sounds
should be quantified. Progressive sounds �il! be heard
only once every 2-4 minutes when the colon has �en
emptied or the horse has not eaten, with normal motil­
ity these sounds are heard every 6-10 seconds. In almost
all horses with abdominal pain propulsive sounds v.'iIl
be reduced. While auscultating the abdomen percus­
sion should he performed to detect pockets of gas in
intestine up against body walL Right paralumbar 'pings'
can indicate cecal tympany, left paralumber 'pings' can
indicate gas within the large colon.
Rectal examination can be a helpful diagnostic prn­
cedure in horses with postoperative pain. Rectal exami­
nation postopen'tiveiy, as preoperatively, should be
done carefully and gently. Postoperatively, special atten­
tion should be paid to minimizing straining in response
to the examination to avoid any increased stresses on
the incision line. Chemical sedation, the use of a twitch,
and rectally administered Ildocaine (lignocaine) may
al! contribute to a reduction in straining.
t:ltr<lsound examination is an extremely useful diag­
nostic [001 forsmal1 iIltestinal problems (see Chapter 2).
V-!hen small intestinal distention is suspected a5 the
cause of pain transabdominal ultrasound is very helpful.
Other diagnostics that should be considered in
assessing postoperative pain are gastroscopy, radiology
(especially in foals), and abdominocentesis. White
blood cell count.� and total proteins should be inter­
preted on the basis of the type of lesion identified in
surgery, the degree of contamination, and the length of
time since surgery. In general, in the author's experi­
ence, white blood cell count and total protein measure­
ment.� in the abdomen postoperatively have not been
higher than 40 000-50 000 cells/�l and 3.5-4.0 gldl,
respectively at approximately 4--5 day; following
abdominal surgery in cases that were progressing well.
TREATMENT
Goals
The goal in treating postoperative pain is to provide
quick effective analgesia, and to eliminate the reflexes
206
(ileus, intestinal spasm) causing the pain. Although
elimination of the problem is not always possible,
reduction of pain with effective analgesics will decrease
the reflex inhibition of motility. This in turn often
resolves the common causes of postoper<ltivc pain such
as distention due to ileus, and inflammation due to
intestinal manipulation. Effective analgesia will also
eliminate or minimize the visceral sensitization or 'wind
up' that ultimately requires higher and more frequent
doses of analgesics resulting in toxic side effects.
Decompression
Decompression is the best way to relieve pain due to a
distended viscus. Nasogastric intubation can reduce gas­
tric tympany or remove gastrointestinal reflux due to
ileus. One of the most common reasons for postopera­
tive pain in the horse is ileus of the small intestine
especially following extensive small intestinal resection.
Nasog-<lstric tubes can be left in place for chronic
decompression, however some clinicians feel that tubes
left in place may also initiate gastric reflux. Regardle�s
of this, ifhorses are suffering postoperative pain, a naso­
gastric tube should be passed and the presence of
reflux determined.
Walking or acupuncture
Walking may also have an analgesic effect on abdominal
pain especially mild pain. This is a common therapy
that appears to increase motility and reduce anxiety.
Some surgeons have also used acupuncture. "VI'hile clin­
ical data are lacking, some clinicians teel that the posi­
tive effects can be appreciated and the risk of hann or
toxic effects is minimal.
Non-steroidal anti-inflammatory drugs
Systemic analgesia is the most common method used to
control colic. Various classes of drugs exist that have
been used for abdominal pain. Clinical trials reporting
anecdotal evidence of efficacy have influenced clini­
cians' choice of drugs. Drug trials also exist that have
used distention models to mimic abdominal pain.
According to these trials drugs exhibiting the best effi­
cacy were flunixin meglumine, xylazine, detomidine,
and butorphanol, see Table 1 1.3.
The most useful and commonly used perioperative
analgesics are the non-steroidal anti-inflammatory
drugs. These drugs reduce the production of throm­
boxane, prostaglandins, and prostacyclin through the
inhibition of cydooxygenase (COX) enzymes. It is now
known that there are two isoforms of COX, designated
as COX-l and COX-2. The constitutive enzyme COX-l
performs 'housekeeeping' activities in platelets, gastro-
 POSTOPERATIVE TREATMENT AND COMPLICAnONS 11

Table l1�Ait"""""" ."dtblfrrNtlYi.��;"'--

",.... io� Udomtn.l-"'� .

An.lgulc DOS.,. Effectlv-n...

Aspirin 20-40 mg/kg p.o. poor

Butorphanol 0.02-0.075 mglkg Lv. good

Chloral hydrate 30--60 mg/kg Lv. titrated fair

Detomidine 1()-.40 mglkg i.v. excellent

Dipyrone 10 mglkg Lv. or tm. fair

Eltenac 0.5--1 mg/kg undetermined

Flunixin meglumine 0.25-1.1 mg/kg Lv. or Lm. exceUent

Ketoprofen 1 .1-2.2 mgikg Lv. good (variable)

Udocaine2% slow Lv. bolus 1.3 mg/kg over good

5 min. then i.v. drip at
0.05 mg kg-' min-1

Phenylbutazone 2.2-4.4 mglk.g Lv. fair

Xylazine 0.2-1. l mg/kg Lv. or i.m. goocH!)(ceUent

intestinal mucosa, and the kidneys. COX-2 is upregu­
lated in inflamed tissues but is found only in small
amounts in normal cells. It is understood that inhibi­
tion of COX-! is the cause of adverse eflects of NSAIDs
and that anti-inflammatory and analgesic effects result
from COX-2 inhibition. Prostaglandins (PGE� and
PGI) sensitize nen:e endings to pain and are poten­
tially responsible for amplification (visceral sensitiza­
tion) of pain during bowel distention, ischemia, and
inflammation. Furthermore. prostaglandins facilitate
transmission of nociceptive impulses peripherally and
affect pain perception in the brain. Flunixin has been
shown to specifically block thromboxane and prostacy­
din for 8---12 hours after a single dose. Its advantages are
the maintenance of normal blood flow to the bowd
during obstruction and a return of intestinal motility.
Flunixin can also be helpful in diminishing the
response to endotoxin release. For these reasons flu­
nixin is the most efficacious and commonly used drug
to control postoperative pain in the horse. Inability to
control postoperative pain with flunixin should alert
the dinician to investigate the source of pain further.
Generic dosages commonly used by this author are
the horse (horses with a low threshold to pain may need
more frequent dosing immediately), and any ongoing
reason for pain (ileus).
Phenylbutazone does not appear to provide visceral
analgesia as effectively as flunixin and does not inhibit
prostaglandin formation as weB nor for as long as flu­
nixin. Furthermore its potential for toxic side effect.� is
greater. Its use appears to be more effective for muscu­
loskeletal problems than for visceral pain, although the
mechanism for this difference has not been elucidated.
Kt:toprofen has also been clinically tested in horses
with colic, the results indicate it provides significant
pain relief similar to flunixin. It also has similar effects
to flunixin in suppressing the effects of endotoxemia
and it reportedly has the least toxic side effects when
compared to phenylbutazone and flunixin.
Dipyrone is another l...;'SAID reported to have anti­
spasmodic effecL� on the bowel due to inhibition of
bradykinin. Some inhibition of prostaglandin forma­
tion does also appear to occur with its use.
Other NSAIDs have not been useful in treating colic.
Aspirin has a shon half life and has little to no effect on
abdominal pain.

• immediately postoperatively 0.5 mg/kg Ll.d. for 2-3

da.,.-;, and then
• 0.25 mg/kg Li.d. for a further 2-3 days.
The dosage and frequency of administration should be
based on the intra-operative findings. the demeanor of
Alpha2 agonists and sedatives
Alpha2 agonists are potent analgesics that bind to and
transduce biological effects of the endogenous
catecholamines epinephrine and norepinephrine.

207
11 COLIC
Recently, alpha... adrenergic receptors have been phar­
macologically characterized into four subtypes
• alpha.a
• alph�b
• alpha2c
• a!pha..,d.
The alph�a and alpha2c receptors are abundant
throughout the eNS and are coexpressed in some sites,
where alphatbs are absent in the brain.
The sedative and analgesic properties of adrenergic
receptor agonists are the result of inhibition of the nOf­
adrenergic input to the hippocampus, thalamus, the
cerebral cortex, which results in behavioral depression
and reduced sensory processing. The central alpha�
adrenoreceptor stimulation thereby modulates the
release of norepinephrine and causes direct inhibition
of neuronal firing. In many cases of postoperative colic
one dose can result in permanent relief of abdominal
pain. Visceral analgesia produced by xylazine at
l . l lllg/kggiven intravenously issimilar to that produced
by opioids and flunixin. however the duration is shorter
( 1 0-40 min). Bradycardia, decreased cardiac output,
hypotension. ileus, and reduced blood floware all poten­
tial side effects. Prolonged effects of xylazine can often
be accomplished with 0.4-2.0 mg/kg intramuscularly.
Detomidine is an alpha2 adrenergic agonist like
xylazine and has profound analgesic and sedative prop­
erties. Similar to xylazine, its actions are centrally medi­
ated. It can completely alleviate signs of colic for up to 3
hours. When compared to flunixin. or butorphanol.
detomidine had 5uperior analgesia. In fact. analgesic
effects can be sufficiently strong to mask an ongoing or
new lesion. The comfort of the clinician in administer­
ing detomidine is often much higher postoperatively
fo!Iowing explordtion of the abdomen than when
attempting to decide ifa patient is a surgical case. Along
with the intense analgesia provided with detomidine.
reduced intestinal motility occurs along with reduced
cardiac output and reduced blood pressure. Other side
effects include sweating. salivation, and snoring.
Opioids
Opioid refers to all drugs. natural or synthetic, that
bind to opioid receptors and exert morphine-like
effects. Classification of opioids is based on a functional
breakdown of activity at opioid receptors. Therefore,
they are classified as agonists, agonist.�-antagonists
(mixed opioids), and antagonists. Opioids exen their
effects on the central nervous system in both the spinal
cord and brain. Antinociceptive pathways are present in
the eNS that descend the spinal cord and prevent
ascending pain-carrying tracts from completing their
208
route. First order neurons are prevented from releasing
excitatory neurotransmitters because of the pre- and
post-synaptic effects on the dorsal horn. Opioid ago­
nists or agonis!S-antagonisl� are helpful in controlling
colic. Pure agonisl� such as morphine are potent
analgesics but they can also cause eNS excitation.
Furthermore, morphine is known to reduce progressive
motility of the small intestine and colon, while poten­
tially increasing mixing movements and sphincter tone.
These concerns often discourage its use in the post­
operative gastrointestinal patient.
Butorphanol is a partial agonist and antagonist
which prmides the most analgesia with the least side
effects. It has been reported to be superior for visceral
analgesia compared to f1unixin but not as efficacious as
the alpha2 agonists. When used in combination with
xylazine or detomidine excellent analgesic effect.� can
be maintained. The dosage postoperatively is usually
0.05 mg/kg to 0.1 mg/kg intravenously. Butorphanol
does reduce small intestinal motility but has no effect
on the cardiovascular system except at higher doses.
Lidocaine (lignocaine)
It has been hypothesized that lidocaine alters sympa­
thetic tone to the bowel by suppres�ing trdnsmission
through afferent sensory pathways. Experimentally
serosal damage. intestinal distention, endotoxemia,
peritonitis. and surgical manipulation have al! been
associated with enhanced sympathetic stimulation.
Lidocaine may prevent reflexive inhibition caused by
one or several of these factors by blocking lransmission
through afferent nerves. These factors have been docu­
mented to increase the release of non-adrenergic and
non-cbolinergic neurotransmitters with alteration in
motility in rats and dogs. Lidocaine may inhibit the
release of neurotransmitters rather than alter sympa­
thetic neurotransmission. None the less, clinical effects
in reducing postoperative ileus and pain have been
reponed in the horse. The dose rate reported is an
intravenous bolus of 1.3 mg/kg given slowly followed by
0.05 mg kg-I min-I. Side effects that may be produced
include muscle fasciculations, ataxia, delayed detection
of laminitis pain and potentially increased incisional
infection rates.
CONCLUSION
Proper postoperative pain management and successful
alleviation of pain is critical in minimizing patient mor­
bidity. Pain increases patient risk during anesthesia
because of the larger amounts of drugs required to
maintain a stable plain of anesthesia. Pain enhances the
 POSTOPERATIVE TREATMENT AND COMPLICATIONS
inflalnmawry response, this in turn increases the pro­
dunion of pain neurotransmitters which further raise
Ihe inflammalory response resulting in an elevation in
the excitahility of sensory neurons. Pain produces a
depressed state, increases inflammation, reduces wound
ilt'alillg, and depresses the immune response.
Pharmacotherapy should be directed at peripheral noci­
ceptofs, primary and secondary spinal neurons, and
pain-proclC'ssing areas in the eNS. These areas include
"pioid receptors, drugs that bind to alphat reLeptors,
and drugs that reduce df! IIIlVD prostaglandin synthesis.
Based on the intraoperative procedures done in
..ach horse, appropriatlC' analgt·sia should hI:' provided
in Ihe perioperative stages. Preventative pain manage­
mellt should be instituted before progression ofdinical
sigm occurs postoperatively in these horses. Often
early, subtle signs of pain lIlay be overlooked. Early
diagnosis and tn�atment of abdominal pain decreases
overall patient morbidit), and the cost of patient care,
thereby allowing tbe clinicians' tilile to be better spent
on illore productilie endeavors.
Ab dominal a dh es ions
SL Fubini
INTRODUCTION
'Adhesions are both the salvation and the bane of the
abdominal sUIgnm' (editorial, Th� I.anal,July 5, 1980).
Formation of a fibrous union beh,'een serosal surfaces is
esselltial for a successful completion of abdominal
surge!)' sucb as an intestinal resection. Howelier,
unwanted adJ:Iesions are responsible for RO-90 per cent
of intestinal obstruction in humans. Adhesions are also
a grave prohlem in urogenital surgery and are responsi­
ble for the frequent failure of infertility surgery' in
WOllle11. Pathological adhesions arc the most common
reason for deatb and repeated episodes of abdominal
pain after small intestinal surgery in horses, There is
speculation in the veterinary literature that the percent­
age of 'symptomatic adhesions' is higher in the horse
than other species. With sucb a high prevalence of
adhesions in humans and hors�s, it is possihle that
studies focusing on adhesion prevention in bumans
could be applied to the horse a'pd vice liersa.
INCIDENCE OF ADHESIONS
It is virtually impossible to aecurately determine the
incidence of postoperatilie adhesions in horses because
11
so many animals are managed medically, remain
asymptomatic, or die or are euthanized without an
examination, Estimates of the incidence of adhesions
are taken from reports following repeat celiotomy and
necropsy, or from experimental studies. Adhesions
were the second-most common (18.9%) reason for
repeat laparotomy in one study, All the horses that had
obstructing adhesions at the second surge!)' had a
small intestinal lesion at the first surgery. Other
reports documenting the incidence of adhesions in
horses following small intestinal surgery range from
6--22 per cent. and 5 per cent follov"oing all equine
intestinal surgc!)'_
It may be that the smali intestinal serosa is more
prone to damage from distention, ischemia, and manip­
ulation. Furthermore, the multiple loops of the small
bowel with its long mesentery' and relatively small
lumen make it more likely to become compromised
from adherence to acUacent loops and subsequent
mechanieal obstfULtion. Other risk factors include
borses that require repeat celiotomy, deyeiop peritoni­
tis, or have prolonged ileus.
There is speculation that adhesions are more com­
mon in foals and Miniature Horses than in adults.
However, without specific, controlled studies concrele
conclusions cannot be made.
PATHOPHYSIOLOGY
Adhesions result when there is an imbalance between
fibrin deposition and fibrinolysis. Trauma to the vis­
ceral or parietal peritoneum results in an inflammatory
response and rdea�e of mediators including histamine,
serotonin, prostaglandin E�, and cytokines causing an
increase in capilla!)' permeability and extravasation of
protein into the abdominal fluid. The tissue inju!)' also
resulL� in release of tissue thromboplastin which acti­
Y<ltes the intrinsic coagulation ca.�cade. This set� the
stage for fibrin deposition bet\veen adjacent surfaces,
Concurrently the fibrinolytic system is activated by tis­
Slle plasminogen activators released from inflammato!>'
cells. Plasminogen is converted to plasmin which, in
turn, lyses fibrin,
This delicate balance is maintained by pla�min (con­
verted from plasminogen), antithrombin III, and pro­
tein C. In altered disease states such as the preselln� of
ischemic bowel or peritonitis, there may be alterations
in these regulators. Antit.hrombin III and protein C
both halie activit)' against coagulation factors. Protein C
also inactivates plasminogen activator inhibitor-l
thereby promoting fibrinolysis. The prima!)' inhibitors
of fibrinolysis are plasminogen activator inhibitor-I.
which prevents the formation of pla�min by inactivating
209
11 COLIC
tisslle plasmi nogen ac.:livlI[Of, and a[ph�-antjplasmin
I,"hkh inaClh�dU� plasmin.
If Ill(" (!lId re.\ult is 311 imrainncllt in fibrinolysi.�,
(hen fibrin()l1� bands become infihrated "llh fibmblasts
whi.-h produn� collagen and a potcntially pt-'ommelll
arlht"�ion. This proccs.� is usually complete by 7-14 clays
Imt lhcn: may I)c rcnwdding 0\"1:( lime:.
EXPERIMENTAL MODELS OF
ADHESION FORMATION
Unfortunately. there is om one completely repro­
dudhlc mudd for adhc�ion production. Over the years,
(�J(p{:rim(!ntal sludic� haW! used either lllodels where
scr(ls<ll trauma i� cn:alC,d or an ischemic insult is
simulated. Typicl1l1)' hthnratory animals arc used and
hrcausc of the diffcrt:nr pathways involved extrapola­
tion !xtwccn species is questionable.
Traul1nuic models include abr.L�i()n oflbe serosal sur­
facCli or p<:ritoTlcum , serosal drying in the presence of
fr�h undolted blood, intcninal di.�tcnli{)n, and sutur­
ing of peri toneal or serosal defecL\, Ischemic models
include it combination of arterial and venOllS occlusion,
or a cI;unping of the intestinal or uteline wall.
SURGICAL PROTOCOL
i
Adherellce to the surgical prlll:ipies of minimizing
'time, tmuma. ltnd nash' is the best way to decrease the
Ji\k of p').�topcratlvc adhe.�ions. Short, efficient surgical
times, "'Iith gentk tissue handling, strict adherenre to
,1\{�ptir t{'(:hniqllc, and minima! foreign material left in
the abdomen i� ideal. Expo.�cd mucosa, drying of the
seTOS", and ischemic tissue all increase the risk of adhe­
sions. SnUle �urgcons adl'ocate omentectomy for adhe­
sion prevention. Horses should be on broad-spectrum
antibintics and non-stcmidal anti-inflammatory drugs
perioperativc1y if abdominal contamination is antici­
pated. Thcrap!:lltic regimens can he aqjusted after
surg(:I1'·
ADHESION PREVENTION
I" a I"el'it:l" 4tnick in 1991, Pijlman 1'1 aI. dc:scribcd 'five
fund:un('nlal attacks' lor ildhcsiun rr�l�ntion first
describc.'d by Bo}'� in 1912, these <Ire Mill thc basis for
t:urrt'llt ildhcsion s!Udies. nlc categorie.� arc 10
• limit or prc'l'Cnt rx-riwneal injury
• rren'lU c'!I<tgulation ofs(;rous exudate
• J"Cmov(' or dissol ve the deposited tibrin
210
• keep the fihrin-coatt:"d peritollea! surfaces apart
• inhibi t the tihrobla.uic proliferation once
csuhlished.
Th� c:alcgmics call be regrouped into four di\i!;iolls.
Hetiur.liQn ofthe injiammntmy 'IJ"uu,n
Dt:c:rcasing peritollC"dl inflammation is best done by
adhering W a.�t'ptic and atrdumatic surgical pr-inciple-s.
I t also hclp.� In avoid dC»iurc of the peritonea! defect ;IS
thi� has been �hown tn i ncrease:: adhC'..sions. One recent
study adl'ocates ptl!'lwpcratil'c pcritonc<l1 lamge <IS a
mechanism to remol'e fibrin that tmps b<lcteria, thereby
preventing peritonitis and subsequent adhesion forma­
tion.
TherdpeU!ic: agents that have been �tudjed as anti­
inflammatory agentq indudc
I . Corticoste roids - studies in laboratory animals arc
poorly controlled and are cOntroversial. Repeated
corticosteroid use is nOI r�ommcndcd in the horse
became of the risk 01" lamini tis and the possibility of
a ncgati\'(' impar.t on wnund healing.
2. NOIH[('roicla\ anti·inflammatorydrugs ..... these are
muli ncly used perioperauvely in horses undergoing
abdominal surgery. Again, sludies in Iilboratory
animals ha\"(� nOI been ctmcillsive.
Inhibit;,,,, ojwnguffllivn
Heparin, a cofactor of antithrOmbin Ill. has �n used
dinically and in one e7t.perimental �tlldy for arlhesioll
prevcu lion. In theory hcparin decrca.';-('s thrombin pro·
duction and �timulaw5 plasminogen :.<Clivdtor activity
which promote5 fibrinolysiS. There is not a consensus
on dosage or route of administrdtion of heparin
(reporLS I'llI"}' from 10--120 [u/kg q. 6-21 h), but it
needs to be administered at the time of �urgery.
Heparin therapy may cause agglutination of red blood
cells :.Ind a drop in packed cell volume.
Enhanunvml ojjibri7/o!-)l"i.\
Studies using plasminogen aCtiv:.ltors including fihrino­
I�in, $trep[okif)a�e, ann urokinase were varied and
inconclusive. More recently, ti�me-type plasminogen
activator appears to be effective and safe in rat� and rab­
bits. FUr/her .�Iud ies are needed and the cost of [he
product is high.
SeparaJ;OIl oflur/al'.l
High molecular "'Ieight substanccs and ph}"Sical barriers
hal'� been used in the peritoneal cavity kcep fibrin­
to
c.overed surface., apart long enoughto allow ror
mesolhelial repair and to pn:vent ad hesions. Sodium
c;uboxymelhyl cellulOSe (SCMC) h� been used most
fommonly in the horr.e a., a 1 % solUTion at a doSt' of
 POSTOPERATIVE TREATMENT AND COMPLICATIONS
7 ;ljkg. It is used to coat serosal surfaces and to help
protect the bowel during intestinal manipulation.
Polyvinylpyrrolidone, dextrans, and hyaluronan are
othn polymer solutions thal have shown some promise
t'xp(�rimentally. For more details on these and physical
barrkrs, see Southwood and Baxter ( 1 997) and
Chapter JO.
ADHESION TREATMENT
Horses with evidence of partial obstftlction (Iow-grade
abdominal pain) may r('spond to medical management
induding demal work and a laxative diet such as
pasture or low-residue feeds.
In some cases of adhesions, euthanasia may be indi­
caled. In other instances, repeat celiotomy with
adhesiolysis and/or bypass of the affected segment may
be successful. Unfortunately, broken-down adhesions
ar{� highly vascular and may re-form unless the involved
tissues are resected.
The long term sunival rate following repeat
celiotomy is poor. Hopefully, as our peri- and intra­
openttive anesthetic and surgical knowledge advanc('s,
so will our understanding and ability to prevent cala­
strophic adhesions.
I leus
P Rakestraw
DEFINITION AND INCIDENCE
lIeus is the impairment of aboral transit ofga�trointe�t.i­
llal contenL'i. The term has been uscd in dillerent ways
in the equine literature, sometimes vel;' broadly to
include both functional and mechanical obstructions,
and sometimes its use is limited to functional impair­
ment of gastrointestinal transit. In this chapter the
author defines the term ileus as a functional obstruc­
tion (adynamic ileus) of aboral gastrointestinal transit.
Ileus is one of the mOSl commonly encountered
complications of equine gastrointestinal surgery. In
ho!"SCs, postoperative ileus (POI) occurs predominantly
after correction of lesions involving the small intestine.
POI may also be seen after correction of ascending
colon lesions, primarily large colon vohulus. Traumatic
handling of the intestine, inte�tinal di�lention, resec­
tion and anastomosis, and intestinal ischemia may con­
tribute to ileus in these cases. Other conditions that
havc been associated with ileus are anterior enteritis,
11
peritonitis, electrolyte imbalances, endotoxemia, and
anesthesia. In a recent report, POI developed in 21 per
cent of horses undergoing surgical lreatment of colic,
and 1 3 per cent of these cases dicd. Although current
management of these cases has improved, postopera­
tive ileus is still associated with 40 per cent of all post­
operative deaths in horses "'�th colic.
PHYSIOLOGY OF NORMAL MOTILITY
Inteslinal smooth muscle cells demonstrate cyclic
changes in membrane eIf'ctrical poto:"lllial that are
called 'slow waves' or 'pacesetter potentials'. The
smooth muscle cells arc connected to each other by gap
junnions which enable the electrical activity of one cell
to affect the activity of an adjacent cell (electrical
coupling) through the movement of ions. Since the
frequency of the membrane oscillations is highest in
proximally located cells. thesc slow waves are initiated
orally and propagated aborally. They are sub-threshold
in that they do not depolariLc the ceIl sufficiently to
reach the threshold to generate an action potential.
111ese sub-threshold fluctuations afe controlled primar­
ily by inlrinsic properties of the smooth muscle cdls.
Additional depolari7:ing (excitatory) input from the
enteric (intrinsic) or autonomic (extrinsic) !lelVOUS
system allows the memhrane to reach the threshold
potential necessary to generale an action potentiaL
'Spike potentials' or spiking activity refer to membrane
fluctuations which exceed the depolariLation threshold
for an anion potential �o are associated with muscle
contraction. Spiking potentials are usually super­
imposed on slow waves since at the peak of slov,' \\�a\'e
depolari/.ation the cell is closest to its threshold for
generating an action potentiaL This is why slow waves
are also called pacesetter potentials.
The activity level of the intestinc is not constant bw
goes through periods of quiescence alternating with
periods of spiking activity. The pattern of these difkr­
em activity periods in the stomach and small imestine is
called the migrating myoelectric complex (MMe).
There are four phases of the \-fMC
• phase 1 describes a period with no spike potentials,
so no contractions occur
• phase 2 is a period of intermittent spike potentials
• phase 3is associated with regular spiking activity
• phase 4 is associated with rapidly diminishing
contracliie activity.
Each phase migrates down thc stomach and small intes­
tine. Phase 3 is generally associated with propulsion of
ingesta, and in the horse phase 2 has also been associ­
ated with propagation of ingesta. In the cecum and
211
11 COLIC
. vcs and spiking aCliviry aIm
large: int("�tjnc. �()W \\"J
occur. H,\\,'c\'CI' M�1C:' arc no. evident. Instead. short
spikt" bursts (SSB) occur during mixing, and long spike
hurm (L5B) rluring pl'Opulsioli ofingcsla.
PATHOPHYSIOLOGY AND
THERAPEUTIC MODIFICATION
It should he e\;nclll from the above description of the
ph)'si{)k�1 of norma] m()tility [hal mallY different rae­
LOrs must he pr('ci�dy coordinated in order to produce
!)I'OdUClive mOlility pa\terns. The intestine must (011-
tract in a CO(lNlinaled manner, while the aboral s.cction
is simuhalH�olLsly inhibited and relaxed to allow pro­
gressive Iran�it to OCCIir. An imbalance in Ihe Eu:tors
conlmUing eXcitaTion and inhihition of gastrointestinal
Iran .smnmh muscle may pn:disposc a horse to ikus.
Cons('qucmly. an attempt ha... heen made to identify
prokint'lic agc-n.. t that wnnld restore the halance
1>('t\\'l'l'n cxduuo!')' and inhihitol)' control of (lmtractil­
ity. Ph,U'ltlaco[ogical modulation aimed at int:rcasing
I');c.llator), <lc.lt\lty has principally inmlvcd Ih� adminis­
.
trUillll HI' par.t'ympathomim�ti(: ag�nl.�,
hClh<lm:cnl or Ilco:"tiglnjnt:. whic:h inne<lSC cholincrgic
Iransmis.�ion. Similarly, cli'<Ipride ....urh as ::In indiTl..'Ct
p<uas)1TIpa[homim('tic h�' �timuhlting serotonin rccep-
10-:'
1 and so cnhandng acetylcholine rc:l�dSC. Aucmpls
In hind, inhihitm), components or contractilily ha\'e
r(lctlSI� (.In the ...ympathctk !ir�tem. S)111pathelic hyper­
act"'i1r shoulct re�pond In alpha adrenergic block.ers
such iU )�)himhlne lind acepromaJ:ine. while adminis­
tration of alpha adrenergic druhT); such as "ylal.ine and
dctomidinc sh(Jultl dt:creasc motility. Metodopramide,
\\'hirh is <In1idopaminergir. among other propcrtie�,
and mJll·str:r()itlal allli.illflammat(H), drugs have also
h('en used 10 intt'ryr:m: ill ilem cases.
DIAGNOSIS
Disruption of propulsil'e motility rcsull� in Ihe seques­
[rati(111 of fluid. gas, and ingesta in the _�egment of the
gasLroint�sliL1al {(';iC! which is dr;fullt:tional and in the
iIHC'stinc proximal m the ahnormal arca. Thi� disten­
lion OC(:UI"!\ primaril)' in Ihe stomach and small intC'5-
lillt', but tan ()<:C.ur in the larJ{c inlt"Sline. especially with
(olilis, enrlotu)(emia, or iKhemia following a large
n,jon �·tJh11111S. The Imljor dinical signs and findin�
secn ill ht)J�'s alTerted by p(lstoperative ileus arc
• rieprc$Sio tl
• anorexia
• aMominal pain
212
• decn:a.'lCd or ah.�ent borblllJ'gmi
• abdominal (Ii�tention
• elcvillCd heart nile
• congeslerl mul,,()us m�mbranes
• prolonged capillalJ' r(.'fiJl time
• na�astric rellux.
11le first signs .....O«Kiatcd
. wllh ilelL'; are riepft's..'liun anri
anor(:)(ia. A� the inlt'stillt! distends the horse demon­
strates inaeasinp; .�igIlN or abdominal distn�ss such a.\
pawing, flank watl:hing, lying down, and rolling:.
Borbor')'gmi arc u.�uaHy dC<:rt:a.�t:d or ahsent.. The hear!
ratc is initiall> Cle\'a!ed becal\�e of the pain associated
'
with t.he distf"nlion. '1'11(: mucous memhranes hccollll'
discolored and capillary refill [ime is prolonged.
Hernoc(JI\cemratio!l is rdIcClcd hy iJl(:rf"<ls(:s ill the
packed c:dl volume and tot.al protein. Decreases in
plasllla (:hloride and potas.
�illm are the most comlllon
electrolyte ahnormalities seen, although sodium and
calcium may also b�� low. As the �everity of the intesti­
nal distention illcl'east's, abdominal distention may
become gro�[r visihle. Rectal examination will help
determine if the small or large imestine is illvolw'd. In
foals, hmh <lbdominal radiograph)' and ultrasO!ln­
such ..., grnphy can be quite hdprul in asst'Ming distention. In
adnlts nast'lgastric decompre�sion orten relrit'\'I_"S 3--1 0
li tt'1'S of IIl1iC\. Tht.' response t o nasl>K'''t'� ric del'omprcs-­
sion provides all important due that Ihe problt:m is a
functional prohlem. Arter decompressiull the horse
should show some improvement such ...� (kcrca.�ed
pain and ht:arl "Ue. Ir no alle\-latioll of signs are
observed, cart:ful lhllught should he gh'en to {he likeli·
hood that the problem may he a mechanical It'Sion
and not a functional ileus.
SUPPORTIVE THERAPY
Although a varll:IY of prokinctir agent.� have hl'en
administered {() hones with ileu� in an attempt to
improve gastrointestinal motility, th(: lack of consenslls
as to which OIlC, if any, are effcctive attests to th�ir
therapemk limitatiolls (Table 1 1 .4) Consequelltly, th�
hallmark ofLreatmc-lIt remains supportive therapy, with
fluid, add-o<lsc, and electrolyte therapy being rnm!
important trCattnenl� In ally hor:t.c with ..olie
Antihiotics are also indicated ir there is compromised
inte.�tine or the pos.�ihility or har.ll'rial ('onlamination ,
CautilJll should be exercised whcn lreating lhesc horses
with the common analgesics (snch as the alpha <ll(onistJ;
")·!<I.,.ine. dClOmidine and romifidinc, and the narcotic­
agonist-antagonist butorphanol) a� these medications
have the potential 10 depress ga�ll'()inlestinal motilit}'
with n:pcatcd usc.
 POSTOPERATIVE TREATMENT AND COMPLICATIONS
TIIbtt 11." Trutments and InInltgelTlent of
postoJMrativeUeus
Fluid, acid-base, and electrolyte therapy
Antibiotics
Nasogastric intubation
Non-steroidal anti-inflammatory drugs
flunixin meglumine
phenylbutazone
ketoprofen
Polymyxin B
Dimethylsulfoxide
Hyperimmune serum/plasma
Prokinetic agents
bethanecol
neostigmine
acepromazine
yohimbine
erythromycin
metodopramide
cisapride
lidocaine
NASOGASTRIC DECOMPRESSION
Rt'pl'ated attempts to relieve gastric distention are
imperative in trcating a suspectcd ilcus case. In certain
(a.,e� reflux may not he obtaincd during thc first
allemp!. In horses \"hcre nasogastric reflux is obtained
the tube can he left in place or reliloved and intermit­
t"'lltly replaced to check for reflux. Tlw frequency of
attempting to decompress a horse with reflux depends
both on the dinical signs and the amount of reflux
Idrit-ved at each session. An increa�ing heart rate is
prohably one of the most sensitive clinical indications to
allempt to retrieve reflux. Increasing abdominal pain is
another indication. As the volume of reflux begins to
decline and reaches less than 1-2 l/h, the interval
h(,tw('en reflux attempts can he increased. It is not
l!llusual to ohw.in a liter or more per hour of rdlux frolll
horses, especially those who have:l nasogastric tube left
in place. This should not be mistaken as a condition that
lll"Ccssarily requires continued tr�atment. II" there is any
doubt, the tube should be withdrawn and the horse's
hean rate and level of pain monitored closely.
ANTI·INFLAMMATORY
'ANTI'·ENDOTOXIN DRUGS
Int('stinal distention, ischemia, and trauma occurring
dllrillg decompression and/or resection and anastomo­
sis all induce inflammation of the bowel wall with an
11
increase in the production of inflammatory mediators
such as prostaglandin 12and Et. and tumor necrosis fac­
tor. Endotoxin can also stimulate production of these
mediators. Each of the�e inflammatory lIlediators has
heen shown to depress motillty when infused experi­
mentally into horses. Consequently non-steroidal anti­
inflammatory drugs are recommended for horses with
gastrointestinal inflammatioll that have ileus or arc at
risk of developing ileus. The most commonly used
NSAID is flunixin meglumine (0.25 mg/kg t.i.d. i.v. or
l . l mg/kg h.i.rl. i.v.). It alleviates some of the systemic
effecL� of endotoxin and also provides some analgesic
relief. The other comlllonly used KSAID is phenylhuta­
zone (2.0-1.1 rug/kg h.i.d. p.o. or i.v.). Although this
drug is not as potent as flunixin in blocking the cardio­
vascular efICcts of endotoxin, it does appear effective in
reducing the motility disturbances associated with
experimental endotoxin infusion. Ketoprofen (2.2 mg/
kg h.i.d. i.v.) has not been evaluated in ileus models,
however because of its anti-prostaglandin and anti­
IcukO!ri{�ne actions, it lIlay also be effective in promot­
ing motility. In addition to blocking cndotoxin effccts,
thc analgesic propertics of these drugs may attenuatc
potential inhibitory sympathetic reflexes. High dosages
and prolonged use of NSAID may inhibit. large bowel
motility.
Another drug that is used at the author's hospital to
treat horses with ileus is polylllyxin B (6000 IV/kg s.i.d.
i.v.) a cationic antibiotic that binds lipid A ,md neutral­
izes endotoxin. Dimethylsulfoxide (DMSO) is a
hydroxyl radical scavenger commonly used to treat
endotoxemia and other inllammatol}' processes in
horses at a dosage of 0.5- 1 . 0 g/kg (10% solution i n 5%
dextrose). Although it has not been evaluated relativc
to promoting gastrointcstinal motility, its anti-inflam­
matory actions may be bendkial in preventing or
decreasing the scverity of ileus. Commercially available
hyperillllllune serum contains anti-I.PS antibodies to
Elrlil'ril'hia loli or Salmonella Iyphimurium. These anti-LPS
antibodies theoretically cross react \\ith endo[Oxins
from all gram-negative bacteria. The evidence for their
efficacy has not been conclusivc.
PROKINETIC AGENTS
Bethanecol
Bethanccol chloride is a muscarinic chdlincrgic agonist
which stimulates acetylcholine receptors on gastro­
intestinal smooth muscle. causing them to contract.
Support for the use of bethanecol in the treatnlt'Cnt of
motility disorders in tht� horse is predicated on ohserva­
tions in normal horses that it increases the rate of
213
11 COLIC
gastric and cecilI emptying as measured by radiolahded
isotopes, and it induces premature MMC phase 3-likc
activity in the ileum. Although its eflicacy in the treat­
ment of experimentally induced mO(.ililY dysfunction
has bet�n questioned in the horse and other species, its
prokinetic effects in normll! horses and the clinical
impres.�ion of its benefit in treating horses with ileus
.�llppons it� usc in the treatment of certain gaslro­
illlcstinal motility dysfunctions such as POI and ceca!
impactions. The recommended dose is 0.025 mg/kg i.v.
or u:" (wry 4-fi hours. The most common side effect of
!he drug is salivation, with abdominal cramping and
diarrhea occurring les.� frequently.
Neostigmine
Neostigmine methylsulfate is a cholinesterase inhibitor
which increases the level of acetylcholine at the synaptic
junction. In studies on normal horses the effects of
neostigmine (0.022 mg/kgi.v.) varied depmdingon the
location of the ga�trointestinal tract examined. It was
shown to delay !fastric emptying and decrease propulsive
motility in the jejunum, to increase propulsive motility
at the pelvic flexure. In another study, neostigmine
increased the amplitude of rhythmic contractions in
both resting and distended jejunum in anesthetized
ponies. More recently, neostigmine (0.025 mg/kg s.c.)
wa.� shown to induce premature phase 3-like activity in
the ileum ,Uld increase the rate ofcecal emptying. There
has heen no consensus as to the recommended use of
this drug. It appears to be an effective drug for large
colon motility problems, but these OCCUI" infrequently.
Some evidence suggeSL'i it Illayalso be useful for POI with
small intestinal motility dysfunction. I Iowever, its usc for
impactions or in cases with excess gastrointestinal dis­
tention has not been recommended because of the
apparent force of drug-induced contractions. The most
COillmon side effect is ahdominal pain.
Acepromazine and yohimbine
Both of these drugs arc alpha adrenergic antagonists.
Elevated serum catecholamines have been associated
with increased synthesis of norepinephrine in the bowel
wall in humans after laparotomy. :\orepinephrine is an
inhihitory neurotransmitter released by post-synaptic
sympathetic Ileurons at the enteric ganglia. It inhibits
the relea.�e of the excitatory neurotr.lllsminer acetyl­
choline by stimulating alpha-2 receptors located on
cholinergic neurons. Acetylpromazine maleate (ace­
promalinc) facilitates small intestinal transit in normal
ponies. Rased on clinical impression. acepromazine
(0.01 mg/kg i.m. q. 4 h) is thought to reduce the sevn­
ity of POI in horses with small intestinal lesiom. Care
.�h()u!d be taken 10 make Sllre the horse is well hydrated
214
as the drug can produce hypotension. Yohimbine
administered at 75 Ilg/kg was demonstrated to attenu­
ate some of the negative effects that endotoxin has on
propulsive motility. Since this dntg is a seJectiw alpha�
antagonist it docs not produce the hypotensive
response seen with acepromazine.
Erythromycin
Erythromycin is a macrolide antibiotic that enhances
gastrointestinal motility by acting on motilin receptors
on smooth muscle, and by acting on enteric neurons
through motilin and/or 5-HT� receptors to stimulate
the relea�e of acetylcholine. It is a commonly used drug
to treat gastroparesis in humans. At 0.5-1.0 mg/kg in I
liter of saline infused over 60 minutes four times daily.
the drug induces small int.estinal phase 3-like activity
and increases the rate of gastric and cecal emptying in
normal horses. Side efl"ccts are infrequent but some
clinicians have reponed obse!\ling abdominal pain and,
in a fCw cases, diarrhea.
Metodopramide
Metodopramide is thought to exert its prokinetic
actions primarily though dopamine receptor antago­
nism. It mily also indirectly stimulate acetylcholine
release and block adrenergic activity. In a POI model,
metodopramide was more efl"enive in restoring gastro­
intestinal coordination, a measurement of motility
strongly correlated to return of normal transit, than
adrenergic antagonists or cholinergic agonists. In
horses the drug is commonly administered al a dosage
of 0.25 mg/kg, diluted in 500 ml of saline, infused over
30-60 minutes. Some evidence suggests that a continu­
ous infusion (0.04 mg kg-I h-I) may be more effective.
Metodopramide (especially at the 0.25 rng/kg dose)
may cause extrapyramidal side cffecb such as excite­
ment, restlessness, and sweating. It may also produce
abdominal cramping.
Cisapride
Cisapride is probably the most commonly used pro­
kinetic in human medicine. It appears to function a� an
indirect cholinergic stimulant by .�electively enhancing
the relea�e of acetylcholine from postganglionic oen­
rons in the myenteric plexus. In numerous trials in
other species cisapride appeared more effective than
metoc\opramide in stimulating progressive smaIl and
large intestinal motility in experimental ileus models. It
has also been shown to be effective in prcvcnting POI in
horses. Unfortunately it is only available as an ofal
preparation which is ullsuiLable for horses \'I1th reflux.
Recently it was found that the drug is not absorbed in a
 POSTOPERATIVE TREATMENT AND COMPLICATIONS
consistent manner rectally ill horses and so this route of
Mlministration should not be rdied on. Lse of the oral
preparation in horses with large colon motility dysfunc­
tion may be efficacious. The bioav:aiIahility of the oral
preparation in the horse is not as good as in humans
and so the recommended dose is 0.3-0.4 mg/kg.
lidocaine (lignocaine)
Lidocaine hydrochloride has four proposed mecha­
nisms 01 action. It may
reduce the concentration of circulating
fatecholamines by supprcssinll; tht>
svmpathoadrcnal response
�. suppress activity of the primary afferent neurons
imol\'ed in reflex inhibition of gut motility
3. stimulate smooth muscle directly
4. decrease the inflammatory response.
Tlw dose used to treat horses is an initial holus of
1.3 mg/kg i.v. administered over 5 minutes followed by
(J.U} mg kg I mire' in saline over 24 hours. Side effects
include muscle fascicul:ations, trembling, and ataxia.
PROGNOSIS
It is the author's impression that the incidence of POI is
decreasing. This may be because of more timely refer­
r<lls and improved anesthetic, surgical, and medical
management of the high risk cases. \Vhen ileus docs
O("(.Ul". the horse is ohen treated with different pro­
kinetic agents depending on \'I,'hich clinician happem to
tah� care of the horse. This author prefers to use lido­
caine in ca�es with significant small intestinal inflamma­
tion as the first prokinetic followed by erythromycin.
Ilowe\'Cr, the author ha� seen other clinicians usc all of
the prokinetic :agents discussed above. It is likely that
each of them will promote motility toa limited cxtent in
certain cascs, but nonc of them will dramatically increa�e
progressive motility in tht'C horse with ilcus. However, it
is also the author's impression that with appropriate sup­
portive therapy the ileus will most likely be transitory and
r{'so]ve in 2-6 days. In cases where it docs not respond,
a serond laparotomy may be indicated.
I mp action at th e anastomos is
P Rakestraw
Impaction at the anastomosis is an uncommon surgical
complication. In one repoft, 53 of 648 cases treat.ed
11
surgically for acute gastrointestinal obstruction were
suqjected to a repeat celiotomy. Only 3 (5.5%) of these
53 repeat celiotomy cases had impaction at an anasto­
mosis. When they occur, they are often associated with
too rapid an increase in the amoum of food ofkred to
the patient in the postoperative period. Although some
cases of 'ileus' may actually involve impactions at the
anastomosis and resolve vlo'ith fluid therapy and time, it
is often necessary to perform a second laparotomy to
correct this condition.
Impaction at the site of anastomosis of the small
intestines occurs early in the postoperative pcriod, i.e.
day 3-7 postoperatively. For small intt>stinal lesions
without nasog:astric reflux, the author often ofIcrs a
small amount of feed (a handf\ll of alfalfa) within the
first 24 hours <Ind slowly increases the amount fed at 3-4
hour intervals over the next 72 hours. It has been sug­
gested that this early return to feed facilitates the return
of normal ga�trointestinal motility, since withholding
feed can decrease gastrointestinal motility. With small
feed increases and careful monitoring of the patient it is
unusual for impactions to develop. If feeding is
increased too rapidly and an impaction occurs, a sec­
ond surgery may be necessary to massage the impaction
pa�t the anastomosis. In most instances it is not neces­
sary to redo the anastomosis, except if there is a stric­
ture or an apparent surgical errOf with the existing
anastomosis. The author has seen the lea�t number of
problems with single layer interrupted end-to-end
jejunqjunostomies. Two layer closures of endow-end
jejUltojunostomies may potentially restrict relaxation
and dilation of the anaswmosis site as a peristaltic wave
aUempL� to propel ingesta across the anastomosis. Some
surgeons feel that jejunoileostomies arc more predis­
posed to functional problems and therefore are more
likely to lead to an impaction. This is why .i�junocecos­
tomies arc preferred. A large stoma in a side-tn-side
jejunocecostomy minimizes the risk of impaction at the
site btl! has the potential to allow reflux of ingesta back
into the jejunum trom the cecum during cecal contrac­
tions. An endow-side jejunocecostomy may decrease
this reflux problem but because of thc smaller stoma it
may increase the occurrence of impaction early postop­
natively. A compromise would be a '/ish mouth' end-to­
side je:junocecostomy anastomosis.
Impaction at an an:astomosis in the large colon usu­
ally occurs because the stoma which was made when the
colon was very inflamed and edematous has decreased
in size over time. Therefore impaction at the site of
anastomosis of the large intestines occurs late in the
postoperative period, i.e. month 1-3 postoperatively.
Surgical correction is necessary to enlarge the stoma.
The sm:all colon is potentially more susceptible to
impaction at the anastomosis (Of enterotomy) because
215
11 COLIC
of the firm consistency of the ingesta in this region.
These impanions at the site of anaswmosis of the small
colon occur early in the postoperative period, i.e. day
3-7 poslopt.'fatively. V·lith careful management, for
example emptying the large (olon at surgery, fluid ther­
ap)" and slow placement hack on feed (small handfuls
of allall"l ) , these also occur infrequently. As with the
small intestine, it is usually not necessary to redo the
anastomosis unless a stricture or surgical error is
apparent.
It should be remembered that appropriate timing 01
a re1aparotomy may make the difference between a suc­
cessful ourcorne or a f;lilure and should IHl!. he delayed
if the horse is not responding as expected medically.
I ncisional comp l ications
NG Ducharme
INTRODUCTION
Approprhnc lluimp<.'dcd wound healing reSU!L� in sum­
clem sln�ngth in the tissue layers to allow a return to
excn:is(� for the various athletic activities that horses are
expected to perform. The prevalence of incisional (Olll­
plirariolls alter gastrointestinal surgery in horses ranges
trom fi-37 per cenl. The I"arious incisional complica­
tions indudc
• d<'hi�cnC{�
• drainage
• hernia.
Ally incisiollal drainage at an incision is suggestive of
abnormal wound healing. Drainage delays wound heal­
ing and weakClls abdominal fascia.
PREDISPOSING FACTORS
The veterinarian and animal a!tendallt� responsible for
postoperative care of palient� should 1:)(' a\vare of the
i]J{H�;\scd risks 10 animals experiencing incisional com­
piic<ltions. Factors that influence th� occurrence of inci­
sional complications are either
• under the cOlllrol of the surgeon, or
• outwith the control of the surgeon.
Farlors in the former group that surgeon� can control
,!re
• use 01 optimal surgical t�chniques and materials
(sec Chapter 10)
216
• duration of surgery, this should be less than 2 hours
• usc of good perioperative pain control
• length of convalescent period, the horse should be
kept out of training until at least 2 months
postoperatively.
Factors that incretlse the risk ofincisional complications
but are beyond the control of the surgeon are
• open bowel procedures involving the large intestine
• repeat incisions in the same animals
• debilitating conditions such as hypoproteinemia
• stormy recovery
• agf' of (he animal, animals less than I year of al{(·
have a lower incisiona! complication rate than older
horses, perhap� because of the lower weight of tlw
animal or the ability to assist the recovery of tJlt�se
patienl.';.
CLINICAL SIGNS
Acute incisional disruption (dehiscence)
Acute incisional dismption generally occurs withill H
days of surgery tlnd, fortunately, is extremely rare. \:':arly
clinical signs arc brown serosanguinous discharge with
a progressive increase in drainage from the incision.
Palpation of the incision with a sterik, gloved hand
will reveal gaps in the incisional wall apposition.
Ohse!\latioll of omentum at the incision site is a grave
sign of impending dehisccnce. In most cases, physical
examination identifies the diagnosis and extent of the
problem. In some cases ultrasound examination will
assist in defining the extent of the lesion.
Incisional hemorrhage
Clinical signs are obvious in so far as blood is draining
from the incision within a few hours after surge!)'.
using physical examination, the clinician can deter­
mine if the hemorrhage is due to tin arterial bleeder
from the incision, one or more venous bleeders
from the incision, or intra-abdominal hemorrhage.
Incisiona! arterial hleeders have a small stream of hem­
orrhage spurting from the incision while venous hleed­
ers 001:(' out of the incision at one or more sites.
Intra-abdominal hemorrhagc is manifested by moder­
ate to large amounts of blood oozing from one ur more
incisional sites. If there is a high rate and volume of
abdominal hemorrhage, allY of tire following systemic
signs of hemorrhage may be seen
• inci.�ional bleeding
• decreased pulse quality
• blanching of mucous membranes
 POSTOPERATIVE TREATMENT AND COMPLICATIONS
• increased respirato!)' rate
• itKre;lsed heart rate
• illtfa-abdominal pain
• decreasing hematocrit after 24 hours.
III addition. the accumulatjon of intra-alxiominal fluid
{ail he fo!Iowed by abdominal ultrasound.
If excess serosanguinous fluid was left in the
abdomen, or one or more linea alba suturees failed, peeri­
tOlwal fluid will leak out of the abdomen. Because of
tht' dye effect of blood on peritonea! fluid, it may be dif­
ficult to diffcreentiate this condition from intra-abdomi­
nal hemorrhage. However. measuring the packed cell
\'()Iume of the fluid draining out of the abdonwn or col­
len(�d by abdomiuocentesis will diffeeremiate thee two
conditions. I n additioll, ultrasound examination of the
inci.�i{)n will identil)' i!l{:isional defects and increasing
pnitoneal lluid volume, The latter would not be
,'xlwcted to on:ur within a few hours of surgez:·.
Incisional drainage and infection
Any incisional drainage, except perhaps Jill' mild blet�d­
ing it few hours postoperatiwly. should be considered
abnormal and may represent an incisional infection.
The preeseellce of serosanguinous fluid or purulent
drainage should be evaluated carefully, and Olle should
dosdy monitor the degree of peri-incisional sweHing
and tenderness. If a large quantity of fluid drips from
the inci,ion. the possibility of peritonitis and partial
dehiscence of the incision should be considered. ASter
sterile preparation at the drainage site. a sample should
Ilt, obtained for cytological and/or bacteriological
cvaillation.
IncisionaI hernias
Incisional hernias may be .�ec[)!ldaz:' to
• >utun' or abdomina! wall failure in the
po�t[)perath·e period
• incisional infection
• carly return 10 exercise.
Tlw last cauS{' of incisional hernia is ,,'en in horses
tumed out too early after surger.., The strength of tbe
abdominal wall does not return to normal until many
months after surgery. Therefore, horses should be
restricted !O a box stall for 6 weeks postoperativdv,
although daily hand walking should be allowed. The
abdominal incision should be eevaluated prior to turn­
ing the animal out to pasture br an additional 6 weeks.
III the author's experience, alter 3 months tbe risk of
incisional hernia is negligible. A ren�nt report suggests
that a 2-month postoperative incision has suHkielll
strength to withstand normal activity.
11
Two types of incisional h(�rnias can be seen post­
operatively.
1 . A Traditional hernia within t.he incision with a
reducible hernial sac, tbese should he surgicalIv
revised.
2. IIerniation tbat is actually a thinning of selected
areas of the inclsioll. In jumpers and br{)[xi mares,
t.hinning of incisiona1 areas should be repaired
6ther by applying a mesh over tbe arca or by a
complete revision of the incision. Other horses,
eveen racehorses, wir.h unrep,\ired thinning of
incisional areas can be regularly oh<>erved. since it
does not necessarily become a true hernia despite
strenuous athletic activity.
TREATMENT
IncisionaI dehiscence
The treatment for incisional dehiscence is smgical
revision. A belly bandage \',i[h a sterile moist dressing
placed immediately on the incision is applied prior 10
induction of anesthesia. Tbe belly bandage alone \\i!l
not prevent evisn�ration and should not sen'e as sole
Treatment. The principles of tn'atment at surgery are
• debridement of the incision
• bacterial sampling of the tissues.
If thee reason for dehiscence is Etilure of a sutnre mater­
ial, tbeen revision with a larger-sized (greater strength)
suturc call he done. Copious lavage of the im;ision site
with sterile physiological solution containing broad­
spectrnm antibiotics should be performed, If significanr
contamination of the incision is present or the body
wall is the reason for dehiscence of the incision, tben
through-and-through sutures should he used (Figllree
1 1 . 1 ) . St(�el sutures with rubber ste!lls are required in
an interrupted vertical mattress of the incision.
If the horse is too weak and sick for general anesthe­
sia, a plastic mesh (e.g. Proxplast, Goshen Laboratories,
Goshen, NY) can be sutured superficial to the skin over
tbe incision (after local anesthesia). This leads to open
peritoneal drainage and requirees all abdominal ban­
dage (Figure 11.2) for support to prevent dehiscence.
The mesb is removed once a bed of granulation tissue is
present underneath the mesh, but continuous abdomi­
nal support is needed fI)r lIlonths.
Incisional hemorrhage
Wheell indsional bleeding is noted the source of the
bleeding must be identificd, A preswre bandage should
treat incisional bleeding associated with incisional
217
11 COLIC

Figure 11.1 Placement of through-and-through steel Figure 1 1 .2 Equine reusable abdominal bandages being
sutures in the repa i r of incisionai dehiscence applied

" esse! leakage. The o�jc<: ri\'� is to arrest. bleeding by identify m

:. appropria te blood donur (cross·match)
app lyi n g counter pressure. It i.'i i mportant thil.t enough should be initiawd. Intr.d\,CClOlIS fl uid adminislralion
pressHre be applied not only to prc\'t'.n t hlood from rat.(�s should be a{ljusl.ccl appropriatc!r (S(,:(: Chaptn 9
(�scaping the incision, but (�qually importan t) to pre­ Fluid and e1ectrolyle therapy and acid-hase balan n;' ill
\'t'l)t subcutaneous hClnorrhage since it predisposc� horses with abdominal pain). If syswmk s igns of illlra­
i m: isi onal illfection (Figure 1 1 .3). ahdominal bleeding appear to in c rease in severity, th{'
If imra-ahdominal hemorrhuge OCCllrs, it is intravenous administration of 4l lIlino capmi c acid ( to g
t'xtn."l1lt:iy r"n� tha t t.he clinician Il(�eds to (or ::;houici) in !4 liter of physiological saline solution, up to th rt'('
fe-anesrhetize the animal to searc:h for [he hleeder. The tlInts rlaily per 450 kg horse) shou l d be considered.
goa[ i'i (() �'prly sufficient pn:ssuTc to sC<l.i the abdomen
and pre\'en t the horiy's loss of red bl ood (elis. 'A'hcn Incisional drainage and infection
serious hemon"hagt' is prest.'n 1 , hlood vl.'ill soak Ihroug-h
IndsionaI infections arc t reated with approprialt:
rhe bell y handages. Rather than r(�moving the bandage,
drainage, removal of selected skin slIttlfcs/stapl<::5i. and
a seculid layer can he applied with mOTe press un:. If this
topical cl eaning and lavage of {he.: i ncision . Sysl('mic
s to ps the hemorrhage or reduces it to a slow d ri p, the
antibio tic.s wmally have alread y been administered a t
hll:ndages can be left in place for G-8 hours. If th is dDe�
the time i n fenions uccur hut may need LO be changed
not stop rhe hemorrhage , the inner handll:ges must he
according to hacH'rial rulturc results. It is import.am to
tuo loose and should be rese!.. On recognition of
remember that incisional infeclions i nc rease tbe risk of
abdominll:1 hemorrhage, any he parin therapy alrt'ady
incisional he rniation from f()ur- to ninelcenfolrl.
initiatt:d should be clisrominued and preparation (0

Incisional hernia
Surgical repai r of a hernia is made either by primary
rtpair or placement of a mesh. Prior to repai r ,til sigll:oi
of infla mmatio n and i nfec.tio n mml be resolved. This
generally entitles the surgeon [() l.'I-<:l it 1-2 mo n t hs
before attempting repair SQ that a finn and defi ned
hernia ring is present. If a suture sinlls is present, (h{�
surgeon mllsi. wait for the suture [0 he absorhed an d tht:
in fec tion lO rcsolV(". If a non-absorbable suture was
used , the suture should be removed prior to attempting
any surgi ca l repair. This can be done with the h()rsc�
standing or under genNai anesthesia. SlIrgical repair
should nOl be attem p ted for itt leas [ I month after
Figure " .3 Postoperative indsional bleeding, not subcuta­ cessation of dr�linage.
neous hemorrhage BCCatlSe of the elfect of l(!nsion (In a hcrniorrhapll)',

218
 POSTOPERATIVE TREATM ENT AND COMPLICATIONS 11

4i 24-hourfasting (feed only) is recommended. The horse

is <Hle�lhelized, and the skin overlying the hernia sac i."
grasped with 2 or 3 Lahey thyroid forceps. After apply­
ing slight u�l1sion on the 11(�mia sac, a fusiform incision
ovt'r lhe ht�rnia ring is made. The incision is exrcn<icrl
to I he hernia ring t",king cart! to ligate or camcfize any
1\igniflt:anl blccders. Asmall 2-3 cm incision iS lh(�n made
through the hernia sac: at the hernia ring. allowing imro­
dU<"liOIl of one of the surgeon 's fingers. The su rgeon
a....sesSCs the prescnc(� or absence of adhesions and pro
..
n:t'ds with the resectiun of lhe hernia !;ac afler proper Figure 1 1 .4 Mesh placement for equine hernia repair.
Iransenion/dissenion of the adhesions. The hernia sac. Note that the edges are folded over with the folded edge
and O\'erlying skin is then resected. Primary repair is used opposite to the abdomi nal cavity

i f t h e.: ('dge of [hc hernia ring (:an tx� re-appo�ed with

minimal tension. All appositional panern (simple
in terrupted or cfuciale) is us(�d (sec Chapter 10 for con­ slire abdominal ba ndages do redu<:e s.....elling and mini­
sickrari on of �ttturc maLerials). The subcuLaneous laver
' mize the likelihood of serumas. They should be llstd
and slin arc clo!ied in an aCC('plable manner. ,,,ith caution and tailored to the individual, as lhc)' are
\k!ih is used when the lension on the incision edge associated with preputjal swelling. In addition, alxiomi­
is signific3m or when it is needed to rt"pair 'spot' thin­ nal bandages c:an increase rhe likelihood of infection
lling of an inc:isiollal are.. . Two types of mesh have been when a male manag(.'S to urinate in t.h� bandage, or ill
used: Marlex (Dowd lnc., Provi<knce, RI) alld hot weather as sweating (><:CUfS, leadi ng to a moist warm
Pn)xplast (Gosht'n l.ahontUlries, Goshen. NY) . Marle x environment nCiir the incision.
ha" a tend(:nc:y to sag and should rhcrcfore be placed
wid1 appropriate (ellsioJl. Absorbable mesh made of
polyglactin 910 or polyglycolic acid IS available, blH to CONCLUSIONS
Lilt' amhor's knowledge iL has not been used in horses.
For humans, Lh�se absorbahle meshes have been The incisional complication r<1lC appcars to be deuea.�­
n:port<'d to ser\'t� as tcmporary suppOrt unti l indsional ing becaw;e of improvenlents in surgical le(:hniqlle �nd,
inkction is resolved. followed b�' plaeemen r ora penna­ prohably. earlier surgical intervention. COlrdui atten­
m:1It mesh. Meshes arc cut. 8 em larg-cr than the (ldecl tion to preven tion and carly recognition ami trealment
tn allm,,' their edges Ie> be folded. and to ()V('r!:IP the her­ are the key in managi ng thc!;.e frequent complications.
Ilia �rlKe by 2-3 em. The mesh call be used as an ovn-ll'l'
ulltier twO conditions

1. to support <\1\ incision that has bc(:11 dosed Postoperative com pl ications
primarily but where signitkam tension is present
2. O\'l'r an incision sitc that has th inning area') whcn: - myopathy/neu ropathy
. : ... .
no primal)' repair is needed.
BA Valentine
�1<:sh contacting Ih<; abdominal cavil}' can resull in
intt.�.stil1e!i adhering to the mcsh. I t is Lllt�rcfore recom­
Ilu:ndcd the me...h be placed snbfascially, blll this is INTRODUCTION
r<.lrdy, if C\.'er, possihle in the horse. Snmetimes the
p(:riwneum (.an be disscc.lt:d free from tht: hernia sac, Post-ancsthclic myopathy/neuropathy rerers 1.0 a range.:
allowing it to form a barri�r between the mesh and the or clinical scenarios in which dysfunction of skeletal
inl(:stines, LJsually t.he mesh is lIsed as :an t·nlay suture d muscle and/ or peripheral nerves occurs in horses fol­
LO tIlt: t:dgc of the defect. Two m<:.�hes an: used with th ei r lowing gen�ral anesthcsia. This dysfunct.ioll may be
t'dges folded o\'t':r with the folds opposite lht: abdominal local ized or generalized, painful or non-painful, and
cavity (Figure 1 1 .4). 111 allca..(�s, mcsht�s are sccuf(�d with clin ical signs may be evident during the immediate
absurhable su ture material, preferably monofilamenl, reco\'ery period or appear da}'s later, ."\.5 suc:h. post­
S()nH� sutures 11IUSt he pr-c-piaccrl in the mesh. anesLhetic myopathy/neuropathy is not a single ciinic()­
Pos(operdtivcly, it is imporlam to minim ire im.:ision<-tl pathologk en tity, bu t rather is a manif�tation or a

s\\,'('lIing. Therefore, mm-stl'roidal anti-inflammatory !ipectrum of induc ed or inherem neuromuscular dys­

d l'llg� are aomini.'il.ered for 3-5 days, By a pplying pres- function evident following anesthesia. I t is estimated

219
11 COlK
that from !�fi per (ent of horses undergoing general
anesthesia lIlay devdop clinical signs of post-anesthetic
myopathy/neuropathy, and that development of these
disorders is the cause of 8--60 per cent of anesthesia­
related deat.hs in horses. It is also likely that subclinical
myopathy occurs, particularly in horses with inherent
defects of muscle function.
PATHOGENESIS
;\Cllromllscular dysfunction may be due to one or more
"I' thl' following
• muscle fiber necrosis
• o\'cra!l musc1e weakness
• peripher,t1 nerve dysfunction.
Muscle fiber necrosis
�Iusck fibt']" necrosis is accompanied by variably
increased serum activities of creatine kinase (CK),
aspart<lIC aminotransferase (AST), and lactic dehydro­
genase (LDH). Lorah/.cd or generalized fiber necrosis
(){'("UfS following ischemia caused by compres.�ion of the
muscle groups during recumbency or by systemic
h�'p<Jtension, and may involve reperfusion injury as well
as ischemic injury. Generation of lipid pcroxidation
prod'lCts following musde membrane damage allow.�
li)r the likelihood that oxidative injury plays a role in
the duration and extent of muscle il-Uury. Mllscle Hber
necrosis may also occur due to, or be exacerbated by,
lllld<,rlying inherent myopathic conditions such as sele­
nium/vitamin E deficiency, ex('nional rhabdomyolysis,
and polysan'baride storage myopathy.
Overall muscle weakness
Owrall muscle weakness may occur because of severe
ckctrolyte imbalances, h),perkakmic periodic paralysis,
or polysaccharide storage myopathy. In these cases,
muscle fiber necrosis may be minimal or inapparent,
imd serum anivities of CK, AST, and LDH may be
normal or only slightly increased.
Peripheral nerve injuries
l'eripheral ller.'e i!-uuries may he due to nerve compres­
sion or swelling of associated soft tissue. Serum activities
of CK, AST, and LDH will be relatively normal.
RISK FACTORS
Risk faClo[s cited for horses include large si7_e, heavy
muscling, high level of fimess, and breed, \v:ith Quarter
220
horses, draft breeds, Thoroughbreds, and Stanrlardhrcds
thought to be at higher risk. Data to support t.hese
hypotheses, however, are scanty and sometimes contra­
dictory. Other, better substantiated, risk factors include
• prolonged duration ofgeneral anesthesia
• type of padding
• positioning during surgery
• systemic hypotension.
The type of anesthetic agent� employed, as well as other
medications administered, may also play a role,
Halothane anesthesia has most often been associated
...,ith post-anesthetic myopathy in the hnrs{'_
Administration of aminoglycoside antibiotics has I)('en
discouraged because of possible neuromuscular block­
ade, however a recent study concluded that a single
high dose of gentamicin sulfate administered perioper­
ativcly did not affect neuromuscular fimctioll in horses
anesthetized with halothane. Delay of elective surgery
in horses with increased serum activities ofCK, AST, or
LDH may decrease the incidence of post-anesthetir
myopathy, but this hypothesis ha� not been carcfillly
investigated.
TYPES OF NEUROMUSCULAR
DYSFUNCTION
Malignant hyperthermia
Los.� of thermoregulatory function, with subsequent
r.!pid increase in body temperatllre and associated mus­
cle rigidity, myonecrosis, and respiratory dysfunction, is
an uncommon but frequently fatal complication occur­
ring during general anesthesia. Susceptible individuals
are those with underlying myopathy resulting in abnor­
mal intramuscular calcium regulation, in \,'hich certain
anesthetic agents, in particular halothane, can trigger a
cycle of unregulated calcium release from the muscle
s;\rcopla�mic reticulum to result in continuous muscle
fibcr contraction and associated heat production. A�
such, this unique disorder is more appropriately classi­
fied under �he heading of 'anesthetic-related myopa­
th(, and should be distinguished fi'om hyperthermia
occurring during the recovel)' period {see below). True
malignant hyperthermia in humans alld swine has beell
fmmd to he due to genetic alterations of the skeletal
lIJuscle ryanodille receptor, a vital link in muscle
excitation-contraction coupling. Other underlying
myopathic disorders, however, have also been found to
predispose individuals to anesthetic-related malignan!
hyperthermia. An anesthetic-related malignant hyper­
thermia-type reaction has b('en reported ill sever.!l
breeds of horses. Quarter horses with hyperkalemic
 POSTOPERATIVE TREATMENT AND COMPLICATIONS
periodic paralysis (HYPP) lIlay be more susceptible to
anesthetic-induced malignant hyperthermia. Sporadic
in l.itro testing of muscle samples from affected horses
has revealed an exaggerated contracture response to
halothane and caflCine, however a specific defect in
skeletal muscle of aflected horses has not yet been iden­
tified. It is interesting to note that several studies have
found evidence for abnormal skeletill muscle calciulIl
regulation in Thoroughbreds prone to recurrent exer,
lional rhabdomyolysis, and it is possible thaI. this t}pe of
defect may predispose aflected horses to ilnesthetic­
rc1;tted malignant hyperthermia.
Post-anesthetic hyperthermia (post­
anesthetic hypermetabolic syndrome)
Development of hyperthermia in horses during the
recovery phase of anesthesia should be diflerent.iated
from 'true' ilnesthetic-induced malignant hyperther­
mia. The term 'post-anesthetic hypermetabo\ic syn­
drome ' is perhaps more appropriate. Post-anest.hetic
hypermetabolic syndrome may he accompanied by vary­
ing degrees of myonecrosis. Ylyopathies resulting in
uncoupling of mitochondria, ill which mitochondrial
oxidative phosphorylation is not properly 'linked' to
the electron transport system, may result in excessive
muscle heat production and hyperthermia. Uncoupled
mitochondria are a relatively non-specitk consequence
of milny different myopathic conditions, and have been
reported in the skeletal muscle of horses prone to exer"
tional rhabdomyolysis. Draft breeds may be more prone
10 development of post-anesthetic hypcrmetabolic
syndrome, possibly because of the high incidence of
polysaccharide storage myopathy in these breeds.
localized myonecrosis
Development of swelling and pain in isolated muscle
groups is perhaps the most common form of post-anes­
thetic myopathy in the horse. Muscle groups under COIl!­
pression from the weight of the hor.;e during surgery arc
most susceptible. As muscle fiber necrosis, in itself, is
neither painful nor results in swelling, i t is clear that
\'asntlilr factors must play a role in this disorder. The
concept that this disorder is a manifestation of a
compartment syndrome, in which increased muscle
pressnre against a tight fascia results in vascular com­
promise, is weI! accepted. Proper padding and position­
ing 01 limbs during anesthesia and recognition and
treatment of hypotension will reduce the incidence of
this phenomenon, but its continued sporadic occur­
rence indicates that other factors are likely to playa roIc.
The possible role of marginal to low levels of antioxi­
dants, in particular selenium and vitamin E, must be
emphasi7:ed, as it is entirely possible that il lack of these
11
compounds may allow a cycle of increasing membrane
i�jury that causes magnification of the low-level muscle
injury that is likely to occur in ally horse undergoing
general anesthesia. I t is suspected thai selenium status
may be more important than vitamin E status in protec­
Lion of equine skeletal muscle from injury. In particular,
masseter myopathy as a post-anesthetic complication
could reflect an underlying selenium deficiency.
Generalized myonecrosis
Horses with generalized myonecrosis and weakness
following anesthesia resemble horses with exertional
myopathy, and these ent.ities mily be related in .�ome
cases. Systemic hypotension, however, has been shown
to induce generalized post-anesthetic myop:Hhy in
apparently normal horses. In addition to weilknl'ss,
affected horses often have hard, painful muscles, which
ilgain suggests that vascular damage must be involved.
Serum ilctivities of CK, AST, and LDH are generally
extremely high, and affected horses may develop overt
myoglobinuria. As with localized myollecrosis, the
antioxidant status of the horse could play a role in pro­
tection or predisposition to development of general­
ized myonecrosis following generAl illlesthesia.
Localized weakness
Localized weakness, most often involving a forelimb, is
considered to be more often a manifestation of periph­
eral neuropathy than of myopathy. Affected horses will
exhibit evidence of partial to complete limb paralysis
with motor and, in some cases, sensory deficits. Muscle
swelling or pilin is generally absent. Proper padding
and positioning of the limb during surw�ry to avoid
compression of peripheral nerve trunks, or pressure
damage to the surrounding muscles, will reduce the
incidence of this disorder. Damilge to nerves may be
structuml or non-structural (conduction block).
Generalized weakness
GeneraIi7(�d weakness, in the absence ofmassive muscle
necrosis, can result in recumbency with inability to rise.
Causes ciled include severe electrolyte imbalance and
altered skeletal muscle energy metabolism. The liltter
is an interesting concept, especially given the altered
energy mcmbo1ism that is thought to Ix the cause of
skeletal muscle dysfunction in horses ".,'ith polysaccha­
ride storage myopathy. Draft horses with polysacchilride
storage myopathy may have prolonged weakness and
prolonged recumbent)" following ane.�thesia, with mini­
mal to no increase in serum activities of musde enzymes
during the recovel�,' pha�e. Continued monitoring of
serum CK and AST, however, may be indicated in these
221
11 COLIC

breeds and in other horses suspected of having polysar­ The placement of the slung horse illlo a pool or foot
charidc storage myopathy, as thefe is evidence that Oll­ 'l.Ilk
t would be ideal.
going muscle ir�tlry can occur up to 5 days Of more Administration of lipids, either intravenomly or
ro!lo\\'ing apparent recovery. This phenomenon may through a nasogastric tube, may benefit horses with
explain cases of sudden onset of recumbency or rhab-­ weakness or rhabdomyolysis due to polysaccharide
dOlTlyoiysis occurring hours or days after apparent full storage myopathy.
n�covcly. Fasciotomy may relieve pressure in localized myo­
pathy due to compartment syndrome.
Splinting or hobbling of limbs that are weak due to
PREVENTION myopathy or neuropathy may be indicated.
In cases with severe myonecrosis, aggressive fluid
Clearly, proper padding and positioning, maintenance therapy to maintain renal function is critic,t!.
of systemic blood pressure, and minimizing total dura­
tion of anesthesia arc the best preventative measures. A
reeeill study suggests that use of dobutamine may
PROGNOSIS
improve intramuscular blood flow during halothane
anesthesia. In selenium deficient areas, administration
Under most circumstances, myonecrosis will be fol·
of selenium and vitamin E prior to surgery may be of
lowed by myofiber regeneration with minimal to no
benefit. The lise of dantrolene prior to surgely, to
scarring. Persistent weakness during the regeneration
reduce calcium release during excitation-(ontractiOll
phase, and the potential for myoglobinuric lIephrosi.�
coupling, is of uncertain benefit. and may, in fad, result
may, however, necessitate aggressive supportive care
ill prolonged postoperative weakness. Given the lack of
for several days fol\ov".jng the onset of myopathy.
data to support the hypothesis that abnormal ealdum
Repeat determination of serum CK and AST activities
fluxes art' involved in every case of post-anesthetk
is useful for evaluation of recovery. The serum half-life
myopathy, ils usefulness in prevention of this disorder
of CK is extremely short, and serum activities follow­
must Iw considered questionable at besi. Preliminary
ing a single bout of muscle il�iUly should be reduced
studies of draft breeds with underlying poly<;accharide
by at least 50 per cent evelT 24 hours. If serum CK
storage myopathY' suggest that a low carbohydrate, high
activity is found 1.0 be persistently high or inneasing,
fat diet may reduce the degree and duration of mnscle
particularly in a horse that is no longer r�nllnbem,
il�jury following anesthesia.
underlying myopathy leading to on-going muscle
injury should be suspected. The prognosi� for recovery
fi·om peripheral neuropathy will depend on whether
THERAPY
there is axonal damage or simple conduction hlock.
Resolution of conduction block may be rapid, whereas
Horses with ohvious signs of muscle necrosis, either
repair of axonal damage, if it OCCllrs at all, may rake
localiwd or generalil:ed, should be treated immediately
weeks to lIIont.h.�.
with intral'enous dimethylsulfoxide(DMSO 1 g/kg
10% solution in 5% dextrose). This free-radical-seav­
enging agent can dmmatically reduce on-going muscle
injury associated \�i th oxidative i!�ury.
Administration of selenium and vitamin l-: may also
aid in reducing fiber necrosis.
Pos toperative com pl ications
Correction of any electrolyte or acid-base alter­ - th rombophleb itis
ations, as wdl as supportive therapy such as analgesics,
tranquilizers, Of sedatives arc indicated to reduce pain
( Walsh
and anxiety.
The decision to hoist a recumbent ho{';e by use of a
tail rope or sling is made depending on the duration of INTRODUCTION
recumbency and the nature of the horse. A calm horse
that is maintaining sternal recumbel!cy should be Thrombophlehiti<; is defined as thrombosis of a I'ein
dose!y monitored, and may regain the strength to rise associated with inflammation of the vessel wall.
within a few hours. For an anxious horse that is Thromhosis rarely occurs witho\lf the presence of
struggling !.o rise, or one that cannot maintain sternal inflammation. Septic thrombophlebitis is the terlll lIsed
recllmlwl!q', use of a hoist and sling may be critical. when the thrombus becomes infected.

222

1ne pathogenesis is multifllctmial. The use
indwelling intravenous catheters, coupled with the fi-e·
quem administration ofirnlant drub
'S ill patients that may
have a coagl.llopathy as a result of their primary disease,
comhine to put horses with severe gastrointestinal disease
at rdatively high risk of developing thrombophlebitis.
The jugular vein is the most frequently affected site
because it is commonly used for venipuncture.
PATHOGENESIS
In the normal animal there is a balance het\\'een prou}­
agulam and anticoagulant activiTy. Thromhosis occurs
when the balance tips in favor of coagulation. Factors
That promote coagulation include
• \ascular intimal damage
• a hypen:oaglliable state
• stasis of blood flow.
Th('�e factors result in inappropriate activation of
!]ormal hemostatic mcchanisms.
Hemostasis
Damage to a blood vessel initiates the process of hemo­
\tasis. This comprises a series of complex events involv­
ing pl,udel plug formation and activation of the
do((in,il; cascade t"wlllually resulting in formation of a
fibrin dol.
(Jlf/ldfl f!lug/omlfllirm
Endothdial ce!Is normally resist adherence to platelets
I)\' a variety of mechanisms. Damage to endothelial (:ells
results in platelet adherence to subendothelial coHagen
and la(tor VI!! (von Willebrand 's factor). This result� in
pla1<"kt activation whidl involves contractioll and secre­
tin!} of granular contents including adenosine diphos­
phal(' (ADP), which in turn attrads and anivates more
platdets. Platelet aggregation is enhanced by throm­
boxant� (TXA,) which is generated from membrane­
d("l'ivcd arachidonic acid. The result is formation of a
plalelet plug.
Blood (i)(/!,'1l/alion
Activation of the coagulation cascade results in the for­
Illation of the fibrin clot. The extrinsic pathway is initi­
awd by tissue factor or tissue thromboplastin which is
d('rived from damaged tissues. The intrinsic pathway is
initiated when blood comes illlo contact with subendo­
thelial collagen or platelels, which are highly negaTively
charged. Apart from tissne factor. all the necessary clot­
ting factors are present in normal plasma, many of
lhem are serine proteases.
P-OSTOPERATIVE TREATMENT AND COMPLICATIONS 11
of The rn'O classically described pathways converge to
activate factor X to Xa. Factor Xa forms prothrombi­
!lase by forming a complex with factor V, platekt phos­
pholipid and ionized cakiulll, Prothrombin<lsc deaw�
prothrombin to form thrombin. Thrombin cleaves
fibrinogen to form fibrin, which undergoes covalent
linkage to form the insoluble clot.
Limitatioll 0/dot/onrwlioll
Clot formation is normally limited to the site of blood
\esse\ il�jury by mechanisms that inhibit clotting factors,
the most important being antithrombin III, and by fib­
rinolytic processes that destroy the clot. Antithrombin
In neutralizes serine protease dotting factors, includ­
ing thrombin, its dlects are potentiated by heparin.
Fibrinolysis is activated al the same lime as coagulation ,
the main fibrinolytic elll_yme bt.�ing plasmin, whose pre­
cursor, plasminogen is incorporated within the dOL as it
forms. Plasminogen is activated by lissue plasminogen
activator derived from endothelial cells and probably
enters the clot bv diffusion.
Thrombus/ormation
&.'veral faclOrs conspire to increase the risk of occllr­
rence of thrombophlebitis in postoperative colic
patients
• patients are frequently in a hypercoagulable state
• mechanical irritatioll of the vessel intima is caused
by venipuncture or by the presence of an
inlravenous catheter
• several of the drugs uscd in colic patients can cause
chemical damage to the endothelium, for example,
thiopentone, phenylbUiazone, and guaifenesin
(GGE).
Hypercoagulability in horses with colic: the
role of antithrombin III
Antithrombin III is a natural inhibilOr of coagulation,
normally accounting for over 70 per cent of the antico­
agulatingeffect of plasma. Antithrombin III forms com­
plexes with activated serine proteases, these are then
removed hy the reticuloendothelial system. On its own
antithrombin III is a weak inhibitor of the activated
serine proteases of the coagulation cascade, especially
thrombin and factor Xa, its activity is markedly
increased by heparin. Antithrombin 1II is thus con­
sumed during the coagulation process.
In equine patients with gastrointestinal disease, [he
most likely cause of coagulopathy is endotoxemia.
Endotoxin has lllallY effects including
• direct damage to endothelium
• platelet aggregation
223
11 COLIC

• activa.Lion of coagulation G1.<;cacl.c and decrease in

i.l1l tilh romhi n III acth·ity.

A nu mh c r of swdi es ha\'t! shown thar horses with sc\'cn�

syslt'mic disease haV(� lower than normal a<:ti\'ity of

antirhrOlnbin HI. I n one study, amilhrnmbin III a<:ti\'ity
was found lO hC" rcdl1ced in horses [hat had undergone
stll'gi<"ltl correction of largl� colon torsion, for 1-3 days
pnsropcnlli\,t·iy. Antithromhin III activit), thell
illcreased lo normal in horses that survived, hut
rt:maincd 1()\It,' in horses that died.
III anolher study it was '()lllld that horses that had
�lOdt'rg:ont" colic surgel}' shO\\lt'd a dCCTcasc in
i\lHilhrombin i l l C\criviry. this fkcreased to ahout 50 pt'r
('l'nl ofiLS no r m al \'allJ(� after �4 days rhen increased to
normal O\·t�r abou[ a week. This (:hang<: w<.t.'i coupled
with a rlccf�a$<: in an i vi ry of coagulation ra<:tors LO

approximalt':ly 25 per (:Cn! of normal '2 days postopera­

li"dy, fiJUowed hy an in<:r(!as(� 10 normal .Kti.... ity over
lhl:' t)e-xt week. Th(' rcsuital1l rende-ncr to coagulation
was c.xplained hy the fan thaI <:oagu\atioll factors are
Fi9ur� 11.5 A 12-year-oJd gelding with 'Swelling of the left
still dfectiv(' at 20 per (('Ill of norma] activity It.'\'d
jugular vein. Septic thrombophlebitis was diagnosed ultra·
wber('a� antilhromhill I I I requin:s ilt kaS! 75 per u�llI.of sonograph i<:ally. The horse had a history of endotoxemia
l1<mnal activity to he cffecr.in: . and the vein had previously been catheterized
In humans, it is well rc(:og-nized Ihilt postoperative..'
patil'lIls with antithromhin If I dcfu:it'llcy are at
in(T('as{'cl risk or t hrom hocmholism: the risk is said to

be modcratt: if antithromhin I I I activit), i!i betweclI

;>0-7:) per cenl ann severe if antithromhin III ;u.:ti\·ity is
less than !l1J pe-r cent. The same may well apply to
horsc..'s. 4 Rare cOlllplications or thrombophlebitis incl lld(�
lhnHnbocmholism :.incl endocarditis.

CLINICAL SIGNS OF Ultrasonographic findings

THROMBOPHLEBITIS
Thrombophlebitis i'i charaClCr1/cd 1IIlra�()n{)grctphi(:all)'
by the pre'icnce of a mass in the \,{�!iscl lllmcn r<lI1ging in
Thrombophlebitis is usuaHy rt!.u1ilr diagll(}�cd 011 the
appearance from hypocchoic w cchogenic (Figurc..$
basis of the following dini<:al signs.
1 1 .6, 1 1 .7}. Thickening of the vessel wall is often pfl'·
I . The affened vei n is hard and cord-lik(� on sene A fibrin sleeve may also be dNecu>d around the
palpatioll. catheter if present, and may ais() be recognized wht�n
2. Sc..'ptic thrombophlebitis �houlct be �nspccl(;d if th(' the cathetcr has becn removcd.
ant-ned vein is hot, swollen. or pa infu l on The thrombus can usually he seen [0 be "-((itched to
palpation (Figure 1 1 .5). If the jugular \'I..! in is t.he endothelium and may parti ally or complt:tt:l�'
alTected the horse m;:\y <t ppear to ha\'e a stiff nt:d. occlude the lumen. Vt:TlOUS <:ongesl.ioTl may h(: disti ll­
Sllppuralion or exudation from sites of skin guishahit· proximal to the thromhus,
P1l11CttIn.' suggests sep tic thromhopllk:hitis. though A s�ptic t.hromhus appears ultrasollographi(:ally as a
u'liui i lis without v<:in invol...t"llwnl' is �Iso a het<:rng('I1<:olls rna.')s in "rhien ancrhoic or hypocrhoi<:
possibility. Septic rhrmnhophlehitls should also he art:as represent areas of fluid or necrosis. AITa.� of pus
suspected in any hor.se with unexplained pyrexia within t.he thrombus appear hypocchoi<: and f1occulclH.
p<lsfoperativelr· Cltrasonography is useful to confirm the presence of
:,t Ril;ucraljllglllar !hromhophlt:hiris may result in septic: thromhophlebitis ann r.o select an art�a of throrn­
t"dt:lIla or th e soft tissues of the Iwad cansing bus w aspirale ror culture.
dysphagia and dysplleit often severt" cnough to Cltrasonography may be usdul in moniLoring: the
l1t!ct!.ssitale lradleosloll1Y. n!!'pollse to therapy.

224
 POSTOPERATIVE TREATMENT AND COMPLICATIONS 11

(a) (b)

Figure 1 1 .6 Transverse (al and longitudinal (b) ultrasonographi< images of the left jugular vein of a mare with a history of
endotoxemia following surgical (orrection of a 360 degree torsion of the large (olon. The vessel wall is slightly thickened.
The lumen of the vein is of normal appearance. The surrounding tissues are unusually hypoechoic and in the transverse
image have a honeycomb (l;ppearance typical of edema. Dr Cel ia M.arr, with permission

(a) (b)

Figure 11.7 Septic thrombophlebitis. Transverse (a) and longitudinal (b) ultrasonographic images of the right jugular vein
of the mare in Figure 1 1 .6. The vein had previously been catheterized. The lumen of the vein is completely filled with a

hete(ogeneou5 thrombu� containing multiple anechoic foci, indicating the presence of fluid pockets (arrows). In the Ion·
gitudinal image. the thrombu� has a laminar appearance caused by the accumulation of layers of blood cells proximally.
Dr Celia Marr with permission
,

225
11 COLIC
PREVENTION
Prevention oj' thrombophlebitis is centered around
• treatmellt of the underlying cause - in horses with
gastrointestinal disease this is usually endotoxcmia
and disst'minaled intravascular coagulation
• measures to minimize venous trauma and scrupulous
management of indwelling catheters - it is advisable
to avoid repeated venipuncture in horst'S at increa,ed
risk of thrombophlebitis due to coagu]opathy
• anticoagulaill therapy is recommended by some
authors hut remains a controversial topic
Catheter management
indwt'lling catheters are commonly used ill horses
undergoing intensive care. Most cases of thrombo­
phlebitis OCfur in veins that are or have been
c<llhetcrilcd. There is little information regarding the
J'reqtwncv of catheter-related thrombophlebitis, One
�tudy reported an incidence of 29 per cent in associa­
tion with !lllid therapy. risk factors including presence
o!' pw('xia and usc' ofhollH>pndun:d fluids.
Pathophysiology of catheter-induced
thrombophlebitis
Endothelia! damage occurs in the area of entry of the
cathNer and at sites of contact of the catheter with the
vessd intima. Platelet aggregation and the coagulation
cascade are initiated by the presence of foreign material
in the bloodstream. Studies suggest that a fibrin sleeve
starts to form on tlw (Catheter within abont. 30 minuws,
beginnillg at its point of enu)' and at the tip where it
cOlltacts the endothelium. There is a marked difference
in lJw thrombogenicity of different catheters resulting
from their surface properties length, gauge, and stifl�
ness. (;ener,IUy, longer and higher gauge catheters are
more thrombogenic because they contact the vessel wall
over a greater area and thus cause more extensive
cndothelial triluma. However, catheters made of softer
materials are less thrombogenic, whatever their size,
because they tend to float fredy within the bloodstream
withont contacting the vt:ssd wall. Readily available
catheters include
• the shorter, stiffer catheters made from
polytetr'-lfllloroNhylene (PTFE), these should not
he Ieli ill for more than 72 hours
• the sofwr catheters available in various lengths, and
incre'lsillgly in higher gauges allowing rapid
iuhlSioll rates, made from polyurethane. lhat can be
maintained fi)r seyeral weeks if carefully managed.
Infectioll mal' ()('cur especially if catheter man;lgement
IS pOOL The incidence of positive bacterial cultUrt�S
226
froIll catheters has b�en estimated at around 70-75 per
cent, with most isolates found to be skin commellSals.
However the relevance of positive culture is unclear as
there appears to be little correlation in these studie�
between positive culture and thrombophlebitis.
Guidelines for catheter use
Good catheter management will reduce the incidem:e
of thrombophlebitis by reducing contamination of the
catheter and trauma to the site.
I . Insertion, surgical preparation of the site, and
placement of the catheter using aseptic technique
minimizes the risk of contamination at tht: tillle of
insertion. There is also a lower incidence of
complications if the catheter is placed by an
experienc�d person, probably because tr,l\lma to
periva.�cular tissues is reduced and there is greater
accuracy in puncturing the vein.
2. The cat.heter should be firmly sutured to the skin to
minimize movement at the site of skin pelletration.
reducing the risk of infection and the degree of
tissue trauma.
3. The use of extension sets is advisable, to avoid the
need to maniplllate the catheter directly, so
reducing its movement and the risk of
contamination from the skin of the horse.
4. Flushing the c_atheter every 4 hours with heparinized
saline soliuiol1 helps to prevent dot formation within
t.h(: catheter. Blocked (or othetwise damaged)
cathet.ers sbould be removed and replaced.
5. The catheter should be removed as soon as it is no
longer required.
5. There are many potential sites of contamination and
infection of catheters, induding thre<:"way taps,joins
in fluid administration sets, fluid bags and any
additions to them. Careful aseptic handling of all
equipment us�d is important. It has been suggested
that all fluid lines should be replaced every 24 hour,.
It is vel)' important to check veins regularly for signs of
thrombophlebitis.
Some authors recommend the use of antiseptic skin
ointl\lent� and dressings while others consider that the
use of antiseptics encourages the development of resis­
tant strains of micro--organisms, or that their use has no
dkct on th� incidenre of thromhophlehitis or positivc
cultures from the catheter.
Anticoagulant therapy
Aspirin
Aspirin given at a dose of 5-15 mg/kg per os (:\'('ry
other day reduces platelet aggregation and may he
givell concomitantly with other :-.ISAlD therapy.
 POSTOPERATIVE TREATMENT AND COMPLICATIONS 11

Heparin • tradlcoswmy lIlay be: nccc::s,'\arr in bilateral

dlrombophlebitis ir dyspnea is $(.'\·ere
The anlicoagubwl dTcct of heparin dqlend� UII the
• surgical drainagE' mar be ncccs-'IiIf)' ifsuppurdtion is
pati'·lIt ha'in� adeqmH.· autithromhin III ani\·ilr.
prest'llI
hq)arin hind� to antithrombin III alltl grcatl�' cuhallces
• \Tin rt'-scctilm rna}' he indicaTed in St.'\'t:rc case!> Ibat
iL� powney as a �(:rin(' prOlc:ll.Sl· inhihilUr. Heparin isnO!
do not resp ond to medical mallagemenl.
!lsd·1I1 for the r('solution of existing Ihrumbi ami has a
limilrd elTect in pn:\·clllinR thcir e"l(�nsion. If used, In IHll·omplic',ued C'dSl.'S or thrombophlebitis,
ahe...·fore. it must he.: �i"en prophylanir.ally. prdiTdhly rccanali7.ation of T.hc I'ein commonly occurs, Ihis may

pre"uperativeiy, hefore the con.�umplion of antitlHom.. I·C1\lrll 10 normal Of there may be.: a degree of stricture.
bin III and librin formation occur, it may then haH· In mOfe severe cases the thrombus may undergo
sonw dfcct in preventing thrombophlebitis in patients organil,atjO!l ....ithout n:canalilation.
'It risk. The �tlgg(:stc::d dl�ag(: rc::gimcn is

• in itial d{)se DO IV/kg s.c.

• 12:, lL' /kg s.c. q. 12 h for six doses P ostoperativ e complications
•
12 h subsequently.
100 IL'/kg s.c. q.
- p eritonitis
Tht· rct\l.Ic:in� dose i� recommended hecause if a uni­
hmn doS(: is u�ed, serum heparin gradually incrcas.cs. T Mair
Thi� d()sinK regimen, when administered to he'llr.hy
hors.:s, resulted in a pla�lna heparin concentration
bt'IWet�!l O.O�-O.2 IU/m1. this is the lhcmpcmic range
INTRODUCTION
o[ 101,· dose heparin prophylaxis used in humans.
l'erilOnili.� is def'ined as inflammation of the peritoneal
Suhnllallt.'OUS adminisu",uion a\'()id� peak.� of plasma
lining of lht" <lbdominal cavir )'. The condition is dis­
Iwp,lIin thai ma�' he more.: likel)' to result in ad\·er$(.'
t·ffefl�.
w.'.-s<.'"(1 in greater detail in Chapter 17. Peritonitis occurs
10 .<,ome nr.grce in all hOfSC.'I following abdominal
Tht' nl(��l comnwlI complication or hqmrin Iher-tp),
sUTKr.ry �ause of the Imtllna associated "ith tht'
is anemia (ren cell lIlaAA may be reduced by 3..� per
surgery, handling of the intestinal tran, etc. In most
u·nl). (lnd rt'd cell agglUlination ill the micrm'a.-.c:lila-
cases this is self-limiting <lnd of little clinical signili­
1Uf(' has been suggt:sted <IS the mllSl likdy callst.'. The
(alice. Ilowevcr, septic PCI'itOliitis is OJ serious and
rcd cdl count rl'l:O\'CI'li ',ithin 96 hou rs of l:e!lSalion of
pott'ntially lifc..d\f("ltelling ctlmp!iC'dtion of abdominal
ht'p;nin the,-"p)'. The signilit:allce of Ihi� oi)s(:n'ation is
SHrg':"), thil( rl'Cluire� prompt and aggres.�iy(' therapy.
unKllown.
Ol.lwr complit:aLioos of heparin adminislr<ltion that
h'l\'(' ht'en dC�(:fibed in horses include fawl Iwmor­
CAUSES OF POSTOPERATIVE
rhag-e (at higher dl)se.� ), thrombo<:·ytopcnia, and PERITONITIS
painful �\\'ening at injection sites.

The mllst C:(llHlllOn cause of postoperative septic peri­

tonitis is leakage of �ndll!uxins and/or bacteria from
the bowel lulTIcn ill to the pc::ritolleal cavity. This may he
TREATMENT
Jue to nCCl·I��is of Ihe entirc howe! wall or a mucosal
injul1' only.
Ont:e thrombophlebitis has been recogni7.cd, sympto­
Contamination c)f the rx.'riloneal cavit}' may also
mal,it- treatmcnt is Tl'commcnded as follows
oc(:ur at, the tim� of surgery espcc:jal!y when entero­
• 1"<'1110\'(' the ler, if prt'$Cnl, and (:ulture th(, tip.
(";llhe tom)" or oov;cI r('section and anasLOmosi.� procedures
dO l111t use the \'ein for \'eniptmClurc:: arc pcrfomled, Some degree of local collt,,-lIlinalion of
• hm packing 111<1)' help by increa$ing blood lIow to the ahdomen at the siles of cntcrolOmr is almost
fhe arca inC\·iahle,
l but pm\ided that the sUll!;cl1' is lK:rfonned as
• II� non"5teroiclal :uui-inllilmmalory dnlgs to rrduce cleanly as possible. this locl'lli7.cd contalllimllion is
inflammatiou unlikely til I:ause scrious dilrusc septic pc::rilonilis.
• lI�e antibimirs {broad spcclnllll or as dinated by 11(>\\c\·c,· if mnrc widespread contamination "(;C\I",,".

(.uhurc and scnsiti\·ity) i n SI.�ptic thromhophll'bitis thcn 'l more S<.'\It.'re diffu�c septic peritonitis mar result.
• L:("cp th(' head ek'\'3.ted, for example by c:ros.o;-rying The causes of peritonitis in the poslop<.'rdti,'c period
irbilateral thromhophl�bitis is prcscnt arc listed iu Table I I ..').

227
11 COLIC
Contamination of the abdomen
at time of surgery from - gut contents
- break in asepsis
- swabs, etc.
leakage of enterotomy or anastomosis
Progressive bowel necrosis following strangulation
Secondary bowel necrosis due to - prior distention
- ileus
- persistent shock
Chronic small intestinal distention and necrosis
Chronic large bowel impaction and necrosis
Non-strangulating intestinal infarction
Enteritis/colitis
Perforated ulcer
Incisional infection and dehiscence
Sever'll studies of postoperative complications in
colic cases have been published, and these have shown
(on !lining results with respect to the rates of postoper­
ative pcritouilis. In the study by Phillips and \VahnsIcy
( I993) generalized septic peritonitis was recorded in 9
of 149 horses (6%) undergoing exploratory laparo­
tomies for colic. The most frequent fatal postoperative
complications that occurred in this study were general­
izt'"d septic peritonitis and bm'l,'el obstruction caused by
adhesions. However, eight of the nine horses with peri­
[())litis had pre-operative ahscessation, rectal tear, or
advanced bowd ischemia.
CLINICAL SIGNS AND DIAGNOSIS
All horses will develop low grade non-septic peritonitis
following colic surgery, and peritoneal fluid total nucle­
aled cell counts and total protein concentnltions are
likd)' to h(� elevated (see Chapter 2 Analysis of peri­
toneal fluid). In IIIOSI cases this will be lIIild and self­
limiting. Howevtcr, diffuse septic peritonitis rC<luires
specific therapy and is potentia!!y life-threatening
unless treatment is instituted early. The early recog­
nition of postoperative peritonitis is therefore impor­
tant. Some or all of the following signs and findings
should alert the clinician to the possibility of septic
peritonitis
• depression
• alxlominal pain
• ileus
• gastric reflux
• intestinal distention
• fever
228
• anorexia
• tachycardia
• leukopenia
• hypoproteinemia
• diarrhea.
None of these findings is specific to peritonitis and al!
of them can be seen in varying degrees in association
with other postoperative complications. However, the
pr�sence of one or more of these signs should be COIl"
sidered as suspicious of septic peritonitis.
Confirmation of the presence of postoperative septic
peritonitis can be difficult because of the non-specific
nature of the clinical signs and the fact that peritonitis
is always present in the postoperative patient. However,
analysis of peritoneal fluid should be performed in
cases suspected of being affected by septic peritonitis.
Exploratory laparotomy (celiotomy) without entero­
tomy will result in an elevated peritoneal nucleated cdl
count for up to 14 days after surgery. The total nucle­
ated cell count of peritoneal fluid can increase up to
400 x 109/1 (400 000 cells/�tl) with more than 90 per
cent neutrophils in healthy horses following surgery
without enterotomy. Likewise, the total protein concen­
tralion may exceed 3.5 gil in such normal horses recov­
ering from surgery. Meamrement of total nucleated cell
coums and total protein levels are therdore unreliable
for the diagnosis of septic peritonitis. However cytology
of peritoneal fluid and examination of a gram-stained
preparation can be more helpful. In particular the iden­
tifkation of one or more of the following abnormalities
should be considered signifi(_ant
• numerous toxic and degenerate neutrophils
• free bacteria in the fluid
• phagocytized bacteria within neutrophils or
macrophages
• food particles and plant materia!
• fibrin particles.
:v1icrobial culture of peritoneal fluid is indicated not
only to identity the pathogens present, but also to help
tailor the antimicrobial therapy more spedfically.
Peritoneal fluid pH and lactate dehydrogenase
{LDH} concentration, and comparison of plasma and
peritoneal glucose concentrations can also be helpful
in determining whether Of not sepsis is present. The
most consistently useful indicators of sepsis includr
• a plasma to peritoneal glucose concentration
difference of more than 2.8 mmol/l (50 mg/dl)
• peritoneal fluid pH less than 7.3
• peritoneal glucose concentration less than
l . 7 mmol/l (30 mg/dl)
• peritoneal fibrinogen concentration more than
2 g/I (200 mg/dl).
 POSTOPERATIVE TREATMENT AND COMPLICATIONS
LDH activity in peritoneal fluid is a less reliable indi­
cator of sepsis than these parameters.
Occasionaliy localized areas of periLOnitis may
become 'walled oW by fibrin, this may result in rela­
tively normal-looking peritoneal fluid in samples
obtained from the ventral abdomen. Thtc absence of
specific abnormalities in peritoneal fluid should !lot,
therefore, rule out the presence of peritonitis and clini­
cal judgment becomes more impof1ant than depcn­
dence on laboratory test resulL�.
Ultrasonographic examination can be helpful in
(,valuating th� patient for septic peritonitis. Excessive
pt·ritoneal lIuid may be present and this often sbows
hetcrogeneous echogenicity. Hyperechoic particles in
t.he fluid an� consis«�nt with the presence of gas bub­
bIes. Fibrin tab
'S on the intestinal stTosa and peri­
toncum cause a roughening of these surfaces. Small
intestinal distention with ,·a�·ing degrees of mural
edema and some evidence of motility is commonly
()bser\'�d in these cases (this contrasts with horses with
small intestinal strangulation that usually have dis­
tenrkd loops with mural edema but no motility). Viscus
rupture is often accompanied by the presence of abun­
d,l!lt fluid that appears hypoechoic and contains hyper­
echoic panicles of ingesta. Pneumoperitoneum may
occur with bowel rupture but can also he seen following
rt·ce!H laparotomy. Free abdominal gas lIlay Ix seen in
a hyperechoic area underlying the body wall in the
dorsal ahdomen. Reverberation artifacts may also he
present.
TREATMENT
In lhe postoperative patient, the diagnosis of septic
peritonitis is likely to be an indication for repeat laparo­
lOmv, unless a specific cause of the peritonitis (such as
known contaminatioll at the time of the initial surge!)')
is recognized. Repeat laparotomy permits identification
of the source of s�psis and this lIlay dictate the appro­
priate treatmelll (e.g. resection of leaking bowd, etc.).
Opt'n peritoneal lavage and use of intra-peritoneal
antibiotics will he helpful, and placement of abdominal
drains to permit postoperative lavage may also be con­
sidered.
Peritoneal lavage and drainage an� helpful in the
treatment of postoperative peritonitis, and may help to
reduce the incidence of intra-abdominal adhesions.
The lavage is continued every 4- 1 2 hours until there is
a decrease in the peritOll(�al lluid cell count and protein
concentration, an increase in pH and glucos{� concen­
tration, and an improvement in the cytological appear­
ann" of the fluid. These and other treatments for septic
peritonitis are described in Chapter 17.
11
P os toperative complications
- l aminitis
CS Cable
INTRODUCTION
Laminitis that occurs in thc postopcratil'e equine
patient can be ont' of the most frustrating and deadly
complications of gastrointestinal disease. Bv definition,
laminitis is an inflammation of the lalllil1at� within the
hoof. The interdigitating laminae create a bond
hctween the hoof wall and third phalanx. Inflammation
and/or necrosis of the laminae can result in a break­
down of this hond, resulting in rotation or ventral dis­
placement of the third phalanx away from the hoof
wall. This rotation is also thought to resuit from [he pull
of t.htc deep digital flexor tendon, which broadly
attaches to th{� palmar surface of the bone, once the
laminae arc no longer holding the third phalanx tightly
against the hoof wall. Laminitis results in pain ranging
widely from mild to severe and unrelenting.
PATHOPHYSIOLOGY
Horses recovering from any gastrointestinal disease that
camed endotoxemi<l afe at risk of developing laminitis.
There are several theories a.� to the etiology of laminitis
in hors{�s with endotoxemia, although experimenml
administration of endotoxin in h()r�s has not re�ulted
in laminitis.
One theory is that laminitis occurs bec.ause of alter­
atiollS in digital circulation. VenoCOllstriction and high
hydrostatic interstitial fluid pressures are thought to
interfere with microcirculation in the foot, resulting in
ischemic necrosis of the epidermal lamcllae and subse­
quent rot.ation, or ventral displacement (sinking), of
the distal phalanx.
A recent theo!)' (introduced bv Dr Christopher
Pollitt) suggests that certain enzymes are responsible
for the destruction of the normal lamellar structure.
The matrix lIlctalloproteinase 2 and 9 (MMP) {�n7.yllles
haw been found in normal hoof tissue in low concen­
trations, but the levels become elevated in laminitic
feet. It is believed that \.,'hen these enzym{�s arc activated
they destroy the lamellar attachments resulting in
laminitis. What triggers the release of these enzymes is
not completely understood, but i t may be substances
released from organisms that normally inhabit. the
equine gastrointestinal tract. For example StuptlJl:(}("'( us
bUlIil has experimentally aC!h·at�d equine MMP-2 and
resulted in lamellar separatioll.
229
11 COLIC
CLINICAL SIGNS
Horses affected with laminitis ;lfe first observed to be
reluctant to move. The front limbs are generally
affected although 011 occasion all four limbs will he
involwd. 1A1l Cll forced to walk, affected horses will shift
their weight to their hind limbs and tend to keep their
front fcc! ahead of their shoulders. They arc especially
reluctant to turn. The diagnosis can ea�ily be made by
the palpation ofa houndi ng pulse in the digital arteries,
increased heat i n both hooves, and the bilateral dinical
signs. Horses arc reluctant to bear weigh t Oil either
front foot when tlK contralateral limb is picked up. If
digital pressure is applied either manually or wi th hoof
testers, pain is elicited diffusely in the toe area,
There are tWO main syndromes that result from pro­
gression of t.he clinical signs.
I. Horses experiencing primary rotation of the pedal
bone may develop a ventral dcpression to th e sole
(outli ning the tip oft.he pedal bone). Fluid and
blood accumulate under the sole . This fluid
accumulation can undermine the entire sole and
drai nage Hlav be observed at the corOllary bands in
the heel area.
2. Horses experienci ng primal)' ventral displacement
can be recognized by the hair at the corona!)' bands
bei ng directed horiwmal and parallel to the
ground as their follicles migrate distally to the kvel
of the COrOlla!)' bands. In addition, one can palpate
a depression at the cranial asp<�CI of the pastern just
above the coronary bands as the coffin joint mOl'es
away from the area.
Radiographic evaluation (lateral view) with a linear
radiodense material taped to the outside of the hoof at
the toe area can help identif}' the manifestation of this
disease and its severity, and demonstrate any fluid and
gas accumulation in the l aminar tissue.
PREVENTION AND TREATMENT
Prevention of laminitis in the postoperative patient is of
paramount importance, since lamellar damage will
have already occurred by the time the horse shows din­
ic;t1 signs of lameness. Horses with endotoxemia should
he considered as likely laminitis candidates, and should
receive anti-endotoxin seHUIl or plasma, and an anti­
cndotoxic dose of fIunixi n meglumine (0.25 mg/kg
t.i.d.). Othcr supporti\'(' trcatments include the applica­
tion of frog pads to aid circulation in the foot and to
apply counterpressure against the pull of the deep digi­
tal flexor t("ndo n . In tht' pa�t horses with laminitis werc
Iwaled wilh acepromazine or nitroglycl'l"ine to bdp
230
increase blood flow to the feet in accordance with the
vasoconstric tion theo!)'. However, i t has been reportcd
that vasodilation occurs in the developmen tal phase of
laminitis and is a possible triggering factor for activating
enzymes responsible for laminitis. Therefore, it is llO
longer dear if vasodilators are indicated because they
could accentuate the laminitic crisis. \-\,ith the currellt
state ofkll owledge the author recommends again.�t t he
use of vasodilators in horses at risk of developing
laminitis. However once the laminitis has developed,
she advocates the use of such vasodilators as acepro­
maline, ni troglycerine, or other vasodilator drugs.
Phenylbutazone should be i mplemen ted in aCUle cases
of laminitis in addition to low doses of fIunixin meglu­
mine for pai n relief. When :\'SAID toxidty is a risk,
dilllte intrav(�noUS D�SO ( 1 00 mg/kg b.i.d.) can be
administered in intravenous fluids for its anti-inflam­
matory dfects.
Horses with acute and progressive laminitis can ben­
efit from a deep digital flexor tenotumy performed in
the standing animal as surgical treatment. The ratio­
nale for this treatment is that in horses '.vith severe lam­
inar de.�truction the unopposed pull of t he deep digital
tlexor tendon can lead to severe rotation of the distal
phalanx.
Return to performance is likely for horses that do
not have si gnificant rotation « 5 degrees) or sinking of
the distal phalanx.
P os topera tiv e compl ica tions
- colitis
TJ Divers
INTRODUCTION
Horses undergoing abdomina! surge!), arc known to he
at increased risk of developing colitis/diarrhea com­
pared to other surgical/anesthetic procedures. This is
not of great surprise since these horses have often
undergone a period of ileus and, in some cases,
ischemic/inflammatory bowel disease. The ileus is fur­
ther aggravated by the i ntended anorexia both prior to
lhe surgery and for one or more days after the surgery.
The lack of normal fermentable fiber r(,aching the
colon dimini shes volati le fatty add productioll which
may permit overgrowth of pathogenic organisms sllch
as Sr.lmOlwllu -'pp. Of CUI.Ilridium diffidll!. Approxim<ltdy
10 per cen t of normal horses arc positive for SlIlmrlnpllfl
spp. when tested by polymerase chain reaction (peR)
yet mure than 40 per cent of horses with ahdominal

disorders are positive indicating that changes in motility
and/or normal flora are important to the proliferation
and/or shedding of the organisms. Additionally most
horses undergoing abdominal surgery afe treated with
ant.ibiotics which may further disrupt intestinal flora
and normal volatile fatty acid production. Finally post­
operative colic patienL� are kept in intensive cafe
environments that might be more likdy to harbor
pathogenic orgimisms such a� Salmone/In spp.
Clo.l/ririium d.ifJirik which arc dillic_ult to eradica1e from
the environment. Other factors that may predispose
postoperative colic patients to infectious diarrhea
include weight loss and deCl"eaSt,d cell"mediated immu­
nity which are likely to occur in many, if not all, POST­
operative colic cases. Small intestinal reflux might also
predispose to the gastrointestinal entrance of infectious
organisms hecause of a persistently high gastric pH.
CAUSES
Causes can generally be divided into olle of two groups
• infectious/inflammatory causes
• motility/dysfunction causes.
The two predominant infeCl.ious causes
Salmonella 'ipp. and Clostridium diUifilf. Both can be
('ndemic or epidemic in critical care hospitals. Both an�
{overed in more detail in Chapter 20.
(;auses of mot.ility dysfunction such as peritonitis or
illlestinal hemorrhage and bowd shortening, especiallv
colonic resection, may result in diarrhea. Iiorses with
colonic res{'ctioll generally have watery k{:es, some·
times hemorrhagic, for several days up tn 2 weeks
f(}lIowing colonic resection. Laxatives and very large vol­
umes of intravenously administered fluids may cause
diarrhea, but this should resolve within l2-24 hours
after discontinuing t.he laxatives, and even more quickly
after discontinuing or slowing the rat.e of intravenous
fluids. Diarrhea may follow resolution oflarge intestinal
impactions. but this is genpr;}l\y the resllit of laxatives
giV('!l per os and should resoh'e promptly If thl"
diarrhea persists an infectious agent should bc strongly
considered.
DIAGNOSIS
The pre_seller of watery feces aft(�r abdominal surgery
should immediately indicate diagnostic tests 10 deter­
mille the cause and severit�' of the prohlem. These
should inclnde
• abdominal ultrasound to determine the volume
and echodensity of the peritoneal fluid
POSTOPERATIVE TREATMENT AND COMPLICATIONS 11
• fecal cultures, gram stain and Clostridium toxin
testing
• complete blood count and serum chemistries
• complete clinical examination.
In most cases of infectious diarrhea the patient will
he febrile and the complete blood count v.,-auld relieal
hemoconcentration, a neutropenia with toxic changes,
and a decreased serum sodium and chloride.
or
Ahdominal sounds may he absent or more 'nuidy' than
normal. !r peritonitis is a (:(Hlcern based on the prior
surgical procedure, clinical and laboratory evidence of
acute inflammatory disease, and ultrasound fIndings,
abdominocentesis should be pen()Hned (see Post­
operath'e complications - peritonitis). There shmtld be
a good indication for this since
• unwarranted abdominocentesis will increase yentral
abdominal s,\'e!ling and negatively affect wound
healing
• interpretation might he difTIcult depending Oil
prior intestinal pr<Keelures that are routinely
expected to cause some degree of peritonitis.
Fresh fecal samples should he submitted to the labo­
ratory for aerobic and anaerobi<: bacterial C_!llture, gram
afe
firil!! toxin assay (ELISA or
stain, and C/usiliriium riif
peR). If a Salmunella spp. is grown, bacterial sensitivity
should be pent>nned. Clm/ridiwH pnfringelll toxin
(cnterotoxin) assay might also be requt>sted, but results
are difficult to interpret. C{o.l/ridiUIIl jll'ljringrtls �� toxin
testing would be desirable, but is nO!. readily available.
peR might also be requested it}r deTection of SflllIIOlid/fI
spp., but it is so sensitive that a positive finding docs nO!
always mean that Sflllllon,lIa spp. is the cause of the diar­
rhea. Likewise, a positive culture of Sa/mllnf/la spp. does
not prove that it is the cause of the diarrhea, hilt this it
makes it more likely than a positive peR.
TREATMENT
Treatm�nts for each disorder are covered in Chapter :i!().
PREVENTION
The prevention of postoperath'e coliti� is not always pos­
sible but its incidence might be f(�duced by
• routine culturing of intensive care patients and
their stalls
• judicious use ofantibiotic_s
• provision of roughage as soon as possible after
surgery.
231
11 COLIC
TIlt' t�<;(: \)l" 01"",1 llIi(;robial iJl()(:i\hml�, although
tmlikcir 1(1 he hannful, are nnt of pm\'cn value. Routine
nthtlrill� of 1)l)slOp"'�r;;ti�e. crilkal ("are palient\ and
thc:ir Slalls allows delce.lion of inft'r(iou'l org,mi..ms.
N('", P:UiCIlIS �IWHld H(X be 1,.·xposerl tn infcdt.,,(j em'i­
I"nnlOt:ots uruil propcr dcanillK pmccdurcs ha\'c been
applkd ;uld the cllvironm('nl i.� cul!un--nq;<uh'c for
known p;;thogcns. Ilypochiorilc lOa)' he used on stall
s\llfac(�. and ghHar,do(:hydc IIscd to disinfect equip­
m('1H th.u can ))('1 � otherwise �Irri!il�d. Fuot haths
('(>lll<!jllin� appmpria\c rl lJ;al<:rnary anullonia disinfcc-
1;1 Il1� should he usee! Oil Illlt,h entering and leaving the
1)()slnrx'l1uivt: I.rilir.. 1 ("art' an:�, and [ht' walking sur­
(;In's rlisinkclcd hut kepI dry and lighted (sunshine or
uhr;\\'iolt:t li!(hl if' possibk) All persollllel should
wash their hands with c:hlorhexidinc or anothcr soap
l)('twt'l"U <:asc"s. use iudh·idnally prcpared equipmem,
for ('xanlpll' slIlmach tuhcs. and takc net:essary precau­
tions to prc:ve-nt tJw spre<ld of <In illknious age-Ilt on
flotlling-. Any horse dl.:\"doping diarrhea should he
mon:d In all i!>o!;ltio(l tildlity.
Alllihimic.5 sh()uld tUlly be U.';t�d if necessary, as cvcn
Jhln'llwr.llly administered ,mtihiotil."S lllight increase
til(' intjdellfC· of wI:H:rial (�()Iitis. �1()Sl onll antimicro­
hi;lls �hul1ld 11111 he lISl'ft until lht: hor1\(' has OC'"C1l on a
nornlal rHllghage (fit·t lilr S(....'(·r..1 dOl}";. �1etronidawle is
ulit:1l ;'ppmpri;m'l)' used rollowing colonic entert,.
(t)]lIil.:
s, hIli [itl: loulille admini�lrati()n or melronida­
.1"011' in the hopI' of pre\'Cllting Clostridium difficil#1
.tp.
di<llTlw:\ should nnt he encouraged and i� nOl ah..�
sun.t:ssll,l.
Postoperativ e compl ications
- cardiac arrh y th mias
M Bowen
INTRODUCTION
em!i;!f arrhph mias durin!( lhe I x�riopcrati\"c pt�riod
art' common and :I!'C usually a rd]('Clion of IIlctabo!il:
ac diSf'a.'ie.
di�lIIrh,\llI:('s mther Ih;m lUll' primar)' cardi
. Many of Ihest: <lnhytiullia1\ art' of lillie or nn COIl.o;e­
li1n:uCt· ami nuly lew cast'S recl uirc specific interven­
tioll, Tlwrapy is imlic:ucd if there is .1 compromise to
c;!nti:,( outpul or pcriplu;r.,1 pcrr"sinn. 00' ir the
rh�,thnt i.� of a tn)t' that ma)' dcsuhilil.C into a more
IIwlilotmtrll life·threatening <trrhylluuia SIKh as \'ClHric­
ul;;r fihrilbtiltl"l.
232
RECORDING AN ELECTROCARDIOGRAM
TIle use of radiotelemetric 01" COlltinuom ambul<lll)l}
(Holter) dectrocardi(lgraphy during the pcriopcnu\'e
period facilit;ues the prompt detection of :llThythmias.
! luw(.'Ver intermittent u� (lr paper (nce c!celro­
GHdiogntph), will be sufficient ror the diagnO!lis nr
persistent rhYlhm disturbance�. Electrocardiogn.ph�' is
indicated in the ponoper"ti\'t'" prriod if either
• a flopid pU!k rate is detec H'(!
.. that cannot be
explained hr lhe le\'el of pain Of cndotoxcmia, or
• the pulse rate is greater than 80 bpm.
Electrocardiography �h(ltL!d also be considered during
the e-v<lluation of horses with reported abdominal pain
but no clinical evidence of gastrointestinal disease, as
horses with primll!)' cardiac disease may presenl with
clinical Sigl1s of di�tres.� that can he mistakcn for abdom­
ina! pain.
A .itandard modified h<lse apcx le<ld s�tem is re("()JIl­
mended for the dUI:umentatioll of arrhythmia.�. Thi.�
comprises placing lhe rig-ht arm (RA or positive) cIcc­
trode over the hean b<tsc l)fi th(' right h'lnd �ide, tht' lel"!
anTI (I.A or nel!:;tti\"l�) e1c<:twde along thejugular gronv('
on the left hand side flf the llt.'Ck. The earth (\el"! lcg)
mlll m:utl'al (righ t leg) can be placed O\'er the scapula.
Recordings.shauld be made in lead I, which will produce
a JX).�i(ivc P wave and a nq�ativc QRS cumplex:. For
details of i nterpretation artln! EKr; readers arc ocferred
to Ihe re<:ommcncied lell:IS <II Ihl: end or this chapt(·r.
PREVALENCE AND CLINICAL
SIGNIFICANCE OF ARRHYTHMIAS IN
THE PERIOPERATIVE PERIOD
Ventricular arrhythmias
Vcntrkular <lrrhythmi<ls represent tht, most common
significant arrhYlhmia in !hl: postoperative period in
the horse. Their ECG ch<lraC:l('ristic;� arc oj" a wide
ahnormal QRS morphology. that is unrelated to a
prcl:eding P wave a.s .�hown in Figure I I .S. Vent.ricular
arrh),thmias can he defined as ventricular premature
dcpo];lTization� with a single (,Hopie COlllpleX, C()up!cL�,
Of trip le ts, reprL'SClIIing tVI() and three consecutive com­
plexes. 01' '·entl'icular t.achycardia as a susained
t velllriL­
Illar arrh)'lhmia wilh an increased nilI.'. Ventricular
t;tchrcardia may he further ddlncd as paroxs)"Inal, per-
1\iMing for up 10 Iwr.nty complexes or slIstained. An
accc:!cr.ttL·d idiO\·cntricular rh)'lhm s
i a sustaiul.'i.l ''CIl­
tricular <ll"rh)'"lhmia wilh a ...tc
... similar 10 sinus rhythm
and a.� such its diagnosis ma)," r:a.�i1y be mi'lli('d �' cardiac
allscultatioll alone.
 POSTOPERATIVE TREATMENT AND COMPLICATIONS 11

" VT RT VF

Figure 11.8 A sample from an ambulatory ECG of a horse 24 hours post-celiotomy, showing sinus tachycardia with isolated
VPDs (P,), a couplet of VPDs (P,), ventricular tachycardia (VT) progressing to R on T phenomenon (RT) and ventricular fib­
rillation (VF) leading to death. Movement artifact is indicated by A. The horse had multiple electrolyte disturbances
(hypocalcemia, hypokalemia, and hypomagnesemia), was acidotic and endotoxemic and had disseminated intravascular
coagulation

Vrnlrirulurprnnfl/uU' tiepoimiUltirm,\ decreased output. The myocardium may become

Sin!(le infrequent isolated ventricular premature depo­
Iaril-ations (VPDs) may be detected in normal horses
during ambulatory monitoring and are not considered
abnormal if they occur infrequently.
Fntlrirular tachycardia
Ventricular tachyc_ardia (VT) at rapid rates may signifi­
cantly reduce cardiac output thus reducing tissue per­
fusion. The increase in heart rate increases myocardial
oxygen demand, but this demand is not met because of
hypoxemic and predispose to further destabili7_ation of
this rhythm into ventricular fibrillation (YF) (Figure
1 L9). VF is usually non-responsive to therapeutic
agents and carries a hopeless prognosis in the adult
horse.
VPDs do not in themselves constitute a significant com­
promise to cardiac output, however they may be a
predictor of a destabilizing arrhythmia. In one clinical
study comparing the incidence of ventricular arrhyth-

5
, _" _
J.
' "Oy , , Y I V , 'j , " ' "'f , I

I --'I V I V ""i • Y -y -y Y , , -1 --;

A
V , , '-y

E
, ,

, ,

I I -, , , ,

-J\ J, J\ � _II II J\
F

, v , v\Jv\ftJ\ANv lv'N"-vJVVVV

Figure 11.9 Ambulatory ECG of a horse 36 hours post-celiotomy that had developed enterocolitis and septicemia. The ECG
shows sinus tachycardia (S) until after the administration of xylazine (100 mg Lv.) as an analgesic. The horse developed
asystole (A) and subsequently electrical-mechanical dissociation (E) and ventricular fibrillation {F}. Each line represents 30
seconds of recording

233
11 COLIC
mias in the postoperative period of both celiotomies
and elective orthopedic surgery, there was an increased
incidence ofvcntricular arrhythmias in the horses with
gastrointestinal disease. In the first 3 days postopera­
tively, H of the 35 horses having undergone a celiotomy
had ventricular premature dcpolarizations, of which
four had paroxysmal ventricular tachycardia, whereas
none of the control group had ventricular arrhythmias.
Despite this incidence, only one of the horses with
paroxysmal ventricular tachycardia warranted specific
anti-arrhythmic therapy. In the remaining horses, the
V1' resolved without therapy and ventricular arrhyth­
mias did not influence sumv,,! mIt's. In another _�ludy
of 21 cases of ventricular arrhythmias in the horse, 7
horses had gastrointestinal tract disease. Four cases
(19%) had ventricular arrhythmias in the 48·hour
period folloVl.ing celiotomy for strangulating or non·
strangulating lesions. Three of these cases died, one
because of gastrointestinal tract disease, one during
treatment for multiform ventricular tachycardia, and
the remaining horse died .3 months after discharge with
c\idence of myocardial fibrosis found on post·mortcm
examination. These studies indicate an increased inci·
dence of ventricular arrhythmias in the postoperative
period after gastrointcstinal disease. However their inci·
dence rarely poses a significant problem and specific
anti-arrhythmic agcnt.� are rarely required. The man­
agement of the underlying problem usually results in a
conversion to normal sinus rhythm.
Atrial fibrillation
Atrial fibrillation (AF) is characterized by an irregularly
irregular heart rate. The ECG characteristics are a lack
ofP waves and the baseline fluctuations around the iso­
e!ectic axis in flOe fibrillation waves (Fwaves). The QR.';;
complex has a normal configuration represcnting a
supraventricular rhythm. AF is occasionally encoun­
tered in the posloperath'c colic patient, but in isolatjon
it is unlikely to have any clinical significance. Therapy
should be delayed as spontaneous conversion may
occur. If AF persists then therapy with quinidine sulfate
should only be considered once the horse is othelWise
healthy. Side effects of quinidine sulfate include
hypotension, supraventricular and ventricular tachy­
cardia, colitis, and tympanic colic.
Bradydysrhythmias
ClinicaHy significant bradydysrhythmias are uncommon
hut can be seen in association with the use of alpha�
agonist.� in horses with underlying cardiovascular dis­
ease or severe cardiovascular compromise (Figure
1 1 .9). Treatment of bradydysrhymias caused by alpha.,
agonisl� should include the use of parasympatholytic
234
agent.� and/or alpha� antagonists. Atipamazole is the
only alpha.., antagonist available in the UK, although it
does not have a veterinary product license for use in the
horse. Following sedation with detomidine (lO-20 Ilg/
kg i.v.), atipamawle should be used at a dose rate of
JOG-I60 Ilg/kg intravenously. Atipamawle causes an
increase in heart rate after 2-4 minutes, although atrio­
ventricular block may still persist. Excessive arousal and
hyperesthesia may be observed. Intramuscular use of
alpha2 agonists causes less profound effects on heart
fate than when given intravenously and should he
considered in 'high-risk' patients where sedation is
reCjuin"d.
PATHOGENESIS OF CARDIAC
ARRHYTHMIAS IN THE
POSTOPERATIVE PERIOD
Horses that develop cardiac arrhythmias in the post­
operative period following celiotomy rarely have any
underlying cardiac pathology. The factors considered
to be important in the pathogenesis of these arrhyth­
mias include
• acid-base or electrolyte disturbances
• hypoxia
• poor myocardial perfusion
• endotoxemia and drug administration.
In humans and dogs it is recognized that autonomic
dysfunction produced by intestinal distention or pain
arising from the gastrointestinal tract may kad to
cardiac arrhythmias but, currently, there is no spccific
cvidence that. this occurs in horses. In horses with poly­
morphic ventricular arrhythmias, primary myocardia!
palholob'Y should be considered.
ELECTROLYTE BASIS OF CARDIAC
AUTOMATICITY
In the normal myocardia! cell the resting potential,
maintaincd by ion-selective membrane channels,
increases because of a slow influx of sodium ions until
the threshold potential is reached. Once the threshold
potential is exceeded there is a large and rapid influx of
sodium ions into the cdl, cau�ing depolarization.
Calcium influx maintains depolarization and causes
muscle contraction. Movement of potassium ions from
the intercellular space leads to repolarization. An
aerobic-encrgy dependent ion pump reSlor'es nOlI!!al
intracellular e!ectronegativity with sodium in the extra­
cellular space and potassium within the cell. Changes to
any ofthes(, ion gradients across the cell membrane will
 POSTOPERATIVE TREATMENT AND COMPLICATIONS
affect t.he automaticity of different parts of the
myocardium and thus enable the production and prop­
agation of an arrhythmia.
Potassium
Hypokalemia can occur due to loss ofsenlm potassium
through the gastrointestinal tract or kidney, or by
dilution of existing serum potassium. Dilutional
hypokalemia can ocnlr due to the prolonged use of
polyionic intravenous fluid therapy solutions, such as
lactated Ringer's solution, that do not provide mainte­
nance requirements for the normal horse. Serum potas­
sium concentrations arc aflccted by the patient's
acid-base status. Potassium is a largely intracellular
{:ation, which is exchanged for extracellular hydrogen
ions during acidosis resulting in an increase in extracel­
lular potassium concentration despite total body losses.
Therefore potassium abnomlalities may go unnoticed
in t.he face of a co-existing acidosis. During prolonged
postoperative ileus, both gastrointestinal losses of potas­
sium and prolonged fluid therapy occur, thus placing
these patients at an increased risk of developing
hypokalemia. Because of gastrointestinal loss of hicar­
bonate there may be co-cxisting metabolic acidosis
which can result in under diagnosis of this electrolyte
disturhance.
Arrhythmia.� associated with hypokalemia are due to a
reduction in the anion gradients of the cell. The reduced
ion gradient of potassium changes the resting potential
so that there is a reduced difference bety,,'een the resting
potential and t.he thre5hold potential. Because there is a
reduced requirement for spontaneous influx of sodium
to reach the threshold potential, the cell becomes more
susceptible to spontaneous excitability which can lead to
ventricular arrhythmias (Figure 11.8).
Rapid intra\'enous administration of potassium chlo­
ride is contraindicated as bradycardias, induding atrial
standstilI, can occur. Potassium should be given by a
slow intravenous infusion at no more than 0.3 mmol
kg I h- I. For maintenance 20 mmo! of potassium chlo­
ride can be added \0 each liter of lactated Ringer's
solution.
Hyperkalemia can occur in patients with hyper­
kaIemic periodic par.l\ysis, anuric renal failure, or
uroperitoneum. These individuals are at particular risk
of developing atrial standstill and third degree atrio­
ventricular hlock, but fatal ventricular arrhythmias may
also occur. Life-threatening hyperkakmia is treated
I'.-ith insulin (0.1 IV/kg) with dextrose (0.5-1 g/kg).
The extracellular concentration of potassium can also
be reduced following the intravenous administration of
sodium bicarbonate ( 1 mrnol/kg) and the slow admin­
istration of cakium (0.2--0.4 mlJkg of a 23% solution of
11
calcium borogluconate) may have a cardioprotective
effect in hyperkalemia.
Calcium
Hypocalcemia occurs due to rapid losses into the
gastrointestinal tract. Calcium is important for cardiac
muscle contractions and for maintaining depolariza­
tiOll after rapid sodium influx into the cell. Profound
hypocalcemia can result in ventricular tachycardia
(Figure 1 1 .8). The detection of hypocalcemia can be
complicated by abnormalities in serum albumen.
Calcium is largely protein bound in plasma, and alter­
ations in serum albumin win be reflected by similar
changes in total serum calcium. Although algorithms
havc been produced to equate ionized calcium to total
serum calcium and serum albumen, their results are
unreliahle in the horse. Determination of ionized
calcium (the metabolically active component) is more
useful (normal ionized calcium 1 .3--1 .6 mmol/I).
Calcium can be administered as calcium boroglu­
conate, given by slow intravenous infusion in saline
(0.2-0.4 ml/kg of a 23% solution of calcium horoglu­
conate, then re-assess calcium status). Excessive admin­
istration can cause atrioventricular hlock at moderate
hypercalcemia, profound hypercalcemia can result in
ventricular fibrillation and death. For maintenance, up
to 40 ml of 23 % calcium horogluconate can be added
to each 5 liters of lac.tatcd Ringer's solution to be given
intravenously over 2-3 hours.
Magnesium
Magnesium is an intracellular cation and therefore
plasma concentrations do not reflect total body con­
centrations. Magnesium has many intracellular func­
tions but its cardiac effects are mediated via its actions
on proton pumps, affecting intracellular calcium and
potassium transport across the cell membr,mes.
Hypomagnesemia was the important electrolyte abnor­
mality detected in horses with ventricular arrhythmias
after colic surgery, particularly when ac.companied
by hypokalemia and hypocalcemia (Figure 1 1 .8).
Magnesium is used in other species as an anti-arrhyth­
mic agent even when no underlying hypomagnesemia is
documented. The exact mechanism of action of mag­
nesium therapy is still to be elucidated but may repre­
sent a calcium channel-blocking ellect. Magnesium
sulfate can be administered by slow intravenous infu­
sion or repeat bolus injec.tions (Table 11.6).
Other factors
Acidosis, myocardial hypoxemia and endOloxemia will
affect the serni-pcrmcable selec.tive ion channels of the
235
11 COLIC

ceIl membrane and can increase cellular automaticity
and therefore predisp(l�e to ectopic foci of depolariza­
tion. Because acidosis is usually a manifestation of
peripheral under-perfusion, intravenous fluid therapy
with polyionic solutions is suitable for correction of
add-base disturbances if there is normal renal func­
tion. Hypoxemia is also likely to reflect hypotension
and should be corrected by administration of crystal­
loids or colloid therapy.
ANTI-ARRHYTHMIC TREATMENT
Specific ami-arrhythmic agents are only indicated In
severe life-threatening arrhythmias. In all cases, allY
underlying cause must be determined and !Teated.
Rapid Of multifocal (more than one contiguration of
ventricular complex) arrhythmias and the presence of
the R on T phenomenon are indications for specific
therapy. Th� R on T phenomenon is a ventricular
rhythm where the QRS complex is associated with the
preceding T wave (Figure 1 1 .9). This rhythm is unstable
because it represents depolarization and repolarization
occurring simultaneously and thus is likely to progress
to fibrillation. Therapy should also be considered if
there is a significant compromise to cardiac output, this
may manifest as weakness, collapse, or increases in
serum creatinine due to poor renal perfusion.
ANTI-ARRHYTHMIC THERAPY IS WARRANTED
IF THERE IS
RAPID VENTRICULAR TACHYCARDIA GREATER
THAN IOOhpm
MULTIFORM VENTRICULAR ECTOPY
Ron T PHENOMENON
SIGNIFlCANf HEMODYNAMIC EFFECTS
Specific agents
Doses of drugs for tbe control of ventricular arrhyth­
mias arc listed in Table 1 1 .6. Ventricular alThyt.hmias
can be treated with class I anti-arrhythmic agent�. These
drugs block sodium channels and therefore stabilize
the membranes of excitable cells The use of c1as. �
IB agents, such as lidocaine (lignocaine), has bl;Tn

Teble 11.i DNoJ-UIed for"" trtattnent of alt'dlac lti'i'hythmils

D.... Indfcftlonlf DOle end .dministr.tion Side effects

Lignocaine hydrochloride Ventricular arrhythmias 0.5 mg/kg Lv. q. 5 min eNS excitability

Quinidine gluconate Ventricular and supraventricular 2.2 mglkg bolus q. 10 min hypotension,
arrhythmias up to 10 mg/kg total, colitis,
or 0.7-3.0 mg kg-' h-1 arrhythmias
diluted in saline

Quinidine sulfate Supraventricular 10 gf450 kg p.o. q. 2-6 h hypotension,

arrhythmias colitis,
arrhythmias

Propanoloi Ventricular tachycardia 0.05-0.16 mglkg Lv. b.Ld. hypotension

Procainamide Ventricular and supraventricular 1 mg kg-' min-' Lv. hypotension

arrhythmias up to 20 mglkg

MagnMium sulfate Ventricular tachycardia 4 mglkg Lv. q. 5 min

Hypomagnesemia up to 50 mg/kg total

Atropine sulfate Bradydysrhythmias up to 0.1 mg/kg Lv. s.c. may induce initial
bradycardia if given
i.v., ileus

Glyoopyrro!ate Bradydysrhythmias 0.01 mglkg Lv. ileus

Atipamazole Alpha, agonist-induced arrhythmias 100--160 IJ.glkg Lv. excitability

�xamethasone Immune-mediated myocarditis 0.02-0.2 mglkg use reduclng dose

or profound AV block regime

236

rt�,omme]J(led for ven t.ricul ar arrhythmias because of
tht short duration of action on sodium channels, which
is Ies.> likely to affect the underlying sinus rate.
Lid(llaille (lignocaine) can lead to focal or generalized
sdnlres, thus horses receiving lidocaine (lignocaine)
should be monitored carefully and the infusion discon"
tinued if muscle fasciculal.ions arc observed. The class
I B drugs, such .IS quinidine and procainamide, which
an� classically reserved for the treatment of supraven­
triclilar arrhythmias, lack the neurological side effects
of lidocaine (l ignocai ne ) and are therefore considered
the dr ugs of choice for the treatment of ventricular
arrhythmias in the consdous horse.
In!r;wenous magn esi um snlfate has been used suc­
n'ssfu ll�' as an an lidysrhythmic agent which is effective
Hl patients evrn with normal serum magnesium
cOllcemrations. Its use in the horse has not heen fully
c\·al uated.
I'mpanolol , a beta-blocker, may he heneficial in
Ire,Uing ventricular tachycardias together with other
ag("nL�, but should be used with care if there is compro­
mised myocardial function as its usc will further reduce
cardiac output.
AFTERCARE AND PROGNOSIS
Onre drug therapy has commenced, the patient should
1)(' ohser,ed carefully for sign> of cardiac and non­
cardiac complications. The underlying calise of the
cardiac arrhythmia must be addressed. Measurement of
the cardiac i�()enzymes of lactate dehydrogenase and
cre<lline kinase can he useful to document myocardial
!It'CH)sis which may ha\"C occurred, and if increased,
<Inti-inflammatory agents are indicated. The prognosis
lill" most arrhythmias occurring in the postoperative
period will depend on the ability to identify and treat
the underlving cause(s). The prognosis \�111 also depend
on the type of arrhythmia, for example if there
lTlultifocal sustain ed ven tricul ar tachycardi a or R on T
phcTlomeno n then the prognosis is guarded. In the
m�jority ofcases with monomorphic ventricular arrhyth­
mias that resolve "'lthout spcdfic therapy, the prognosis
is good and the arrhythmia is unlikely to recur once the
primary g-astrointestinal lesion has resolved.
BIBLIOGRAPHY
Treatment of endotoxemia
Baflon M 1-1, Bruce E 1-1, �loore.J "", �I al. ( 1 99S) Effect of
Ilimor Ilec)"()_si� ranof antibody giv(�n to horses during
"arl�' experimentaHy induced endotoxem ia. Am.J. V;'I. &.
'i():7�)2-7_
POSTOPERATIVE TREATMENT AND COMPLICATIONS 11
Barton :\1 H, :\1oure H :-J, 1\orton N ( 1997) Effecl� of
pentoxi!yliine infusion on response of horse� to in vivo
challenge exposure with endotoxin. Am. .f. Vtl. /Us.
58:1291-9.
(;argilc .1 1., MacKay R .l, Dankcrt.! R, Skclley L ( 199.'i) Effect
of trealment of Miniature Horses with a monoclonal
antihody again�t equine tumor necrmi� fact (T:\,F) on
clinical, hematologic and circulating T:">:F H,spnme� giwn
endotoxin. Am.J. Vtl. JUl. 56:1151-9.
Durando M M, MacKay R.J. Linda 5, Skelley l.A (1994)
HfecUi of polymyxin B and Salmonella Iyphimurium
,mlherurn on h()r�('� given ('ndO(oxin intra\·enous!y. Am. f.
\'el. Hr.. 55,921-7.
Olson :\ C, l leIl),er P W and DodamJ R ( 1 995) Mediators and
vascular drecl� in respome to endotoxin. 8r. \/el. .f.
151:489-.>;22.
Shuster R, Trauh·Dargatz.J, Baxler G (1997) Su"'''y of
diplomates .of the American College ofVrterinary Internal
Medicine and the American College of Veterinary
Surgeons regarding clinical aspects and treatment of
endotoxemia in hurses. .f. ,1m. I'fl. Mfd. ,bsoc. 210:87-92.
Spapcn H, Zhang Ii, Vincent J J. ( 1 997) Potential therapeutic
arnid� in endoroxemia and mh(,r f.orm• .of
'-ah", of laz
sepsis. SIwek 8,321-327.
Nutritional support after alimentary tract
surgery
l.<:,wis, I . D ( 1 995) F.quine Clinical Nutrilion. Williams and
Wilki"" Philadelphia, pp. 389-417.
Ralston, S L (1991) Fe<!ding sick horses. In Large Animal
Cli"icallVu/rilion, .J M �aylor, S L Ralslon, (cds). Mosby
Yearbook, St Loui�, MO, pp. 432-46.
Postoperative shock and organ failure
Arden W A ( 1 999) Circulatolj' Shock. In Equint SUTgt1)' 2nd
cdn,j A Aucr and.! A Stick (cd.). \II B Saunders,
Philadelphia, pp. 40-5.
Byars T D ( 1 999) :\fultiple organ dysfunction syndrome. In
l'rortl'dings oflilt Blv.rgms:; f;qui.w Mtdiriru and Crilical Dm
S),mposium. Octoher 24--27, Lexington, Kentucky.
llumJ M, Ed"·.lrds G B and Clarke K W (1986) lncid<!nce,
diagnosis and treatmem of postoperalivc complications in
colic cascs. f;quint Vel. .J. IS( 4) :264-270.
Moore.! A ( j 99()) Pathophysiology of Circulatory Shock. In
is a
Tilt EqllilU' Acul� Abdomen, l\ A \',-'hite (ed). Lea and
Febiger, Philadelphia, pp. 90-9.
MooreJ A ( 1 999) Fndotoxemia and Ihe _<y_'temic
inllammatory response syndrome. In Procftdi"gs oftht
Blufgrass Fquin� M�didn' "",I en/iml e,m S)'mpo,ium,
October 24--27, Lexington, Kenlucky.
Orsini J A ( 1 99(1) Shock. In I-AplilU' Surgtry, ht edn. J A AU<!f
(ed) \Ai B Saunders, Philadelphia, pp. S I -5.
Postoperative pain
C!.lrk.! 0, CI Hrk T P ( l 999) Analgesia. In V;'I. elin. N. "'m.
�"inePracl., S A Turner (ed.). W B Saunde�,
r
Philadelphia, 15(3):705-23.
Drossman D A ( 1 998) Chronic funnional abdominal pain. In
Gastroj"te.,linai and Liv"Disrase6th "dn, �I Feldman, B F
Scharschmidt, M H SIeisenger (eds) W B Saunders,
Philadelphia, 1998, PI' 90-7.
237
11 COLIC
Glasgow R E and Mulvihill SJ ( 1 99R) Ahrlominal pain,
induding (he acute abdomcn. In Gll-llroinuslillal and LiTltT
Dismlf 6!h edn, M Feldman, B F Scharschmidt, "'1 H
Sleisengcr (cds). lA' B Saundns, Philadelphia, PI' 80-89.
Muir W W ( 1 99S) Anaesthesia and pain management in
h(>r�c�. l:'qw'ne Vft. j.,-duc. 10(6):3:1.1-340.
,
\\ hit� :-: A ( 1990) Examination and diagn"-'is of th" acute
abdomen. In 17lt Equint Actlln\bdmnn!, N A While (cct.) .
Lea and Fcbigcr. Philadelphia, PI" 102-42.
While ;-.; A and Byars D T ( 1 990) Analgesia. In The Equine
Awlr tlbdmllro, 1\ A White (cd.). Lea and Fcbig-cr.
Philadelphia, pp 154-9.
Abdominal adhesions
Baxter G M (199J) intra-abdominal adhesions in horses.
Compo Uml. Edur. Pmcl. I'd. 13:1587-97.
!�axter G M, Broome T E, Moore J :\ ( 1 989) Abdominal
adh('sions �fu�r small intestinal surg('I)' in the horse. V�I,
SUTf{. 1 8 409-414.
Raxter G M,Jackman R R, Eanes S C, �I aL ( 1 993) F�i!ure of
calcium channel hlock,,,]e to prevent intra-abdominal
adhl�sions in ponies. 1i.1. S"rg. 22:496-�O.
Baxter G M, Parks A H. Prasse K W (1991) Effecl� of
explor�to[1' l�parolOm}' on plasma �nd peritoneal
",,�guJati()n/!ibrinoJysi� in horse.�. Am.]. V,I. lV.I. fi2:1121-7,
(:oll�I'" C, Barton M H, I'rasse K W, �I al ( 1 99,,) Intravascular
and peritoneal coagulation and librinolysis i n horses with
anile !!;as!roimestinal tract disease. ./. .-i.m. l'ft. Med, Ass",..
2()7:46!>-70.
DiZ.".ega G S ( 1 994) C(lnt('mpor�ry arihe,ion prn'e!ltion,
Fnhl. SimI. 61;219--3fi.
Du{'harme N G, Hackett R P, Ducharme G R, ,I aI, ( 1 983)
Surgic�1 lre�lment of colic: Results in J il l horses, V,/. Surg.
12:206-209.
Ellis H ( 1 982) The c�uses and prewnlion of inf.estinal
adh<'sions, Br. ./. '<;"'g. 69:241-3.
I lague B A, Honna� C M, Berridge B R, E�ster.! l. ( 1 998)
�:valuation of pos\openltive perit{}ne�l lavagl' in standing
horses for prevention of exp�rimentally induced
abdominal adhesions. J,"I. Sur/<. 27:122-126.
Hay W 1', Mueller P O E ( 1 998) Intra-abdominal adhesiom.
In Cunml Tnhniqutl ill Equillt SUTW')· alld l..ammm 2nd
"dn, N Whiw ..! Moore (cds) W B Saunders, Philadl']phia,
PI'. 307-310.
Holtz G ( 1 984) Prel'ention and manag('mem of peritoneal
adhesions. FroiJ. StniL 41;497-:>07.
Kuebdhe{'k K I .. Slone D E, May KA ( 1 998) Dfect of
OIl1('ntectomv on adhesion formation in horses. \",,1. Surf{.
�7:132-137. . metodopramide for the treatment of ileus in horses
I.ullflin C, Sullins K E, White N A, ,I aL ( 1 989) Induction of
periloneal anhesions with small intestinal ischemia and
di�tention in the foal. fquinr Vel.}. 21 :451-458.
MacDonald M H, 1'�5COC./ R. Stover S M, tI aL ( 1 989) Survival
after small int.c.�tine H'.":ctinn and anaqomosis in horses.
I'd. SUI"f{. 18:415-23.
Moll II I), Schumacher.!, \Vright.l C, el al. (1991) Evaluation
of sodium carboxymethylceHulo;;e for prevention of
""perimentaHy induced abdominal adhesions in ponies,
Am. f. \'�I. Rr;, :'>2:88-91.
.\-fudlel: P 0 �:, l lunt R 1, Alkn D, Parks A H. H�\' W P ( 1 995)
·
Illlfapt'riloneal use or sodium rarboxymethylcellulo'l' in
horses undergoing exploratory celiotomy. Vel. Surg.
24:112-117.
Parker.! E, Fubini S i., Car B D, el "t. (1987) Th" liSt' 01
238
Ilcparin in preventing intra-abdominal adhesions
secondary to �xperimentaHy induced peritonitis in the
horse. Vf/, Surg. 16:459-62.
I'arker./ E, Fubini S L, Todhunter R./ ( 1 989) R<,trmp"cti\'e
evaluation of repeat celiotomy in 53 horses wilh acme
gastrointestinal disease. \'.1. SuW, 18:424-3 1.
Pbillips T./, WalmsleyJ P ( 1 993) Retrospective analysis of the
results of 151 exploratory laparotomks ill horsl's witb
gastrointestinal dis('ase. J-."qui'lf VH}. 2.�:427-3l.
I'ijlman H M, Oil)")" P j , Brommer E.! P, Verner I I M ( 1 994)
Prevention of adhesions, t�·um. .f. Olistrl. Gyntml, l&prod.
BioI. 53:155-{j3.
Ragle C A, SnyderJ R, Meagher D M, fI al. ( 1 992) Surgical
treatment. of colic in American ),finiature Horses: 1 fi cases
( 1 9BO-I9H7).). Am. IItl. Med. Assof. 201:329-31 .
Sch�..mme M, Bul�on R ( 1 997) Abdominal adhesions - h..v"
we made any progress? t Jjuint Vfl, J. 29:252-254.
Southwood L I" Ba"ter G M ( 1 997) Current concepts in
management of abdominal adhesions. \.,,/ r.lin .>,,'• •;m.
Equine Prado 13:415-35.
Southwood L L, Bax!.er G :\1 , Hut<hison .l :\:I, Shuster R ( 1 997)
Survey of diplomates of the American College of
Veterinary Surg<'ons regarding postoperative intra­
ahdominal adhesion formation in borses undergoing
abdominal "'rgery. J. Am. \fet. ,"',d. As.<or. 2 1 1 : 1573--fi,
Sullins K E ( 1 990) Inwstinal adh{,.,ion r<,dunion. In Th�
f:quilit Amlf Abdomen, ?\I A \Vhite (ed.) Lea and Febiger.
Philadelphia, p. 245,
Sullins K E, White 1\ A, Lundin CS, tl al. (1991) Treatment of
iSLhemia induced pnitoncal adhesions in fnab. Vet. Surg.
20:348.
Swanwick R A, Milne F./ ( 1 973) The non-suturing of parietal
peritoneum in abdominal surgery of the horse. V,I. /Vr.
93:328-35,
Vachon A M, Fisdln A T ( 1 995) Small intestinal herniation
through the epiploic foramen: ,,3 Ca5{" ( I 9R7-1993)
t
Jjuine Vtl,j. 27:373-80.
Yaacobi Y. Israel AA, Goldberg E I' ( 1 993) Preve"tion of
postoperative abdominal adhesions by tissue precoating
with polymer solutions. J. Surg. Rts. 55:422-6.
Ileus
Adams S B, I.amarC H, Masty.! ( 1 984) Motility of the distill
ponion of the j�junmn and pelvic t1exure in ponies:
En..,c�� of six drugs. Am. J. Vft, He,I, 45:795-799.
Hliks!ager A T, Bowman K F, Levin .! F, el a[ ( 1 994) Evaluation
of factors associated "ith postoperative ileus in horses: 31
c�ses ( 1 990-1992). j. Am. Vtl. MFd. ..hsllC. 205:174B-1752.
Dart AJ, l'eauroiJ R, Hodgson D R ( 1 996) Hficacy of
following small int...stinal surgery: 70 cases ( 1 981-1992).
AU,I'. V,t.}. 74:280-284.
Davies.! V, Gerriug E L ( 1 983) EITect of spasmolytic analgesic
drug., on the motility patterns of the equine small
intestine. {k,. V.t. Sci, 33:334-339.
Eades S C, MooreJ :-.I ( 1993) Blockade of endotoxin-induced
cecal hypoperfusion and ileus with an alpha"amagonist in
horses. Am,). Vtl. lVJ. 54:586-590.
Gcrring E L, HuntJ M ( 1 986) Pathophysiology of (,quint·
ilells: elTI'ct of adrenergic blockade, parasympathetic
stimulation and mctodopramidc in an eXpt'rimental
model, l�quinf �ffl. J. I8:249-25.�.
Gerring r: L, King.! 1\, Edwards G B (1991) A multicenter Inal
of cisaprirle in the prophylaxis of equine postopt'ralive
ibiS. Equ;". ""I. i';duc, 3:143-145,
 POSTOPERATIVE TREATMENT AND COMPLICATIONS 11

KingJ �', C.crrinM }: L (1<Ja9) A",Utgollism of endotoxin­
i"dun:d di�rtl plion of cqui ne howd mUlilif)' by f1un;>:;n
.md phcn�·In..llaJ.on('. f"ijllm" l'H.). snppl. 7:81-5.
l.t�,·r (; U. ;\kniu A M, :-':c\,wirth L. tl nl. (1998) Effect of
Alpha.-adrenc!l,';c. clloline!").
';!". anri nOIl-steroKial anl.i­
,nll,,,,,mamry dn'!;'''o myc>(:kClrical 3CI;"ily of ilcum,
(ccu.n. and right "('nlTal colon and creal emMillg of
roldinlJbded markc'r,; in dinicillly normal ponies . .1m.J.
lit. IV... 59::-IW-:-I:l7,
1.(.'\I",r (; D, Merrh ,\ M, �eu..�rth I� d nl.. (1998) Effect of
" 1�1hr<lInydn t�ClObi"n3!e 0" ",yuck-cuic acthity of
ikum, cecum. and l'ij::;h t venLral col"n, lind n:ntl emptying
ot ntdinJaix'led mark.cl"$ m clinically norm�1 ponies. .4"'-1-
I'". I�. ;19:�28-�34.
:\\al",\., E D. TurnrrT ,\. Wibon J H (19911) !llIral'('nOm
lior><:Ain.:: for Ill(! treatmen t of i!cu•. Sj.�lh Colic SY'''f''>,<;um
/(',ll'lIrrit ,1/lllram; amtr,ICI 42.
N.l\'afr.. C B, ROll.....I AJ ( 1 9�16) Ganroinlestinal moti lity and
discasl' in \;II'gc ;uo!tllals,). V,t Inlml. Mtd. 10:51-,';9.
!>"rk� A II. StickJ A, Arden W A, ,1 al. ( 1 9119) Effects of
distcillion �nd nCtlSlil!'minc on jejunal '-asn>iar rcsist.mec,
H"ygl'!l uplaltl: and intraluminal pressure fhang'" in
p"llic�. Am.). 11ft. JVl, :'10:.'i4-!',1!.
}kynold'J C. Putman ? E ( J �)2) Pmkinclie agcnt\.
(;all,,,,,qll!l'(l/. r.lin. N. Alii. 2J :567_:'196,
Sama S K, (llt.emn<ln M F (1993) .l.iYC:lClectriC ;md collU-dctik
a'li"ilil':5. In AIIII.I nt (;Il'/>Ilinl�.<linal Alo/iii/] h, H,allh AmI
IJi.lrtl.II', � M Schusler «(."(1.). Williams am Wilkin�.
I\ah imnrl�. pp. �42.
Wi..cman L. Fauld� D (1994) CjSllpridt,= an updated re,;ewof
'IS pharmacology and Ih"r"p"III ;" cflk;lq a.� a prokinclic
in ga,\trOintCllinal motili!)' d;�onlcB. Dru,, 47:116-152.
Impaction at the anastomosis
Frt't'mll:n D F. ( 1997) Suq;:cry <IfIhe sman illiestine. (.. In_
Ui". N. A"I, i':-f,,;qf l'I'«rl. Surgical M.1I"a�"'rnl ofCa/it
11:261-:\01 .
rar"�'I'J E , FlO!>ian S L Ttldhunlc,' R J ( (989) Retro('p<,<:(i,'"
" '"<lIUaliol1 of repeal ccliowm)' in 53 hm""es ....ith acute
g�.<.Irnilll�_'tin..l di�a�. I'n, SUfi:, [11:424-431
Ros, M W. Cullcl! K K. RUI !c.o"'skiJ A (1990) Myoel«tric
",.til'il)' of dot: il l'um. (" 'nun. and right "cntral colon in
),'>!lits dul'lng illtt:rdigestil" :, llonf" " ding, and dig,,,ti,,,,
pcriod�. ,1m,.!, I'", }V,. 51:5t;].
Incisionai complications
Ducharme :'" G, Freeman D E, Ste�!c.d R R, Dean P W, Young
\) R ( I ('192) Principles of in(C$Lina! surge,)". In r:qui"F
"",,,1,.'"1. lsI eeln) AAu"r (cod.), W B Saund"r�.
Philadelphia, p, :.125.
l1"nl1;\� C M, Cohen N ( 1 997) Ris!c. f.telon for wound
inf..ctinn foll".,ing .;elfntom)' in hOr.ln. 1 Am. V,I. M,d.
:'-'w·. 21O:7�t.
InKk-Feh rJ Eo 8;0>:,..,' (; M, I·!<,.,...
n! R n. Trnuc:r C W.
..
Sla�hak T S (1m) B3cler,al eul tminp; of"cnlraJ m..-dian
'TliolOmics for prcdK:lioli ofpt�lop.,r.!lil'L' ;nci�Jonal
t"CJlnplicatioJls in horses. �'". .""�. 26:7-13.
Ko.Iw�" (: E, 5t�ha" T S (19��) Preclisposin.: factors.
Wilson D A, Baker GJ, Boel'<) MJ (1995) C..omplicalion, of
celiotomy inci.<.ion$ in horK$. V". SU11l. 24:506-514.
Postoperative complications -
myopathy/neuropathy
Bloom 8 A. Valentine BA, Glc(."(1 R D, Cable C S (1999)
Poslal1lteSl.hell<: re(:umhenq in a Belgian filly with
'SiH:.-hari(k .'II!>r"ge mynpalh)'. VI'I'. IW.. 144:73--7�.
p<>I)
(;1=<1 R D ([996) J>u,;tal�"ht'l;" my"palhy. In r:qwn' Orthofxdic
S"rn-A Nixon (ed,j. M�by. SI 1..<I..;';, MO, pp 343---349_
f faguc H A, ;\1artinc1. t: A, lbrtslidd S M ( !Y9H) HlecL� of
high·dose gt:ntamkin wl fale on neuromuscular blockade
in halothan_Il��hetiled hona. Prrx. Am, Anoc, t'quirtt
/1'ad. 44;240-241 .
Harris I' A (willi COntnbUliollS hy :\la¥hew J G ) (199M)
Ylu�culO!kelcllll dire;ase. In fquil11 fl1lrrnal Mfdiril1t, S M
R"cd, W M n;ayl)' (erM. W B Saunders, Philadelphia, 1998,
pp. 388-91 .
Johnson B 1) , H�alh R IJ , Bowman B , Phillips R W, Rich L D,
VO.IS.! I. ( 1 978) Serum chemistI)' chan ge� in ho,,,,,es during
am,'1thcsia: A pilot study im'es{i galing Ihc pos.�ibk c;1U�es
of postanesthetic m)'osi ti� i n hor�s. J. Equint MId. SlIrg, 2:
10')... 122.
1,,,,, Y-I l L, Clarke K W. Alihl,ai H I K, Song D ( 1 99H) EIl"cn_
"f dopamine, clohUl.1mine, dopexaminr., phenylephrine,
and !ialine soIulion on intrnmwcu lar blood flow and olher
c.ardi<Jpulmonal'}' ......rt..blt::s in ha!ulh..nc.....anl"!jthcti7ed
pO" le�. ;,,,,.). 1'''' J&,� f>9: 146.'-72.
Postoperative complications -
thrombophlebitis
BaYlyW M and Vale 8 H (198'1) Intr.l.W'nous cathclcrizalion
. ';nd associau!d problems ill the horse_ Co",p. Oml. I-AI«.
l'mrl, \tl, 4 Sm-2�7.
fl;I<Oll I. R (19!lIJ) JU�lIlar Ihr(lmbophlebili.� (,,-wlting fmRl an
a'LlIe.sth"lic inducti()(l tech nique in the horse. l':q..itu Vd..J.
22(3) 177-179,
EttlingerJJ, PiI!merJ 1:: ami BeuSt'" C (199'.1) Ba<et.eria found
on !nlr.."enolls ealheleN removed from hOl'se�, \on. RI!<.
1:'10248-:249.
Gerhards II (1987) (Antithwlnbin 11\ determination in the
hor�. Refenmct' "allit's and acqllir"rl ant.ithromhin III
dclkienq'.) TlpnrlLI. Pmx. E'i 47_:;5.
Cuhards 11 ( 1 9f!7) (1IYI'H"""gLllahiliLY _ an eLiologica! faclor
ill the deyclupmt:llt ofjllj::;ulu "ein lhrombmis in horSt'S.)
D/,o;cit. l;m",.I. WIC/lr, 94 173_174,
Gerhards H and �:b�rhardt C ( 1 9R8) PI<lsma hepari n values
and hemostlt!is in e{luid� after subclIIaneous
admini....:rati<>tI nft',...·. d.»e calcium heparin. Am.J. \/tl. !Us.
4913-18.
Holland M. Kcll)' A B tl ",I. (1986) AllIithrombin III a((h'ity in
hor�C:$with large colon tOl"$ilJO . ..l,rn.)' VtJ. &. 47(4)
897-900.
Mum., B R and HinchcHf K W (lW'l) Heparin: a review of ilS
phamlat:nlog)' and ther..[Xlllic 'IS(' in hOl�s.J \w. lnl.
Mtd. 8( 1) 2�:V->.
Morris D 0 (1989) Thrombophlebitis in horsn: the
conuibutioo, ofh"moslalK: d)",fu""I>O., 10 p;< 11">g
..nes.is.

diagnosh. and mll:llilgc:mcnl of large ahdorninal dt:fc:clS in C4I>Ifp. Coni. F4uf. Pm" . I'lf. II 13S6-1394.
hflrstsalld call1e. ). ,t'''. Yd. ,\1,,1. A�......., 2()(":607�i11. ;\torri� J) J) (I!)!II) F.nrlllloxemia in hones
.. ). Yd. Inf. Mm. :>
I'hillips TJ, \\!am�k1'J I' (1995) RCUUSPCCli\"c ana!)'Sis ofthe 167-181.
r..�"h\ of 151 uplorn\omies in holYS ..itll gastroim�tina[ �un"t\< R ( 1 99tH F.ndnlO�.,mia ill hu,.,;c;.. III Pr",'icr2() {21
c\i.'<:'<I'K·. fA(vilit \'�. J. \!5:4Zi-43L ��.

239
11 COLIC
Reef, V B ( 1998) Cardiovd..,wlar ultra.onography. In Equine
D;"R"OMic Ultrasound, VB Reef (I'd.). IN B Saundt'r�,
Philadelphia, pp. 215-72.
Spurlock S L and Spurlock G H (1990) Risk factors of
catheter related complications. Comp. ConI. Edu(, l'rod.
\·..1. 12(2);241-24H.
Spurlock S L, Spurlock G H �I ,,{. ( 1990) Long-term jugular
vein catheterization in horses. J. Am. Vfl. Med. AlI"". 196
425..-43().
Traub-Darga!]J L and Dargatz D A ( 1 994) A rctr<Jspcctivc
study of vein thrombosis in hor.o;c. treated with
intraw�nous fluids in a veTerinary teaching hospitaL J. Vet.
Inl. Mfd. 8(4):264--256.
Postoperative complications - peritonitis
Blackford] T, Schneiler H L, van StcenhouseJ L and Sanders
W L (1986). Equine peritonea! fluid analysis following
celiotomy. PrrK. Equin' Colic &s. Symp. 2:112-115
Fontaim, G L, Rodgerson, D H, Hanson, R R and Steiger, R
( 1 999). Ultrasound evaluation of cquine gastrointestinal
disorders. Conlp_ Gmt_ Edw;. Pme/. V�I. 21,253-262
McIlwraith C W (l982). The acute abdominal patient,
postoperati.'e management and complications. �ret, Clin.
N. Am. l.argeAnim. Praet. 4:167-184
Phillips TJ and Walm�leyJ P ( 1 993) Retrospective anal�is of
the ,-esults of 151 exploratory laparotomie.� in hor�es wilh
g:utrointcstinal disea.�es. £l[ui1U' Vel.J. 25:427-431
S;Hlt.\chi E M, Grindem C n, Tate L I' and Corbett W T
(1988). Peritoneal fluid anal�'sis in ponies after abdominal
surg{'ry. Vtl. Surg. J 7:fi.-9
Van Hoogmoed L, Rodger L D, Spier SJ, Gardner I A,
Yarbrough T B and SnyderJ R (1999). Evaluation of
peritoneal fluid pl!, gIUC08{' concentration, and la<:tate
dehydmgenase activity for detection of septic peritonitis
in horse.� .J. Am. Vrt. Mtd. Assoc. 214:1032-1036
White N A (1990}. lnten�ivc care, monitoring, and
comp!ication� ofanilC abdominal disease. Peritonitis. In
Thl F"l',ine Arlll" Abdm1um, N A Whit(' (cd_) Lca and
Febiger, Philadelphia, pp. 323---5.-
240
Postoperative complications - laminitis
Eastman TG, Honnas C M, Hague B, tl aL ( 1999) Ikep
digital flexor tenotomy a� a treatment for {'hron;c
laminitis in hor�es: 3� ca�es ( 1 98B-1997}. J. Am. Vet. M,'d.
Anac. 214(4), 517-9.
Pollitt C C ( 1 999) Equine laminitis: A revised
pathophysiology. Proc. ."-m. As.IOC. Eqllim Pract. 45: I H8-192.
....'. hite :\ A { l 990} Intensive care, monitoling, and
compIkatioTlS of acute abdominal di�ease_ In Tlu F.quillf
Aru/t' Abdomrn, :\ A \\-'hite (cd.). Lea and Febiger,
Philadelphia, pp. 32fi.-30.
Postoperative complications - colitis
l'arraga M E, Spier Sj, Thurmond M, Hir<h 0 ( 1 997) A
dinkal t.rial of probiotic administnttion for prevention of
Salmonella shedding in the postoperative period in hon;('_�
with colic. I Vtt. In/. M�d, I I (I) 36-41.
RUlala W A, Cole E C, Thomann C A, Weber DJ ( 1 998)
Stability and bactericidal acti�itj' of chlorine WitttiOTlS.
In/tri. Control Hosp. Epidmtial. 5:323-327.
Postoperative complications - cardiac
arrhythmias
BonaguraJ D. Diagnosis ofcardia<: arrhythmias. In Cum'nl
Thuah in Equine l"mdiu, :\ E Robinson (I'd.). W B
Saunders, Philadelphia, pp. 240-249.
Man C M. Treatment of cardiac arrhythmias and cardiac
failure. In Cun-rot Therapy in Equine Practice, N E Robinson
(cd.). W B Saunders, Philadelphia, pp. 250-254.
Man C M, Reef V B (1991) ECG of the month.i- Am \"1. Mtd.
A",ae. 198(9}, 1533-1534
ReimerJ .\1, ReefV B, Sweeney R W ( 1 992) Ve!llricular
arrhythmias in horses: 21 cases ( 1 984-1989) I Am. V�1.
Mtd. Assoc., 201(8}:1237-1243
RedV B ( 1 999) Arrhythmias. In CrmiiDingy nftluHmw, C .\1
Marr (d.) W B Saunders, London, pp. 179-209.
 12
Diseases of the stomach
MJ Murray
Gastric ulceration in the
adult
INTRODUCTION
Gastric ulceration is the most common disorder of the
equine stomach and in recent years the widespread
nature of this disorder has gained increased recogni­
lion. Gastric ulceration can manifest itself in many ways
in horses, and varies in severity from mild and inconse­
quential to severe and debilitating.
ETIOPATHOGENESIS
The equine stomach is lined dorsally by a stratified
squamous epithelium and ventrally by a glandular
epithelium; these epithelia have different functions and
different susceptibilities to peptic injury. The squamous
portion of the stomach has no secretory or absorptive
function, and appears to serve as a reservoir for ingesta.
Because the equine gastric squamous mucosa has no
surface barrier to hydrochloric acid, and the epithelium
has limited properties to prevent peptic injury, its pro­
tection from peptic injury depends on limited exposure
to acidic gastric secretions.
The equine gastric glandular epithelium is histologi­
cally and physiologically similar to the lining of the
stomach of other animals and humans. It secretes
hydrochloric acid and pepsin as well as some water and
electrolytes, and a variety of endocrine mediators are
produced within this mucosa. The gastric glandular
mucosa has evolved elaborate mechanisms to protect
itself from peptic injury, including a mucus/bicarbon­
ate barrier that prevents back diffusion of hydrochloric
acid, mucosal blood flow, cellular restitution, and
growth factors that promote mucosal healing. Blood
flow is dependent on mucosal prostaglandins and nitric
oxide synthesis.
Hydrochloric acid is secreted by parietal cells via an
H+-K+-ATPase pump, of which there are more than one
million per cell. Hydrochloric acid is secreted by the
stomach under the influence of vagus nerve stimula­
tion, gastrin, and histamine, with histamine appearing
to be the most potent stimulus of gastric acid secretion
in horses. In addition to stimulating hydrochloric acid
secretion by the stomach, gastrin appears to stimulate
secretion of water, sodium, chloride, and bicarbonate
from the pancreas into the duodenum; some of these
secretions normally reflux into the stomach.
The equine stomach secretes hydrochloric acid con­
tinuously, even when the horse is not eating. Gastric
acid secretion is pronounced even in neonatal foals.
Gastric acidity is least when the horse eats, because eat­
ing stimulates secretion of bicarbonate-rich saliva that
can neutralize some gastric acid, and roughage absorbs
the gastric secretions so that they do not contact the
mucosal surface. Once a horse stops eating, gastric acid­
ity can rapidly increase, with pH falling below 2.0, and
acidity remaining high while the horse does not eat.
The gastric mucosa is damaged by excessive expo­
sure to hydrochloric acid and the proteolytic enzyme
pepsin. Lesions in the gastric squamous mucosa form
within 24-48 hours if horses are prevented from eating,
because the gastric hydrochloric acid comes into con­
tact with the mucosal surface and there is no inherent
protection from hydrochloric acid-induced injury. Feed
deprivation per se does not induce lesions in the
241
12 COLIC
glandular mucosa, because it is protected from
hydrochloric acid.
Lesions in the gastric glandular portion of the
stomach occur when there is impairment of mucosal
resistance, permitting exposure of the mucosa to
hydrochloric acid and pepsin. This can occur with ill­
ness or from administration of excessive NSAIDs, and
possibly intensive exercise. In one study, during intense
treadmill exercise blood flow in the gastric antrum was
reduced by a greater proportion than in any other
abdominal organ. Factors that impair mucosal resis­
tance in the glandular mucosa of adult horses are
poorly understood, but studies in laboratory animals
have implicated reperfusion injury as a cause of
impaired mucosal resistance and ulceration. The rela­
tively high prevalence (25%) with which lesions in the
antral mucosa of adult horses have been observed by
the author is suggestive of underlying factors that are
affecting mucosal blood flow in that part of the
stomach.
In humans Helicobacter pylori bacteria have been
determined to be the predominant cause of gastric and
duodenal ulceration. Helicobacter spp. bacteria have
been found in several domestic animal species, but not
in equine species.
EPIDEMIOLOGY
Horses of all breeds and uses can have gastric ulcers.
The prevalence of gastric lesions is influenced by the
management and use of the horse. Horses turned out
onto pasture and used lightly typically have normal
stomachs or only very mild erosions. In contrast, horses
kept in box stalls and trained intensively have a high
prevalence, up to 90 per cent, of gastric lesions. Most
lesions are seen in the gastric squamous mucosa, but
the prevalence of lesions in the gastric glandular
mucosa has ranged from 10-40 per cent in different
endoscopic studies. Endoscopic studies have found that
the prevalence and severity of lesions in the gastric
squamous mucosa, but not the glandular mucosa,
increases as the intensity of training (exercise)
increases. Recent studies have demonstrated that
intense exercise, for example American Thoroughbred
race training, can induce and maintain gastric
squamous mucosal ulcers.
Whereas the prevalence of gastric lesions is greatest
in horses used intensively, clinical problems associated
with gastric ulcers occur in horses used for many activi­
ties, including breeding. Management is probably a
factor, because type of food eaten and eating behavior
can influence gastric ulceration. Restricting access to
roughage or feeding a large amount of concentrate,
242
thus reducing the amount of time a horse consumes
roughage, promotes increased gastric acidity and dam­
age to the gastric squamous mucosa. Feeding concen­
trates stimulates a greater post-prandial serum gastrin
response than feeding roughage, and gastrin is a potent
stimulus to hydrochloric acid secretion. In one study,
feeding alfalfa hay was associated with less gastric injury
than feeding brome grass hay, and it was speculated
that the protein content of the alfalfa might act as a
buffer. In another study, horses moved from pasture
turnout to stall confinement with free access to timothy
grass hay suffered from gastric lesions within 7 days.
CLINICAL SIGNS
The signs of gastric ulcers in horses can be vague and
non-specific, they include
• abdominal discomfort, indicated by mild-to­
moderate colic and frequent lying down
• poor appetite, Le. not eating well, picking at feed,
or not finishing feed
• poor body condition, rough hair coat
• attitude changes (dull, 'sour', or agitated)
• belching, this is a sign of impaired gastric emptying
and involvement of the pylorus.
There is often poor correlation between ulcer sever­
ity and clinical signs. Horses with deep, bleeding ulcers
may have relatively mild signs, whereas horses with
superficial erosions may have greater discomfort.
DIAGNOSIS
Endoscopy is the most reliable method for diagnosis. A
3 m-long, 10-11 mm diameter endoscope is preferred
as an all purpose gastroscope. Most gastric lesions
develop in the squamous mucosa, usually adjacent to
the margo plicatus (Plate 12.1) along the right side or
the lesser curvature (Plate 12.2) of the stomach. Lesions
also develop in the glandular mucosa, and in adult
horses most of these are found in the antrum (Plate
12.3). Lesions affecting the pylorus are typically
thought of as a problem unique to foals, but with
increased use of 3 m endoscopes, pyloric ulceration and
fibrosis has been found in adult horses (Plate 12.4).
Duodenal ulcers appear to be very uncommon in adult
horses.
In lieu of an endoscopic examination, the veterinar­
ian will need to rely on clinical signs and response to
treatment that suppresses gastric acidity to make a
diagnosis of gastric ulceration. With simple gastric ulcer
disease, clinical signs should subside within 1-2 days.

For example, if a horse's appetite is poor because of
ulcers, treatment to suppress acid will result in improved
appetite within 24-48 hours. If abdominal discomfort is
caused by ulcers, this should resolve within 24 hours of
beginning treatment. With gastric emptying disorders
or duodenal ulceration, response to treatment may be
less satisfactory. Also, because the signs of gastric ulcers
are vague, one may incorrectly perceive a response to
treatment and neglect the true diagnosis.
When a horse is evaluated for a condition for which
gastric ulceration is a possible cause, the veterinarian
should obtain a minimum database consisting of a com­
plete blood count (CBC), serum chemistry profile, and
preferably a urine analysis. Gastric ulceration in itself
will not cause changes in any blood parameter in adult
horses, with the exception of severe pyloric ulceration
with fibrosis and restricted gastric outflow in which
there may be anemia and mild hypoproteinemia. If
abdominal discomfort is a clinical problem, a rectal
examination should be done. Peritoneal fluid analysis
and abdominal ultrasonography should be considered
in cases of colic in which gastric ulceration is a possible
diagnosis. Fecal occult blood will not be an indicator of
gastric bleeding in horses because the large intestinal
microflora will have excessively digested heme pigment
rendering the fecal occult blood test ineffective.
TREATMENT
The primary principle of treating gastroduodenal
ulcers in horses is to reduce gastric acidity; this provides
symptomatic relief and creates an environment that is
conducive to ulcer healing. Natural processes that pro­
mote ulcer healing are initiated within hours of peptic
injury, and individual ulcers can heal without treat­
ment. However, in an acidic environment, new ulcers
can form, and in trials examining the effect of the
proton pump inhibitor omeprazole, acid suppression
always resulted in markedly superior ulcer healing com­
pared to vehicle or sham treatment. Therefore, in a
horse that has clinical signs referable to gastric ulcera­
tion, treatment is recommended.
Treatments that reduce gastric acidity include
antacids, histamine type-2 receptor antagonists (H2
antagonists), and the proton pump inhibitors.
Antacids, such as magnesium oxide and aluminum
hydroxide, neutralize existing gastric acid but only for a
brief time (30-120 min). Antacids can provide sympto­
matic relief, but must be given in large volumes every
2-4 hours to facilitate ulcer healing. The H2 antagonists
block hydrochloric acid secretion by gastric parietal
cells by competitively inhibiting the histamine type-2
receptor on parietal cells. The effect of the H2 antago-
DISEASES OF THE STOMACH 12
nists is dependent on plasma levels and at recom­
mended doses gastric acidity is reduced for 1-8 hours.
There is considerable variability between horses in the
magnitude and duration of effect of H2 antagonists.
The drugs cimetidine and ranitidine have been used
most extensively in foals and horses, and both drugs
have poor bioavailability « 20% ) after oral administra­
tion. Reducing the dose of an H2 antagonist, even by
one-third, from its recommended dosage can render
the drug completely ineffective in suppressing gastric
acidity in many horses.
The proton pump inhibitors omeprazole and lanso­
prazole irreversibly bind to the parietal cell H+-K+­
ATPase (proton pump) that secretes hydrochloric
acid. At recommended doses omeprazole can block
hydrochloric acid secretion for 24 hours in horses.
Omeprazole, both in the enteric-coated granule for­
mulation available for human use and in a new paste
formulation for horses, has been shown to be highly
effective in promoting gastric ulcer healing in horses.
In several trials, ulcer healing in omeprazole-treated
horses was substantially superior to healing in con­
trols. Importantly, in one set of trials, ulcer healing
occurred in more than 77 per cent of omeprazole­
treated horses that remained in race training, and
this has not been noted in horses treated with H2
antagonists.
Sucralfate, the major components of which are
sucrose octasulfate (SOS) and aluminum hydroxide,
can facilitate healing of gastric and duodenal ulcers in
humans. Clinical experience suggests sucralfate can
promote healing of lesions in the gastric glandular
mucosa of horses. Sucralfate binds to gastric glandular
mucosa and enhances mucus production, mucosal
prostaglandin synthesis, and mucosal blood flow.
Sucralfate can be administered concurrently with an H2
antagonist. Concurrent administration may reduce H2
antagonist absorption by 10 per cent, but this has not
appeared to affect efficacy in horses. Importantly,
sucralfate can substantially interfere with the absorp­
tion of other drugs, particularly fluoroquinolones, and
thus its use with other medications should be deter­
mined on a case-by-case basis.
Aluminum hydroxide has been shown to enhance
gastric mucosal nitric oxide, and this should promote
mucosal blood flow. Misoprostol is a prostaglandin El
analog that may promote healing of gastric glandular
mucosal lesions by increasing mucosal blood flow.
Misoprostol can cause inappetance, diarrhea, and
abdominal discomfort, and for these reasons it is not
used routinely to treat gastric ulcers. However miso­
prostol has been used together with other medications
to treat severe gastric glandular mucosal ulcers in a
small number of foals and horses with apparent success.
243
12 COLIC

The treatments that enhance mucosal resistance to

peptic injury and appear to facilitate healing are only
appropriate for the gastric glandular mucosa. Squamous
mucosal lesions can occur while a horse is being treated
with sucralfate. If an endoscopic examination has not Drug (size) Recommended
dosage
been performed, treatments such as sucralfate should
always be accompanied by acid-suppressive therapy.
Antacid
In some horses, ulceration will affect the pylorus and MaaloxTC 240 ml (8 oz), q. 4 h
gastric emptying will be impaired. Often, severe squa­ Mylanta double strength 240 ml (8 oz), q. 2 h
mous mucosal ulceration will accompany impaired gas­
tric emptying. Treatment with an acid-suppressive drug Ha antagonist
may result in improved clinical signs, but gastric ulcera­ Cimetidine (800 mg tablets) 25 mg/kg p.o.,
tion will persist or worsen. Treatment to improve gastric q. 6 h
emptying will usually result in improved clinical signs (150 mg/ml) 7 mg/kg Lv.,
and facilitate ulcer healing. Bethanecol has been shown q. 6-8 h

experimentally and clinically to enhance gastric empty­

Ranitidine (1 SO, 300 mg 7 mg/kg p.o., q. 8 h
tablets)
ing and facilitate ulcer healing. Chronic administration
(25 mg/ml) 1.5 mg/kg i.v.,
of bethanecol may be required and appears to be safe.
q. 8 h
Cholinergic signs (salivation, diarrhea, abdominal dis­
comfort) are rare at the recommended dosages. Proton pump inhibitor
The duration of treatment required for ulcers will Omeprazole (20 mg capsules 1 mg/kg p.o.,
vary depending on the severity of lesions and the man­ of enteric coated granules) once daily
agement of the horse. Gastric erosions are more super­ Omeprazole (paste 4 mg/kg p.o.,
ficial than ulcers (erosions can cause significant clinical formulation) once daily
signs!) and thus will heal more quickly. Deep ulcers may
Mucosal protectant
require weeks to heal because granulation of the ulcer
Sucralfate (1 9 tablets) 10-20 mg/kg p.o.,
bed followed by epithelial contracture is necessary for
q. 8 h
complete healing. Time required for healing also will
Misoprostol (200 IJg tablets) 1.5 IJg/kg p.o.,
be dependent on the magnitude and duration of acid
q. 8-12 h up to
suppression. Because of its unique mode of action, 2.5 lJg/kg p.o.,
omeprazole can suppress gastric acidity for 24 hours, q.8h
and in a study examining the enteric-coated granule
formulation of omeprazole considerable healing of the Motility modifier
gastric squamous epithelium was apparent within 4-7 Bethanecol (5.15 mg/ml) 0.02 mg/kg s.c.,
days of starting treatment. If there is delayed gastric q. 6-8 h
emptying (pyloric or duodenal stricture, etc.) a longer Bethanecol (50 mg tablets) 0.35 mg/kg p.o.,
q.8h
duration of treatment may be required.

PREVENTION

Prevention of gastric ulcers can be very challenging.

Some horses appear to develop ulcers more readily
than others, and these horses are likely to have recur­
rence after successful treatment. The medically ideal
preventive measure is to take a horse out of work and
turn it out onto pasture. In many cases this is neither
desirable nor possible. Feeding management can be
modified to promote more continuous roughage
consumption and less concentrate consumption. In
one study, alfalfa hay appeared to offer some gastric
protection compared to brome grass hay. Nutritional
management to prevent gastric ulcers is incompletely
understood at this time.
Antacids are not effective in preventing gastric
ulcers, particularly in race horses. In a feed deprivation
model, ranitidine prevented ulcer formation, but clini­
cal experience with race horses suggests that ranitidine
is not effective in treating or preventing gastric ulcers in
race horses that remain in training. Omeprazole, in a
new paste formulation, was found to prevent formation
of gastric ulcers in horses in intensive race training at a
dosage of 2 mg/kg, once daily. This is an impressive
accomplishment for the compound, but may not be
practical on a widespread basis.

244
 DISEASES OF THE STOMACH 12

Endoscopic Squamous Glandular

examination lesions lesions Treatment recommendation

No ? ? • omeprazole paste, 4 mglkg p.o., once daily for 3-4 weeks, or

• 7 mg/kg p.o., q. 8 h for 4 weeks, or
ranitidine,
• cimetidine, 25 mgfkg p.o., q. 6 h for 4 weeks

Yes Yes No • omeprazole paste, 4 mg/kg p.o., once daily for 2-3 weeks, or
• ranitidine, 7 mg/kg p.o., q. 8 h for 3-4 weeks, or
• cimetidine, 25 mg/kg p.o., q. 6 h for 3-4 weeks
Repeat endoscopy after treatment

Yes No Yes • sucralfate, 10-20 mglkg p.o., q. 8 h for 2-4 weeks

Repeat endoscopy after treatment

Yes Yes Yes • omeprazole paste, 4 mg/kg, once daily for 2-3 weeks, or
• ranitidine, 7 mglkg p.o., q.8 h for 3 weeks, or
• cimetidine, 25 mg/kg p.o., q. 6 h for 3 weeks, and
• sucralfate, 10-20 mglkg p.o., q. 8 h for 2-4 weeks
Repeat endoscopy after treatment

Gastric impaction CLINICAL SIGNS AND DIAGNOSIS

The clinical signs of gastric impaction are those associ­

Gastric impaction can occur as a primary condition, but
often it is diagnosed at surgery as a finding secondary to
other disturbances in the intestinal tract. In some cases
there may be predisposing causes, such as ulceration or
fibrosis at the pylorus, whereas in other cases gastric
impaction may occur spontaneously. Gastric impaction
can proceed to rupture.
ETIOPATHOGENESIS
Factors that predispose to gastric impaction include
• ingestion of certain feed stuffs, including beet pulp,
bran, straw, wheat, and barley - beet pulp and bran
can become desiccated within the stomach and may
not become rehydrated by water or gastric
secretions
• dental disorders - roughage may be incompletely
masticated
• keding a horse that has signs of colic - there may
be poor gastric emptying associated with
generalized decreased gastrointestinal motility.
ated with abdominal discomfort. If the signs are mild
and resolve spontaneously or with analgesics, owners
are often inclined to feed the horse, worsening the
impaction. Most stomach impactions are diagnosed
at surgery, presumably because they become so large
that the degree of pain warrants surgery. A stomach
impaction may be suspected during an examination for
colic if it is difficult to pass a nasogastric tube into the
stomach. With gastric distention, the gastroesophageal
junction can become distorted, making it difficult to
pass a nasogastric tube. If poorly macerated or digested
feed material is recovered from the nasogastric tube
when the horse has not eaten for several hours, a gastric
impaction may be suspected. On rectal examination,
the spleen may be displaced caudally and medially,
although this finding is not specific for gastric
impaction or dilation.
Endoscopy may be helpful in the diagnosis,
although simply identifying a stomach full of ingesta is
not diagnostic for an impaction, and it is difficult to
assess distention by endoscopy. Radiography may be
useful in some cases, when the impacted stomach will
be noted to displace the diaphragm cranially (Figure
12.l).

245
12 COLIC
Figure 12.1 Radiograph of the caudal thorax and cranial
abdomen of a horse that presented with colic. The stom­
ach is full of a radio-opaque material and there is accumu­
lation of gas. Gastric lavage recovered desiccated bran,
which had been fed to the horse as a putative laxative
after the horse had been mildly injured after falling from
a jump on a cross-country course. The horse had fallen on
its sternum, note that the diaphragm appears irregular
cranially
TREATMENT
If gastric impaction is suspected, the horse should be
transferred, with a nasogastric tube in place, to a facility
at which surgery can be performed if necessary.
Medical treatment can include gastric lavage to remove
as much ingested material as possible. This may need to
be done repeatedly. Instillation of 100-200 ml of 8%
dioctyl sodium sulfosuccinate (DSS) may facilitate
hydration of desiccated ingesta. Treatment with anal­
gesics and intravenous fluids should also be done, as
needed, although it is doubtful that intravenous fluid
administration will substantially increase the hydration
of desiccated gastric contents. Gastric motility stimu­
lants should be avoided if the extent of the impaction is
not known, because of a possibility of inducing gastric
rupture. We have treated gastric impactions that were
diagnosed at surgery with bethanecol, 0.02 mg/kg, S.c.,
q. 8 h, with no adverse effects.
Surgical treatment can include direct infusion of
balanced polyionic fluids into the impaction through
the stomach wall. The stomach is massaged to break
down the impaction and facilitate movement of fluid
into the ingesta. Alternatively, fluid may be infused via a
246
nasogastric tube, followed by massage of the stomach.
Postoperatively, the horse should be held off feed for
48-72 hours. A gastroscopic examination is indicated,
both to document resolution of the impaction and to
determine whether there is an underlying disorder in
the stomach.
Gastric dilation
ETIOPATHOGENESIS
Dilation of the stomach with fluid or gas usually
results from another intestinal disturbance. Normally,
a small amount of duodenal contents, consisting of
gastric effluent, bile, and pancreatic secretions,
refluxes back into the stomach. If there is excessive
intestinal secretion or intestinal obstruction, a large
volume of fluid can move from the duodenum into
the stomach. It is possible for fluid to spontaneously
reflux from the stomach into the esophagus, but with
distention, the gastroesophageal junction is distorted
such that it is tightly closed. This promotes progressive
gastric distention as fluid continues to move into the
stomach from the duodenum.
Primary gastric dilation may occur if a horse eats
highly fermentable material, generating a large volume
of gas. This is dissimilar to frothy bloat in ruminants, in
which a stable gas/fluid froth develops in the rumen as
a result of plant/rumen microbial interactions. Gas also
may accumulate secondary to generalized impaired
gastrointestinal motility from a variety of disorders.
Normally, excessive gas in the stomach exits either via
the small intestine or it can be belched. If gastric dis­
tention is excessive, the normal release mechanisms
may be impaired and the gas will continue to accumu­
late.
CLINICAL SIGNS AND DIAGNOSIS
The clinical signs are the same as those for gastric
impaction, although the onset may be more acute and
the signs more severe. Affected horses are often tachy­
pneic because of compression of the thorax by the dis­
tended stomach. Diagnosis of primary gastric dilation
can be presumed if passage of a nasogastric tube
releases a large volume of gas, relieving the colic
episode. If a large volume of fluid is retrieved, gastric
dilation may have been resolved, but the underlying
cause of enterogastric reflux will need to be deter­
mined.

TREATMENT
Treatment is removal of excessive fluid or gas via a
nasogastric tube, or at surgery via needle aspiration. An
underlying reason for the gastric dilation should be
determined and treated appropriately. Because the
cause of gastric dilation in horses is dissimilar to frothy
bloat in ruminants, treatments designed for frothy bloat
are not indicated for gastric dilation in horses. Also,
products designed to treat 'stomach gas' in humans,
such as simethecone, are not indicated for horses with
gastric distention.
Gastric rupture
Gastric rupture occurs as a sequel to gastric distention
from ingesta, fluid, or gas. The adult equine stomach can
hold up to 20-25 liters when maximally distended. With
distention, gastric rupture can occur from simple
excessive distention, but also the integrity of the wall of
the stomach may become compromised because of
decreased blood flow. Distention of the small intestine
has been demonstrated to significantly reduce mural
hlood flow, and it is likely this occurs in the stomach with
distention. In some cases, it has appeared that rupture
occurred as a result of an infarction of a portion of the
stomach wall, without apparent substantial distention.
Gastric perforation from ulceration happens rarely in
adult horses. Because of extensive contamination of the
peritoneal cavity with stomach contents, treatment is not
possible and humane destruction of the horse is required.
Gastric squamous cell
carcinoma
INTRODUCTION
Squamous cell carcinoma affects the esophageal and
gastric squamous mucosa. The neoplasm is uncommon
and by the time clinical disease associated with squa­
mous cell carcinoma is recognized treatment is rarely
possible.
ETIOPATHOGENESIS
Neoplastic cells originate in the squamous epithelial
mucosa of the esophagus or stomach. In humans there
DISEASES OF THE STOMACH 12
are dietary, genetic, and environmental factors that
may contribute to esophageal cancer, but because
esophageal and gastric neoplasias are so uncommon in
horses contributing factors are not known. The rate of
growth and aggressiveness of alimentary squamous cell
carcinoma in horses is variable. In some horses tumors
remain localized within the stomach, whereas in other
horses tumors may extend through the stomach wall
and spread to other abdominal viscera or metastasize to
other locations in the body.
CLINICAL SIGNS
Typical signs associated with, but not diagnostic for,
squamous cell carcinoma include
• chronic weight loss
• poor appetite
• abdominal discomfort
• lethargy.
Ascites or edema may occur in some cases. If the
esophagus is involved, dysphagia or ptyalism will be the
predominant signs. Involvement of the stomach with
squamous cell carcinoma at the cardia may also result in
dysphagia, while involvement at other sites in the stom­
ach may result in signs of obstruction to outflow (colic)
and/or weight loss. In some cases tachypnea will be a
prominent sign, either because of metastasis to the
thorax or pressure on the diaphragm from an enlarged
tumor.
DIAGNOSIS
Neoplasia is one of a number of potential conditions to
consider when presented with a horse with chronic
weight loss (see Chapter 18), recurrent colic (see
Chapter 17), and/or chronic diarrhea (see Chapter
21). The diagnostic evaluation should consist of a com­
plete physical examination including rectal examina­
tion, routine blood work (CBC, serum chemistry
panel), urinalysis, and peritoneal fluid analysis.
Endoscopy (Plate 12.5), ultrasonography, laparoscopy,
and laparotomy can be used to further evaluate the
patient.
Many horses with squamous cell carcinoma will have
anemia, leukocytosis, and hyperfibrinogenemia. Some
will have hypoproteinemia due to bowel inflammation
and protein exudation, whereas other cases will have
hyperglobulinemia.
Peritoneal fluid will vary from normal, if the tumor is
confined within the stomach, to an exudate if the tumor
has spread. Neoplastic cells from a primary gastric
247
12 COLIC

squamous cell carcinoma occasionally will be observed BIBLIOGRAPHY

in a sample of peritoneal fluid, and will be large, poorly
differentiated epithelial cells with a bluish, ground­ Gastric ulceration in the adult
glass-appearing cytoplasm (Wright's stain).
Andrews F M,Jenkins C, Frazier D, BlackfordJ (1992) The
If gastric squamous cell carcinoma is suspected, effect of oral omeprazole on basal and pentagastrin­
cytology of aspirated stomach contents may reveal stimulated gastric secretion in young female horses. Equine
large, poorly differentiated squamous carcinoma cells. Vet.]. supp!. 13:80-3.
Endoscopy can be useful, particularly in diagnosing Hojgaard L, Mertz N A, Rune SJ (1996) Peptic ulcer
pathophysiology: acid, bicarbonate, and mucosal function.
esophageal or gastric squamous cell carcinoma. A
21:10-15.
Scand.]. Gastroenterol. supp!.
biopsy will usually be diagnostic, even on the small McCarthy D M (1990) Sucralfate. N. Engl.]. Med.
tissue specimen that can be obtained through an 325:1017-25.
endoscope. Ultrasonography can be used to determine Murray MJ (1992) A comparative review of the
whether there is excessive abdominal fluid, to possibly aetiopathogenesis and treatment of peptic ulcer. Equine
Vet.]. supp!. 13:63-74.
identifY a mass, and to detect any abnormalities within
Murray MJ (1997) Suppression of gastric acidity in horses.
the parenchyma of the liver or spleen (occasionally, ]. Am. Vet. Med. Assoc. 211:37-41.
gastric squamous cell carcinoma will metastasize to the Murray MJ, Haven M L, Eichorn E S, et al. (1997) The effects
spleen). of omeprazole on healing of naturally-occurring gastric
ulcers in Thoroughbred race horses. Equine Vet.].
29:425-9.

Squamous cell carcinoma

Successful treatment of esophageal or gastric squa­ Campbell-Beggs C L, Kiper M L, MacAllister C, Henry G,

mous cell carcinoma has not been reported in horses. RoszelJ F (1993) Use of esophagoscopy in the diagnosis of
esophageal squamous cell carcinoma in a horse.]. Am. Vet.
If small, localized tumors are found, surgical excision Med. Assoc. 202:617-18.
or endoscopic laser ablation may be attempted. McKenzie E C, MillsJ N, BoltonJ R (1997) Gastric squamous
Intralesional injection of cisplatin can be successful cell carcinoma in three horses. Aust. Vet.]. 75:480-3.
for cutaneous squamous cell carcinoma and, Olsen S N (1992) Squamous cell carcinoma of the equine

although not reported for the treatment of gastric stomach: a report of five cases. VetRec. 131:170-3.
Tenant B, Keirn D R, White K K, et al. (1982) Six cases of
squamous cell carcinoma, could be done through an squamous cell carcinoma of the stomach of the horse.
endoscope. Equine Vet. J 14:238.

248
 15
Diseases of the large colon that can
result in colic
Impactions
RR Hanson
INTRODUCTION
The large colon, with distinct motility patterns coordi-
nated by a myoelectrical pacemaker at the pelvic flex-
ure has distinct non-rhythmic haustral movements and
stronger well-defined rhythmic retropulsive and propul-
sive contractions to move ingesta along the gastro-
intestinal tract. These complex functions require the
coordination of motility patterns to facilitate digestion
as the large colon serves as the primary site for water
resorption and microbial fermentation of carbohy-
drates to produce volatile fatty acids. Abnormal rhyth-
mic contractions of the large colon result in partial or
complete simple intestinal obstruction and often
develop at sites of narrowed lumenal diameters just
orad to the pelvic flexure or the transverse colon.
The pathogenesis of colonic impaction likely
involves dysfunctions of the myoelectrical pacemaker at
the pelvic flexure. Dissociation of the normal sequences
and dysfunctions of motility patterns are theorized to
result in abnormal transit and fluid resorption, predis-
posing the horse to functional abnormalities such as
colonic impaction. In horses with colonic impaction,
the digesta appears to be retained just orad to the pelvic
flexure, involving a long segment of the ventral colon
and does not simply involve the pelvic flexure alone.
The digesta is usually firm and contains fibrous feed
material, although sand and gravel can cause a similar
obstructive lesion.
EPIDEMIOLOGY
In one hospital study of large colon impactions in
horses, the median age of the horses was 7.1 years
(range 1-29 years), with most of the affected horses
being female (63%). No breed predisposition was iden-
tified. In another study impaction of the large colon
accounted for 13.4 per cent of 1100 colic cases referred
to a university hospital and for 9 per cent of cases in a
normal farm population.
ETIOLOGY
Large colon impactions may be promoted by
• reduced water intake
• poor quality feed
• limited exercise
• participation in show activities
• foreign material in the hay
• poor dentition
• foaling
• colonic motility alterations.
Cold weather may reduce water consumption or freeze
the water source entirely. Horses provided with water
from tanks, buckets, and automatic waterers are signifi-
cantly associated with an increased risk of colonic
impaction, compared to horses that drink from natural
water sources. Winter pasture may force consumption
of poor quality roughage. Changes in management con-
ditions, such as sudden restriction of exercise because
of musculoskeletal injury, stable change, a move from
pasture to barn housing, shipping, and systemic disease,
may also predispose to colonic impaction. In one study,
279
15 COLIC
more than 50 per cent of the horses examined for
colonic impaction had an increase in the duration of
stall confinement in the 2 weeks preceding the colic
episode.
Amitraz, a formamidine acaricide that interrupts
colon motility, has been used to experimentally induce
colonic impactions in horses. Its mechanism of action
may involve the mediation of intrinsic enteric neuro-
modulators that affect the coordination of myoelectri-
cal activity from the pacemaker regions in the large
intestine and, possibly, fluid and ion transport.
Cockspur hawthorn fruit ingestion and naturally occur-
ring impaction colic could have similar pathogenesis.
The incidence of colonic impaction is influenced by
soil composition and geographic region. Foreign mate-
rials, such as nylon cord stripped from rubber feeders,
fence pieces, or bailing twine left in hay, combine with
fecal material to form impactions that usually require
surgical correction. Impactions may accompany other
conditions such as non-strangulating displacement of
the colon.
CLINICAL SIGNS
Horses with colonic impaction usually have intermittent
clinical signs of abdominal pain with a gradual onset,
and are often partially or completely anorexic. Some
horses show acute signs of abdominal pain while others
have mild or no signs of abdominal pain. Mild signs,
such as rolling the lip, playing with water, looking at the
abdomen, stamping the feet, or backing up, may occur
while the obstruction is incomplete. Abdominal pain
becomes more severe as the mass becomes larger,
heavier, the colon muscles spasm, or obstruction causes
gas distension.
The heart and respiratory rates are initially normal,
but increase with progressive signs of abdominal pain
and endotoxemia. The mucous membranes are pink or
blanched, while the capillary refill time is usually nor-
mal. These indicators of perfusion remain normal until
the bowel deteriorates releasing endotoxin. Most
horses with a large colon impaction have decreased or
absent intestinal borborygmi on auscultation, but
normal or increased intestinal sounds can occur.
Transrectal palpation is useful for diagnosing
colonic impactions. In most cases, a large doughy-to-
firm mass is palpable in the area of the pelvic flexure or
the left ventral colon while transverse colon impactions
or more isolated sand impactions are not usually palpa-
ble. Gas distention of the ascending colon or cecum is
common. Nasogastric reflux may be obtained if the
impaction is located in the right dorsal colon and is
impinging on the duodenum.
280
CLINICAL PATHOLOGY
Clinical laboratory values are initially normal but
abnormalities may develop over time. An increase in
the systemic packed cell volume and total protein con-
centration may be evidence of mild dehydration in
some horses. If the dehydration goes undetected or is
untreated, the impaction may progress or become
refractory to medical treatment. An increase in the
peritoneal fluid total protein concentration and low
systemic white blood cell counts can occur if the
impaction causes devitalization of the colonic mucosa.
Therefore peritoneal fluid total protein concentration,
as an indicator of colonic wall degeneration, should be
followed closely in horses that are treated medically for
long periods.
DIAGNOSIS
The diagnosis is usually made on transrectal examina-
tion where an ingesta-filled pelvic flexure is palpated in
most cases. Alternatively either the impaction is out of
reach or gas distention of the colon and cecum prevents
transrectal palpation of the impaction. Horses with a
history of recent increase in stall confinement and mild
intermittent signs of abdominal pain should be
examined closely for large colon impaction.
TREATMENT
Colonic impaction is a common cause of colic and often
responds to medical management directed at
• restricting diet
• controlling pain
• maintaining hydration
• reducing muscular intestinal spasms in the area
around the impaction
• hydrating the colon ingesta to allow passage offeces
and establish normal colon function.
Feed should be withheld until transrectal palpation
findings are normal and there is evidence of intestinal
transit. Very small amounts of hay or grazing may stim-
ulate bowel motility, but further addition of ingesta to
the impaction should be avoided. Most horses respond
to sedation, analgesia, and intragastric administration
of laxatives. Aggressive medical treatment for 3-5 days
may be necessary, although softening and movement of
the impacted mass should be felt sooner than this dur-
ing transrectal palpation.
Intravenous fluid therapy may be necessary in horses
that do not respond to initial treatment with analgesics
 DISEASES OF THE LARGE COLON THAT CAN RESULT IN COLIC
and laxatives. Most horses with colon impactions are
slightly dehydrated. Aggressive oral administration of
fluids (4-8 liters per nasogastric tube every 6 h) is help-
ful but labor is intensive. Intravenous fluid administra-
tion may increase the water content of the impacted
ingesta in horses by altering the passive forces that gov-
ern transmucosal fluid transport, raising the capillary
hydrostatic pressure, and decreasing plasma protein
concentration. Intravenous fluids should be adminis-
tered at 2-5 l/h or three to five times the recommended
maintenance rate through a large bore (l4-gauge x 12.5
cm) jugular catheter. Over-hydration can be monitored
by assessment of the horse's packed cell volume and
total protein concentration which should be main-
tained at 5.0-5.5 g/dl. In a study of 147 horses hospital-
ized with colon impactions that did not respond to
initial farm treatment, the mean duration of medical
treatment with xylazine, flunixin meglumine, and intra-
venous fluids was 2 days (range 1-8 days). Eighty per
cent of these hospitalized horses responded to medical
treatment.
While the ingesta is being hydrated to soften the
impaction, it is often necessary to relieve visceral pain.
Relief of visceral pain helps moderate the effects of
adrenergic inhibition of intestinal motility. Xylazine
hydrochloride, an alpha, adrenoceptor agonist, modu-
lates the release of norepinephrine and directly inhibits
neuronal firing, causing sedation, analgesia, bradycar-
dia, and visceral pain relief. Xylazine may cause a cessa-
tion of intralumenal pressure changes and reduce
jejunal and colonic motility for up to 2 hours. This
effect may be beneficial in relieving intestinal spasms
around the impaction mass. The latter may, in turn,
allow fluid absorption and passage of gas. Treatment
with xylazine (0.2-0.4 mg/kg i.v, or i.m.) can be
repeated. Butorphanol (0.01-0.02 mg/kg i.v. or i.m.) or
detomidine (0.01-0.02 mg/kg i.v, or i.m.) is also bene-
ficial for similar reasons, but close monitoring of the
horse is essential to ensure that the analgesics are not
masking signs indicative of the need for abdominal
surgery.
Flunixin meglumine reduces prostaglandin-medi-
ated visceral pain during intestinal obstruction or dis-
tention and reduces the systemically evident effects of
endotoxin without inhibiting intestinal motility.
Because flunixin meglumine can mask clinical signs of
endotoxemia and intestinal strangulation obstruction,
careful monitoring of the horse after the drug is admin-
istered is essential. The recommended low dose
(0.25-0.5 mg i.v. q. 6 h), however, enables treatment of
horses with colonic impactions without masking impor-
tant clinical signs that are indicative of a failing cardio-
vascular system. Treatment with flunixin meglumine
should be continued after correction of the colonic
15
impaction until horses are eating regularly and intesti-
nal transit has returned to normal.
Laxatives, cathartics, and emollients are given to
alter fecal consistency and to promote transit of ingesta
in horses with colonic impactions. The stomach should
first be siphoned and if more than 2 liters of fluid is
obtained, small-intestinal ileus or delayed gastric emp-
tying is likely. Instillation of additional fluid should be
done cautiously, if at all, in these patients.
Mineral oil (2-4 liters p.o.) is a common, non-toxic
emollient that acts to lubricate the ingesta and coat the
intestine to facilitate the passage of ingesta through the
intestine. Mineral oil can be used as a fluid marker to
determine the speed ofintestinal transit. The oil usually
appears in the feces 12-24 hours after nasogastric
administration. However, since the oil may pass around
a firm mass of ingesta, the presence of oil in the feces
does not always signify resolution of the impaction.
Mineral oil should not be given to horses with nasogas-
tric reflux or if strangulation obstruction is suspected.
Bulk cathartics (bran, psyllium mucilloid, methyl-
cellulose) cause hydrophilic retention of colonic water;
this retention stimulates intestinal transit. Psyllium
mucilloid is non-toxic and may be used for 1-3 weeks if
necessary. Bulk laxatives, however, can take days to
begin working and should not be relied on for all
colonic impactions. Magnesium sulfate (l g/kg p.o. q.
24 h for 2-3 days) is a saline cathartic that acts largely
via an osmotic effect to increase fecal water content.
Magnesium sulfate may cause more gastrointestinal
distention and thus stimulate a greater gastrocolic
response than other laxatives. It can affect systemic
hydration and should be administered only to well-
hydrated horses, or preferably in combination with
intravenous or intragastric fluid administration.
Magnesium sulfate is associated with the risk of devel-
opment of diarrhea, and effective safe dosing of this
product is debated.
Dioctyl sodium sulfosuccinate (DSS) is an anionic
surfactant that stimulates fluid secretion from the
intestinal mucosa and reduces surface tension allowing
water to penetrate impacted material. The usual dose is
10-20 mg/kg of a 5% solution mixed with 2-8 liters of
water given via a nasogastric tube. Toxicity occurs at
doses ranging from 0.5-1.0 g/kg. Repeated dosing of
DSS may cause mucosal irritation, dehydration, and
toxicity. For these reasons, DSS should be used no more
than twice during a 48 hour interval. DSS can be used
alone but is frequently mixed with mineral oil. It is not
known whether mixing the two compounds is advanta-
geous or detrimental to the treatment of impactions.
The use of prokinetic drugs to treat horses with
colonic impactions is controversial. Intestinal contrac-
tions induced by neostigmine, which acts on the large
281
 DISEASES OF THE LARGE COLON THAT CAN RESULT IN COLIC
Ingested sand may cause foreign body enteritis or it may
accumulate in the ventral colon, pelvic flexure, and/or
transverse colon causing impaction. The inflammatory
response, associated with accumulation of a sufficient
volume of sand, can result in colonic rupture.
EPIDEMIOLOGY
Sandy environments such as those found in Florida,
California, and Arizona, are common locations for
horses with this disorder. Young horses and horses with
indiscriminate eating habits occasionally consume sand
voluntarily, making them more prone to developing the
condition.
ETIOLOGY
Horses stabled in a sandy environment and fed from
the ground appear to be at risk. Offending sand is gen-
erally fine beach sand or clay, but gravel or bluestone
shale can occasionally be found. Sand is also found in
the feces of clinically normal horses.
CLINICAL SIGNS
Clinical signs range from mild to severe pain and nor-
mal to deteriorating cardiovascular status. Most horses
with clinical signs of sand colic are older than I year of
age. Sand impactions of the ventral colon may be
substantial (25 kg); however, they are often difficult to
palpate transrectally because of their location in the
cranial portion of the gastrointestinal tract and hence
may be out of reach. Cecal and large colon gas disten-
tion is inevitably present. Horses with this condition
may have small amounts of diarrhea and clinical signs
of endotoxemia.
Abdominal paracentesis should be conducted cau-
tiously since the sand-impacted colon can be inadver-
tently lacerated. An abdominal paracentesis should not
be performed in horses that clearly require surgical
intervention or in horses in which the procedure may
be of low diagnostic value. Sand present within an
enterocentesis is pathognomonic for the disease.
Auscultation of the ventral abdomen of horses with
sand impaction may reveal 'friction-like' rub sounds
compatible with sand borborygmi.
DIAGNOSIS
Sand impaction can be difficult to differentiate from
feed impaction, and tests for fecal sand do not correlate
15
well with the presence of sand in the colon. History or
observation of sand in the feces only indicates exposure
to sand. Sand may be detected during transrectal palpa-
tion or it may be found on the rectal sleeve. Dissolving
feces in water and observing for sand in the bottom of a
bucket or on a rectal sleeve may provide evidence of the
possibility of sand impaction. Although small amounts
of sand are frequently found in feces and do not neces-
sarily reflect sand impaction, large amounts of sand are
more indicative of sand accumulation. Comparison of
the normal discharge of sand in normal horses from
that of the diseased horse may assist in the diagnosis of
sand impaction.
Ultrasonographic examination of the ventral
abdomen along the midline caudal to the xiphoid
process with a 5-MHz ultrasound probe may reveal the
presence of sand in the ventral colon, appearing as
floating starburst spicules as the sand is suspended in
the ingesta. Abdominal radiographs, if available, can
aid in the diagnosis of sand impaction.
TREATMENT
Psyllium mucilloid (0.5-1.0 g/kg p.o. q. 6-24 h) has
been implemented to lubricate the gastrointestinal
tract and assist in the movement of sand out of the
body. A solution of psyllium mucilloid and 4-8 liters of
water must be pumped rapidly into the stomach via a
nasogastric tube before the psyllium mucilloid forms a
gel. The treatment is maintained for several days to a
week depending on the severity of the case. The feces
should be monitored for the rate of expulsion of the
sand. Psyllium, however, had no effect in hastening
sand evacuation from the large intestine in a controlled
experimental study in six normal ponies. Further
studies on the effect of psyllium in the diseased colon
are needed.
Intravenous fluid therapy may be necessary in horses
that do not respond to initial treatment with analgesics
and laxatives. Intravenous fluid administration may
increase the water content of the impacted ingesta in
horses by raising the capillary hydrostatic pressure and
decreasing plasma protein concentration. The recom-
mended administration rate for intravenous fluids is
2-5 l/h or 2.5 times the maintenance rate.
Horses with sand impactions often do not respond
to medical treatment alone and require surgical inter-
vention. In many horses surgical exploration must be
undertaken without an accurate pre-operative diagno-
sis; because of abdominal pain, large colon distention,
and deteriorating cardiovascular signs. Sand impactions
most commonly involve the pelvic flexure and/or the
right dorsal colon. A colotomy along the pelvic flexure
283
15 COLIC

allows for tap water lavage and drainage of colonic Administration of a moist bran mash containing 450 g
ingesta and sand. To prevent abdominal contamination of psyllium mucilloid, once a week, is a useful prophy-
it is important to deliver most of the large colons from lactic measure to prevent the occurrence of sand
the abdomen before beginning the colotomy. It can be impaction colic in horses exposed to sand.
difficult to remove excessive sand present in the right
dorsal colon through a pelvic flexure colotomy.
However, the use of a large bore nasogastric tube
inserted into the colon lumen from the pelvic flexure Displacement of the large
colotomy to the right dorsal colon can aid in the colon
removal of the sand. Copious lavage of the right dorsal
colon, with manipulation of the colon to suspend the
RP Hackett
sand in the lavage, is needed to adequately dissipate the
sand. Judicious technique eliminates the need for mul-
tiple colotomies which prolong the surgery and compli- INTRODUCTION
cate the recovery period. Septic peritonitis can be
minimized by using aseptic technique, atraumatic han- The large colon in an adult horse is approximately
dling of the intestines, and appropriate supportive care. 3.4 meters in length (11 % of the total gastrointestinal
Sand impaction of the pelvic flexure may act as a tract) and has a capacity of approximately 81 liters
pendulum, predisposing the horse to volvulus of the (38% of the total). The large size and mobility due to
colon. Cranial displacement of the pelvic flexure and sparse mesenteric attachments of the ascending colon
non-strangulating and strangulating colonic displace- predispose it to a variety of displacements. The colon is
ments are associated with this condition. Postoperative looped back upon itself at the pelvic flexure and then
complications include the recurrence of the disease, folded at the sternal and diaphragmatic flexures to fit
septic peritonitis, diarrhea, and incisional dehiscence. within the abdomen (Figure 15.1). Colonic mobility is
restricted only by attachments to the cecum and trans-
verse colon. Colon diameter varies from approximately
OUTCOME
The mortality rate is higher with sand impactions than
ingesta impactions of the large colon. In recent studies,
44 of 48, and 30 of 40 horses with sand impaction were
discharged from the hospital, and at 12 months follow-
ing discharge 38 of 48 horses and 24 of 40 horses were
alive. If the sand can be completely removed from the
colon without unnecessary contamination, the progno-
sis for horses with sand impaction is no worse than for
those horses with ingesta impaction.

PREVENTION
Minimizing exposure to sand is important in preventing
recurrence. This requires that horses eat their feed
raised off the ground (in a manger or in buckets) or
separated from sand (on rubber mats or in feeding
troughs). Hay containing sand should not be a part of
the horses' diet. Feeding hay free of sand prior to pas-
ture turnout lessens the horse's desire for aggressive
grazing and their exposure to sand.
Intermittent administration of psyllium mucilloid
for several weeks may be indicated to remove accumu-
lated sand. Longer term administration often results in Figure 15.1 Normal equine cecum and colon viewed with
an increased rate of degradation of the mucilloid by the horse in dorsal recumbency. The dorsal colon is shaded
colonic microbes and a decrease in the laxative effect. dark gray

284
 DISEASES OF THE LARGE COLON THAT CAN RESULT IN COLIC
Figure 15.4 Entrapment of the colon over the renosplenic
ligament is relieved by using the arm and back of the hand
to displace the spleen axially and ventrally while the palm
and grouped fingers are used to sweep the colon dorsally
then laterally
sweep the colon dorsally then laterally (Figure 15.4).
Once entrapment is relieved, the left colon is exterior-
ized for direct inspection. Vascular injury to the
entrapped segment is rare. Pelvic flexure enterotomy
for relief of secondary impaction is rarely necessary.
The survival rate following surgical treatment of LDDC
is extremely favorable (92% in one study).
Relief of LDDC via standing flank celiotomy may be
attempted under certain circumstances. Left flank
celiotomy should be employed only in those cases in
which a diagnosis of LDDC is absolutely certain as diag-
nosis or treatment of other forms of displacement or
other causes of obstruction can rarely be accomplished
by this approach. The standing approach is ordinarily
used in patients who are poor candidates for general
anesthesia either because of advanced pregnancy or
physical size (large draft horses), or because of eco-
nomic constraints. Following phenylephrine infusion as
described above, a left flank celiotomy (gridding the
internal oblique and transversus abdominus muscles) is
performed. The left colon is needle decompressed of
gas as much as possible, lifted over the splenic base and
manipulated ventrally to a position axial to the splenic
apex. This procedure is markedly facilitated by phenyle-
phrine-induced splenic contraction. Normally, the apex
of the spleen is near or even across the ventral midline,
well beyond the reach of most surgeons.
Horses successfully treated for LDDC are at
increased risk of one or more recurrences. The actual
prevalence of recurrence is unknown, rates from 2-22
per cent are reported. These recurrence rates do not
justify additional surgical procedures to prevent recur-
15
Kidney
Edge of
L- incision
Figure 15.5 Schema representing obliteration of the reno-
splenic space. Five or six sutures are placed in a cruciate
pattern between the capsule of the dorsal aspect of the
spleen and the renosplenic ligament
renee following a single episode of LDDC however such
procedures should be considered in horses experienc-
ing a second bout of LDDC. Obliteration of the reno-
splenic space via a left flank celiotomy or an 18th or
17th rib resection approach has been successfully used
to prevent recurrences of LDDC. This procedure does
not prevent other types of colonic displacement, as
compared to colopexy or elective colonic resection, but
may be more satisfactory in horses used for athletic pur-
poses. For this procedure, the horse is anesthetized in
right lateral recumbency. The authors prefer an 18th
rib resection (see Chapter 10). Once the abdomen is
entered, the renosplenic entrapment is relieved without
the use of phenylephrine. An assistant's hand is then used
to lift the body of the spleen so that the tension between
the dorsal aspect of the spleen and the renosplenic liga-
ment is reduced. Five or six sutures of #2 polypropylene
material are placed in a cruciate pattern between the
capsule of the dorsal aspect of the spleen and the reno-
splenic ligament (Figure 15.5). The space is closed from
ventral to dorsal with the aim of eliminating the space at
its most dorsal and caudal aspect such that the colon
cannot be entrapped in this location.
Right dorsal displacement of the colon (RODe)
Displacement of the large colon between the cecum
and right body wall (Figure 15.6) results in signs of
colic due to obstruction. The cause of this problem is
unknown. Most commonly the pelvic flexure and left
colon pass in a craniocaudad direction between
cecum and right body wall. These structures then turn
287
15 COLIC

Large colon volvulus

~Rm!!l~ilil$lI!iI~dlilM.n.·IT1ml]!WI.~~

RP Hackett

INTRODUCTION

Volvulus of the large colon can occur anywhere along

the length of the colon. In a report of 109 cases of volvu-
lus,47 (43%) occurred at the level of the cecocolic fold
and ampulla coli, 33 (30%) in the left colon or sternal
and diaphragmatic flexures, 26 (24%) across the cecal
base and transverse colon and 3 (3%) affected the right
colons cranial to the cecocolic fold (Figures 15.7, 15.8,
15.9). The twist is typically clockwise as viewed from
behind the horse. Clinical signs associated with volvulus
of the colon are largely attributed to the degree of
volvulus as outlined in Table 15.1.
Based on the clinical signs, the degree of volvulus
appears to remain relatively static over time in many
Figure 15.6 Right dorsal displacement of the colon viewed horses. In some horses however, the twist appears to
with the horse in dorsal recumbency progress with time (hours or even days) resulting in
intensification of clinical signs. Depending on the
degree of vascular obstruction, large colon volvulus is
defined as either non-strangulated colon volvulus or
craniad placing the pelvic flexure in the cranial strangulated colon volvulus.
abdomen. Less commonly, the pelvic flexure and left
colon pass caudocraniad between the cecum and body
wall, also with the pelvic flexure in the cranial
abdomen. Either type may be accompanied by
180°-360° volvulus of the large colon. As with LDDC,
the clinical signs of right dorsal displacement of the
colon are extremely variable ranging from a pro-
longed course of very mild colic to an acute episode of
severe pain and tympany. Rectal examination reveals
large colon segments with variable tympany passing
from between the cecum and right body wall, behind
the cecum and then forward. The pelvic flexure ordi-
narily is not palpable. In cases accompanied by 270°
or greater volvulus, edema in the wall of the colon
may be evident by rectal palpation. This finding may
be confirmed ultrasonographically.
The treatment of RDDC is surgical. Exploratory
celiotomy under general anesthesia confirms the diag-
nosis. In most cases, the colon can be repositioned
after gas decompression of the colon and cecum. In
cases accompanied by severe impaction, evacuation of
the colon by pelvic flexure enterotomy and lavage may
Figure 15.7 Schematic representation of the equine large
be necessary to safely manipulate and reposition the
colon viewed with the horse in dorsal recumbency, show-
colon. Resection of the colon will be necessary in the
ing the regions most commonly involved by torsions. 1 =
rare case in which colonic viability has been compro- area at the base of the colon where torsions may origi-
mised by an accompanying volvulus. The prognosis for nate; the cecum is often involved in these cases. 2 = area of
RDDC unaccompanied by colonic ischemia is very right colon where torsion may originate and does not
good. involve the cecum

288
 DISEASES OF THE LARGE COLON THAT CAN RESULT IN COLIC
Figure 15.8 Volvulus of the large colon involving the ster-
nal and diaphragmatic flexures, viewed with the horse in
dorsal recumbency
Figure 15.9 Volvulus of the large colon and cecum, viewed
with the horse in dorsal recumbency
15
Degree of Effect
colon rotation
None
90°-270° Obstruction of lumen to
passageof ingesta (partial
obstruction)
Obstruction of lumen to
passageof ingesta and gas
(complete obstruction). Mild to
moderate venous compromise
resulting in colonic edema
>360° Strangulation obstruction of
colon
NON-STRANGULATED COLON
VOLVULUS
The clinical presentation of horses with colon volvulus
varies widely as might be predicted from the above dis-
cussion. Horses with a twist of 90-270° resemble those
with impaction colic. Abdominal pain is usually mild
and readily controlled with analgesic medications. Vital
signs, hydration, and peripheral perfusion remain
within normal limits. There is no evidence of abdomi-
nal tympany and borborygmi are normal. Signs may
remain static for days or progress over 12-24 hours.
Rectal examination in many horses is normal early in
the course of disease. Mild tympany of the left colon or
cecum may be evident in some horses. Feed impaction
of the left colon may be evident in some cases of longer
duration. This can be distinguished from pelvic flexure
impaction because the left dorsal colon is empty in a
pelvic flexure impaction and filled with ingesta in a left
colon torsion.
Clinical signs in horses with a 270-360° colonic
volvulus are more intense, largely because of progres-
sive gaseous distention of intestinal segments proximal
to the twist. Signs of pain are more profound and are
more refractory to analgesic drugs. Moderate tachy-
cardia (60-90 bpm) is common. Indicators of hydration
and peripheral perfusion are relatively normal.
Abdominal distention is evident. The occasional horse
will have nasogastric reflux. Rectal examination typi-
cally reveals moderate to marked tympany of the left
ventral and dorsal colon. Colonic bands may be ori-
ented transversely if the pelvic flexure has shifted to the
right of midline as the left colon distends. Tympany of
289
15 COLIC

the cecal base is typical. Mild edema of the colonic wall its junction with the transverse colon. Horses with long-
may be evident on rectal palpation or ultrasonographic standing non-strangulated colon volvulus will often
evaluation. have secondary impaction of colonic segments with
firm ingesta. Manipulation of the heavy, distended
Treatment colon in these horses is difficult and bears a substantial
risk of colonic rupture. Evacuation of the colon via
The treatment for non-strangulated colon volvulus is
pelvic flexure enterotomy and lavage is prudent before
surgical. Progressive colon tympany and signs of severe
correction of the volvulus is attempted (Figure 15.10).
abdominal pain clearly indicate the need for surgery in
Correction of volvulus involving the left colons and of
horses with 270-360° colonic volvulus. In horses with a
the right colons between the cecocolic fold and sternal
90-270° volvulus, clinical signs are relatively mild and
and diaphragmatic flexures is readily accomplished
resemble those of colonic impaction. Such horses are
under direct visualization. Relief of volvulus across the
often treated conservatively for many days. However,
cecal base and right dorsal colon-transverse colon junc-
unless the presence of a treatable impaction is con-
tion is accomplished blindly. While an assistant holds
firmed by rectal examination, mild colonic volvulus
the right dorsal colon as vertically as possible, the sur-
should be strongly considered in horses with signs of
geon places a hand on both sides of the ampulla of the
mild to moderate abdominal pain that persists for
right dorsal colon just dorsal to the twist. The colon is
longer than 24-48 hours. Surgical exploration is
rotated in an anticlockwise direction to correct the
warranted in such horses.
typical clockwise volvulus (Figure 15.11) Correction of
The surgical approach for management of non-
volvulus is confirmed by ability to trace the cecocolic
strangulated colon volvulus is ventral midline
fold from the cecum onto the right ventral colon and by
celiotomy. Following needle decompression of the
palpation of a normal junction between the right dorsal
cecum and large colon, the colon is exteriorized for
colon and transverse colon. If the latter procedure is
inspection. Volvulus affecting the left colons or of the
not performed, a 360° volvulus across the cecal base
right colons between the cecocolic fold and sternal and
and transverse colon may be left in place.
diaphragmatic flexures are apparent by direct inspec-
tion. Volvulus across the cecal base and right dorsal
colon-transverse colon junction is evident only by pal-
pation. The right dorsal colon is followed distally to
determine a twisting where its ampulla funnels down at

Figure 15.11 Schematic drawing showing manipulation

Figure 15.10 Evacuation of the colon via pelvic flexure
enterotomy in a horse with large colon volvulus
required to correct the typical large colon volvulus. While
an assistant holds the right dorsal colon as vertically as
possible, the surgeon places a hand on both sides of the
ampulla of the right dorsal colon just dorsal to the twist.
The colon is rotated in an anticlockwise direction to
correct the typical clockwise volvulus

290
 DISEASES OF THE LARGE COLON THAT CAN RESULT IN COLIC
OTHER NON-STRANGULATING COLON
DISPLACEMENTS
In addition to those described above, other non-stran-
gulating abnormalities of colon placement have been
described. The most common of these is retroflexion
(cranial displacement) of the left colon such that the
pelvic flexure is located in the cranial abdomen. Also,
herniation of the colon through large internal defects
(diaphragm, gastrosplenic ligament, mesocolon) may
be considered a form of non-strangulating displace-
ment. Clinical signs associated with such problems
mimic those of the more common forms of non-
strangulated colonic displacement.
STRANGULATION OF THE LARGE COLON
Strangulation of the large colon is typically due to volvu-
lus, although strangulation due to internal hernia may
occur rarely. Volvulus of the large colon exceeding 360 0
results in peracute abdominal crisis that is rapidly life
threatening. This degree of volvulus leads not only to
complete colonic obstruction but also to endotoxemia
and sequestration of blood in the strangulated segment.
Strangulated colonic volvulus constituted 6.5 per cent
of surgical colics at university referral centers. The fatal-
ity rate for these cases was 72 per cent. Periparturient
mares are particularly at risk. Volvulus of the colon is
typically hemorrhagic rather than ischemic - venous
drainage of the colon is compromised but arterial
inflow is relatively intact. This results in engorgement of
the colonic wall with fluid and blood. Mild signs of
colic, perhaps due to non-strangulated displacement,
occasionally precede signs of severe colic by hours or
even a couple of days. In most cases however, there is an
acute onset of severe abdominal pain and rapidly pro-
gressive abdominal distention. Signs of cardiovascular
compromise including tachycardia, dehydration, pro-
longed capillary refill time, and deterioration of
mucous membrane color rapidly ensue. Rectal exami-
nation commonly reveals marked colonic tympany,
thickening of the colonic wall and, often, orientation of
colonic tenia transversely across the abdomen.
Strangulated large colon volvulus is a surgical emer-
gency and the prognosis is substantially enhanced by
early surgical intervention. The approach to surgical
treatment generally parallels that for non-strangulated
colonic volvulus as described above. The colon is
decompressed, evacuated through pelvic flexure
enterotomy and the volvulus is corrected. In addition,
the surgeon's assessment of colonic viability will influ-
ence case management. Although a number of tech-
niques for objective asse~sment of equine intestinal
15
viability have been described (fluorescein perfusion,
surface oximetry, intralumenal pressure, frozen sec-
tions histopathology, Doppler blood flow), these proce-
dures are not in common practice, however, because of
either lack of availability or concern about their relia-
bility. Subjective parameters (color, thickness, motility,
mesenteric pulse) are ordinarily employed but are of
limited accuracy. Often colonic damage is overesti-
mated because of the color changes and edema typical
of hemorrhagic strangulation. Gross appearance of the
colonic mucosa at the enterotomy site is a more reliable
subjective criterion, as postoperative outcome is largely
dependent on mucosal survival. Intact reddish mucosa
suggests a favorable prognosis. A black mucosa, particu-
larly when coupled with blood staining of colonic con-
tent, indicates loss of mucosal integrity and a poor
prognosis. Cases with a clearly viable colon are man-
aged as for non-strangulated volvulus (described
above). Resection of colon that is non-viable or of ques-
tionable viability is indicated in cases with volvulus of
the right colon at the level of the cecocolic fold or in
the left colon or sternal and diaphragmatic flexures.
Resection is not possible in cases with non-viable colon
due to volvulus across the cecal base and transverse
colon, and euthanasia is indicated. Cases with unre-
sectable colon of marginal viability should be given a
chance through recovery from anesthesia and intensive
therapy for endotoxic shock. In these cases, pharmaco-
logical intervention is often used to combat postopera-
tive hypoperfusion of the large colon - medications
such as heparin are used to decrease vascular resistance
by minimizing intravascular coagulation in low flow
states and dimethylsulfoxide (DMSO) to reduce
endothelial swelling. In addition these animals become
progressively hypoproteinemic associated with the
mucosal necrosis and plasma therapy is needed. These
cases may respond over several days as surviving cells
in the mucosal crypts regenerate to restore mucosal
integrity and prevent endotoxin absorption and colonic
water loss. Such cases are candidates for a 'second look'
surgery if not responding positively after 2-3 days.
PREVENTION OF COLON VOLVULUS
The recurrence rate for colonic volvulus in non-brood
mares is approximately 5 per cent, brood mares are at a
higher risk. Mares that have had one volvulus have a 15
per cent chance of a second one. Mares that have expe-
rienced a volvulus two or more times have an 80 per cent
chance of another recurrence. Such mares are candi-
dates for colopexy by fixation of the lateral band of the
left ventral colon to the cranial ventral abdominal wall
about 15 ern to the left of the ventral midline. A contin-
291
15 COLIC
Ventral
midline incision
I RP Hackett
Figure 15.12 Colopexy. The lateral taenia of the ventral
colon (line of x's) is sutured to the ventral abdominal wall
about 15 cm to the left of the ventral midline (dotted line).
Inset: relationship of fixation to ventral midline incision.
uous or simple cruciate pattern of no. 2 non-absorbable
monofilament suture is ordinarily used. This procedure
has been described through a ventral midline celiotomy
or via laparoscopy and prevents recurrence of volvulus
(and other types of colonic displacement) (Figure
15.12). Complications of this procedure are not uncom-
mon and include colic, incisional hernia, catastrophic
rupture of the left colon, and enterocutaneous fistula.
The safety of this procedure in horses used for athletic
endeavors has not been established. Some surgeons pre-
fer elective resection of the large colon near the termi-
nation of the cecocolic fold to prevent recurrence of
volvulus and other displacements in athletes. Weight
loss and soft stools are early complications of this pro-
cedure but normal nutritional performance can be
expected to return within 5-6 months.
292
Primary colonic tympany
II
Primary colonic tympany is a functional colic - there is
no mechanical bowel obstruction yet there is distention
of the large colon, or the large colon and cecum, with
gas. Tympany is often idiopathic but may arise from
either overproduction of gas or, more commonly, from
delayed evacuation of normal gas. Gas overproduction
has been associated with a rapid dietary change to
highly fermentable concentrates or forages. Delayed
evacuation of gas may be associated with a number of
factors leading to diminution of colonic motility
• parasitism
• lack of exercise
• colitis
• peritonitis
• stressors such as transport or surgery
• parasympatholytic agents including drugs, toxins,
or plants.
The severity of clinical signs is proportional to the
degree of colonic distention. Cases with mild to moder-
ate colonic distention exhibit signs of mild to moderate
abdominal pain and corresponding tachycardia. Such
cases may spontaneously resolve or be successfully man-
aged medically through treatment with analgesics and
with mineral oil to promote colonic evacuation and
reduce gas production.
In severe cases of colonic tympany, signs include
marked colic pain, abdominal distention, tachycardia,
tachypnea, and cardiovascular deterioration. Marked
distention of the colon is evident on rectal and ultra-
sonographic examination but colonic mural thickness
is normal and there is no evidence of displacement or
lumenal obstruction. Peritoneal fluid is typically unre-
markable. The veterinarian must be aware that such
horses cannot be readily distinguished from those
affected with colonic tympanyt0.05 263472n
 DISEASES OF THE LARGE COLON THAT CAN RESULT IN COLIC
preparation and local anesthesia, the catheter is placed
into the distended viscus. Suction accelerates the
decompression but is not essential. After decompres-
sion, as the catheter is withdrawn, a broad spectrum
antibiotic solution such as neomycin or gentamicin
should be injected through the catheter to reduce like-
lihood of local peritonitis or cellulitis along the needle
track in the body wall. If clinical signs of tympany
return, it is likely that tympany is secondary rather than
primary and surgical exploration is indicated.
Non-strangulating infarction
of the large colon
RP Hackett
Infarction of the large colon in the absence of
mechanical strangulation has most commonly been
associated with arteritis of the cranial mesenteric artery
due to Strongylus vulgaris infection. The failure of post-
mortem examinations to demonstrate emboli has led
to the speculation that vasoactive mediators released
from the arteritis at the mesenteric root lead to spasm
of colonic vessels and, in some cases, to colonic infarc-
tion. The higher prevalence of non-strangulating
infarction in younger horses as well as the observation
that it appears to be less common with modern
anthelmintic therapy, support the role of Strongylus vul-
garis in its etiology. Clinical signs associated with
verminous arteries vary markedly. Intestinal ischemia
results in signs of abdominal pain and motility dis-
ruption (increased or decreased) and may account
for many self-limiting, undiagnosed cases of colic.
Infarction leads to bowel necrosis and accompanying
clinical signs due to ileus and endotoxemia. Horses
with acute colonic infarction demonstrate moderate to
severe signs of pain, progressive abdominal distention,
tachycardia, and reduced peripheral perfusion. The
colon is often fluid or gas distended on rectal examina-
tion. Peritoneal fluid early in the course of the disease
may be normal or slightly hypoproteinemic. In
advanced cases, the fluid may be serosanguinous with
high white blood cell counts. A serious or deteriorat-
ing clinical status, particularly when accompanied by
abnormal peritoneal fluid findings, should lead to
exploratory celiotomy. Surgical resection of infarcted
bowel, if possible, is warranted.
Ischemia and infarction of bowel has also been
associated with disseminated intravascular coagulation
and other systemic coagulation disorders, shock, and
embolization of thrombi from remote sites.
15
Enterolithiasis
AT Fischer, Jr
INTRODUCTION
Enterolithiasis in horses has been reported over the last
several hundred years. Recent articles have suggested
that the frequency of enterolithiasis is increasing in
California. In the same article, the authors reported
that horses with enteroliths represented 15 per cent of
the horses presenting with colic, and 27 per cent of
the horses that underwent exploratory laparotomy.
Enteroliths are composed of ammonium magnesium
phosphate which is supplied both by the digestive
processes of intestinal bacteria and by feeds. The
enteroliths typically form around a central nidus.
DIAGNOSIS
Enterolithiasis is most common in Arabian horses,
Arabian crosses, and Quarter horses but it has been
documented in all breeds. In the author's population of
horses with enteroliths between 40-50 per cent are
Arabian or Arabian crosses. If Quarter horses are added
to this group, 63 per cent of the cases are included.
There does not appear to be any sex bias but stallions
are reportedly underrepresented. Enteroliths are rare
in horses less than 3 years of age but have been reported
as early as I year old. Enteroliths are most commonly
diagnosed in middle-aged horses. In our hospital popu-
lation, any horse presenting with colic over 4 years of
age undergoes abdominal radiography unless other
factors dictate that this is unnecessary.
Horses presenting with enterolithiasis may have
• recurrent colic
• an attitude change
• scant, mucus-covered feces, no feces, or soft pasty
feces.
In some horses with enteroliths, the first change noted
by the owner is that the horse goes offits feed and stops
eating. Some of the horses with enterolithiasis will have
passed enteroliths or the owners will have found
enteroliths on the pasture. Most horses with enteroliths
will present with a moderate amount of discomfort but
some will be severely uncomfortable because of either
total obstruction of the bowel and gas accumulation
oral to the obstruction, or deterioration of the bowel
wall due to pressure necrosis.
Physical examination of horses with enteroliths is
rarely diagnostic. Most of the clinical signs shown by
293
 DISEASES OF THE LARGE COLON THAT CAN RESULT IN COLIC
The small colon should be examined to make sure that
there are no enteroliths present. If enteroliths are pre-
sent in the small colon, they are most commonly
removed without moving them inside the bowel as they
are usually firmly lodged. If the part of the small colon
where the enterolith is lodged is easily exteriorized, the
procedure for removal is the same as for removal from
the right dorsal colon. If the enterolith is lodged in the
proximal small colon and cannot be exteriorized, an
antimesenteric teniotomy may be performed to mobi-
lize the enterolith and bring it to an area more
amenable to removal. Alternatively, the enterolith may
be removed from where it is lodged after appropriate
isolation of the bowel with laparotomy sponges and
drapes. The bowel should be stabilized with stay sutures
and an assistant's hand placed underneath the
enterolith. An antimesenteric enterotomy is performed
and the enterolith is removed. The bowel is closed in
two layers and lavaged. It is helpful to remove the horse
from the ventilator and allow spontaneous non-assisted
respiration when removing enteroliths from the proxi-
mal small colon as the diaphragmatic excursions can
contribute to tearing of the bowel and contamination of
the abdomen. The closure of the abdomen is routine.
POSTOPERATIVE CARE
The care for a horse following surgical removal of an
enterolith is identical to any other abdominal surgery.
Acid-base and electrolyte status should be assessed reg-
ularly until the horse is back on full feed and supple-
mented appropriately with intravenous fluids. Early
return to feeding is believed to be beneficial. As soon as
the horse shows an interest in food, a limited amount of
grazing is allowed. Gradual return to full feed occurs
over the first few days after surgery. Mineral oil is
administered by nasogastric intubation if there are
large amounts of ingesta left in place at surgery. Dietary
restriction usually only occurs when there is compro-
mise to the intestinal wall that is unable to be removed
at surgery. Horses with compromised intestinal wall are
fed small amounts of feed for the first 5-7 days after
surgery while allowing the bowel wall to heal. Repeated
doses of mineral oil are administered during this time.
The horses are exercised by walking in hand for the first
30 days after surgery. Turnout into a small pen occurs
for 30-60 days after surgery.
COMPLICATIONS
Intra-operative complications include rupture of the
intestinal tract while trying to manipulate the enterolith.
15
Ifthis occurs deep in the abdominal incision, gross con-
tamination of the abdominal cavity occurs and the horse
is euthanized. Serosal tearing occurring during manip-
ulation of the intestine may be repaired by direct sutur-
ing or placing omental grafts over the area. Frequently
when serosal tearing occurs, the bowel is friable and
attempts to suture the tear only result in more tears. The
serosal tears may be left unsutured if necessary. Some
horses may have extensive pressure necrosis where
enteroliths have been lodged in the proximal small
colon. The affected bowel is usually discolored black and
green. If the section of bowel can be removed by either
a wedge resection or full-thickness section, then this is
done. More commonly, the damaged bowel is within the
abdominal cavity and cannot be exteriorized. In these
cases, as long as the bowel is thickened and has not
started to thin with total necrosis, the bowel may be left
in place and the horse fed small quantities for the first
week after surgery. Most of these horses will have an
uncomplicated recovery with no future complications.
The most frequent postoperative complications
include colitis and incisional drainage. Colitis is man-
aged by returning to early feeding, attention to fluid
and electrolyte abnormalities, and administration of
plasma (see Chapter 11). If the horse is not eating,
force feeding of a complete ration is helpful to ensure
that enough nutrients are available to the horse and
subjectively this seems to decrease the duration of the
colitis. Incisional drainage is best managed by daily
cleaning of the discharge from the incision with dilute
betadine or chlorhexidine in saline. Peritonitis is
another reported complication but is decreasing in
frequency because of earlier surgical intervention and
earlier recognition of the presence of enteroliths by
abdominal radiography.
PREVENTION AND RECURRENCE
Abdominal surgery for the removal of enteroliths is very
rewarding with high success rates. Future research
should examine the role of diet and genetic predisposi-
tion toward the development of enteroliths. Recurrence
has been reported in 7.7 per cent of horses operated on
for enterolithiasis and these horses were less likely to
have undergone dietary modification. A genetic predis-
position is possible because breed predilections have
been reported. In a recent study 9.6 per cent of horses
with enteroliths had siblings that were also affected. The
effect ofenvironment must be examined in these horses.
Dietary management should include feeding a minimal
amount of alfalfa hay or pellets, and increasing the per-
centage of grass-type hay in the diet. Alfalfa has been
considered a contributing factor because ofits high mag-
295
15 COLIC
nesium content and protein content contributing to the
liberation of ammonium during digestion by the intesti-
nal microflora. Wheat bran has been similarly impli-
cated because of its high phosphorus and' magnesium
content. Alkaline pH in the colon of horses undergoing
surgery for enteroliths has been demonstrated and this
was felt to be a factor in the formation of enteroliths.
Studies involving the implanting of enteroliths into
fistulated ponies with acidic pH in their colons demon-
strated that the enteroliths would dissolve. This obser-
vation led to administration of apple cider vinegar (one
cup given orally twice daily over hay or grain) in an
attempt to lower colonic pH. Personal observation has
not validated this therapy as most of the horses that are
operated on at the author's hospital have been given
apple cider vinegar for several years prior to surgery. The
magnesium content of water might be contributory, but
Lloyd et at. (1987) calculated that water with a very high
magnesium content would supply only 10 per cent of the
magnesium in an alfalfa hay diet, making it a less impor-
tant concern in prevention of enteroliths.
Increased vigilance by veterinary surgeons for the
presence of enteroliths by routine abdominal radiogra-
phy of horses admitting with colic allows for earlier
surgical intervention with more successful outcomes.
Segmental eosinophilic
colitis
GB Edwards
INTRODUCTION
Segmental eosinophilic colitis is an uncommon disease
that results in a local obstructive lesion of the colon
wall. Affected segments of bowel show variable mucosal
necrosis, submucosal oedema, and eosinophil infiltra-
tion of the lamina propria and deeper layers of the
colon wall. No cause has been established although a
parasite-associated etiology is suspected.
CLINICAL SIGNS
Affected horses usually present with mild to moderate
intermittent colic. The pain is responsive temporarily to
analgesics, but recurs as the action of the analgesic
wears off. There may also be varying degrees of abdom-
inal distention for a few hours to several days. The heart
rate varies depending on the duration of disease, but is
usually in the range 36-75 (mean 52) bpm. Capillary
296
refill time and mucous membrane colour are normal
unless the horse has become dehydrated or is affected
by toxemia secondary to peritonitis.
RECTAL EXAMINATION
Rectal examination typically reveals varying degrees of
large colon and cecal distention, and a relatively soft
impaction of the pelvic flexure and left ventral colon.
Mural edema may be evident in the pelvic flexure and
left dorsal colon, and in some cases the corresponding
mesocolon may also be edematous. This is sometimes
accompanied by a segmental, firm enlargement
(approximately 10 em diameter) of the left dorsal
colon.
ABDOMINOCENTESIS
Peritoneal fluid shows evidence of non-septic peritoni-
tis. It is usually turbid and yellow I orange colored. In a
few cases sanguinous peritoneal fluid is obtained. The
total nucleated cell count is elevated (10-250 x 109 / 1)
and consists predominantly of neutrophils. The total
protein concentration is also elevated (> 30 gil).
SURGICAL FINDINGS AND TREATMENT
At surgery, cecal and small intestinal distention may be
present, this should be relieved prior to lifting the left
colon and part of the right colon from the abdominal
cavity. Serosal lesions are usually present in the left
dorsal colon just aboral to the pelvic flexure. These
changes vary from slight petechiation, to erythema, to a
discrete well-defined area of serosal necrosis. The
lesions are usually well demarcated. Occasionally
lesions may be found oral to the pelvic flexure, or there
may be multifocal lesions involving the left dorsal, left
ventral, and right ventral colons. The colonic contents
are usually relatively soft and can be removed via an
enterotomy in the left ventral colon without recourse to
lavage (which reduces the risk of peritoneal contamina-
tion). On the mucosal surface, the lesions are charac-
terized by edema and dark discoloration. In some cases
there may be areas of necrosis evident on the surface.
Treatment consists of removal of the impaction, and
surgical resection of the affected segment of colon. In
very mild cases where the lumenal occlusion is minimal,
resection of bowel may not be necessary, although there
is a risk of subsequent worsening of the disease postop-
eratively. In cases where the segment of abnormal colon
is short, a wedge resection may be performed with liga-
 DISEASES OF THE LARGE COLON THAT CAN RESULT IN COLIC
tion of segmental vessels but leaving the colic artery and
vein intact. When resection of longer lengths of left
dorsal colon is required, the colic vessels should be
double ligated and the compromised segment of bowel
transected at an oblique angle. Following resection, the
colon is repaired by end-to-end anastomosis. The defect
in the colonic mesentery should be closed with a simple
continuous suture pattern.
In horses in which the segment of compromised left
dorsal colon is too long to allow resection and end-to-
end anastomosis, and in horses with lesions affecting
both the left dorsal and left ventral colons, a partial
resection of both the ventral and dorsal colons should
be performed. Following double ligation of the colonic
vessels, a side-to-side anastomosis 15-18 em long is
created between the left dorsal and left ventral colons,
prior to resection of the affected bowel segment and
closure of the proximal ends with a double layer of
inverting sutures.
PROGNOSIS
In one review of 22 cases of segmental eosinophilic col-
itis, long-term follow-up information was available for
18 cases. Of these horses, 16 were alive and well, with no
history of colic, 3 months to 7 years following discharge
from the clinic. One horse in which resection of the
colon was not performed had recurrence of colic
symptoms.
BIBLIOGRAPHY
Impaction
Dabareiner R M (1998) Impaction of the ascending colon
and cecum. In Current Techniques in Equine Surgeryand
Lameness, N A White,J N Moore (eds). W B Saunders,
Philadelphia, pp. 270-2.
Dabareiner R M, White N A (1995) Large colon impaction in
horses: 147 cases (1985-1991).J Am. Vet. Med. Assoc.
206(5):679-85.
Freeman D E, Granger D N, Taylor A E (1992) Comparison
of the effects of intragastric infusion of equal volumes of
water, dioctyl sodium sulfosuccinate, and magnesium
sulfate on fecal composition and output in clinically
normal horses. Am.J Vet. Res. 53(8):1347-53.
KaneeneJ B, Miller R, Ross W A, Gallagher K, MarteniukJ,
RookJ (1997) Risk factors with colic in the Michigan
(USA) equine population. Prevo Vet. Med. 30(1):23-6.
Roberts M C, Seawright A A (1983) Experimental studies of
drug induced impaction colic in the horse. Equine Vet.J
15(3):222-8.
Ross M, Hanson R R (1992) Impaction of the Ventral Large
Colon. In Auer J A (ed): Equine Surgery, W.B. Saunders,
Philadelphia, pp 390-2.
Sellers A F, LoweJ E (1986) Review of large intestinal motility
15
and mechanisms of impaction in the horse. Equine Vet.J
18(4):261-3.
Sullins K E (1999) Diseases of the Large Colon. In Calahan
P T, Mayhew I G, Merritt A M, MooreJ N (eds): Equine
Medicine and Surgery, Mosby, St Louis, MO, pp 741-2.
Young R L, SnyderJ R, PascoeJ R, Olander HJ, Hinds D M
(1991) A comparison of three techniques for closure of
the pelvic flexure enterotomies in normal equine colon.
Vet. Surg. 20(3):185-9.
Sand impaction
Hammock P D, Freeman D E, Baker GJ (1998) Failure of
psyllium mucilloid to hasten evacuation of sand from the
equine large intestine. Vet. Surg. 27(6):547-54.
Ragle C A, Meagher D M, Lacroix C A, Honnas C M (1989)
Surgical treatment of sand colic. Results in 40 horses. Vet.
Surg.18(1):48-51
Ross M, Hanson R R (1992) Sand impaction of the large
colon. In Auer JA (ed.): Equine Surgery, W.B. Saunders,
Philadelphia, pp 393-4.
Specht T E, Colahan P T (1988) Surgical treatment of sand
colic in equids: 48 cases (1978-1985).J Am. Vet. Med.
Assoc. 193(12):1560-4.
Young R L, SnyderJ R, PascoeJ R, Olander HJ, Hinds D M
(1991) A comparison of three techniques for closure of
the pelvic flexure colotomies in normal equine colon. Vet.
Surg.20(3):185-9.
Displacement of the large colon
Left dorsal displacement of the colon
Baird A N, Cohen N D, Taylor T S, WatkinsJ P, SchumacherJ
(1991) Renosplenic entrapment of the large colon in
horses: 57 cases (1983-1988).J Am. Vet. Med. Assoc.
198:1423-6.
White N A, Lessard P (1986) Risk factors and clinical signs
associated with cases of equine colic. Proc. Am. Assoc.
Equine Pract. 32:637-44.
Santschi E M, Slone D EJr, Frank W M II (1993) Use of
ultrasound in horses for diagnosis of left dorsal
displacement of the large colon and monitoring its
nonsurgical correction. Vet. Surg. 22:281-4.
Sivula NJ (1991) Renosplenic entrapment of the large colon
in horses: 33 cases (1984-1989) J Am. Vet. Med. Assoc.
199:244-6.
Right dorsal displacement of the colon (RODe)
Hackett R P (1983) Nonstrangulated colonic displacement in
horses.J Am. Vet. Med. Assoc. 182:235-40.
Large colon volvulus
Barclay W P, FoernerJ J, Phillips T N (1980) Volvulus of the
large colon in the horse. J Am. Vet. Med. Assoc. 177:629-30
White N A, Lessard P (1986) Risk factors and clinical signs
associated with cases of equine colic. Proc. Am. Assoc.
Equine Pract. 32:637-44.
Fischer A T, Meagher D M (1986) Strangulating torsions of
the equine large colon. Compo Cont. Educ. Pract. Vet.
8S:25-30
Harrison I W (1988) Equine large intestinal volvulus. A review
of 124 cases. Vet. Surg. 17:77-81
297
15 COLIC
Hance S R, Embertson R M (1992) Colopexy in broodmares:
44 cases (1986-1990).J Am. Vet. Med. Assoc. 201:782-7
Enterolithiasis
Blue M G, Wittkopp R W (1981) Clinical and structural
features of equine enteroliths.]. Am. Vet. Med. Assoc.
179(1) :79-82.
Blue M G (1979) Enteroliths in horses - a retrospective study
of 30 cases. Equine Vet.]. II (2) :76--84.
Fischer A T (1990) Enterolithiasis. In Current Practice ofEquine
Surgery, N A White,] N Moore (eds).] P Lippincott,
Philadelphia, pp. 348-51.
Hassel D M, Langer D L, Snyder] R, Drake C M, Goodell
M L, Wyle A (1999) Evaluation of enterolithiasis in equids:
900 cases (1973-1996).]. Am. Vet. Med. Assoc.
214(2):233-7.
Hassel D M, Yarbrough T B (1998) A modified teniotomy
technique for facilitated removal of descending colon
enteroliths in horses. Vet. Surg. 27:1-4.
298
Hintz H F, Lowe] E, Livesay-Wilkens et al; (1988) Studies on
equine enterolithiasis. Proc. Am. Assoc. EquinePract. 34:53-9.
Lloyd K, Hintz H F, Wheat] D, Schryver H F (1987)
Enteroliths in horses. Cornell Vet. 77(2): 172-86.
Peloso] G, Coatney R W, Caron] P, Steficek B A (1992)
Obstructive enterolith in an l l-month-old miniature
horse.]. Am. Vet. Med. Assoc. 201 (1l):1745-6.
Rose] A, Rose E M, Sande R D (1980) Radiography in the
diagnosis of equine enterolithiasis. Proc. Am. Assoc. Equine
Pract.26:211-9.
Yarbrough T B, Langer D L, Snyder] R, Gardner I A, O'Brien
T R (1994) Abdominal radiography for diagnosis of
enterolithiasis in horses: 141 cases (1990-1992).]. Am. Vet.
Med. Assoc. 205(4):592-5.
Eosinophilic colitis
Edwards G B, Kelly D F, Proudman C] (2000) Segmental
eosinophilic colitis in horses a review of 22 cases. Equine
Vet.]. 32:86--93.
 16
Diseases of the small colon and rectum
J Schumacher
Diseases of the small colon
ENTEROLITHS
Enteroliths, or intestinal calculi, are mineralized con-
cretions that develop in the large colon by concentric
deposition of salts around a central nucleus, usually a
small silicon stone or metal object. Enteroliths can
remain within the large intestine for long periods unas-
sociated with signs of clinical disease, and it is only when
they obstruct the lumen of the large or small colon that
the horse shows signs of abdominal pain.
Enteroliths are primarily composed of ammonium
magnesium phosphate crystals (struvite). Because
ammonia is constantly produced from microbial activity
within the large intestine, and phosphates are abundant
in common horse feeds, the concentration of magne-
sium, rather than ammonia or phosphate, in the feed
may influence the formation of enteroliths. Diets of
alfalfa hay containing a high concentration of magne-
sium have been incriminated in the formation of
enteroliths.
Epidemiology
The prevalence of enterolithiasis is high in the south-
western US, and university teaching hospitals in
California, Florida, and Indiana have twice the preva-
lence of enterolithiasis as other schools in the US. The
Arabian seems to be the breed most commonly affected
by enterolithiasis, and females of all breeds are more
likely than males to develop enteroliths. The reason for
the predisposition of females to the development of
enterolithiasis is unknown, but fluctuations in the con-
centration of prostaglandins in the serum associated
with the reproductive cycle may affect gastrointestinal
motility, thereby predisposing females to the formation
of enteroliths.
The time required for an enterolith to form is
unknown, but reports of enterolithiasis occurring in
horses younger than 4 years old are rare. Enterolithiasis
in an II-month-old miniature horse has been reported.
The mean reported age of horses requiring abdominal
surgery because of an obstructive enterolith is 10 years.
Clinical signs and diagnosis
Diagnosis of obstructing enterolithiasis is based on clin-
ical signs and physical examination. An obstructing
enterolith blocks the passage of feces but may allow pas-
sage of gas and intestinal lubricants, such as mineral oil.
An enterolith within the small colon typically causes
complete obstruction, and affected horses tend to show
signs of more severe abdominal pain than horses with
partial or intermittent obstruction of the transverse or
right dorsal colon. Palpation of an enterolith in the
small colon is usually possible only when it is lodged in
the rectum or distal portion of the small colon. An
enterolith in the proximal aspect of the small colon is
usually beyond the reach of the examiner, and small
colon distal to the enterolith is usually flaccid and diffi-
cult to identity. If the enterolith has lodged in the mid-
dle or distal portion of the small colon, loops of
gas-filled small colon may be recognized.
Diagnosis of enterolithiasis in horses showing clini-
cal signs of the disease can sometimes be confirmed by
radiography. Radiography is less helpful in the diagno-
sis of enterolithiasis of the small colon than it is for
diagnosis of enterolithiasis of the large colon (i.e.
299
16 COLIC

transverse colon), however, and the absence of radi- Prognosis

ographic findings does not preclude the presence of
Prognosis for survival of horses undergoing surgery for
an enterolith.
enterolithiasis is determined by the cardiovascular
health of the horse and the in tegrity of the affected area
Treatment of intestine. In one study, 58 per cent of 24 horses oper-
ated on for enterolithiasis survived, and in another
Treatment of horses suffering from obstruction of the
study of 34 horses treated surgically for enterolithiasis,
small colon by an enterolith is by removal of the
survival following surgery was 70.6 per cent. In another
enterolith through a laparotomy (celiotomy). If possi-
report, over 85 per cent of horses operated on for
ble, the enterolith should be manipulated a few cen-
timeters distally or proximally so that the enterotomy enterolithiasis survived.
can be made in a normal portion of intestine. Studies
show that longitudinal enterotomies made through the Prevention of recurrence
antimesenteric tenia of the small colon are superior to To prevent enterolithiasis from reforming following
those made adjacent to the tenia, as determined by surgery, the feeding area should be elevated or free of
maintenance of the diameter of the lumen, ease of clo- gravel, and the amount of alfalfa fed to the horse (and
sure, and minimal interruption of the blood supply. the rest of the herd) should be decreased and replaced
Enterotomy performed through the antimesenteric by another type of hay. Colonic pH below 6.6 tends to
tenia results in less hemorrhage and less inflammation. prevent the formation of enterolithiasis, and decreasing
and sutured incisions through the tenia are stronger the amount of hay and increasing the amount of grain
than sutured incisions adjacent to the tenia at 96 hours. in the diet tends to decrease the pH of colonic contents.
Closure of the mucosa as a separate layer offers no Adding vinegar to the diet is another method of
advantage or disadvantage in healing in normal horses. decreasing colonic pH.
Complications associated with enterotomies of the
small colon include leakage, visceral adhesions, and
stricture formation. Factors that may adversely affect FOREIGN BODY OBSTRUCTION
the outcome of surgery of the small colon in the horse
include the small colon's relatively poor blood supply, Foreign materials involved in obstruction of the small
its high concentration of collagenase, its high intralu- colon include nylon fibers from halters, hay nets, or
menal concentration of bacteria (including large con- twine, cords from rubber material, synthetic fencing
centrations of anaerobic organisms), its muscular material, disposable plastic sleeves, and tops of feed
activity; and the presence of particulate feces. The sacks (Figure 16.1). The foreign material becomes
mesocolon of the small colon is relatively short, making coated with mineral precipitate increasing its bulk. The
exteriorization of the proximal and distal ends of the resulting masses are irregular. often containing projec-
small colon difficult or impossible. The risk of peri- tions that cause necrosis of the obstructed intestine.
toneal contamination is high if enterotomy or resection The ingested foreign material may remain within the
and anastomosis are necessary for those parts of the
small colon that are difficult to exteriorize.
An enterolith in the proximal end of the small colon
must often be repelled into the right dorsal colon and
then into the left dorsal colon for removal through an
enterotomy. An enterolith can be most easily and safely
dislodged and repelled proximally by retrograde infu-
sion of water into the small colon. To repel an
enterolith proximally, a stomach tube is inserted into
the rectum and passed into the small colon. The tube is
guided to the obstruction by the surgeon and. while the
small colon is occluded by holding it tightly to the tube,
water is infused into the intestine until the lumen
expands to a size large enough to allow the enterolith to
be dislodged proximally. The enterolith is then
repelled into the left dorsal colon where it can be
removed safely via enterotomy remote from the abdom- Figure 16.1 Ingested plastic trash can liner occluding the
inal cavity. rectum and small colon

300

large colon for a considerable period of time before
passing into and obstructing the small colon.
Obstruction of the small colon caused by ingestion of
foreign material occurs generally in horses 3 years old
or less, probably because young horses are less discrim-
inate in their eating habits.
Clinical signs and diagnosis
Obstruction of the small colon by a foreign body usually
results in a gradual onset of vague signs of anorexia,
dullness, and abdominal pain. If the obstruction is
located in the most distal part of the small colon, tenes-
mus may be observed. Systemic effects of the obstruc-
tion are minor initially, even in horses showing signs of
marked pain, and the hematocrit may remain
unchanged for many days. Affected horses remain unre-
sponsive to medical therapy. The obstruction may be
difficult to locate by palpation per rectum, owing to its
small size and tendency to lodge in the proximal por-
tion of the small colon. The obstruction is usually asso-
ciated with an impaction that extends into the large
colon.
Treatment
The obstruction must be removed before the small
colon surrounding it becomes necrotic. At surgery, the
obstruction should be manipulated a few centimeters
distally or proximally so that the enterotomy can be
made in normal intestine, but if the involved segment
cannot be exteriorized, the obstruction should be
repelled proximally by retrograde infusion of water into
the small colon and removed through an enterotomy at
the pelvic flexure of the large colon.
FECAL IMPACTION
Fecal impaction is the most common disorder of the
small colon. Ponies, American Miniature Horses, and
Arabians, especially female Arabians, appear to be
affected by fecal impaction of the small colon more fre-
quently than are other breeds, whereas the condition is
less common in Quarter horses. Impactions of the small
colon appear to be most common in aged horses and
yearling ponies.
Fecal impaction of the small colon may be related to
ingestion of bedding or poor-quality hay, poor denti-
tion, inadequate hydration, parasitic damage, or disor-
ders of intestinal motility. The small colon becomes
impacted most frequently during the fall and winter,
and this seasonal predilection may be related to inade-
quate water consumption or dietary changes. Old
horses may be predisposed to impaction of the small
DISEASES OF THE SMALL COLON AND RECTUM 16
colon because of deterioration in dentition and gas-
trointestinal function. Because of the narrowing of the
lumen of the large colon through the transverse colon
into the small colon, this area of the intestine may be
predisposed to impaction. Predilection for obstruction
by ingesta of the small colon may also result from
decreased moisture content of the ingesta in this loca-
tion.
Clinical signs and diagnosis
Horses with fecal obstruction of the small colon initially
exhibit mild signs of colic. Deterioration in physical
condition progresses slowly and results from distension
of viscera with gas and fluid proximal to the impaction.
Deterioration progresses slowly because the location of
the small colon at the distal end of the intestinal tract
provides a large space for ingesta, gas, and fluid to accu-
mulate proximal to the obstruction.
Diagnosis of impaction of the small colon on the
basis of clinical signs and clinicopathologic data is fre-
quently difficult. Consistently observed clinical features
of affected horses are reduced production or absence of
feces and absent or reduced borborygmi. Abdominal
distension is often present, and nasogastric reflux can
be obtained occasionally. Although the heart rate is
usually high, clinicopathologic data are normal, this is
consistent with experimentally induced obstruction of
the small colon in horses. White blood cell count, con-
centration of electrolytes, hematocrit, and concentra-
tion of plasma total protein show little deviation from
normal.
Examination per rectum is often helpful in the diag-
nosis of fecal impaction of the small colon. One or
more loops of tubular, firm, digesta-filled intestine can
be identified during examination per rectum, and the
single, free tenia can often be identified on the colon,
confirming the segment of intestine involved.
Treatment
Objectives of medical treatment of horses with fecal
impaction of the small colon are to maintain hydration,
stimulate gastrointestinal motility, to soften the
impaction by the administration of osmotic laxatives or
lubricants, and to control pain. Intravenous administra-
tion of a balanced electrolyte solution is used to overhy-
drate the horse and to initiate fluid secretion into the
intestine to directly hydrate and soften the mass of
ingesta. Intestinal motility is stimulated by exercise,
fluid therapy, and replacement of potassium and cal-
cium. Frequent urination can be used to clinically assess
the response to overhydration.
Treatment of horses with fecal impaction of the
small colon by administration of an enema has been
301

Figure 16.4 Trichobezoar removed from the small colon
have an uneven, furrowed, velvet-textured surface. The
smooth surface of phytoconglobates and bezoars may
allow them to obstruct the lumen for relatively long
periods without causing severe damage to the mucosa.
Obstruction caused by ingestion of fibrous, non-
digestible material is seen most commonly in horses less
than 3 years old and in horses with poor dentition.
Treatment
Treatment of horses affected by fecaliths, phytoconglo-
bates, or bezoars is by surgical removal of the obstruct-
ing mass. If the obstructed segment of small colon
cannot be exteriorized, the mass should be repelled
into the large colon by retrograde infusion of water and
removed through an enterotomy at the pelvic flexure.
INTRAMURAL HEMATOMA
An intramural or submucosal hematoma is an uncom-
mon lesion of the small colon or rectum caused by hem-
orrhage between the mucosa and muscularis.
Hemorrhage occludes the intestinal lumen and dissects
along the intestine producing intestinal necrosis. The
condition occurs most commonly in old horses.
Histological examination of lesions reveals no evidence
ofthe cause, and the source of hemorrhage contributing
to the formation of mural hematoma is not evident dur-
ing gross or microscopic examination of resected colon.
The condition causes signs of abdominal pain, and
because the hematoma obstructs the lumen, examina-
tion per rectum of affected horses may reveal tympany
of the large colon. The rectum is usually devoid offeces,
but various amounts of clotted blood may be found.
Treatment of horses with the condition is by resec-
tion of the affected intestinal segment followed by an as-
DISEASES OF THE SMALL COLON AND RECTUM 16
tomosis of the proximal and distal segments of colon. At
surgery, the lesion is recognized as a dense, circum-
scribed mass attached to the wall of the small colon or
rectum. If the affected segment cannot be exteriorized
a colostomy may be necessary.
MESOCOLIC RUPTURE
Mesocolic rupture and subsequent segmental ischemic
necrosis of the small colon occur as a complication of
foaling and are the result of direct trauma caused by the
foal as it positions itself for delivery. During late preg-
nancy, the fetus is positioned ventrally, but during the
first stage of labor, the foal rotates into dorsal position
for delivery using vigorous reflex movements of its neck
and forelimbs. During these movements, the small
colon of the mare may become trapped between uterus
and dorsal body wall, causing the mesocolon to tense
and tear.
Mesocolic rupture can also result from type IV rectal
prolapse, a condition sometimes associated with partu-
rition. The vascular arcade of the mesocolon may
stretch and tear when more than 30 ern of the rectum
and small colon prolapses through the anus (see
Diseases of the rectum, Rectal prolapse).
Regardless of the cause of mesocolic rupture, infarc-
tion results, causing functional obstruction and pro-
gressive signs of colic. Segmental ischemic necrosis of
the small colon caused by disruption of the meso-
colonic vasculature should be considered when exam-
ining post-parturient mares that show signs of
abdominal pain, particularly when the cardiovascular
health of the horse deteriorates slowly and concentra-
tion of protein and the nucleated cell count in the peri-
toneal fluid increase. A consistent finding in affected
horses is failure to pass feces.
STRANGULATING LESIONS OF THE
SMALL COLON
Segments of the small colon may strangulate when they
become involved in a volvulus or intussusception, or
more commonly when entwined with a pedunculated
lipoma or the pedicle of an ovary. Volvulus occurs when
a segment of intestine twists around its mesentery. The
condition has been associated with adhesions and
abscesses. Volvulus of the small colon is unusual, pre-
sumably because it has a short mesentery.
Strangulating pedunculated lipomas are rarely seen
in horses younger than 9 years, and they most com-
monly affect horses greater than 15 years. In the US,
Quarter horses and Morgans appear to be the breeds
303
16 COLIC
most at risk of strangulation of the small colon by a
pedunculated lipoma, and females are more commonly
affected than males. Compared to other segments of
the mesentery, the mesocolon and mesorectum may be
predisposed to formation of lipomas because of the
large amount of fat in these areas, but even so, the small
colon is much less likely than the small intestine to
become strangulated by a pedunculated lipoma.
Clinical signs and diagnosis
Signs ofcolic initiated by strangulation of the small colon
are sudden in onset, but the general clinical course of
physiological deterioration may occur more slowly than
when more proximal segments of the gastrointestinal
tract become strangulated. Serosanguinous fluid con-
taining increased concentration of nucleated cells and
total protein is obtained during abdominal paracentesis
of affected horses, and tympany of the large colon and
absence offeces are evident on examination per rectum.
Treatment
Treatment of horses with a strangulating lesion is by
reduction of the volvulus or entrapment followed by
resection of the infarcted segment of small colon and
anastomosis of the proximal and distal segments.
Horses seem able to compensate for the considerable
loss of absorptive capacity that occurs when a long seg-
ment of small colon is removed.
NON-STRANGULATING INFARCTION OF
THE SMALL COLON
Primary vascular lesions with segmental infarction
caused by mesenteric thromboembolism are uncom-
mon because the small colon receives most of its blood
supply from the caudal mesenteric artery, this is rarely
affected by occlusive verminous arteritis. Often, during
abdominal exploration or at post-mortem examination
of horses affected by non-strangulating infarction of the
small colon, no evidence of arteritis of the caudal
mesenteric artery can be found. Treatment of affected
horses is by resection of the infarcted segment and anas-
tomosis of the proximal and distal segments. If the
affected segment of small colon cannot be exteriorized,
colostomy or transrectal exteriorization followed by col-
orectostomy must be performed.
INTESTINAL ATRESIA
Intestinal atresia of foals results in complete occlusion
of the intestinal lumen. The condition is rare, except in
304
crosses between predominantly white Overo Paint sires
and dams.
The etiology of intestinal atresia is unknown, but the
condition may be the result of a simple recessive gene,
developmental arrest, or vascular compromise to the
fetal gut resulting in ischemic necrosis of the affected
portion of intestine. The condition has been associated
with other congenital abnormalities, such as renal age-
nesis or hypoplasia, cerebral gliomata, hydrocephalus,
schistosomas reflexus, and infection with equine her-
pesvirus Type I. The distal portion of the large colon
and proximal end of the small colon are the segments
most commonly missing.
The types of intestinal atresia are classified accord-
ing to the tissue involved. In type I atresia, or mem-
brane atresia, a diaphragm or membrane occludes the
intestinal lumen. In type 2, or cord atresia, the proximal
and distal blind ends are joined by a small cord of con-
nective tissue, with or without mesentery. In type 3, or
blind-end atresia, the proximal and distal blind seg-
ments of colon are completely separated, and the cor-
responding mesentery is absent.
Clinical signs and diagnosis
Clinical signs of intestinal atresia are recognized within
a few hours after birth and may include depression, pro-
gressive abdominal distension and discomfort, tenes-
mus, absence of feces, no response to administration of
enemas, and an empty, blind-ending rectum as deter-
mined by digital palpation or endoscopic examination.
The anus is usually normal. Intestinal atresia can usually
be diagnosed by observation of clinical signs, proc-
toscopy, and contrast radiography using barium ene-
mas. Definitive diagnosis is made during exploratory
laparotomy (celiotomy).
Treatment
Foals suffering from intestinal atresia have a poor prog-
nosis for survival, and for white Overo Paint foals with
aganglionosis, the prognosis is grave. Surgical correc-
tion following early diagnosis offers the only chance of
survival for the affected foal. Untreated foals die within
the first days of life after developing endotoxemia,
severe metabolic disturbances, and occasionally fibri-
nous peritonitis. The blind ends can be resected, and
the proximal and distal segments of colon anastomosed
if the atretic segment is located in an exteriorizable part
of the intestine and is not extensive. Alternatives to
resection and anastomosis include colostomy or pulling
the blind-ended small colon through an incision in the
rectum and suturing it to the anus. The foal should be
examined for other congenital abnormalities before
intestinal atresia is corrected.

Diseases of the rectu m
RECTAL TEARS
Causes
Rectal tears occur most commonly during palpation per
rectum of reproductive structures to assess fertility or
diagnose pregnancy, and during palpation per rectum
of the abdomen to determine the cause of intestinal or
urogenital disease. Palpation per rectum is not without
risk of injury to the wall of the rectum or small colon,
and experience in examining the contents of the
abdomen per rectum does not preclude the possibility
of causing a rectal tear. Iatrogenic rectal tears and their
complications are a leading cause of malpractice suits
against veterinarians.
Rectal tears can also occur during administration of
an enema, especially in foals, as a result of either exces-
sive hydrostatic pressure or puncture of the rectum by
the enema tubing. Rectal tears have also been associ-
ated with dystocia, rupture of a mural hematoma of the
small colon, and accidental entry of the stallion's penis
into the rectum of the mare during copulation.
Perforation of the mare's rectum by the penis of a stal-
lion is most likely to occur when breeding is forced or
when angulation or tipping of the labia makes vaginal
entry difficult.
Spontaneous rupture of the rectum is rare and diffi-
cult to substantiate, but it has been reported to result
from ischemic necrosis due to thrombosis of the caudal
mesenteric artery and its branches, caused by migration
of Strongylus vulgaris. Neurogenic fecal retention and
extensive perineal and rectal melanomas can predis-
pose to spontaneous rupture of the rectum. In a few
cases, histological examination of tissue surrounding an
iatrogenic rectal tear has demonstrated a lesion that
weakened the wall of the rectum.
Progression
Complications associated with tears that occur caudal to
the peritoneal reflection include perianal fistulae, dis-
secting cellulitis, and formation of rectal diverticulae
and strictures. Tears of the intraperitoneal portion of
the rectum or small colon frequently cause fecal-
induced septic peritonitis resulting in death, even with
the best medical therapy.
Epidemiology
Rectal tears occur in horses of all ages, but the injury
occurs most frequently in young horses. Young horses
may be at risk of incurring a rectal tear because of their
DISEASES OF THE SMALL COLON AND RECTUM 16
small size, nervousness, resentment to palpation, and
excessive straining. Stallions and geldings are at greater
risk of receiving a rectal tear during examination per
rectum than are mares. Repeated examination of mares
may make them more accustomed to the procedure
and less likely to resist, also the diameter of the rectum
of males is smaller than that of mares. Arabian horses
are at increased risk of rectal injury, perhaps because
they have a relatively small anus and rectum and seem
to resist palpation more than horses of other breeds.
Anatomy
The rectum extends from the pelvic inlet to the anus, a
distance of approximately 30 cm in a 450-kg horse. The
cranial portion of the rectum is approximately 15-20
ern long, is attached to the mesorectum, and is covered
by peritoneum. The caudal portion, which includes a
flask-shaped dilatation, the ampulla recti, is approxi-
mately 10-15 ern long and is not covered by peritoneum
but is attached to the surrounding structures by con-
nective tissue and muscular bands. Because the peri-
toneal reflection extends caudally to within 15-20 cm of
the anus, rectal tears most often occur within the peri-
toneal segment of the rectum or small colon, with sub-
sequent development of septic peritonitis. The distance
from the anus to the caudal end of the peritoneal space
is longer in old and fat horses than in young and thin
horses, however, and thus a rectal tear of an old, fat
horse has a greater chance of involving the retroperi-
toneal, rather than the peritoneal, portion of the rec-
tum than does a tear in a similar location in a young,
thin horse.
In a study of 42 horses affected by a rectal tear, the
distance from the anus to the tear varied from 7.5-60
cm, and most tears occurred at the pelvic inlet, a dis-
tance of 25-30 em from the anus. The tears occurred
most often in the dorsal aspect of the rectum, between
10-12 o'clock, and the direction of the tear was usually
longitudinal.
The pelvic inlet, besides being the most common site
of the rectum at which the reproductive organs are pal-
pated, is where the rectum narrows and is deflected
downward. The rectal wall is often stretched forward at
this point, reducing its pliability. Tears in this location
are at the junction of the rectum and terminal part of
the small colon, and many tears are, in fact, located in
the caudal portion of the small colon.
Tears often occur along the edges of the dorsal
mesocolic band, because in this area, as the longitudi-
nal muscle thickens to form the mesenteric tenia, the
thickness of the circular muscle decreases. In addition,
microvascular studies of the small colon of horses indi-
cate that the area adjacent to each side of the band may
305
16 COLIC

be inherently weak because at this area, the short termi- litis and separation of tissue. Tears that perforate all lay-
nal arteries penetrate the wall. ers and extend into the peritoneal cavity are classified as
grade 4 (Figure 16.9). Grade 3 rectal tears commonly
Classification progress to grade 4.
Rectal tears are classified according to the layers of the
rectal wall disrupted. Tears restricted to just the mucosa
or the mucosa and the submucosa are classified as
grade I (Figure 16.5). In grade 2 tears, only the muscu-
laris is torn, causing a mucosal-submucosal hernia to
develop (Figure 16.6). The mucosa and submucosa,
because of their elasticity and numerous folds, can
stretch without perforation, while the overlying con-
tracted muscles rupture. Although grade 2 rectal tears
result in no contamination of the peritoneal cavity, they
could contribute to development of an iatrogenic grade
3 or 4 rectal tear.
Grade 3 tears involve the mucosa, the submucosa,
and muscularis and include tears that extend into the
mesentery. Tears that cause formation of a serosal diver-
ticulum are classified as grade 3a (Figure 16.7), and
tears that enter the mesentery are classified as grade 3b
(Figure 16.8). The intact serosa or mesorectum of a
grade 3 rectal tear prevents particulate fecal matter
from contaminating the peritoneal cavity, but bacteria
are not excluded and septic peritonitis results. Grade 3
rectal tears are often accompanied by dissecting cellu-
Figure 16.6 Grade 2 tear: the muscularis is torn, but the
other layers of the rectal wall remain intact

Figure 16.5 Grade 1 tear: only the mucosa or mucosa and Figure 16.7 Grade 3a tear: all layers except the serosa are
submucosa are torn torn, forming a serosal diverticulum

306

Figure 16.8 Grade 3b tear: the tear enters the mesentery
Prevention
Failure of the rectal wall to relax during palpation is a
major factor in the development of a tear. Producing a
rectal tear in the relaxed rectum is difficult, and so the
best way to prevent a rectal tear is to ensure that the rec-
tum is relaxed before proceeding with palpation.
Horses should be adequately restrained to perform pal-
pation per rectum, and if the horse is fractious, it
should be sedated, or a twitch or lip chain should be
applied. The hand and arm should be lubricated liber-
ally. The fingers should be introduced in coned fashion
and feces evacuated from rectum. The hand should be
inserted to slightly beyond the desired site of palpation
so that by dragging the rectal wall caudally, tension on
the rectal wall is reduced, allowing structures to be pal-
pated through a relaxed rectum. If the horse strains
excessively or if a strong contraction occurs, the hand
should be withdrawn. If the horse continues to strain or
if deep palpation is required, epidural anesthesia or a
parasympatholytic drug should be administered.
Extreme caution should be exercised when examin-
ing young horses and small ponies per rectum, because
their fractious nature and small size put them at high
risk for rectal damage. To avoid perforating the fragile
rectal mucosa of the newborn foal during treatment for
impaction of meconium, enema tubes should be
DISEASES OF THE SMALL COLON AND RECTUM 16
Figure 16.9 Grade 4 tear: the tear perforates ali layers and
extends into the peritoneal cavity
smooth, well-lubricated, and never forced into place,
and solutions should be administered by gravity flow.
Clinical signs, diagnosis and immediate
treatment
Tachycardia, intestinal ileus, pyrexia, sweating, reluc-
tance to move, and signs of abdominal discomfort after
palpation per rectum, administration of an enema, or
breeding indicate that the horse may have received a
serious rectal injury. A small amount of blood-tinged
material on the examiner's sleeve usually indicates that
only minor trauma has occurred, but the presence of
whole fresh blood on the sleeve or sudden relaxation of
the rectum, especially when the horse is straining, indi-
cates that the rectum has been seriously injured.
If a tear is suspected, the horse should be sedated,
peristalsis slowed, and the rectum evaluated carefully by
digital examination. Administration of parasympa-
tholytic drugs or caudal epidural anesthesia may be
effective in stopping peristalsis of the rectum and relax-
ing the rectum and anal sphincter. Propantheline bro-
mide, 30-35 mg per 450 kg body weight, given
intravenously, produces rapid, effective reduction of
peristalsis for up to 2 hours and prevents straining to
allow digital and endoscopic evaluation of the tear.
Precise evaluation of the layers of the rectum involved
307
16 COLIC

in the injury is best gained by digital palpation, using a vived. Horses given adequate first-aid were admitted
well-lubricated surgical glove or bare hand. Feces with less severe peritoneal inflammation, as demon-
should be removed carefully from the tear and acljacent strated by lower mean and median concentrations of
portion of the rectum. Palpation of a thin, flap-like white blood cells in the peritoneal fluid.
membrane indicates that the tear probably extends only
through the mucosa, but the presence of a thick-walled, Definitive treatment
cavity-like depression bounded by a thin, tough mem-
Grade 1 tears usually heal without serious complica-
brane that prevents extension of the hand into the
tions, and horses suffering from a grade 1 tear are usu-
abdominal cavity is characteristic of a grade 3 tear.
ally treated conservatively by administration of
Failure to recognize that a grade 3 or 4 tear has
broad-spectrum antibiotics and a stool softener. Horses
occurred can delay treatment and increase legalliabil-
with a grade 1 tear should not be palpated per rectum
ity. Immediate and intensive treatment not only
unless absolutely necessary for 3 to 4 weeks. Horses with
increases the chances of the horse's survival but also
a grade 2 tear are treated similarly to horses with a
aids defense against a malpractice action. Negligence is
grade 1 tear, but antimicrobial therapy is unnecessary.
difficult to disprove when a serious tear is not recog-
Horses with a full-thickness tear into the retroperi-
nized immediately. Circumstances in which the horse is
toneal portion of the rectum have a better prognosis for
managed initially may make the difference in winning
survival than do horses with similar tears in the peri-
or losing a case in court. The client should be informed
toneal region. They tend to heal with the main compli-
immediately that the rectum has been torn and the
cations being the formation of perirectal abscesses.
gravity of the condition should be described.
Dorsally positioned perirectal abscesses can be drained
Survival of the horse depends largely on the course
rectally or perianally, and ventrally positioned abscesses
of action instituted at the time of injury. Unless mea-
can be drained through the dorsal wall of the vagina.
sures are taken immediately to prevent peritoneal cont-
Treatment options for horses with a grade 3 tear into
amination and progression of a grade 3 tear, endotoxic
the peritoneal region of the rectum include conserva-
shock and death usually result. The tear should be care-
tive (medical) management, primary closure with
fully packed with medicated gauze sponges, and the rec-
access either through the rectal lumen or via celiotomy,
tum should be carefully packed from the anus to cranial
or diversion of feces to prevent fecal contamination of
to the tear with 3-inch (7.5 ern) stockinette filled with
the tear so that healing can proceed by second inten-
0.25 kg of rolled cotton. A purse-string suture or towel
tion. Feces can be diverted by colostomy (end or loop
clamp should be placed in the anus to keep the packing
colostomy) or with a temporary indwelling rectal liner.
material within the rectal lumen. A parasympatholytic
If second intention healing has begun in horses with a
drug or caudal epidural anesthesia should be adminis-
grade 3 tear, then continued medical management,
tered to stop peristalsis and prevent straining.
including packing the tear with medicated gauze
Before being transported to a surgical facility, a
sponges or repeated manual evacuation of the tear
horse that has suffered a grade 3 or 4 rectal tear should
(under epidural anesthesia), and intensive antibiotic
receive a fecal softener, such as mineral oil, tetanus pro-
therapy can be successful.
phylaxis, and broad-spectrum antimicrobial therapy,
Grade 4 tears usually result in contamination of peri-
using such drugs as penicillin, gentamicin, and metron-
toneal surfaces with particulate fecal material, making
idazole. The horse should also receive flunixine meglu-
euthanasia of horses with a grade 4 tear justified. If the
mine for its analgesic, anti-endotoxic, and
peritoneal surfaces have not been contaminated with
anti-inflammatory effects, and fluid therapy should be
particulate fecal material, then the same techniques
administered. Peritoneal fluid should be obtained by
used to repair grade 3 tears can be used. If the horse
abdominal centesis to assess the degree of peritoneal
incurred a grade 3 or 4 tear during evaluation of colic,
contamination, and for bacterial culture and sensitivity
an exploratory celiotomy should be performed to deter-
testing. Comparison of this fluid with fluid obtained
mine if intestinal obstruction requiring surgical correc-
later at the surgical facility may help determine the seri-
tion is present.
ousness of the tear and the extent of peritoneal conta-
mination.
Primary repair
In a study of 35 horses that had received a grade 3
rectal tear, first-aid measures taken at the time the tear Primary closure of grade 3 rectal tears is considered
occurred had a marked influence on outcome. First-aid contra-indicated by some surgeons because of the likeli-
measures were considered adequate in 14 horses, of hood of creating a dead space which may predispose to
which 11 (79%) survived, whereas only 50 per cent of formation of an abscess, and because attempts to close
those horses that did not receive adequate first-aid sur- tears primarily per rectum with the horse standing may

308

cause the tear to enlarge or perforate and may increase
contamination of damaged tissue. In one study, how-
ever, primary closure of the rectal tear, used as the sole
means of repair or used in conjunction with other tech-
niques, was shown to improve chances of survival, and
formation of an abscess during convalescence was not
evident. Primary suture closure was successful in six of
seven horses for which it was the principal method of
treatment. In this study, the tear was repaired primarily
only if it was minimally contaminated with feces. The
tear was not sutured if the ability of the tissue to hold
sutures was in doubt, either because of extensive sepa-
ration of tissue layers or marked edema.
If the tear is close to the anus, it can be sutured per
rectum with the horse standing or recumbent. Repair
can be performed using a blind, one-handed suturing
technique, but the disadvantage of this technique is the
difficulty with which it is performed by those inexperi-
enced in this method. Ineffective attempts to suture the
tear in this manner may cause the tear to enlarge or per-
forate. An alternative method of suturing the tear per
rectum involves the use of an expandable and
adjustable speculum that allows visual and surgical
access to the tear, however this speculum is not widely
available.
A grade 3 tear was sutured successfully on an anes-
thetized experimental horse by prolapsing the rectum.
The distal end of the small colon was intussuscepted
into itself, and the rectal mucosa exteriorized through
the anus, allowing the tear to be seen from the mucosal
side. Intussusception was accomplished by introducing
a hand into the rectal lumen and advancing it 4-5 cm
proximal to the tear. An assistant, working through a
laparotomy (celiotomy), initiated the intussusception
by pushing a saline-soaked gauze sponge into the finger
tips of the hand inside the rectal lumen. This allowed
the palpator to grasp the rectal wall and retract the rec-
tum through the anal orifice. The tear was then lavaged
and sutured directly. A rectal tear, located approxi-
mately 40 cm proximal to the anus, of another horse
was successfully repaired with the horse standing, by sta-
pling the tear after intussuscepting the affected portion
of the rectum toward the anus with stay sutures placed
on either side of the tear.
When exposing the damaged segment of rectum by
intussusception, the rectum should not be exteriorized
under tension for a prolonged time to avoid tearing or
thrombosis of the mesenteric vessels. The short meso-
colon and large amounts of mesenteric and retroperi-
toneal fat may prevent intussusception and
exteriorization of the damaged segment of rectum in
most horses, but the technique may be useful if the
horse is young and thin. The technique should be
attempted only if the tear is recent, because the manip-
DISEASES OF THE SMALL COLON AND RECTUM 16
ulations may worsen the tear if the surrounding tissue is
edematous.
Grade 3 or 4 tears can be sutured through a laparo-
tomy (celiotomy), but the ability to see and repair the
tear by direct suturing from the abdomen depends
largely on the distance of the tear from the anus. In
mares, a midline prepubic incision between the mam-
mary glands may provide good exposure of tears more
than 25 ern from the anus. Exposure may be improved
by elevating the hindquarters. A paramedian incision is
used to expose rectal tears of geldings and stallions.
The incision is extended caudally as far as possible, but
exposure of the distal end of the small colon and rec-
tum is less than exposure achieved in the mare. Few
tears can be sutured from a flank approach, but certain
conditions, such as advanced pregnancy or excessive
edema of the udder may make a flank approach neces-
sary. If the tear extends into the dorsal mesentery, as
many do, suturing the tear through a ventral midline
celiotomy is difficult. The dorsal position of the tear
limits the exposure of the tissue, and fat in the mesorec-
tum makes the edges of the tear difficult to identity.
Creating an enterotomy in the antimesenteric tenia of
the small colon or the rectum opposite a dorsal tear
permits surgical access to the tear.
If a tear cannot be adequately closed primarily using
any of these suturing techniques, the horse should be
considered a candidate for a colostomy or installation
of a temporary, indwelling, rectal liner.
Temporary, indwelling, rectal liner
A temporary, indwelling, rectal liner can be implanted
to divert fecal material from a grade 3 or 4 tear until the
tear is healed sufficiently by secondary intention to pre-
vent bacterial contamination of the peritoneal cavity.
To construct the rectal liner, each end of a 5 x IO-cm
plastic rectal ring is trimmed to form a 5 x 7.5-cm ring.
Holes are drilled 1.5 cm apart around the circumfer-
ence of the ring at one edge of the central groove, and
a no. 5 polyester suture is laced through these holes.
The hand is removed from a plastic palpation sleeve,
and the rectal ring is inserted into the small end of the
sleeve. A rubber band is placed around the sleeve and
over the central groove in the ring at the end opposite
the polyester suture. The sleeve is glued to the end of
the ring with cyanoacrylate, and the sleeve is inverted
over the ring.
To implant the prosthesis, a laparotomy (celiotomy)
is performed, and the rectal ring is passed through the
rectal lumen by a non-scrubbed assistant and posi-
tioned proximal to the rectal tear by the surgeon per-
forming the celiotomy. The portion of small colon
containing the ring is exteriorized through the
309
16 COLIC
celiotomy. Care is taken to position the rectal ring in
the most distal portion of the small colon that can be
exteriorized at the celiotomy to ensure that the end of
the liner extends beyond the anus when the horse
recovers from anesthesia. A strand of heavy chromic
catgut is passed circumferentially around the intestine
over the groove in the ring close to the polyester suture,
through a small perforation in the mesocolon, and tied
sufficiently tight to initiate pressure necrosis of colon
beneath it. Four interrupted absorbable sutures are
placed equidistantly around the circumference of the
colon to include the circumferential suture, the intesti-
nal wall, and polyester suture in the rectal ring. These
four retention sutures and the circumferential ligature
are oversewn with 2-0 synthetic absorbable suture, using
an interrupted Lembert pattern. This inverting suture
line maintains continuity of the intestine when the ring
and encircling ligature slough 9-12 days after surgery.
The small colon is lavaged with water through a
stomach tube passed retrograde up the sleeve, and 4
liters of mineral oil is infused into the right dorsal por-
tion of the large colon. The contents of the large colon
should be removed through an enterotomy at the pelvic
flexure to decrease the amount of ingesta passing
through the rectal ring. Either before or after the pros-
thesis is implanted, the rectal tear is sutured, if possible,
to prevent a grade 3 tear from progressing to a grade 4
tear or to prevent a grade 4 tear from forming a
mucosal-to-serosal fistula.
A reduced volume of soft feces is maintained by feed-
ing a pelleted ration and by administering mineral oil
via stomach tube until the ring and liner detach.
Because the end of the liner tends to disappear into the
rectum when the horse assumes recumbency, horses
can be kept standing until the rectal tear heals, or an
embroidery hoop can be attached to the end of the
liner to prevent the liner from retracting into the rec-
tum.
The primary advantage of a temporary, indwelling,
rectal liner over a diverting colostomy is that use of a
rectal liner requires one surgical procedure, whereas a
colostomy requires a second surgical procedure to re-
establish continuity of the small colon after the tear has
healed. The temporary, indwelling, rectal liner should
not be used if more than 25 per cent of the circumfer-
ence of the rectum is torn, if the rectum is too small to
accommodate the rectal ring, or if the tear is too far
proximal to accommodate the rectal liner. The tempo-
rary indwelling liner requires continuous postoperative
maintenance to prevent impaction of the ring with
feces and retraction of the distal end of the liner into
the rectum. Complications of this technique include
separation of the prosthesis from the rectal wall before
the rectal tear is sufficiently healed, insufficient length
310
of the rectal liner, and conversion of a grade 3 to a
grade 4 tear.
Colostomy
Colostomy can be used to treat horses with a grade 3 or
grade 4 rectal tear by temporarily or permanently
diverting feces to allow the rectal tear to heal by second
intention. The colostomy is termed a loop colostomy or
an end colostomy, depending on whether an intact
loop or a transected segment of small colon is used to
create the stoma. Both techniques of colostomy require
two surgical procedures - one to form the stoma and
the other to restore continuity of the small colon after
the tear has healed. Both techniques allow complete
diversion of feces, but loop colostomy may be more eas-
ily and quickly performed and revised, and atrophy of
the distal segment of the small colon is more easily pre-
vented with this technique of colostomy.
Loop colostomy is performed in the left flank, cra-
nial to and level with the fold of the flank, using either
a single or double-incision technique. Horses are anes-
thetized and positioned in lateral recumbency, or
surgery is performed with the horse standing. Marking
the proposed site for the stoma on the skin with sutures
before the horse is anesthetized ensures that the stoma
is created in the proper location.
To perform a single-incision colostomy as described
by Freeman et at. (1992), an incision is made at the pro-
posed site of the stoma and extended 12-15 em dorsally
through the skin, subcutaneous tissue, and fascia of the
external abdominal oblique muscle, parallel with the
costal arch. The internal abdominal oblique muscle
and aponeurosis, the transversus abdominis aponeuro-
sis, and peritoneum are perforated bluntly, and a loop
of small colon, located at least 1 meter from the peri-
toneal reflection, is exteriorized. Both arms of the loop
are apposed with absorbable suture, using a continuous
pattern, for 8 em, at a third to half the distance from the
mesentery to the antimesenteric tenia. The suture line
is angled toward the mesentery at the end of the loop so
that the antimesenteric tenia can be exposed through
the cutaneous incision. The loop of small colon is then
positioned in the ventral aspect of the abdominal inci-
sion so that the loop protrudes 2-3 em above the skin.
The proximal part of the loop is positioned ventral to
the distal part.
The seromuscular layer of the colon is apposed to
edges of the abdominal musculature and fascia by sev-
eral interrupted sutures. The abdominal wall is closed
dorsal to the loop, forming a snug fit around the loop
but without impinging on the lumens. The antimesen-
teric tenia of the exteriorized segment of small colon is
incised longitudinally to expose the lumen of the small
 DISEASES OF THE SMALL COLON AND RECTUM 16
colon, and the incised edge of the small colon is
sutured to the skin with simple interrupted, non-
absorbable sutures.
The double-incision technique may reduce the risk
of peristomal herniation and stomal prolapse. To create
a double-incision colostomy as described by Freeman et
at. (1992), a 12-15 em incision is made approximately
10 cm below the left tuber coxae. A loop of small colon
is exteriorized, and the arms of the loop are apposed
with absorbable suture as described for the single-inci-
sion technique. A second incision, 6-8 em long, is made
in the lower region of the flank, and the sutured loop of
colon is manipulated from the upper incision through
the lower incision until the loop protrudes above the
skin for 2-3 cm. The loop is incised and sutured to the
body wall as described for the single-incision technique.
The stoma should be no larger than the diameter of the
small colon to avoid prolapse. To decrease contamina-
tion of the rectal tear following colostomy, feces in the
distal segment of small colon should be removed by
lavage through the stoma.
Following colostomy, the horse should be fed a laxa-
tive diet, and ointment should be applied to the skin
around the stoma. A cradle should be applied if the
horse has a tendency to mutilate
16 COLIC

obstruction and dehiscence can develop because of donut at the anus. Type 2 prolapse, sometimes referred
shifting of muscle layers when the horse stands. to as a complete prolapse, is an eversion of all or a por-
tion of the ampulla recti (Figure 16.12). A type 2 pro-
Postoperative treatment lapse is generally larger and more cylindric than a type
1 prolapse.
Regardless of the manner by which a horse with a grade
Type 3 prolapse is also an eversion of all or a portion
3 or 4 rectal tear is treated, the horse should receive
of the ampulla recti, but it is accompanied by intussus-
broad-spectrum, bactericidal, antimicrobial drugs and
ception of the peritoneal portion of the rectum or
flunixin meglumine. The peritoneal cavity should be
colon (Figure 16.13). Type 4 rectal prolapse is an exten-
lavaged daily with copious amounts of a balanced
sive intussusception of the peritoneal portion of the
polyionic electrolyte solution or physiologic saline solu-
rectum or colon through the anus (Figure 16.14 and
tion (Figure 16.10), and horses should receive a bal-
Plate 16.1). With type 4 prolapse, the exposed intestine
anced polyionic electrolyte solution at sufficient rate to
is frequently ischemic because of vascular compromise
correct dehydration. The horse should be fed a com-
caused by stretching and tearing of mesenteric blood
plete pelleted ration and no hay to reduce bulk, and
vessels as the mesocolon is forced into the pelvic canal
mineral oil should be administered, as needed, to pre-
by the intussusception. In the first 3 types, the prolapse
vent production of formed feces. Table salt can be
is continuous with the mucocutaneous junction of the
added to each feeding to encourage water consump-
anus, but if a finger can be introduced for several
tion.

Prognosis for survival of horses with rectal

tears
In a report of 42 horses with a grade 3 or 4 tear of the
rectum or small colon, mortality was 64 per cent. This
study found that horses with a tear into the mesentery iii i
(grade 3b) had a better prognosis for survival than did
horses with a lateral or ventral tear (grade 3a). In
another study, however, horses with grade 3b tears had

c
a worse prognosis for survival than did horses with a
grade 3a tear. Of the horses with a grade 3b tear, 44 per
cent were discharged compared to 74 per cent of the
horses with a grade 3a tear. In both studies, horses with
a grade 4 tear had a grave prognosis for survival.

RECTAL PROLAPSE Figure 16.11 Type 1 prolapse: the rectal mucosa alone is
prolapsed
Cause
Rectal prolapse in the horse is sometimes associated
with conditions that cause tenesmus, such as constipa-
tion, diarrhea, neoplasia, dystocia, urethral obstruction,
or colic. Factors that may predispose to rectal prolapse
include loss of tone in the anal sphincter, loose attach-
ments of the mucous membrane to the muscular coat of
the rectum, or loose attachments of the rectum to
' ' ' ",,,l,, " ! I ! CI

perirectal tissues. Females are more likely than males to

i II j i j
I I C
develop rectal prolapse.

Classification
"<:" "
Rectal prolapses are classified according to the tissue
involved. Prolapse of the rectal mucosa alone is classi-
fied as a type 1 prolapse (Figure 16.11). Type 1 prolapse Figure 16.12 Type 2 prolapse: all or a portion of the
is usually seen as a circular swelling, resembling a large ampulla recti is everted

312
16 COLIC
ANORECTAL LYMPHADENOPATHY
Enlargement of the anorectal lymph nodes, which are
situated dorsally along the rectum in the retroperi-
toneal space, can cause extralumenal obstruction of the
rectum resulting in signs of abdominal pain. Other clin-
ical signs associated with the condition include
anorexia, lack of production of feces, tenesmus, and
pyrexia. Anorectal lymphadenopathy occurs primarily
in young horses, and although the cause is usually
unknown, it may develop secondary to rectal or vaginal
trauma or from gravitation of an abscess in the gluteal
muscles into the perirectal tissues. Sepsis of an anorec-
tal lymph node can extend into the peritoneal cavity
causing septic peritonitis. Bacteria cultured most com-
monly from perirectal abscesses are Streptococcus zooepi-
demicus and EScherichia coli.
Diagnosis of anorectal lymphadenopathy is con-
firmed by digital palpation per rectum, transrectal
ultrasonography, and cytologic examination of an aspi-
rate or biopsy from an affected lymph node. Peritoneal
fluid, obtained by abdominocentesis, should be exam-
ined cytologically to determine if sepsis extends into the
abdominal cavity.
Treatment of affected horses is aimed at relieving,
and then preventing, fecal obstruction of the rectum.
Laxatives, such as mineral oil, should be administered
orally to keep feces soft, a complete pelle ted ration
should be fed to reduce intestinal bulk, and broad-spec-
trum antimicrobial drugs should be administered.
Celiotomy is warranted when signs of pain cannot be
controlled by relieving constipation, or when secondary
complications necessitate abdominal exploration.
When a mature abscess is detected ultrasonographi-
cally, it should be lanced using a perianal incision.
BIBLIOGRAPHY
Archer R M, Parsons] C, Lindsay W A, Wilson] W, Smith 0 F
(1988) A comparison of enterotomies through the
antimesenteric band and the sacculation of the small
(descending) colon of ponies. Equine Vet.]. 20:406--413.
Arnold] S, Meagher 0 M (1978) Management of rectal tears
in the horse.]. Equine Med. Surg. 2:64-71.
Arnold] S, Meagher 0 M, Lohse C L (1978) Rectal tears in
the horse.]. Equine Med. Surg. 2:55-61.
Ayres S L, Wagner P (1994) Perirectal abscess in an American
Miniature horse. Equine Pract. 16:33-5.
Beard W L, Robertson] T (1989) Enterotomy technique in
the descending colon of the horse. Effect of location and
suture pattern. Vet. Surg. 18:135-140.
Blikslager A T, Bowman K F, Haven M L, Tate L P, Bristol
D G (1992) Pedunculated lipomas as a cause of intestinal
obstruction in horses: 17 cases (1983-1990)]. Am. Vet.
Med. Assoc. 201:1249-1252.
Blikslager A T, Bristol 0 G, Bowman K F, Engelbert T A
314
(1995) Loop colostomy for treatment of grade-3 rectal
tears in horses: seven cases (1983-1994).]. Am. Vet. Med.
Assoc. 207:1201-1205.
Blue M G (1979) Enteroliths in horses - a retrospective study
of 30 cases. Equine Vet.]. 11: 76--84.
Blue M G, Wittkopp R W (1981) Clinical and structural
features of equine enteroliths.]. Am. Vet. Med. Assoc. 179:
79-82.
Byars T 0 (1993) Management of impaction colics in the
horse. Equine Pract. 15:30-34.
Dart A], Pascoe] R, Snyder] R (1991) Mesenteric tears of the
descending (small) colon as a postpartum complication in
two mares.]. Am. Vet. Med. Assoc. 199:1612-1615.
Dart A], Snyder] R, Pascoe] R, Farver T B, Galuppo L 0
(1992) Abnormal conditions of the equine descending
(small) colon: 102 cases (1979-1989) 200:971-978.
Edwards G B (1992) A review of 38 cases of small colon
obstruction in the horse. Equine Vet.]. supp!. 13:42-50.
Evard] H, Fischer A T, Greenwood L 0 (1988) Ovarian
strangulation as a cause of small colon obstruction in a
foa!. Equine Vet.]. 20:217-218.
Fischer A T (1990) Enterolithiasis. In Current Practice of Equine
Surgery, N A White,] N Moore (eds). Philadelphia.] B
Lippincott, pp. 348-51.
Freeman 0 E (1996) Comments on loop colostomy in horse.
]. Am. Vet. Med. Assoc. 208:336.
Freeman 0 E, Richardson 0 W, Tulleners E P, et al: (1992)
Loop colostomy for management of rectal tears and small-
colon injuries in horse: 10 cases (1976--1989).]. Am. Vet.
Med. Assoc. 200:1365-1371.
Gay C C, Spiers V C, Christie B A, Smyth B, Parry B (1979)
Foreign body obstruction of the small colon in six horses.
Equine Vet.]. 11:60-63.
Guglick M A, MacAllister C G, Ewing P], Confer A W (1996)
Thrombosis resulting in rectal perforation in a horse . .f
Am. Vet. Med. Assoc. 209:1125-1127.
Herthel 0] (1975) Colostomy in the mare. Proc. Am. Assoc.
Equine. Pract. 21:187-191.
Hintz H F, Lowe] E, Livesay-WilkinsP et al. (1988) Studies on
equine enterolithiasis. Proc. Am. Assoc. Equine. Pract.
24:53-59.
Hjortkjaer R K (1979) Enema in the horse. Distribution and
rehydrating effect. Nord. Vet. Med. 31:508-519.
]effcott L B, Rossdale P 0 (1979) A radiographic study of the
foetus in late pregnancy and during foaling .[. Reprod.
Fertil. supp!. 27:563-569.
Johnson H W (1943) Submucous resection for surgical
correction of prolapse of rectum.]. Am. Vet. Med. Assoc.
102:113-115.
Keller S 0, Horney F 0 (1985) Diseases of the equine small
colon. Camp. Cant. Educ. Pract. Vet. 7:S113-S120.
Livesey M A, Keller S 0 (1986) Segmental ischemic necrosis
following mescolic rupture in postparturient mares. Camp.
Cont. Educ. Pract. Vet. 8:763-768.
Lloyd K, Hintz H F, Wheat] 0, Schryver H F (1987)
Enteroliths in horses. Cornell Vet. 77:172-186.
Magee A A, Ragle C A, Hines M T, Madigan] E, Booth L C
(1997) Anorectal lymphadenopathy causing colic,
perirectal abscesses, or both in five young horses.]. Am.
Vet. Med. Assoc. 210:804-807.
Mason T A (1978) Strangulation of the rectum of a horse by
the pedicle of a mesenteric lipoma. Equine Vet.]. 10:269.
Mazan M R (1997) Medical management ofa full-thickness
tear of the retroperitoneal portion of the rectum in a
horse with hyperadrenocorticism.]. Am. Vet. Med. Assoc.
210:665-667.

McClure] T, Kobluk C, Voller K, Geor R], Ames T R, Sivula
N (1992) Fecalith impaction in four miniature foals.J Am.
Vet. Med. Assoc. 200:205-207.
Meagher D M (1972) Obstructive disease in the large
intestine of the horse: diagnosis and treatment. Proc. Am.
Assoc. Equine Pract. 18:169-179.
Murray R C, Green E M, Constantinescu G M (1992) Equine
enterolithiasis. Compo Cont. Educ. Pract. Vet. 14:1104-1112.
Nappert G, Laverty S, Drolet R, Naylor] (1992) Atresia coli in
7 foals (1964-1990). Equine Vet.]. supp!. 13:57-60.
Pearson H, Waterman A E (1986) Submucosal haematoma as
a cause of obstruction of the small colon in the horse: a
review of four cases. Equine Vet.J 18:340-341.
Peloso] G, Coatney R W, Caron] P, Steficek B A (1992)
Obstructive enterolith in an l l-month-old miniature
horse.J Am. Vet. Med. Assoc. 201:1745-1746.
Rose] A, Rose E M, Sande R D (1980) Radiography in the
diagnosis of equine enterolithiasis. Proc. Am. Assoc. Equine
Pract.26:211-220.
Ross M W, Stephens P R, Reimer] M (1988) Small colon
intussusception in a brood mare.J Am. Vet. Med. Assoc.
192:372-374.
Ruggles A], Ross M W (1991) Medical and surgical
management of small-colon impaction in horses: 28 cases
(1984-1989).JAm. Vet. Med. Assoc. 199:1762-1766.
Sanders-Shamis M (1985) Perirectal abscesses in six horses.J
Am. Vet. Med. Assoc. 187:499-500.
Sayegh A I, Adams S B, Peter A T, Wilson D G (1996) Equine
rectal tears: Causes and management. Compo Cont. Educ.
Pract. Vet. 18:1131-1143.
Slone D E, Humburg] M,]agar] E, Powers R D (1982)
Noniatrogenic rectal tears in three horses.J Am. Vet. Med.
Assoc. 180:750-751.
Speirs V C, Christie B A, van Veenendaal] C (1980) The
management of rectal tears in horses. Aust. Vet.J
56:313-317.
DISEASES OF THE SMALL COLON AND RECTUM 16
Spensley M S, Meagher D M, Hughes] P (1985)
Instrumentation to facilitate surgical repair of rectal tears
in the horse: a preliminary report. Proc. Am. Assoc. Equine
Pract.31:553-563.
Spiers V C, van Veenendaal] C, Christie B A, Lavelle R B, Gay
C C (1981) Obstruction of the small colon by intramural
haematoma in three horses. Aust. Vet.]. 57:88-90.
Stashak T S, Knight A P (1978) Temporary diverting
colostomy for the management of small colon tears in the
horse: A case report. J Equine Med. Surg. 2:192-200.
Stauffer V D (1981) Equine rectal tears - a malpractice
problem.J Am. Vet. Med. Assoc. 178:798-799.
Stewart R H, Robertson] T (1990) Surgical stapling for repair
ofa rectal tear.J Am. Vet. Med. Assoc. 197:746-748.
Taylor T S, Valdez H, Norwood G W, Hanes G E (1979)
Retrograde flushing for relief of obstruction of the
transverse colon in the horse. Equine Pract. 1:22-28.
Taylor T S, Watkins] P, Schumacher] (1987) Temporary
indwelling rectal liner for use in horses with rectal tears. J
Am. Vet. Med. Assoc. 191:677-680.
Turner T A, Fessler] F (1980) Rectal prolapse in the horse. J
Am. Vet. Med. Assoc. 177:1028-1032.
Watkins] P, Taylor T S, Schumacher], Taylor] R, Gillis] P
(1989) Rectal tears in the horse: an analysis of 35 cases.
Equine Vet.J 21:186-188.
Welker B, Modransky P (1992) Rectal prolapse in food
animals. Part II. Surgical options. Compo Cont. Educ. Pract.
Vet. 14:554-558.
Wilson D G, Stone W C (1990) Antimesenteric enterotomy
for repair of a dorsal rectal tear in a mare. Can. Vet.J
31:705-707.
Yarbough T B, Langer D L, Snyder] R, Gardner 1 A, O'Brien
T R (1994) Abdominal radiography for diagnosis of
enterolithiasis in horses: 141 cases (1990-1992).J Am. Vet.
Med. Assoc. 205: 592-595.
315
 17
Other conditions

Abdominal distention in the

adult horse
Gaseous distention Gastrointestinal tympany
T Mair (distentionttympanitic cOlic)
Intestinal obstruction!
impaction
INTRODUCTION Ileus
Pneumoperitoneum
Abdominal distention is classically regarded as being
caused by one of the 'seven f's' Fluid distention Ascites
Peritonitis
• fat • feces Uroperitoneum
• fetus • flatus Hemoperitoneum
• food • foreign body Fetal hydrops
• fluid
Weakened body wall Ventral body wall hernias
Although pregnancy (Figure 17.1) or obesity can be Ruptured. prepubic tendon
regarded as 'normal' or 'physiological' causes of Cushing's disease

abdominal distention in adult horses, other conditions

that result in an enlarged abdomen are pathological,
and may be associated with serious and possibly life-
threatening disease. The most common and most
important diseases associated with abdominal disten-
tion in the adult horse are listed in Table 17.1.

GASTROINTESTINAL TYMPANY
(DISTENTIONITYMPANITlClFLATULENT
COLIC)
$W~%MillIfIW:%_~WW:S~f%IW~%i®fBIl(IiiIII!II@*""i~"j_ _ '",,='M@MJilM&'i@('MM!M.,"'lI!I,"*i>B)l'='~!W'i0iI'ii@MII",'ffi;;;i=£5j

Figure 17.1 Abdominal distention and ventral edema in Gastric, cecal, or colonic tympany occur as a result of
late gestation accumulation of excessive gastrointestinal gas due to

317
17 COLIC
Feeding highly fermentable substrate (especially
soluble carbohydrates), e.g. grain, lush grassand
clover, wilted grass/grass clippings
Abrupt change in feeding (especially forage)
Feeding horse when it is exhausted or overheated
Electrolyte abnormalities, e.g- hypocalcemia,
hypokalemia
Cold water engorgement
Therapeutic administration of atropine
Aerophagia
Inadequate mastication
Rapid feed engorgement
Interruption of GI motility from stress, excitement,
or pain
Impactions
Displacements
Late pregnancy
Ileus secondary to anE1sthesia, surgical manipula-
tion of the intestines (see Chapter 11), vascular
compromisE1 (thromboembolic colic) and liver
disease. Adult horses rarely exhibit abdominal
distension after small intestinal obstruction,
unlike foals.
increased fermentation and/or ineffectual gastroin-
testinal motility (see Chapters 12,14, and 15). Overcon-
sumption of readily fermentable food stuffs such as
fresh grass, grain, or beet pulp results in the production
of large amounts of lactic acid and volatile fatty acids.
Volatile fatty acids inhibit gastrointestinal motility and
thereby promote further fermentation and production
of gas. If the rate of gas production exceeds the ability
of the gastrointestinal tract to move the gas through, or
if progressive motility of the intestinal tract is impaired,
then gas will accumulate in the stomach, cecum,
and/or large colon. Distention inhibits vagal motility,
while fermentation continues. Moderate to severe dis-
tention may increase the contractility of other segments
of the gastrointestinal tract, resulting in spasms that
may cause pain.
Factors associated with distention colic are summa-
rized in Table 17.2.
Clinical signs and diagnosis
The clinical signs and degree of pain with distention
colic vary depending on the rate of gas accumulation
and the part of the gastrointestinal tract involved. In
mild cases there may be only vague signs of dullness and
inappetence. In more severe cases there is often inter-
mittent colic that is most severe with intestinal spasm. In
318
the most severe cases, especially where there is gastric
tympany, there is acute distress and signs of severe
uncontrollable pain.
Heart and respiratory rates are often elevated if the
pain is severe, or if the distention compromises respira-
tory function (due to pressure on the diaphragm) or
venous return. The heart rate may reach 100 bpm or
more. The mucous membranes are usually pale but may
become cyanotic.
Abdominal distention is most likely in cases of large
intestinal tympany. Large colon tympany tends to result
in bilateral abdominal distention, whereas cecal tym-
pany results in distention of the right flank and right
paralumbar fossa. Abdominal borborygmi may be
increased in frequency if the distention is mild or mod-
erate, but with severe distention, borborygmi may be
absent. Tympanitic, 'tinkling' sounds may be heard as
the horse breathes or moves. Percussion of the
abdomen may be helpful in identifying the region of
the gastrointestinal tract that is distended. In cases of
cecal tympany, percussion with a stethoscope over the
right flank reveals high-pitched pinging sounds.
Rectal examination reveals gas-filled sections of the
gastrointestinal tract. In primary gastric tympany, the
spleen may be displaced caudally by the enlarged stom-
ach. Primary gastric tympany needs to be differentiated
from cases of gastric distention secondary to small
intestinal obstruction; in the latter cases, several loops
of distended small intestine may be palpable. In cases of
cecal tympany, the distended cecum is palpated in the
upper right caudal quadrant of the abdomen. The ven-
tral band of the cecum stretches across the pelvic inlet
from cranial in the right dorsal quadrant to ventral in
the left ventral quadrant. Distention of the large colon
is readily identified by the location of the distended vis-
cus, its size, and the presence of longitudinal bands
except at the pelvic flexure.
Uncontrolled, progressive distention of the stomach
may result in rupture. The rupture is usually located
along the greater curvature. Signs of impending rup-
ture include severe pain, tachycardia (usually> 100
bpm), abdominal distention and retching. Cyanotic
and pale mucous membranes are usually present.
Commonly, once the stomach ruptures, the signs of
severe pain disappear, but signs of shock, sweating, and
collapse rapidly follow. Ingesta is evident in the
peritoneal fluid, and the serosa of the intestines feel
roughened on rectal examination; euthanasia is recom-
mended in such cases.
Treatment
The primary objective of treatment is to evacuate the
gases from the region of distention and to prevent
17 COLIC

• foreign body obstruction (see Chapter 16)

• sand impaction (see Chapter 15)
• non-strangulating intestinal infarction (see Chapter
15).

ILEUS
Intestinal ileus is characterized by a decrease in propul-
sive motility, an increase in fluid and particulate transit
time, and distention of the intestine. Horses with small
intestinal ileus have ongoing nasogastric reflux and the
presence of distended loops of small intestine that are
palpable per rectum; such cases may have mild to mod-
Figure 17.2 Ascites and ventral edema due to multicentric
erate abdominal distention if the intestinal distention is
lymphosarcoma in a horse
severe and affects the majority of the small intestine.
Horses with ileus of the large intestine are more likely
to have significant abdominal distention due to tym-
pany. Conditions that may predispose to intestinal ileus
and abdominal distention include
• primary large intestinal tympany (see above)
The diagnosis of ascites is achieved by identification
• postoperative ileus (see Chapter 11)
of abdominal distention, fluid ballottement, diagnostic
• non-strangulating intestinal infarction (see Chapter
ultrasonography, and abdominal paracentesis. Fluid
15)
ballottement of the adult equine abdomen is not easily
• grass sickness (see Grass sickness)
performed but it is relatively easier in ponies and minia-
• peritonitis (see Peritonitis)
ture horses than in larger horses. Diagnostic ultrasound
• therapeutic administration of atropine
is useful to confirm the presence of large quantities of
• electrolyte abnormalities (hypocalcemia,
anechoic free peritoneal fluid. Abdominal paracentesis
hypokalemia)
yields clear, watery fluid with a total nucleated cell
• colitis (see Chapter 20)
count less than 10.0 x 109/1 (usually < 2.0 x 109/1) and
• stress.
total protein concentration less than 25 g/I (usually <
15 g/I). In some cases the fluid may have the appear-
ance of a modified transudate (i.e. fluid has the charac-
PNEUMOPERITONEUM teristics of a transudate but has a modest increase in cell
count or total protein concentration).
Pneumoperitoneum, the presence of free gas in the Ascites has been reported to occur in association with
peritoneal cavity, is usually caused by gastrointestinal lymphosarcoma, squamous cell carcinoma, mesothe-
rupture and per-acute peritonitis (see Peritonitis). lioma, and various other carcinomas and adenocarcino-
Affected horses present with signs of severe shock, mas. Mesothelioma is extremely rare, but may cause the
tachycardia, sweating, reluctance to move, and rapid greatest amount of abdominal fluid accumulation since
death. it is a tumor of the fluid-producing cells of the peritoneal
lining. Abdominal neoplasia commonly produces other
clinical signs such as weight loss and abdominal pain (see
Gastrointestinal neoplasia).
ASCITES
Hypoproteinemia and hypoalbuminemia due to
protein-losing enteropathy (see Chapter 21), hepatic
Ascites associated with the accumulation of a transuda-
disease (see Chapter 19) and renal disease are more
tive effusion in the peritoneal cavity is uncommon in
commonly associated with peripheral edema, but may
horses. The causes of ascites in the adult horse include
occasionally present with ascites. Likewise, horses in
• neoplasia (Figure 17.2) right-sided heart failure usually present with signs of
• hypoproteinemia exercise intolerance,jugular pulse, and ventral abdom-
• right-sided heart failure inal and limb edema, but ascites may sometimes be
• uroperitoneum. evident.

320

PERITONITIS
Peritonitis rarely causes severe abdominal distention
due to fluid accumulation, but intestinal ileus associ-
ated with per-acute or acute peritonitis may result in
abdominal distention (see Peritonitis). In cases of
per-acute peritonitis due to bowel rupture, gas accu-
mulation in the peritoneal cavity (pneumoperi-
toneum) (see above) may also produce abdominal
distention. Other clinical signs associated with acute
peritonitis include colic, tachycardia, tachypnea,
pyrexia, guarding of the abdomen, reluctance to
move, scanty diarrhea, and reduced gut sounds (see
Peritonitis) .
UROPERITONEUM
Uroperitoneum is rare in adult horses (see Chapter 22
for discussion of uroperitoneum in foals), but urinary
bladder rupture occasionally occurs following trauma,
in peri-parturient mares, and in male horses following
urethral obstruction by a calculus. Diagnosis ofuroperi-
toneum is based on identification of a high peritoneal
fluid creatinine:serum creatinine ratio, possibly with
the presence of calcium carbonate crystals in the peri-
toneal fluid. Hyponatremia, hypochloremia, and hyper-
kalemia are often present. Identification of the site of
urinary tract disruption is usually achieved by
endoscopy. Ultrasonography can also be helpful in the
evaluation of uroperitoneum. Free urine in the
abdomen usually presents as anechoic fluid, but
because of the large amount of calcium carbonate crys-
tals and mucus, it may also appear as hypoechoic fluid.
The site of bladder rupture may sometimes be visual-
ized by transabdominal ultrasound in foals, or transrec-
tal examination in adults.
HEMOPERITONEUM
Hemoperitoneum due to rupture of the middle uter-
ine artery in mares, splenic rupture following trauma,
rupture of a verminous aneurysm of the cranial mesen-
teric artery, etc., may cause abdominal distention and
pain due to fluid (blood) accumulation in the
abdomen. However, other clinical signs related to
hypovolemic shock (tachycardia, tachypnea, cold
extremities, pale mucous membranes, weakness) will
predominate. The causes, diagnosis, and management
of hemoperitoneum are discussed elsewhere in this
chapter.
OTHER CONDITIONS 17
FETAL HYDROPS
Fetal hydrops results from the accumulation of exces-
sive amounts of fluid within the amnion (hydrops
amnion or hydramnios) or chorioallantois (hydrops
allantois or hydrallantois). These are rare conditions
that occur in the last trimester of pregnancy of multi-
parous mares. Hydrallantois is the more common of
these two dropsical conditions. Typically there is a sud-
den onset of abdominal distention and ventral edema
with affected mares showing variable degrees of colic
and difficulty in defecation. Dyspnea and cyanosis may
also be present. Rectal examination should be per-
formed with care since passage of the forearm will be
impeded by pressure from the large fluid-filled uterus.
The fetus is usually not palpable due to the massive
quantities of fluid. Transabdominal ultrasonography
can be used to verify the presence of excessive fluid, and
an examination from both sides of the abdomen can be
helpful to eliminate the possibility of twins. Feces tend
to be covered with mucus because of prolonged passage
through the lower gastrointestinal tract. Ventral
abdominal rupture may result from the presence of an
excessive weight of fetal fluid, and there is a further risk
of uterine rupture. Affected mares usually abort, and
recommended treatment involves induction of parturi-
tion with administration of intravenous fluids and grad-
ual removal of excess allantoic fluid. The foals are often
abnormal and affected by a variety of congenital abnor-
malities.
VENTRAL BODY WALL HERNIAS AND
PREPUBIC TENDON RUPTURE
Defects of the abdominal wall in pregnant mares may
involve stretching and/ or rupture of the transverse
abdominus and oblique abdominal muscles, the rectus
abdominus muscles and the prepubic tendon. Apart
from those associated with hydropic conditions (see
above) or twin pregnancies, most cases occur in mares
close to term. Draft breeds and older mares appear to
be at greater risk. In extreme cases rupture may lead to
hemorrhage, shock, and death. Typical clinical signs
include a sudden change in the contour of the ventral
abdomen, ventral edema, reluctance to move, and
intermittent colic. If the prepubic tendon is ruptured,
the pelvis will appear tilted and a lordosis will be pre-
sent. The mammary gland may be displaced craniad
and ventrad because of loss of its caudal attachment to
the pelvis. Confirmation of the tentative diagnosis can
be difficult. Palpation of the defect per rectum is usually
not possible because of the advanced stage of preg-
nancy. External palpation is often unrewarding due to
321
 OTHER CONDITIONS 17
• septic or non-septic - whether or not bacteria are
present.
Primary peritonitis (bacterial infection without an
Grossappearance Clear or slightly turbid obvious intraperitoneal source) is rare in adult horses
Straw colored or colorless but may be associated with immunodeficiency or
Specific gravity < 1.016 immunosuppression.
Total protein <25 gil (usually <15 gil) Secondary peritonitis may be caused by numerous
(mainly albumin) diseases including external trauma, diseases of the gas-
Total nucleated < 10.0 x 109/1 (usually trointestinal tract, breeding and foaling injuries, intra-
cell count < 2.0 x 109fl) and postoperative infection, etc. (Table 17.4).
Differential cell 20-90% neutrophils Peritonitis in the horse is most frequently secondary,
count 5-60% mononuclear/mesothe-
acute, diffuse, and septic. The severity of the disease is
lial cells
0-35% lymphocytes related to a number of factors including the underlying
0-5% eosinophils cause, the nature of the infectious agent(s), the resis-
0-1 % basophils tance of the host, speed of recognition and interven-
Total red cell count Negligible tion, and the response to initial therapy.
Fibrinogen Negligible « 0.1 gil) (does not A variety of different bacterial species have been iso-
clot on standing) lated from the peritoneal fluid of horses with septic
Glucose 5.0-6.4 mmol/l (90-115 mg/dl) peritonitis. Mixed bacterial infections are common.
Creatinine 161-237 ~mol/l (1.8-2.7 mg/dl) Common isolates include
Urea nitrogen 3.9--8.2 mmolll (11-23 mg/dl)
Lactate 0.4--1.2 mmolll (3.8-10.9 mg/dl) • Escherichia coli
Total bilirubin 5-13 ~mol/l (0.3-0.8 mg/dl) • Streptococcus zooepidemicus
Amylase 0-14 lUll • Staphylococcus spp.
Lipase 0-36 lUll • Actinobacillusequuli
• Rhodococccus equi
• Bacteroides spp. (especially B. fragilis)
• Peptostreptococcus spp.
Peritoneal fluid from normal foals is significantly dif-
• Clostridium spp.
ferent to adult horses with respect to total nucleated
• Fusobacterium spp.
cell count. In the foal, a nucleated cell count greater
than 1.5 x 109/1 (1500/1.11) should be considered as ele-
vated.
PATHOPHYSIOLOGY
Dispersal of fluid within the peritoneal cavity is
rapid, aided by peristalsis and movement of the horse. It
Peritonitis is an inflammatory disease. The inciting
is absorbed from the abdominal cavity mainly by lym-
cause, be it septic or non-septic, results in the activation
phatic vessels beneath the mesothelial basement mem-
of macrophages and other cells, with the subsequent
brane on the surface of the diaphragm. Small stoma in
release of eicosanoids, histamine, serotonin, and other
the mesothelial lining provide access to the lymphatics.
mediators. These lead to vasodilation and increased vas-
The constant production and clearance of peritoneal
cular permeability followed by the migration of inflam-
fluid ensures an effective clearance mechanism for bac-
matory cells and transudation of fluid containing fibrin
teria, cells, and foreign material entering the peritoneal
and clotting factors, complement and immunoglobu-
cavity.
lins, into the peritoneal cavity. The inflamed peri-
toneum becomes a freely diffusible membrane,
allowing a massive outpouring of fluid and plasma pro-
CLASSIFICATION AND ETIOLOGY OF teins from the circulation. This is a defensive reaction
PERITONITIS that may result in the neutralization and phagocytosis
of bacteria, and rapid lymphatic clearance from the
Classifications of peritonitis are
abdomen. The fibrinolytic activity of mesothelial cells is
• primary or secondary - indicating the origin of the reduced and fibrin is deposited to seal off perforations
disease and to localize areas of infection. Intestinal ileus may
• peracute, acute, or chronic - depending on the also occur as a result of sympathetic stimulation, and
onset and duration this further helps to reduce dissemination of contami-
• diffuse or localized - indicating the region affected nated peritoneal fluid.

323
17 COlle

.
. ...
'.>. hi. .« .

Infectious or Septic Non-septic Parasitic Traumatic Iatrogenic

Surgical complic ations; Ruptured bladder, Verminous Breeding or Recta! tear

ureter or kidney arteritis foaling
-anastomosis failure injury Uterine
-non-viable tissue Parasitic larval perforation:
- poor asepsis migration Penetrating -Infusion
- wound infection and larval abdominal -biopsy
cyathostomosis wound -AI
Intestinal accidents with Chemical agents: Perforating lesions
transmural movement of -bile (ascarids, Blunt Enterocentesis
bacteria -gastric juice tapeworms) abdomina!
- pancreatic juice trauma Cecal
Abdominal, renal, or trocharization
retroperitoneal abscess Foreign body Ruptured
diaphragm Liver
Uterine rupture Neoplasia: biopsy
or perforation -ovarian
-abdominal

Metritis

Urachal
infection

Post·castration infection
Enteritis

Septicemia

Cholangitis

If the peritoneal defenses are successful at contain· SIGNALMENT AND HISTORY

ing the inflammatory process, the disease may be con·
trolled and a period of cellular repair begins with a
return of mesothelial cell fibrinolytic activity and
removal of fibrin deposits. However, if the defense
mechanisms arc ovenvheImed or contamination of the
peritoneum continues, the inflammatol)' process per­
sists and becomes generalized throughout the peri­
toneum. Blockage of the lymphatic drainage channels
with fibrin and inflammatory debris leads to the accu­
mulation of fluid and bacterial toxins within the peri­
toneal cavity. Plasma sequestration within the abdomen
may result in the development of hypovolemic shock,
and absorption of bacterial endotoxins may result in
sew'n' metabolic derangements associated with endo­
toxemia. Prolonged inflammation and fibrin deposi­
tion may be followed by fibrous scarring and adhesion
formation (Plate 17.1).
Peritonitis may occur in horses of either sex. and all
ages and breeds. A predisposing cause may be noted in
some cases, for example abdominal surgery, trauma,
breeding, or foaling injuries. Peritonitis secondary to
internal abscessation is most commonly seen in young
horses, less than 5 years of age. A prior respiratory infec­
tion, such as Siuptococcus equi subsp. equi (strangles) may
have preceded the onset of peritonitis in some cases.
CLINICAL SIGNS
The presenting clinical signs in individual cases of peri­
tonitis vary depending on the nature and extent of the
peritonitis, and t.he severity of systemic signs associated

324
 OTHER CONDITIONS 17
with hypovolemia and endotoxemia. From a clinical Acute peritonitis is, therefore, an important differ-
standpoint, cases may be classified as peracute, acute, or ential for horses presenting with colic, especially if
chronic, although there can be considerable overlap there is concurrent pyrexia. In the absence of thera-
between these categories. Localized peritonitis may be peutic intervention, signs of endotoxemia and circula-
present with few or no overt clinical signs, whereas dif- tory collapse become more pronounced and death may
fuse septic peritonitis usually causes severe clinical dis- ensue after a period of several hours to several days.
ease.
Chronic peritonitis
Peracute peritonitis The clinical signs of chronic peritonitis may be low
In peracute peritonitis (e.g. following gastric rupture), grade and non specific, and include
the horse may be found dead or present with profound • depression
toxemia rapidly leading to circulatory failure and death • inappetence
within a few hours. The clinical signs of peracute peri- • progressive weight loss
tonitis are • reduced fecal output
• profound depression • low grade chronic or intermittent abdominal pain
• cold extremities • persistent or intermittent pyrexia
• congested to cyanotic mucous membranes • decreased gut sounds
• tachycardia • chronic diarrhea
• weak, thready pulse • ventral edema.
• tachypnea The presence and severity of these signs are very vari-
• sweating able from case to case.
• colic
• ileus
• collapse
• death within several hours INVESTIGATION AND DIAGNOSIS
and are overshadowed by signs of endotoxemic and The diagnostic procedures used in peritonitis are
hypovolemic shock.
• abdominal paracentesis
• hematology
Acute peritonitis
• serum/plasma electrolytes and biochemistry
In acute peritonitis with diffuse bacterial contamination • rectal palpation
of the abdomen, for example following perforation of • ultrasonography
the gastrointestinal or female reproductive tracts, the • urogenital examination
clinical signs may include • laparoscopy
• exploratory laparotomy.
• depression
• colic Abdominal paracentesis
• inappetence
• pyrexia A definitive diagnosis is usually made by examination of
• congested mucous membranes peritoneal fluid (Plate 17.2). Abdominal paracentesis is
• weak peripheral pulses generally a safe and simple technique (see Chapter 2).
• tachycardia The peritoneal fluid should be collected into EDTA
• tachypnea and plain containers for cytology, gram stain and pro-
• ileus or decreased gut sounds tein estimation, and into aerobic and anaerobic blood
• reduced fecal output culture bottles for bacterial culture. Use of an antimi-
• excessive nasogastric reflux crobial removal device may be helpful for culture of
• abdominal distention fluid from horses that have already been treated with
• sweating antibiotics.
• diarrhea A diagnosis of peritonitis can frequently be made by
• abnormal rectal findings direct visual examination of the fluid. The fluid may be
• guarding of the abdomen yellow to white and turbid, indicating a high nucleated
• reluctance to move, defecate, or urinate cell count. If left to stand, the cells will settle at the bot-
• muscle fasciculations. tom of the container and fibrin clots may develop. If the

325
17 COLIC
fluid is shaken, the high protein concentration causes it
to froth. Alternatively, the fluid may be homogeneously
blood stained suggesting hemoperitoneum or intestinal
infarction, or turbid and brown-green in color suggest-
ing contamination with intestinal contents.
Normal peritoneal fluid usually has a total nucleated
cell count ofless than 2.0 x 109/1 with a predominance
of neutrophils (Table 17.3). Peritonitis is characterized
by an elevation of the total nucleated cell count (fre-
quently > 100 x 109 11) with a high proportion of neu-
trophils (frequently> 90%). In chronic peritonitis, in
addition to a neutrophil reaction, an increase in
macrophages or mononuclear cells, and the presence
of reactive mesothelial cells may be seen. Reactive
mesothelial cells may be mistaken for neoplastic cells,
and consultation with an experienced clinical patholo-
gist may be prudent in such cases.
Microscopic evaluation of the fluid is important in
addition to performing total and differential cell
counts. Toxic or degenerative changes to neutrophils
are common in cases of sepsis. Free or phagocytized
bacteria may be observed in a proportion of cases, and
gram staining can be helpful to guide the initial antimi-
crobial therapy. Bacteria will be cultured or identified
cytologically in only about 70 per cent of cases, and fail-
ure to identify or culture bacteria from peritoneal fluid
does not, therefore, rule out septic peritonitis. The
presence of multiple bacterial species during micro-
scopic examination or following culture usually indi-
cates intestinal leakage or rupture. The presence of
food material or intestinal protozoa indicates either
inadvertent enterocentesis or bowel rupture.
The normal total protein concentration of peri-
toneal fluid is less than 25 gil, and this rises rapidly in
acute peritonitis (frequently> 50 gil). Peritoneal fib-
rinogen concentration may be increased, especially in
chronic peritonitis; concentrations greater than 0.1 gil
(10 mg/dl) are significant. It should be noted that fib-
rinogen concentration will also be increased by blood
contamination of the sample.
Peritoneal pH and comparison of plasma and peri-
toneal glucose concentrations can also be useful to eval-
uate if the peritonitis is bacterial in origin. A
plasma-peritoneal glucose difference of greater than
2.8 mmol/I (50 mg/dl), or a peritoneal pH less than 7.3
with a peritoneal glucose of less than 1.7mmol/l
(30 mgl d1) are both highly suggestive of septic peri-
tonitis.
Serial analyses of peritoneal fluid samples obtained
during the course of treatment are helpful in monitor-
ing the success of therapy. Serial cultures may be neces-
sary to identify emerging or resistant strains of bacterial
species. Bacterial cultures are frequently negative
despite the presence of bacteria in the peritoneal fluid.
326
In order to improve the culture rate, peritoneal fluid
should be collected into blood culture medium - if the
horse has already been given antibiotics, fluid should
first be passed through an antimicrobial-removal
device.
Hematology, serum/plasma electrolytes and
biochemistry
The hematological and biochemical changes that may
be seen in peritonitis are listed below, these changes
vary depending on the stage, severity, and type of peri-
tonitis.
Peracute peritonitis
1. Elevation of hematocrit and red cell figures occur as
a result of hemoconcentration.
2. Endotoxemia causes leukopenia, neutropenia, and a
degenerative left shift.
3. Plasma fibrinogen values are likely to be normal or
low.
4. Protein sequestration into the peritoneal cavity may
result in hypoproteinemia, but this is often offset by
the concomitant dehydration; serum protein levels
may, therefore be normal or elevated.
5. Electrolyte imbalances are often present, including
hypocalcemia, hyponatremia, hypokalemia, and
hypochloremia.
6. Metabolic acidosis.
7. Raised creatinine concentration as a result of pre-
renal or renal azotemia.
Acute peritonitis
1. There is often an initial leukopenia and neutrope-
nia, which is followed by leukocytosis, neutrophilia
and left shift.
2. Plasma fibrinogen will be normal in the early stages
of acute peritonitis, after which it is likely to be ele-
vated (up to 10 gil); it can take 48 hours for peak
concentrations to be reached.
3. Hypoproteinemia, often with a decrease in the albu-
min:globulin ratio, reflects protein sequestration
into the abdomen; if dehydration is present, hyper-
proteinemia may be observed.
4. Electrolyte imbalances may be present as for pera-
cute peritonitis.
Chronic peritonitis
Laboratory values are extremely variable.
1. Hematology may show normal white cell figures, or
there may be a leukocytosis and neutrophilia (with
or without a left shift). Occasionally a monocytosis
will be present.

2. There may be anemia due to chronic inflammation
and bone marrow suppression.
3. Plasma fibrinogen is likely to be elevated « 5 gil).
4. Hyperproteinemia due to hypergammaglobuline-
mia may be present in some cases. The
albumin:globulin ratio may be decreased. Serum
protein electrophoresis may demonstrate elevation
of alpha, beta and gamma globulin ratios indicative
of chronic inflammation.
Rectal palpation
In peracute cases where there has been contamination
of the abdominal cavity with gastrointestinal contents, a
gritty feeling to the serosal surface of the bowel may be
felt, and in some cases crepitus may be present due to
free gas within the cavity. Distended large and small
intestine may occur secondary to ileus.
In acute and chronic peritonitis, rectal findings may
be non-specific. In many cases the examination will
elicit pain. An impression of bowel floating in abdomi-
nal fluid may be detected in some cases. Distended
bowel or secondary impaction of the pelvic flexure may
be palpable. In mares with uterine rupture, a fibrinous
adhesion may be identified over the affected area.
Occasionally abdominal masses or abscesses may be pal-
pated, and mesenteric lymph nodes may be enlarged.
Ultrasonography
Abdominal ultrasonography frequently reveals an exces-
sive quantity ofhypoechoic to echogenic peritoneal fluid.
The echogenicity of the fluid increases with the cellular
content. In the presence oflarge amounts of fluid, loops
ofintestine and intra-abdominal organs appear separated
from one another and lifted from the ventral aspect of
the abdomen. Particles observed floating freely in the
peritoneal fluid may be caused by fibrin or ingesta. Fibrin
tags or adhesions between bowel and the parietal peri-
toneum or between the abdominal organs may be evident
in some cases. The presence of free gas in the abdominal
cavity is suggestive of either bowel rupture or the pres-
ence of gas-producing bacteria.
Urogenital examination
A urogenital examination should be performed in
mares with a history of recent covering or foaling to
identify vaginal, cervical, or uterine tears. Recently cas-
trated males should also be evaluated for an infected
castration wound.
Laparoscopy and exploratory laparotomy
Diagnostic laparoscopy is most helpful in cases of sus-
pected abdominal abscessation or neoplasia, where a
OTHER CONDITIONS 17
mass is palpable per rectum. Only the dorsal part of the
abdominal cavity can be explored in the standing horse,
allowing visualization of the serosal surfaces of the
colon, small intestine, and stomach, and parts of the
urogenital tract, spleen, and liver. The technique is con-
traindicated in cases where gross bowel distention or
adhesions are present in the area where the laparo-
scope is to be introduced.
Exploratory laparotomy (celiotomy) should be con-
sidered for diagnostic, therapeutic, and prognostic rea-
sons. The procedure should not be undertaken until
stabilization of the patient and treatment of hypov-
olemia and endotoxemia have been accomplished.
TREATMENT
Prompt and aggressive treatment is required. The treat-
ment objectives in peritonitis are to
• reverse endotoxic and hypovolemic shock
• eliminate infection
• correct the primary cause of peritonitis
• relieve pain
• correct metabolic and electrolyte abnormalities
• correct dehydration
• correct hypoproteinemia
• provide nutritional support.
The first treatment priority is to stabilize the patient.
Hypovolemia and endotoxemia need to be addressed
early and aggressively. Restoration of cardiovascular
function is essential before further treatment priorities
such as antibiotic therapy, peritoneal lavage and
drainage, and surgical treatments.
Fluid therapy
Intravenous fluid therapy is necessary to correct hypov-
olemia, metabolic acidosis, and electrolyte imbalances.
The principles of fluid therapy are described elsewhere
(see Chapter 9). Regular monitoring (every 4-6 hours)
of the packed cell volume (PCV), total plasma protein
(TPP) , blood gas analysis, and electrolyte concentra-
tions is necessary to assess the response to this therapy.
Plasma therapy
If the total plasma protein concentration falls to less
than 45 gil, slow intravenous plasma therapy (2-10
liters) is indicated to maintain plasma oncotic pressure
and to minimize the risk of pulmonary edema during
rehydration with intravenous fluids. Fresh equine
plasma is also beneficial in the treatment of endotox-
emia by supplying fibronectin, complement, antithrom-
bin III, and other inhibitors of hypercoagulability.
327
17 COLIC

Antibiotic therapy Antibiotic therapy should be continued until the

Antimicrobial therapy should be initiated immediately
after peritoneal fluid samples have been obtained for
culture. Antibiotic therapy, therefore, needs to be
started before the results of culture and susceptibility
are available. In most cases of septic peritonitis a mix-
ture of gram-positive and gram-negative aerobes and
anaerobes will be present, and the antibiotic therapy
must have sufficient spectrum to control the antici-
pated flora.
Antimicrobial combinations commonly used in ini-
tial therapy include
I. Na.' or K+ penicillin 22000-44000 IV/kg i.v., q. 6 h
or
ceftiofur 2-4 mg/kg i.v., q. 8-12 h
plus
2. gentamicin 2.2 mg/kg i.v., q. 8 h, or
6.6 mg/kg i.v., q. 24 h
or
amikacin 6.6 mg/kg i.v., q. 8 h, or
15 mg/kg i.v., q. 12 h
plus
3. metronidazole 15-25 mg/kg p.o., q. 6 h.
This regime may be modified once the results of cul-
ture and sensitivity are available. These antibiotics will
achieve adequate levels within the peritoneal fluid,
intraperitoneal administration of antibiotics is there-
fore unnecessary.
Toxic side effects of aminoglycosides, especially
renal tubular necrosis, are important considerations in
the hypovolemic septic horse. Routine pharmacological.
monitoring should be undertaken in such cases to min-
imize the risk of toxicity.
Other antimicrobials that can be useful in the treat-
ment of some cases of peritonitis (dependent on the
culture and sensitivity results) include
clinical signs have resolved and clinicopathological
parameters (peripheral white blood cell count, plasma
fibrinogen, and characteristics of the peritoneal fluid)
are normal. Generalized septic peritonitis may require
antimicrobial therapy of 1-6 months.
Gastric decompression
Nasogastric intubation to allow gastric decompression
should be performed in all cases with evidence of gas-
trointestinal ileus. Repeated nasogastric intubation
every 3-4 hours, or placement of an indwelling naso-
gastric tube may be necessary in some cases.
Anthelmintics
Anthelmintic treatment is indicated in all cases with a
suspected parasitic etiology (verminous arteritis due to
migration of Strongylus vulgaris larvae or larval cyathos-
tomosis). Fenbendazole (10 mg/kg p.o. daily for 5 days)
or ivermectin (0.2 mg/kg p.o.) are recommended.
Analgesic and anti-inflammatory therapy
Analgesics may be required to control the pain associ-
ated with peritonitis. Commonly used analgesics
include flunixin meglumine (0.5-1.0 mg/kg i.v.) and
xylazine (0.2-1.1 mg/kg i.v). Flunixin meglumine
should also be used for its anti-inflammatory and anti-
endotoxin effects; a dose rate of 0.25 mg/kg, q. 6 h is
effective for this purpose.
Heparin therapy
Heparin therapy has been recommended to prevent
adhesion formation and to render bacteria more sus-
ceptible to cellular and non-cellular clearing mecha-
nisms. A dosage of 40-80 IV /kg, q. 8 h is suggested.

I. sodium ampicillin 25-100 mg/kg i.v.,

Abdo'minal drainage and lavage
q. 6-8 h
2. trimethoprim-sulfadiazine 15 mg/kg p.o., q. 12 h The aims of abdominal drainage and lavage include
3. enrofloxacin 1.5-2.5 mg/kg p.o.,
• removal of bacteria, enzymes, and toxins from the
q. 12 h.
peritoneal cavity
Enrofloxacin should be used in adult horses only, • removal of degenerative neutrophils and cellular
because of its adverse effects on cartilage in young debris
horses. • removal of blood
The duration of antibiotic therapy depends on sev- • removal of ingesta and foreign material
eral factors including • dilution of adhesion-forming substrates such as
fibrinogen and fibrin.
• the severity of the peritonitis
• the underlying cause of the peritonitis Although drainage and lavage can be performed rel-
• the degree of loculation of infection by fibrin atively easily, some doubts exist about how effectively
• the etiological agents the large peritoneal surface area can be treated in this
• the response to treatments. way because of the size and limited access to many parts

328
 OTHER CONDITIONS 17

of LIH: abdominal c.wity. In <tdditioTl then." arc (OI}ccms

thal lavage may disseminatc a localized infection

th roughout tht: (:avity. Oesl}ile t.hese concerns peri.
tonciillavagc and drainage arc conside red by man}' din­
icians. to be beneficial ill ac ute CaSCs of pc:-rilOllilis where
there is a purulel l t effusion and poor response to initial
Tllt'<iicallhc:-rapy.
The process is usually performed 2-3 tinu:s a day fot'
2-3 days uTllil the pel;toneal fluid whitt: cell count and
I()tal pn)tein concentration s how an improvement.
Both peritoneallav.1ge and rh"ainage em he perf<mned
c..fft�cti\'c1y using a single ingress!egress catheter placed
on (he ve ntral midline at the most de pend ent aspect of
I.he abdomen (Figure 17.4). A..ltcmativdy, two catheters
("an he used - one egress calhett:"r on the ....entral mid­ Figure 17,4 Foley catheter inserted in the ventral midline
to permit abdominal lavage and drainage
IiIH' and one ingress catht·I.(·r in one of the paralurnhar
fos..'ia('. A variety of fcnc!ltrated d rains can he use d stich
a.� a nmshroom cirdin, thoracic ('annula (e.g. 32 French
gauge), Foley catheter, or sH.'rilized sc-gmf'nI. of naso­ sue irriracion and cellulitis. 2scending infection,
gastric lube. After sedati ng the horse.�, the site for draill obstruction of the.: drain hy fihrin, and hcrni<,tion of
ill,><'rlion is prepa red aseptically, and the ..,kin and suh­ omentum OJ' illlcStine !hTO\lgh the drain or drditI .�ite.
CLH.aneous tissue is infiltrated with local anesthetic. A I All hors�s treated by peritoneal lavag-e and dr.:linagc arc
ern stab incision is made through the skin, subcma­ Sus(cplible to hemoconcentration, plasma protein loss
)lelllIS {issue, and linea alba to a llow insertion of the and electrolyte disturbances. FrequeIlt mon i LOring of
drain. If a mushroom drain or Foley catheter is being these param(:ters, and. repl at:cm cnt therapy as neces­
used, it can be stretched over a metal probe { sm:h a'i a sary, arc required.
felliale can ine or Chambers marc catheter) lO aid its The addition of povidone-iodine or antibiotics to the
insertion. If the howel is inadvertently punnured dur� lavage fluid is unnecess,ary and lIlay cause a chemical
Illg insertion, the drain should not he removed until r.ht'" peritoni tis and increasen morbidity. Their usc is there­
il�jlll)' can be repaired surgically under general ane!t­ fore not recomm(:nded.
tbesia. The risk of penetrating rhf> bowel (or lIlcrwj in
the.' pregnant rnan�) can Iw rt�duced by uitrasono­ Surgical treatment
graphic sc anning of the area prior to placing the drain.
The aims of surgical th erapy of peritonitis are to ideo­
When rhe drain is being used as an ingn�ss cannula,
,.if)' and rt::J'nove the source of a bdominal (.oo13mination
1 O-:�O iilen; of warmed Javag<.· solution (balanced
and to remove s.eplic material. Many cases of per itoni tis
polyionic fluid) is infused, anrl th e drain is flushed WiIh
will recover wlthout resorting to surgical invasion of lhe
heparinized saline and closed. If the horse stans to show
abdominal cavity. alth ough the source or peritoneal
signs of abdominal discomfort when the fluid is being
contamination may remain undiagnosed. 1n those ca.�es
infllsed, the infusion should be stopp��d at a smaUer vol­
where no un derlying c.ause of the peritonitis (.an be
lime Lhan intended. Heparin may he added to rhe lavagt.'
est.ablished, surgical explora{ion may help to identify
fluid (5000 IU/l) in an allcrnpt to decrease peritoneal
the <:31lSe; however, in many other cases, no ohvious
flbrin formation and so to allow beltel' an:ess of amibi­
source of contamination will be found. The decision to
otics lO the bacleria. The ho rse is then walked fur 15 to
perform or not to perform an exploratory lap a rotomy
30 minutes prior to opening th<� catheter to allow the
can, therefore, he ....er)' difficult. Some surgeons may opt
fluid to drai n otLL The volume of fluid rC«(lYered should
to penorm surgery in every C:i:1..i' e in the hope of ide ntify­
he measured; approximately the SaTJl(� v(}lum� should be
ing and treating the underlying (ause. Alternatively,
recovered as was infused. Following drainage, the
su rgi cal explora ti on of the abdOIIlt:n may be lim ited to
c.tfheter should be filled with heparin, closed and pro­
the following si tuations
a'ned with a sterile bandage Unlit the neX llreatment. If
ahdominal pain occurs when the lavage fluid is being I. cases where an abdominal mass of unknown e tiology
infused, the rate of infusion should be slowed, or tlll.' has been identified
hors(' may be {f('awd \\'lth an analgesic such as xylazinc. 2. cases where an ahdo minal abscess has been identi­
Complications of peritoneal drainagc indude vis­ fied and where surgical removal, drai nage. or marsu­

rnal puncture during insertion, local subcutaneous tis- piali la

. (ion is consi.dered possible

329
17 COLIC
3. mares with a ruptured uterus
4. cases with abdominal wall trauma
5. postoperative horses where anastomosis failure is
considered possible
6. cases where intestinal perforation is considered
likely (e.g. where food material or intestinal proto-
zoa are identified in the peritoneal fluid)
7. cases with severe and intractable or worsening
abdominal pain
8. cases where medical therapy and abdominal drainage
fail to result in improvement within 24-48 hours
9. cases which demonstrate a deterioration in the clini-
cal features, despite aggressive medical therapy,
within 12 hours.
Surgical exploration of the abdomen permits effec-
tive open abdominal lavage via the laparotomy wound.
Open peritoneal drainage via a small abdominal wound
loosely sutured with monofilament stainless steel reten-
tion sutures has also been described, but the risk of
ascending infection is considerable with this technique.
PROGNOSIS
The prognosis depends on many factors including the
etiology, severity, duration, and treatment. The mortal-
ity rates in published series of peritonitis range from 25
to 70 per cent.
No single clinical or laboratory parameter can be
used reliably in an individual case to assess the progno-
sis. However, horses with peracute peritonitis, and those
cases which show a poor response to initial therapy tend
to have the highest mortality rate. Horses with postop-
erative peritonitis are also reported to have a high mor-
tality rate. Other factors that may have a detrimental
effect on survival include severe endotoxemia, severe
dehydration, severe colic, laminitis, diarrhea, paralytic
ileus, and coagulopathies. Horses with peritoneal fluid
that has a very low glucose concentration also tend to
have a poorer prognosis. Abdominal adhesions or
abscess formation can also have a negative effect on
long-term prognosis.
Abdominal abscesses
T Mair
INTRODUCTION
Internal abscessation of the mesentery or of parenchy-
mous abdominal organs is recognized most commonly
330
as a complication of Streptococcus equi subsp, equi infec-
tion (strangles) (Plate 17.3). However, mesenteric
abscessation can also arise spontaneously in horses that
have no previous history of overt respiratory infection,
or as a consequence of intestinal leakage (e.g. following
penetration by a foreign body, or adjacent to an anasto-
mosis leakage) or surgical contamination. These
abscesses are most commonly located in the small
intestinal mesentery. Other bacteria that are commonly
isolated from mesenteric abscesses include Streptococcus
equi subsp. zooepidemicus, Escherichia coli, Salmonella spp.,
Rhodococcus equi (in foals), and anaerobes.
Abscess formation following strangles is believed by
some to be more likely if the horse received inadequate
antibiotic therapy during the acute respiratory disease
(compared to horses that received no antibiotics at all),
but it may also occur in horses that received no treat-
ment during the acute stage of infection.
SIGNALMENT AND HISTORY
Horses of any age and either sex can develop abdomi-
nal abscesses, but they are most common in young
adults (less than 5 years of age). A history of recent
strangles infection (within the preceding few months)
may be present. In foals less than 6 months of age,
Rhodococcus equi infection may result in abdominal
abscessation, and these foals may demonstrate other
signs of pulmonary infection. A history of recent
abdominal surgery or castration may be significant.
Heavily parasitized horses may also be at increased risk
of developing abdominal abscesses, since migrating par-
asite larvae (large strongyles) can carry bacteria with
them as they migrate through the mesenteric tissues.
CLINICAL SIGNS
The clinical signs associated with abdominal abscesses
are very variable, and are dependent on the size and
position of the abscess, the degree of bowel involve-
ment, and the degree of associated peritonitis.
The common clinical signs include
• chronic weight loss
• inappetence or anorexia
• persistent or intermittent pyrexia
• pyrexia of undetermined origin
• acute colic
• chronic or recurrent colic
• depression
• diarrhea (especially foals infected by Rhodococcus
equi).

Colic may be caused by external cmnpn:ssio ll ohhe
itllestinal lumen, tmction on th(� mesentery. or adhe­
sions lO the intesLint! or omentum (Plate
Abscesses are an uncommon cause of acute colic, and
were recorded in 0.4 per cent of one large !ieries of sur­
gicaJ colics compiled in the l'SA.
DIAGNOSIS
Horses with abdominal abscesses can be difif culllO dif­
fen�1l1iate from animals with otht!f <:auses of chronic
weight loss or chronic/imermittent colic (see The
difT{�rentiaI diagnosis and evaluation of chronic and
recurrent colic), The following techniques rna)' he
h elp/iIi in making a rliagnosis
• reClai examination
• hematology :dnd serum biochemistry
• ahdominal paracenlesis
• ultrasonography
• laparoscopy
• t"xpioralory laparotom y (celiotomy)
• nuclear scintigraphy.
Rectal examination may reveal an abnormal mas.."i
that may be painful to palpation. These ma.�ses arC uSu­
all)' palpated in the midline or in the ventral qu:.tdranrs.
l.oups of adherent and distended small intestine may be
palpated acHacenr to the abscess. However. many
abs(:esses will not be palpabl<: per rectum.
H e matologic al changes are frequently non-specific., hut
may include leukocytosis, neutrophilia, monocytosis,
and hyperfibrinogenemia. J lyperproteinemia, hyper­
globulinemia, hypoalbumincrni:.t. and hypocalcemia
may be derccted by serum bim:hcmistl)'. Peritoneal fluid
changes are not consistenr in all cases, but there is
ally evidence of low-grade peritonitis with elevated total
nucleated cell count, neutrophil count, and prolein con­
centration. Bacteria are not reliably present in the fluid.
Allor th<! se abnormalities may be _"cen ,,,·jlh other dis­
east's, including some cases or abdom inal neoplasia, and
differentiation bern'een absn:ssation and neoplasia can
be a significant challe nge . Both neoplasia and abscesselO
rna)' sometimes be present in the same horse.
Enlargement of the anorectal lymph nodes and sub­
sequent abscess formacion can calIse excralumenal
obstruction of the rectum resulting in sig ns of abdomi­
nal pain (see Chapter 16). Other clinical signs associ­
<lted with the cOlldition include anorexia, lack
production of feces, tenesmus. and pyn:xia. Anorectal
abscesses arc most (:ommonly identified -in foals, but
thf")' can sometimes anecl "dull horses. Sepsis can
extend inlO the peritoneal cavity causing septic peri­
lonitis. Diagnosis of anorectal abscess ation is confirmcd
OTHER CONDITIONS 17
17.4).
Figure 17.5 Ultrasonogram obtained tramrectally showing
a large multilowlated post-castration absce55
by digital p alpatio n per rcc[Um, I.ransrectal ultrasonog­
Ti:lphy. and cyto logic examination of an aspirate or
biops)' from an affected lymph n o de. Peritoneal Auid,
obtained by abdominocemesis, should be examined
cytologically to determine if sepsis extends int.o the
abdomina! c:avit)- ,.
Lltrasound examination (transrcclal and/or trans­
ahdominal) may he helpful. espc(:ially if a ma� is palpa­
ble per rec:rum. Post-c<t!ollration (including
cl)'prorchidt:cr,omy) abscesses are usually located adja·
cent to one inguinal canal ( Fig ure 17.5). Mesenteric
abscesses may he difficuh to image. depending on their
location. Confirmation of an ahdominal abscess may
require surgical exploration, eithcr by .....ay of diagnostic
laparoscopyor explora.tory laparotomy (celiotomy).
�udcar scintigraphy u s in g tcchnctium-99m labeled
white blood cells can sometimes be used to identify an
lISll­ abscess lhat cannot be localized by other tt:chniqm::s
(see Chapter 2).
TREATMENT
SuccessrUI treatment may be achieved in some (ase s by
prolonged antibiotic therapy. AtteI'C1pts to culture the
offendin g organism should always. be made to help
select the appropriate anlibiolic(s). Peritoneal fluid
should be coll cc ted for bOlh aerobic and anaerobic cul­
ture. If feasible. a needle aspirace of the absccss should
be made percultl.ncously, utili1.ing ultrasound guidance.
of AJternativd y . samples llIay be obtained by centesis via
exploratory laparotomy (cdiotomy) or laparoscop)'.
Antibioric therapy will be re<:]uiced fOT Ci minimum of 30
days, and not infrequently for 2-6 months. Procaine
penicillin (22000 Ie/kg b.i.d. Lm.) is the antibiotic of
choice [or cases involving St-rtptor.oCCU.f equi. However,
331
17 COLIC
prolonged courses of intramuscular penicillin are likely
to result in muscle soreness and resentment by the
patient. Switching to an oral antimicrobial medication
is preferable in horses that require prolonged courses
of antibiotics. Potentiated sulfonamides (30 mg/kg
s.i.d. or b.i.d.), enrofloxacin (7.5 mg/kg s.i.d. or 4.0
mg/kg b.i.d.), metronidazole (15 mg/kg q.i.d. or 20-25
mg/kg b.i.d.) and rifampicin (5.0-7.5 mg/kg b.i.d.)
can be useful in this regard. Treatment should be con-
tinued until such time as the clinical and laboratory
changes (including fibrinogen) have returned to nor-
mal. If the abscess is palpable per rectum or can be
imaged by ultrasound, treatment should be continued
until such time as the abscess is no longer appreciable.
In foals with suspected or confirmed Rhodococcus equi
infection, oral treatment with erythromycin ( 25 mg/kg
t.i.d.) and rifampin (5-10 mg/kg b.i.d.) is indicated.
Other treatments for peritonitis (see Peritonitis)
may be indicated depending on the degree of peri-
toneal inflammation and sepsis.
Surgical therapy is frequently not possible owing to
the location of the abscess, but may be indicated in
some circumstances. In particular, surgery may permit
• intestinal by-pass in cases of small intestinal
obstruction
• abscess resection
• abscess drainage by needle aspiration
• marsupialization of abscess to the body wall.
PROGNOSIS
The prognosis for horses with abscesses uncomplicated
by intestinal obstruction is guarded to good. Many such
horses will recover with prolonged medical therapy. In
one report of 25 cases of abdominal abscesses, 17 of the
horses recovered following prolonged antibiotic treat-
ment. A clinical or laboratory improvement after 2
weeks of treatment is a positive and encouraging sign.
The prognosis is much poorer in cases where intra-
abdominal adhesions form. The prognosis for foals
affected by Rhodococcus equi mesenteric abscessation is
generally very poor.
Hemoperitoneum
'UP
FT Bain
CAUSES
Hemoperitoneum (hemorrhage into the peritoneal
cavity) can be caused by a variety of conditions in horses
332
Neonate
Rupture of umbilical vessels
Rupture of spleen
Fractured ribs
Older foal and adults
Idiopathic
Splenic rupture
Hepatic rupture
Kidney rupture
Uterine or ovarian artery rupture
Coagulopathy
Idiopathic -associated with liver orkidney biopsy
post-surgery
Splenic and other neoplasia
Lacerated iliac artery (pelvic fracture)
of all ages. Some of the common causes of hemoperi-
toneum are listed in Table 17.5.
In neonates, rupture of the internal umbilical struc-
tures is the most common cause of hemoperitoneum.
Hemoperitoneum can also occur secondarily to rup-
ture of the spleen or liver, or it can be caused by frac-
tured ribs and diaphragmatic tearing during dystocia.
In older foals and adult horses, idiopathic hemo-
peritoneum is occasionally seen as a clinical entity; this
appears to be most common in older horses, rupture
of a mesenteric vessel being suspected in these cases.
External trauma can also result in hemorrhage into
the peritoneal space of foals and adults as a result of
rupture of the spleen, liver or kidney, or due to frac-
ture of one or more ribs. Hepatic rupture may also
occur in association with hyperlipemia and fatty infil-
tration of the liver (see Chapter 19). A common cause
of hemoperitoneum is hemorrhage from the uterine
or ovarian artery in aged brood mares during the peri-
partum period. In the male horse, severe abdominal
hemorrhage following castration may occur occasion-
ally, although the more common hemorrhagic compli-
cation following castration is external hemorrhage.
Almost all horses have some blood in the abdomen fol-
lowing castration. Intra-abdominal hemorrhage due to
severe coagulopathy may also be considered (although
this is not as common as arterial rupture), and it can
occur iatrogenically after biopsy procedures on the
liver or kidney. Abdominal neoplasia may cause intra-
abdominal hemorrhage because of invasion and rup-
ture of local vessels or hemorrhage from the tumor
itself; the latter occurs commonly in cases of heman-
giosarcoma (Plate 17.5).

CLINICAL SIGNS
The most common clinical signs of hemoperitoneum
are those related to hemorrhagic shock due to acute
loss of blood volume
• profound sweating
• tachycardia
• tachypnea
• weak peripheral pulses
• pale mucous membranes
• trembling
• distress.
In some situations, there are signs of abdominal
pain, and some horses with intra-abdominal hemor-
rhage may resemble a horse affected by severe colic.
Abdominal distention may also be seen.
DIAGNOSIS
The most useful and rapid diagnostic aid for hemoperi-
toneum is the abdominal ultrasound examination
(Figure 17.6). A routine, comprehensive evaluation of
the abdomen should be performed including imaging
both sides of the abdomen to include a scan of all major
anatomic structures of the patient. In peripartum
brood mares, this includes examination of the caudal
flank and inguinal areas for evidence of a hematoma in
either uterine broad ligament. In all patients, the
spleen should be examined closely for any evidence
that it is the origin of the hemorrhage. Tears of the cap-
sule of the liver or spleen can sometimes be appreciated
Figure 17.6 Ultrasonogram of the abdomen in a horse with
hemoperitoneum showing a large quantity of echogenic
peritoneal fluid
OTHER CONDITIONS 17
by ultrasonography. The ultrasound appearance of
hemorrhage is that of a cloudy, homogenous echogenic
swirling fluid (swirling in a manner similar to smoke
which is very characteristic of active bleeding). The ori-
gin mayor may not be evident, but the swirling may be
most active adjacent to the ruptured vessel. Clotted
blood may gravitate ventrally and be seen as variably
dense, laminated, echogenic material beneath a more
echolucent fluid (Figure 17.6). In neonates, the umbil-
ical structures should be closely examined.
Abdominocentesis may be useful for diagnosis and
characterization of hemorrhage. The presence of
platelets may reflect recent or active hemorrhage,
whereas the presence of erythrophagocytosis suggests
that the blood has been present for at least several
hours. Cytologic identification of inflammatory cells
may suggest rupture of an organ such as the uterus or
bowel in a postpartum mare. More often abdominocen-
tesis with cytologic evaluation is helpful in identifying
the complicated hemorrhagic abdominal effusions
other than simple vascular rupture.
TREATMENT
The treatment options for hemoperitoneum are
• keep patient quiet
• intravenous fluid therapy with
whole blood
polyionic fluids
polymerized bovine hemoglobin
fresh plasma
• autotransfusion
• corticosteroids
• naloxone
• epsilon-aminocaproic acid
• analgesics
• intra-nasal oxygen
• surgery.
Treatment of the hemoperitoneum depends on the
origin of the hemorrhage as well as the severity of blood
loss. In patients with acute hemorrhagic shock, replace-
ment oflost blood volume and oxygen-carrying capacity
is critical. In certain situations, medical treatment alone
is deemed best. This includes most mares with sus-
pected uterine artery hemorrhage where surgical explo-
ration may be ineffective and result in additional and
possibly fatal hemorrhage. In some foals, medical man-
agement alone is useful. Application of a belly wrap or
abdominal support bandage may be helpful in increas-
ing intra-abdominal pressure and reducing hemor-
rhage. Transfusion with compatible, fresh, whole blood
is the most common approach. This provides oxygen-
333
17 COLIC

carrying capacity as well as fresh coagulation factors these patients. Abdominal ultrasound remains a critical
from the plasma. Time is often a factor in the acquisi- diagnostic tool for this problem.
tion of whole equine blood since storage of equine
blood is not practiced. In some instances, the adminis-
tration of polymerized bovine hemoglobin (Oxyglobin,
Biopure Corporation, Cambridge, MA, USA) may be Gastrointestinal neoplasia
effective in providing sufficient oxygen-carrying capac-
ity until whole blood transfusion can be arranged. The M Hillyer
author has used doses of 7.5-15 ml/kg in foals with
hemoperitoneum with beneficial effects as evidenced INTRODUCTION
by decreased heart and respiratory rates and improved
attitude and alertness. Neoplasia ofthe gastrointestinal tract of the horse is not
The question of fluid resuscitation in hemorrhagic common. While neoplasms have been reported in
shock is a controversial one. The phrase 'hypotensive almost all of the tissues of the equine gastrointestinal
resuscitation' has been discussed in the literature. This tract, some locations and types of neoplasia are more
is based on the concept that rapid normalization of common than others, the common types tending to
blood pressure may lead to dislodgment of the develop- produce characteristic syndromes with typical clinical
ing clot and further bleeding. An extensive discussion signs. The recognition of such signs in a horse helps to
of the therapy of hemorrhagic shock is beyond the raise the index of suspicion of a gastrointestinal neo-
scope of this section, however it is worth noting that this plasm, in turn allowing a more targeted approach to the
concept may be critical to the outcome of the patient in investigation and an earlier diagnosis. For example, the
some situations. Another modality for transfusion ther- presence of chronic weight loss, recurrent colic and/or
apy in these cases is autotranfusion. This can be accom- choke after feeding, and fecal occult blood would raise
plished with the use of a variety of vacuum blood the suspicion of a gastric carcinoma, while an acute
collection systems with an anticoagulant (approxi- strangulating obstruction of the small intestine in an
matelyone fifth of the quantity normally used for whole aged pony would be suggestive of a strangulation by a
blood transfusions) and filtered administration set. pedunculated lipoma. These 'typical' scenarios are
Concern for infection is critical and evaluation of the described later in this section.
collected blood for leukocytes and evidence of sepsis is
mandatory prior to readministration.
Medications that are considered supportive of hem-
orrhagic shock include corticosteroids (prednisolone
sodium succinate 2 mg/kg) and naloxone (0.03 mg/kg
i.v.). Aminocaproic acid has been used as an inhibitor Primary gastrointestinal Reported sites of
of fibrinolysis in hemoperitoneum due to uterine artery neoplasms occurrence
rupture in the mare at an initial dose of 20 g/450 kg (in Lipoma Mesentery
fluids) followed by 10 g/450 kg q. 6 h (in fluids). The Wall of small and large
use of hypertonic saline and colloid fluids is considered intestine
controversial because of the rapid rise in arterial blood Squamous cell carcinoma Stomach
pressure caused by these fluids. Fresh plasma may be
beneficial in replacing clotting factors lost into the peri- Lymphosarcoma Small and large Intestine
toneal space during massive hemorrhage. Adenocarcinoma Small and large Intestine
In some patients, the decision for surgical explo-
Leiomyoma Duodenum
ration might be necessary. This will depend on the clin- Jejunum
ical determination as well as ancillary diagnostic aids Small colon
that indicate a reasonable ability to identify the source
and control the hemorrhage. Drainage of the blood Leiomyosarcoma Stomach
Duodenum
may be required in order to lessen abdominal pain, but
Jejunum
this should not be performed routinely as the fluid pres- Rectum
sure in the abdomen may slow the bleeding and some
of the red cells may be resorbed. Neurofibroma Large Intestine
The most critical factor of all is the early recognition Myxosarcoma Cecum
of hemoperitoneum as the cause of the clinical signs.
Adenosarcoma Not specified
Delayed recognition is a common cause of death in

334

Secondary gastrointestinal neoplasms
Melanoma
Mesothelioma
Testicular seminoma
Teratoma
Transitional cell carcinoma
Gastrointestinal neoplasms are usually classified
according to their cell type and site of origin (Table
17.6). This section will concentrate on the primary neo-
plasms, although metastasis to the gastrointestinal tract
of other tumors may also occur (Table 17.7).
PREVALENCE
Previous reports of equine pathology studies suggest an
estimated incidence of gastrointestinal neoplasia of less
than 0.1 per cent of routine post-mortem examinations
and about 5 per cent of horses with clinical signs of
abdominal disease.
The most common neoplasm of the gastrointestinal
tract is the mesenteric lipoma. However, it is often clin-
ically insignificant and therefore not included and
hence under-represented in many surveys of abdominal
neoplasia. When significant the lipoma may produce
signs only related to its physical properties, namely as a
space-occupying mass causing a simple intestinal
obstruction, or more commonly as a pedunculated
mass causing a strangulating intestinal obstruction.
The two most frequently reported neoplasms of the
equine gastrointestinal tract are the gastric squamous
cell carcinoma and the alimentary lymphosarcoma
(although most surveys of gastrointestinal neoplasia
have failed to record lipomas). It is probable that there
is an approximately equal prevalence of both of these
tumors, but it is interesting to note an apparent higher
incidence of gastric squamous cell carcinomas in North
America, while the alimentary lymphosarcoma may be
relatively more common in Europe.
ETIOLOGY
As with many neoplasms in other species, the etiology of
gastrointestinal neoplasia in the horse is still poorly
understood. Gastric squamous cell carcinomas have
been associated with geographical areas and linked to
conditions causing chronic gastric mucosal irritation
such as parasites and physical irritants, but the true
OTHER CONDITIONS 17
etiology is likely to be multifactorial. The etiology of
lymphosarcoma and the other gastrointestinal neo-
plasms is presently unknown.
PRESENTATION AND CLINICAL SIGNS
Horses with a gastrointestinal neoplasm will usually pre-
sent with a chronic and insidious history of weight loss.
Weight loss will usually be seen as a result of one or
more of the following events
• reduced feed intake
• altered digestion and/or absorption from the
intestinal tract
• increased protein loss into the intestinal tract or
peritoneal cavity
• increased nutrient requirements of the neoplasm
• altered energy requirements as a result of effects of
the neoplasm.
Recurrent colic, diarrhea, and poor performance or
exercise intolerance may also be features of gastroin-
testinal neoplasia, together with an intermittent
pyrexia. Typically the neoplasms occur in mature or
aged animals.
The exception to this is the pedunculated mesen-
teric lipoma causing an intestinal strangulation and
signs of acute colic, described in more detail elsewhere
(see Chapter 13).
INVESTIGATION
Clinical signs and history
As previously stated, horses with a gastrointestinal neo-
plasm will usually present in poor body condition with a
history of progressive weight loss. Careful questioning
of the owner may be needed to elucidate other signs
such as reluctance to feed, low grade abdominal dis-
comfort, or altered fecal consistency. An intermittent
pyrexia may also be present. Physical examination of
the horse is often unrewarding but is essential, together
with a thorough history, in order to eliminate other
more common causes of weight loss (see also Chapter
18) such as
• inadequate or unsuitable feeding
• dental or swallowing disorders
• excessive exercise/energy demands
• parasitism.
In addition the clinical examination may reveal the
involvement of other tissues/organs as well as the gas-
trointestinal tract.
335
17 COLIC
Clinical pathology (see Chapter 2)
Non-specific changes are often seen in the clinical
pathology results from blood samples of horses with gas-
trointestinal neoplasia.
Anemia may be present as a result of non-specific
chronic inflammatorydisease orin association with blood
loss. The blood loss may be marked as in cases of gastric
squamous cell carcinoma where red cells may be lost into
both the bowel lumen and the peritoneal cavity.
White blood cell parameters are usually normal or
may reflect the chronic inflammation which may
accompany a gastrointestinal neoplasm. Intestinal lym-
phosarcoma will rarely be associated with abnormal
lymphocytes circulating in the blood.
Reduced plasma protein concentrations may be seen
in conjunction with the weight loss and altered nutrient
metabolism. Low albumin concentrations are often
seen with malabsorption syndromes/protein losing
enteropathies such as the diffuse intestinal lymphosar-
coma. However, in many cases the total protein concen-
tration remains in the normal range as a result of
increased globulin concentrations associated with the
chronic inflammatory response.
Increased concentrations of the intestinal fraction of
the alkaline phosphatase enzyme (lAP) may also indi-
cate the presence of intestinal disease.
Hypercalcemia has been reported in association with
both lymphosarcoma and gastric carcinoma.
Rectal findings (see Chapter I)
Rectal examination is essential in the investigation of any
case with suspected gastrointestinal neoplasia. Although
normal findings may be present in many animals, an
increased volume of peritoneal fluid, distention of the
intestine, or an abnormal tissue mass or masses will
increase the index ofsuspicion of gastrointestinal disease
and allow further directed investigations to be selected.
Abdominal paracentesis (see Chapter 2)
Collection of a sample of peritoneal fluid is another
important part of the investigation of a case of sus-
pected gastrointestinal neoplasia. Many cases, such as
intestinal lymphosarcoma or adenocarcinoma, may
have normal or non-specific inflammatory peritoneal
fluid. But other cases, typically the gastric squamous cell
carcinoma, may have exfoliated neoplastic cells in the
peritoneal or pleural fluid from which a diagnosis of
abdominal neoplasia may be made.
Ultrasonography (see Chapter 2)
Percutaneous or per rectum ultrasonography can pro-
vide additional information on the volume and charac-
336
ter of the peritoneal fluid. Intestinal distention may be
recognized together with abnormal bowel wall thicken-
ing and abnormal tissue masses. Ultrasonography also
allows guided collection of fluid or tissue samples for
further evaluation.
Laparoscopy (see Chapter 3)
Laparoscopic examination of the equine abdomen is a
useful minimally invasive technique for visualization of
the abdominal organs and for collection of tissue sam-
ples for histological examination. The primary site of
the neoplasm may be seen or secondary effects such as
bowel obstruction or abdominal metastasis recognized.
OTHER INVESTIGATIONS
Sugar absorption tests (see Chapter 2)
Glucose or xylose absorption tests are useful to demon-
strate a state of malabsorption from the small intestine
that may occur with a diffuse intestinal lymphosarcoma.
Although not diagnostic, a reduced uptake curve of the
sugar is highly suggestive of an infiltrative condition of
the small intestine.
Nuclear imaging (see Chapter 2)
Despite not being widely available the use of radio-
labeled markers may provide a novel method of identi-
fying a gastrointestinal neoplasm.
Exploratory laparotomy/celiotomy
Although expensive and highly invasive, exploratory
laparotomy provides the ultimate method for explo-
ration of the abdomen and collection of tissue samples
for histological examination. In clinical practice it is
often used as the last stage of the investigation, when
other, less invasive, techniques have failed to give a
definitive diagnosis. It also may provide the opportunity
for surgical removal and hence treatment of a discrete
neoplasm. Laparoscopy may allow direct visualization of
a neoplasm/mass and biopsy in some cases without
needing to resort to a laparotomy.
CASE SCENARIOS
Mesenteric lipoma (Figure 17.7)
Mesenteric lipomas
• are often clinically insignificant in older horses
• occasionally cause a simple intestinal obstruction
• usually cause a strangulating intestinal obstruction

• affect middle-aged and older animals, especially
ponies
• have an acute onset colic related to intestinal
obstruction
• are successfully removed by early surgery.
OTHER CONDITIONS 17
• local metastasis is common and abnormal tissue
masses may be palpable per rectum
• gastroscopy allows identification and biopsy of the
neoplasm
• a primary mass on the greater curvature of the
stomach may be identified by ultrasound or
visualized laparoscopically.

Lymphosarcoma (Figure 17.9)

Features of lymphosarcomas include the following:
• any age of horse can be affected, often young adults
• progressive weight loss is the major sign and may be
the only sign
• diarrhea may be present if the large intestine is
involved
• hypoalbum0 0909 Td 26d ( i4a5e)Tm (v418.64 Tm r9(the)Tj 8sual48.8

Figure 17.7 Post-mortem photograph of a pedunculated

lipoma causing a small intestinal strangulation in an aged
pony

Gastric squamous cell carcinoma (Figure 17.8)

Features of gastric squamous cell carcinomas include
the following:
• they affect middle-aged and older horses
• there is a proposed increased incidence in males
• weight loss and inappetance are major features
• pyrexia and colic are also common
• esophageal involvement may cause recurrent choke
• anemia is often a marked feature
• they are usually exfoliative therefore abdominal or
thoracic paracentesis is often diagnostic

Figure 17.8 Post-mortem photograph of a gastric squa-

mous cell carcinoma in the stomach of a horse
 OTHER CONDITIONS 17
persists for 48 hours or longer. Recurrent colic refers to
bouts of abdominal pain which recur at variable inter-
vals from hours to days to weeks. As with other types of
colic, the abdominal pain usually emanates from the
Gastric Condjtjons
gastrointestinal tract, but may also arise from other
• gastric ulceration
body systems.
• squamous cell carcinoma
The diagnosis of the cause of chronic and recurrent • chronic gastric impaction
colic can be difficult to achieve, even after exhaustive
Partial gbstructjonsQf the bowel lumen
investigations including, in some cases, surgical explo-
Small intestine
ration of the abdomen. Chronic and recurrent colic
• pyloric/duodenal stenosis
cases are often frustrating to deal with, but the under-
• ileal hypertrophy
standable concern of owners place the veterinarian • hypertrophy of cecal mucosa
under some pressure to find an explanation for the • intestinal neoplasia (Plate 17.6)
clinical signs. Pregnant mares affected by recurrent • ileocecal intussusception
colic seem to be at increased risk of abortion and • other ileocecal obstructions
owners of such animals should be made aware of this • adhesions
possibility. • mesenteric abscess
• Meckel's diverticulum
Large Intestine
• cecocecal intussusception
• cecocolic intussusception
CAUSES OF CHRONIC AND RECURRENT • recurrent large bowel displacements, e.g.
COLIC nephrosplenic entrapment
• colonic torsion (180° or less)
Abdominal pain is usually caused by one of the follow- • enteroliths
• adhesions
ing mechanisms
• diaphragmatic hernia
• bowel wall (mural) stretching • sand impaction
• mesenteric traction Inflammalgrydjseases
• mucosal, parenchymal, or peritoneal inflammation. • cyathostomosis
• colitis
Stretchingof the bowel wall • NSAIDtoxicity/right dorsal colitis
The majority of conditions causing stretching of the MotUtty dj~Qrgel]
bowel wall and chronic pain are forms of simple • spasmodic colic
obstructions. Strangulating obstructions and infarctive • cranial mesenteric arteritis
conditions usually have a much more rapid course and • thromboembolic disease
are unlikely to lead to chronic or recurrent pain. These • chronic grass sickness
simple obstructions can be physical (e.g. gastric and • cecal dysfunction
colonic impactions or ileal muscular hypertrophy) or • color'lic impaction
functional (e.g. spasmodic colic). • small colon impaction

Mesenteric traction
Conditions that result in pain due to traction on the
mesentery include chronic impactions, neoplasia,
abscessation, and splenomegaly.
Inflammatory lesions
Mucosal inflammatory diseases include sand irrita-
tion, colitis, and cyathostomosis. Parenchymal inflam-
matory disorders include hepatitis and cholangitis.
Peritoneal inflammation can be caused by septic peri-
tonitis, abdominal abscessation, and intra-peritoneal
neoplasia.
The common causes of chronic and recurrent colic
are listed in Tables 17.8 and 17.9.
INVESTIGATION OF CHRONIC AND
RECURRENT COLIC
The clinical examination of the horse with chronic or
recurrent colic is similar to that carried out in horses
with acute colic (see Chapter 9). Following a routine
clinical examination it will often be determined that
immediate surgery is not required and that time is avail-
able to undertake further diagnostic tests and labora-
tory investigations. Clinical examination of horses
demonstrating recurrent bouts of transient colic

339
17 COLIC

Liver conditiqos History

• hepatitis • pain -duration
• cholangitis onset
• cholelithiasis frequency
time interval between bouts
Pancreas
is it related to feeding?
• chronic pancreatitis
• previous medical - previous abdominal
• pancreaticneoplasi.a
history surgery
Urogenjtjl tract previous colic history
• cystitis respiratory infections
• urolithiasis drug therapies (e.g.
• bladder neoplasia NSAID)
• ovulation weight loss
• granulosa cell tumor • in-contact horses
• testicular teratoma • management - exercise
grazing
SW.un anthelmintic treatments
• splenic neoplasia (lymphosarcoma,
hemangiosarcoma) dental prophylaxis
• splenic hematoma • nutrition
• splenomegaly • access to water

Perjtqoeal cAvity Signalment

• peritonitis • age
• intraperitoneal abscess (Plate 17.7) • color
• intraperitoneal neoplaSia Clinical examination
ThorAcicdjsejse • gastrointestinal tract
• pericardial effusion • other body systems
• pleuritis Laboratory investigations
• hematology
• biochemistry
• monosaccharide absorption tests
• fecal analysis
should, wherever possible, be undertaken during an
episode of abdominal pain. Abdominocentesis
The evaluation of horses with chronic and recurrent Endoscopy
colic may include some or all of the procedures listed in
Radiography
Table 17.10. A careful assessment of the history and a
thorough clinical examination are essential compo- Ultrasonography
nents in every case. Biopsy
Response to treatment
History
Diagnostic laparoscopy
Pain
Exploratory surgery
The onset of pain associated with lesions such as intus-
susceptions is frequently sudden; there may be an initial
episode of severe pain, followed by milder and inter-
mittent bouts of colic. With other slowly developing trate). Bouts of pain that show an association with feed-
lesions, such as neoplasms, the onset of clinical signs is ing may indicate gastric ulceration, neoplasia, or a par-
usually more insidious. An increasing frequency of tial obstruction of the bowel lumen. Recurrent bouts of
recurrent bouts of colic with a shorter time interval pain in mares at regular intervals of about 3 weeks
between bouts may indicate a progressively worsening would suggest ovulation-related pain.
obstruction of the bowel lumen (e.g. external compres- In recurrent colics it is useful to know the duration
sion from a space-occupying mass or an intramural infil- of bouts of pain and whether or not the pain resolves

340

spontaneously, and also whether or not the pain
responds to simple spasmodic drugs.
Previous medical history
Previous abdominal surgery or injury can predispose to
intra-abdominal adhesions, which can result in recur-
rent bouts of pain. Likewise, a history of previous peri-
tonitis or abdominal abscessation might indicate the
possibility of adhesions or recurrence of the original
disease. A history of a respiratory infection (especially
strangles) in the recent past could suggest the develop-
ment of an abdominal abscess.
The recent or current administration of drugs
should be recorded. Non-steroidal anti-inflammatory
drug (NSAID) therapy can predispose to gastrointesti-
nal ulceration. Recent administration of an
anthelmintic might suggest a parasite-associated prob-
lem (such as cyathostomosis).
A history of chronic or recent weight loss may be pre-
sent in cases of abdominal neoplasia, abscessation, and
chronic peritonitis.
In-contact horses
Similar disease problems in in-contact horses is suspi-
cious of infectious, parasitic, nutritional, toxic, or man-
agement problems.
Management, nutrition, and access to water
Access to and quality of water should be evaluated.
Inadequate access to water can predispose to intestinal
impactions. Rations excessively high in carbohydrate
can result from overfeeding grain and concentrates,
and underfeeding roughage, likewise access to lush
grass can result in high carbohydrate ingestion. These
diets may result in excessive gas production within the
bowel and may cause diarrhea. Group feeding may
allow aggressive horses to overeat in preference to less
dominant individuals. Sudden changes in feeding prac-
tices and irregular time interval between feeds may also
result in intestinal complications.
Poor quality roughage, eating coarse bedding mate-
rials, and inadequate mastication of roughage resulting
from dental disease can result in colonic impactions.
Sandy pastures or feeding horses in sand schools can
result in excessive ingestion of sand.
Inadequate parasite control can result in a signifi-
cant parasite burden, which can predispose to several
types of colic.
Signalment
Young foals and yearlings are particularly prone to
gastric ulceration, as are young adult horses in race
OTHER CONDITIONS 17
training. Intussusceptions, foreign body ingestion, and
cyathostomosis are also more common in young horses.
Older horses are more likely to suffer from motility dis-
orders and neoplasia. Pedunculated lipomas are most
common in old ponies. Grey horses may be more at risk
of developing melanomas.
Clinical examination
A thorough physical examination should be carried
out, paying particular attention to the gastrointestinal
tract (see Chapter 9), but also including evaluation of
other body systems. Repeated examinations are likely to
be required, and examination while the horse is show-
ing signs of pain is preferable. Hospitalization of
affected horses can be extremely helpful to allow
repeated examinations over several days or weeks.
Rectal examination is likely to be the most useful
diagnostic technique. Some significant findings that
may be identified by rectal examination in horses pre-
senting with chronic or recurrent colic include
• pelvic flexure impaction
• abnormal masses such as neoplasms and abscesses,
enteroliths, intussusceptions, cystic calculi, and
broad ligament hematomas can also be detected in
some cases
• muscular hypertrophy of the small intestine can
occur within a period of 2-3 weeks in the segment
of intestine proximal to a partial obstruction, this
may be palpable as several loops of thickened,
rubbery-feeling bowel
• distended small intestine proximal to a (partial)
bowel obstruction
• segments of small intestinal hyperperistalsis are
occasionally palpable in horses with spasmodic
colic.
Abdominal auscultation may be helpful in the diag-
nosis of some conditions. A characteristic 'sand and
water' sound may be heard in the ventral rostral
abdomen in cases of sand impaction. A loud 'fluid
through a pipe' sound can be heard with spasmodic
colic or chronic distention of a portion of the small
intestine proximal to a partial obstruction such as ileal
hypertrophy.
Laboratory investigations
Unlike the horse with acute abdominal disease, in
animals with chronic or recurrent colic there is often
time to perform routine clinicopathological evalua-
tions. In many cases laboratory results will be unre-
markable or reveal non-specific changes, but in some
cases laboratory results may be diagnostically helpful
341

undiagnosed. Exploratory surgery via a ventral laparo-
tomy / celiotomy or diagnostic laparoscopy are often
performed as a final attempt to diagnose the cause of
the problem. However, even these procedures may fail
to yield a diagnosis in some cases and owners of affected
horses should be warned of this possibility prior to
surgery being undertaken.
Grass sickness
RS Pirie
INTRODUCTION
Grass sickness is a dysautonomia of Equus spp. charac-
terized by damage to neurons of the autonomic,
enteric, and somatic nervous systems. The disease was
first reported in the east of Scotland in 1907. Although
the northeast region of Scotland still has the highest
incidence of grass sickness, the disease has been recog-
nized throughout the United Kingdom as well as in
many other northern European countries including
Norway, Sweden, Denmark, France, Switzerland, and
Germany. No histologically confirmed cases have
occurred in Australasia, Asia, Africa, North America, or
Ireland. All members of the Equus spp. appear to be
susceptible to grass sickness, with the disease having
been reported in horses, ponies, donkeys, and captive
exotic equids. A clinically and pathologically indistin-
guishable disease known as mal seco (dry sickness) has
also been reported in the Patagonia region of
Argentina and in Chile and the Falkland Islands. Many
clinical similarities exist between grass sickness and
other dysautonomias in man (familial dysautonomia)
and other domestic species (feline dysautonomia,
canine dysautonomia). Although equids were previ-
ously thought to be the only herbivores susceptible to
dysautonomia, recently a clinically and pathologically
similar disease has been identified in the brown hare in
the UK (leporine dysautonomia) and the constipated
form of mucoid enteropathy of caged rabbits has also
been classified as a dysautonomia.
Grass sickness can be divided into three subdivisions
(acute, subacute, and chronic) which are characterized
clinically by varying degrees of gastrointestinal immotil-
ity and dysphagia, although it should be emphasized
that there is a continuum between these divisions. The
acute and subacute forms of the disease are invariably
fatal, however a proportion of mildly affected horses
with the chronic form may survive. Despite extensive
research the cause of grass sickness still remains
unknown.
OTHER CONDITIONS 17
EPIDEMIOLOGY
Age
Grass sickness has been confirmed in horses from 4
months of age onwards, however the peak incidence
occurs in 2-7-year-olds and is therefore considered pre-
dominantly a disease of the young adult horse.
Gender
Traditionally, no gender predisposition was thought to
occur, however results from a recent epidemiological
study suggested that mares were at a slightly reduced
risk.
Body condition
At the onset of disease, grass sickness cases are usually in
significantly better body condition than would be
expected from a reference population. Very rarely will
an animal in poor body condition contract grass sick-
ness.
Season
In the northern hemisphere, the highest incidence
occurs in the spring and summer months, with the peak
number of cases in the UK occurring between April and
July. Despite this obvious peak in incidence, cases will
occur in every month of the year. In the southern hemi-
sphere (e.g. Argentina), the highest incidence occurs
from October to February.
Grazing
As the name implies, grass sickness is almost exclusively
a disease of grazing equids with reported cases being
extremely rare in housed animals. Occasionally a strong
association will exist with certain premises.
Movement to new premises
Animals on a property for less than 2 months are at
greater risk and many cases will occur within weeks fol-
lowing movement to a new pasture or premises.
Climate
Cool (7-10°C), dry weather tends to occur in the 10-14
days preceding outbreaks.
Anthelmintic history
Recent evidence suggests that grass sickness is encoun-
tered more commonly in horses receiving frequent
anthelmintic treatments compared to those animals
which do not. This finding is independent of the effect
343
17 COLIC

• the potential involvement of an ingested mycotoxin

Geographical location
Age
Gender
Body condition
Season
Grazing
Movement to new premises
Climate
Anthelmintic history
of increased frequency of changing pastures. The rea-
son for this apparent association is unclear, however it is
not considered likely that anthelmintic drugs them-
selves are directly responsible and decreasing the use of
anthelmintics is clearly not advisable.
ETIOLOGY
The etiology of grass sickness is unknown. Numerous
epidemiological studies have found no evidence for a
conventional infectious agent. Considerable evidence
exists to suggest that a natural neurotoxin may be
implicated and the presence of a neurotoxic compo-
nent in the plasma of acute cases has been demon-
strated experimentally. Investigations into the possible
role of toxic plants, viruses, and fungal, chemical, and
bacterial toxins has failed to identify the cause. Current
investigations include
• the possible role of toxin release from Clostridium
botulinum
• an oxidative stress-mediated neural damage.
To date none of these investigations have yielded
conclusive results.
CLINICAL SIGNS
Acute form
The onset and progression of clinical signs in the acute
form is rapid with death occurring in less than 48 hours.
Animals will usually present with depression/somno-
lence, inappetance, and rapid progression to varying
degrees of abdominal pain in many cases. The degree
of colic may however be relatively mild and inconsistent
with the profound elevation in pulse rate. The pulse is
usually weak and may exceed 100 bpm in many cases.
Pyrexia (up to 40°C) and bilateral ptosis mayor may not
be present. Muscle fasciculations of the triceps and
quadriceps muscle groups may be observed and sweat-
ing may be generalized or localized to the flanks, neck,
and shoulder regions. Dysphagia is almost invariably
present but can be difficult to appreciate due to co-
existing inappetance. It may be apparent however,
when observing the animal attempting to drink when
many cases will flick their muzzle through the water or
'paw' at the water bucket, presumably through frustra-
tion. Excessive dribbling of saliva is often present and
probably results from a combination of excessive saliva
production and the reduced ability to swallow.
Dehydration is usually present which can be demon-
strated by prolonged tenting of the skin. Some horses

Acute Subacute Chronic

• depression/somnolence • 'tucked up' abdomen • severe weight loss
• distended abdomen • weight loss • markedly 'tucked up' abdomen
• ileus • dysphagia • base-narrow stance
• tachycardia • tachycardia • rhinitis sicca
• salivation • colic (as disease progresses) • bilateral ptosis
• gastric reflux • gastric reflux (as disease progresses) • slightly elevated heart rate
• muscle tremors • patchy sweating « 60 bpm usually)
• ptosis • ptosis • muscle tremors
• patchy/generalized sweating • muscle tremors • patchy sweating
• dysphagia • colon Impaction • mild colic
• small intestinal • reduced gut motility • reduced gut motility
distension
• colic (occasionally)
• colon impactions (occasionally)

344
 OTHER CONDITIONS 17
will show spontaneous gastric reflux with foul smelling
green or brown fluid exiting from both nostrils, and in
those that do not, passage of a nasogastric tube will
invariably result in the retrieval of many liters of mal-
odorous reflux. A generalized, marked reduction in
intestinal motility is evident during abdominal ausculta-
tion. As the disease progresses, abdominal distention
becomes apparent in most cases. Rectal examination in
acute cases will reveal a dry rectal mucosa and some
cases will strain excessively during the rectal examina-
tion. Frequently, distention of the small intestine can be
appreciated and consequently the rectal findings in
many acute cases can appear similar to those encoun-
tered in some surgical colic cases with associated small
Figure 17.10 Chronic grass sickness case showing a typical
intestinal obstruction. In some cases, a hard secondary
'tucked up' abdomen, this sign may occur early in the
impaction of the large colon can be palpated in the cau-
course of the disease before profound loss of body condi-
dal abdomen. The distinct corrugated nature of this tion becomes apparent
structure will often distinguish it from the relatively
smooth outline of a primary colonic or cecal impaction.
The prognosis in acute cases is hopeless, therefore
euthanasia is required after this diagnosis is made. acterisuc 'elephant on a tub' posture (Figure 17.11).
Some cases will show apparent weakness and a reduced
Subacute form anterior phase to the stride will result in occasional toe
dragging. Bilateral ptosis is often present resulting in a
Generally the clinical signs in subacute cases are similar sleepy, depressed expression. Persistent tachycardia is
but less severe than those of acute cases. The duration present, however the heart rate is lower than in acute
of clinical signs is longer and the outline of the and subacute cases, rarely exceeding 60 bpm. Varying
abdomen quickly develops a marked 'tucked up' degrees of muscle tremor, patchy sweating, and abdom-
appearance. This finding does not appear to be entirely inal pain are present. Signs of colic are usually mild and
due to loss of body condition, although significant transient. Varying degrees of dysphagia are common
weight loss does become apparent. Affected animals are but the associated reduction in appetite can make this
almost invariably dysphagic. Persistent tachycardia is difficult to appreciate. Frequently, affected horses will
present with or without any evidence of abdominal accumulate chewed food between the cheeks and molar
pain. Patchy sweating, usually around the flanks, neck teeth, often resulting in a fetid odor to the breath.
and shoulder, and muscle tremors of the triceps and Abdominal auscultation usually reveals a reduction in
quadriceps muscle groups are often present. intestinal motility. Small intestinal distention and
Nasogastric reflux and small intestinal distention are
usually absent early on in the course of the disease, how-
ever these may develop in a small number of cases as the
disease progresses. Also as the disease progresses many
subacute cases will exhibit worsening episodes of colic.
Colonic and cecal impaction is common and readily
appreciated during rectal examination. Although a
small number of cases that present initially as subacute
cases will gradually progress to the chronic stage, the
vast majority will die or require euthanasia within 7 days
of the onset of signs.

Chronic form
The clinical signs in the chronic form are more insidi-
ous in onset. The most obvious signs include severe
weight loss with the development of a distinct 'tucked
up' abdomen (Figure 17.10). Affected horses will often Figure 17.11 Chronic grass sickness case adopting a base-
have a very base-narrow stance, thus adopting the char- narrow ('elephant on a tub') stance

345
17 COLIC
colonic impaction are rare, therefore rectal examina-
tion usually reveals a lack of contents within the palpa-
ble regions of the colon and cecum. Many chronic cases
will have severe rhinitis with the accumulation of dry
hemorrhagic mucoid material on the nasal septum and
nasal turbinates. Although this can be appreciated by
close inspection of the rostral nasal septum using a pen
torch, often the animal will have a distinctive 'snuffling'
sound during breathing that originates from the nasal
cavity. Until relatively recently, the mortality in chronic
cases was reported to be 100 per cent, however strict
selection of treatment candidates and adherance to
good management protocols has considerably
improved the prognosis in some chronic cases (see
below). The suggested criteria for selection of cases for
treatment are summarized in Table 17.14.
CLINICAL PATHOLOGY
No alterations in blood clinical chemistry or hemato-
logic parameters are pathognomonic for grass sickness.
As one of the major differential diagnoses of grass sick-
ness is colic, most of the comparisons of clinical chem-
istry parameters have been made between grass sickness
cases, normal controls, and colic cases. Plasma cortisol,
catecholamine, and histamine concentrations are sig-
nificantly higher in acute and subacute grass sickness
cases than in colic cases and normal animals. This find-
ing has been attributed to increased sympathoadrenal
activity. The acute phase proteins, haptoglobin and oro-
somucoid, are increased in all three forms of grass sick-
ness but not in the majority of colic cases. Also the
protein content of peritoneal fluid is higher in grass
sickness cases compared with medical colics. The
author, however, considers that none of these analyses
is of value as a clinical diagnostic tool.
PATHOLOGY
Gross pathology
Acute grass sickness cases have a stomach distended
with green/brown fluid. The small intestine is usually
normal in color but distended with fluid throughout its
entire length. In some acute cases and the majority of
subacute cases the colon is impacted with hard, dry
digesta. When the colon wall is peeled away from the
firm impaction, a black coating is usually left on the sur-
face of the impacted ingesta (Plate 17.8). Examination
of the mucosal surface of the distal esophagus will often
reveal longitudinal linear ulceration as a consequence
of gastric reflux. In chronic grass sickness cases, the
346
main feature is profound emaciation with the gastroin-
testinal tract lacking in contents. Interestingly, some
chronic cases of mal seco have colonic impactions at
post-mortem examination.
Histopathology
Characteristic neuronal lesions occur in multiple auto-
nomic ganglia such as the cranial, cervical, stellate, and
coeliacomesenteric, in dorsal root ganglia, in specific
brain stem nuclei, and ventral horn and intermedialat-
eral gray matter of the spinal cord. In the acute lesion
affected neurons show a chromatolytic change, staining
homogenously with dyes such as hematoxylin and eosin
(H&E) and cresyl violet. There is loss of Nissl granules,
neuronal swelling, and vacuolation, and sometimes
pyknotic nuclei are evident. Degeneration and loss of
enteric neurons also occur in the submucous and
myenteric plexuses. In acute and subacute cases, this
damage is widespread throughout the jejunum, ileum,
and small colon (and possibly the large colon) with the
ileum being the most severely affected. In chronic cases
however, the distal small intestine, particularly the
ileum, may be the only severely affected area of the gas-
trointestinal tract.
DIAGNOSIS
Confirmation of a diagnosis of grass sickness can only
be made by demonstrating the characteristic
histopathologic lesions in the autonomic or enteric
ganglia at post-mortem examination, or by ileal biopsy
at laparotomy. This latter technique can be useful in the
ante-mortem diagnosis of acute and subacute cases
where surgical colic is a major differential diagnosis. In
chronic cases however where subsequent treatment is
being considered, anesthesia and surgery are likely to
adversely affect the outcome. Rectal biopsy is not yet a
reliable technique in grass sickness as the enteric neu-
rons in the rectum are only mildly affected and only a
small sample can be obtained.
In most cases therefore, an ante-mortem diagnosis is
made on clinical signs and history. Although no single
clinical sign is truly pathognomonic for the disease and
many clinical signs may overlap with other diseases,
repeated clinical examinations and thorough rectal
examinations can be extremely accurate when consid-
ered in conjunction with the animal's recent history.
Dysphagia in a horse with continuous or intermittent
colic, nasogastric reflux, a firm corrugated colon
impaction, and small intestinal distention is strongly
suggestive of acute or subacute grass sickness. Rapid
weight loss with the development of a marked 'tucked

up' appearance in a horse with dysphagia and rhinitis is
highly suggestive of the chronic form. Other signs that
will aid in the diagnosis include patchy sweating, muscle
tremors, salivation, and ptosis.
Because surgical colics are the major differential
diagnoses with respect to acute and subacute grass sick-
ness, careful consideration of the entire clinical presen-
tation is extremely important. Table 17.13 highlights
some of the most significant findings which may aid in
the differentiation between surgical colics and acute or
subacute grass sickness cases. It should be noted how-
ever that these differences do not necessarily apply to
all colic cases requiring surgical intervention.
Other ancillary diagnostic techniques which may aid
in the diagnosis of grass sickness include esophageal
endoscopy and contrast radiography. Endoscopic
examination of the distal esophagus of acute and occa-
sionally subacute cases may reveal longitudinal linear
ulceration of the mucosa and intermittent retrograde
flow of gastric fluid. Abnormal esophageal motility has
also been demonstrated by the use of radiographs and
image intensification following barium swallow. In
these cases a large reservoir of contrast material is seen
to pool in the distal esophagus.
Depression/somnolence more apparent than signs of
abdominal pain
Presence of gastric and small intestinal distension in
the absence of pain or in the presence of!11iJJJ.
/intermittent pain
High pulse rate in the absence of pain or in the
presence of mildliatermittent pain
Grossly normal peritoneal fluid
TREATMENT
Any attempts to treat acute and subacute cases have
failed and these cases should be euthanased following
diagnosis. Consequently only chronic cases should be
considered for treatment. In some apparently mild, sub-
acute cases it may be necessary to observe the animal for
up to 7 days in order to establish whether it will develop
into a chronic form. If the animal is completely dys-
phagic, refluxing gastric fluid, and/or showing signs of
severe colic, euthanasia is required before this observa-
tion period is complete. Table 17.14 summarizes the
OTHER CONDITIONS 17
S2.t:lle. ability to swallow
A ~ of intestinal motility
None or only mild/intermittent colic
S2.t:lle. appetite present
Pulserate < 60 bpm
suggested criteria for the selection of treatment candi-
dates with the chronic form of grass sickness. It is the
opinion of the author that by far the most significant
criteria necessitating euthanasia in chronic cases are
severe dysphagia and total inappetance.
General management
Nursing provides the mainstay of the treatment, and
the recovery rate for chronic cases has improved dra-
matically with the instigation of a good management
regimen as detailed below. Housing is advisable in the
early stages of the disease. The use of palatable high
energy, high protein feed is indicated, however the
animal's individual preference will often dictate the
food consumed. This preference will often change
from day to day and even from feed to feed. The fre-
quent provision of feed is indicated with a recommen-
dation of 4-5 feeds per day. Preferred feeds include
molasses-containing feeds, crushed oats, and high
energy cubes. Soaking these feeds may facilitate swal-
lowing in some cases, however whether to dampen
the feed or not is again dependent on the individual
animal's preference. The energy content of the feed
may be improved by the addition of up to 500 ml of
corn oil, however this should be done gradually.
Palatability can be improved by adding dilute
molasses or succulents such as cut grass, carrots, or
apples. It should be noted that these items are to
improve palatability only and contain insufficient
energy to form the whole diet. The consumption of
concentrate feed in order to minimize excess weight
loss is vital to the survival of the individual case.
Nasogastric feeding has been attempted in some cases
with extremely limited success and therefore the indi-
cation for such treatment remains questionable. The
importance of nursing, frequent human contact, fre-
quent grooming, and regular walking out and hand
grazing cannot be overemphasized. Occasionally it
may be necessary to hand feed some cases when
appetite is especially poor. In many cases despite a
moderate degree of food intake, the body weight will
continue to decrease quite dramatically during the
347
17 COLIC

firSI 2-4 wt:cks. The prognosis however is con.�ider.tbl)' OUTCOME

poofer if this decrease in body W('ight continw:s
beyond 6 ....
·
Cek.5 duration. �OSI swviving chronic gran sid:.nC5S cases are capable
of rC$uming normal work. Residual abnormalities may
Therapeutic agents however PCT":'iilil in some survivors, including mild dys­
phagia. excessive s�'ealing, long silky coat growth, and
Intestinal motility enhancers
multiple small areas of pil�rection. Although most of
Cisapride is an indirect cholinergic agent which fadli­ the residual proble ms lend to improve with time, they
Iltles acetylcholine release from the myenteric plexus of may fail to rewlve completely.
the gut. Unlike the related compound metoclo­
pramide. cisapride lacks central antidopaminergic
propenies. The use of cisapride (0..5-0.8 mg/kg p.o. PREVENTION
toLd. for 7 days) has been shown to increase gut motility
in chronic case s of grass sickness. Because cisaprirlc may Although no guaranteed mC'lhod� uf prevention 3re

increase colic signs approximately :2 hours after admin­ known, consideration of the associated ri�k factors

istration, it may indirectly interfere with the overall allows certain precaUlions to be taken. This is panictl­
demeanor and appetile of the animal. Any decision larly relevant in high risk areas during March to July.
therefore to adminislcr cisapride should take into These precautions include
account the pOIcntial beneficial versus detrimental • h[)using new arrival$ for a 2-month period. before
effects on the individual clinical signs; i.e. increased turn out
inl('stinal motility versus colic and inappetance. The • avoiding any change in pasture during the high risk
apparent contribution of the severity of each clinical
5eason
sign to the over-ill seventy of lhe di�ase will therefore • avoiding the use of plI.slure where lhe disea...e ha�
delermine whether cisapride lherapy is required. In occurred before
adrlil.ton, chapride i� expensive and is not currenlly • hnusing hon;es may alliO be advisable in high·risk
licensed for \ eterinary usc.
'
areas, if the preceding 7-10 comccutive days have
been cool and dlj'.
Analgesics
A1llhese pr�aution$ are especially rele\'3nt ror 2-8-
Nun·steroidal antl-inflammatory drugs are suitable for year-olds.
analgesia in �.h ronic cast'S as they do nO[ adversely affect
inte�tinal motility. Chronic cast's may have mild, tran­
sienl episodes of colic fonov.ing feeding and fiuni"in
meglumine (0.5-1.1 mg/kg Lv.) or phenylbutazone
Pancreatic diseases
(2.2-4.4 mg/kg) may he administered under such cir­
cumSlance5. T Mair

Appetite stimulants INTRODUCTION

Inappetance is a mOljor ddermining factor in the sur­
\';\,al of many cases of chrunic grASS sickness. It is impor­
tant however. to dt':tcrmine if the lack of food intake is
mainly because of inappctance or dysphagia. Diazepam
has prov..n to be mildly beneficial as an appetite stimu­
lant in a very limited number of chronic cases. The
effective dose varies \\-ilh the individual hut 0.05 mg/kg
;'\'. q. 2 h, or as nccewry, is .. sugge'ilcd litarting
A liimilarcompound, brnlil.olam (2IlR/kg slow i.\'.) has
recently heen use d as lI.n appt'tite stimulant in chronic
grass sickness casC$ with sligh tly more suc cess than
diaupam. BrotilOlam iii not however licensed for use in
ho rses and no co ntrol trials have been conducted 10
assess its full wurth in the treaunenl of chronic grass
sickness (ases.
The pancreas i§ a triangular shaped organ that lies
transversely on the d()r�al wall of the abdomen, the
greater part being to the right of the midline. It has an
averdge weight of ahout 3SO g. It is attached dorsally by
conne<:tive tissue \0 the kidneys and adrenals. the IfdS­
trophrenic ligament, the suspensory ligament of the
spleen, Ihe poslerior vena cava. the portal fissure, and.
point.
Inc gastropancreatic fold. The ventral 5urbce i� adja­
cent 10 the base of Ihe ce..:um and the large colon.
There are tWO ducts
• Ihe larger pan&T8C.(jc dIU' opens inlo the duodenal
cti\'eniculum alongside the bile duct
• Ihe (J(cn.w')pancr(alic duet ends on a papilla in Ihe
duodenum opposile the main pancreatic duct.

348
 OTHER CONDITIONS 17
The pancreas is a compound gland that has impor- • chronic weight loss despite good or increased
tant exocrine and endocrine functions. Digestion in the appetite
small intestine is partly dependent on pancreatic secre- • depression
tions, but also on biliary secretions and mucosal enzymes. • inappetence
The volume ofpancreatic fluid secreted by a 100 kg pony • intermittent colic
is approximately 10-12 IIday. Secretion is under both • persistent or recurrent pyrexia
neural and hormonal control. Pancreatic juice contains • jaundice.
bicarbonate ions, amylase, lipase, and peptidases.
If there is concurrent insulin-dependent diabetes
The islets of Langerhans account for only about 2
mellitus, polyuria and polydipsia may also be observed.
per cent of the total weight of the pancreas. Two major
Clinical pathological abnormalities are inconsistent,
cell types are present in the islet tissue
but may include
• a cells secrete gastrin and glucagon
• raised serum amylase
• ~ cells are the source of insulin.
• raised serum lipase
The rate of insulin secretion is highly dependent on • raised peritoneal fluid amylase
blood glucose concentration. The major effect of • increased fractional excretion of amylase
insulin is to increase the utilization of glucose by most • hypocalcemia
body tissues. This is achieved by increasing the trans- • hyperglycemia
portation of glucose across the cell membrane. • glucosuria
• hypertriglyceridemia
• raised serum gamma glutamyl transferase
DIABETES MELLITUS • hyperbilirubinemia.
Reference values for amylase and lipase acnvines
Five separate forms of diabetes mellitus are recognized
should be established by each laboratory. Serum amy-
I. insulin-dependent diabetes mellitus lase activity for normal horses usually ranges from
2. non-insulin-dependent diabetes mellitus 14-35 IU /1, and values less than 50 IU /1 are generally
3. secondary diabetes mellitus considered to be normal. Peritoneal fluid amylase activ-
4. gestational diabetes mellitus ity is usually slightly lower than serum activity. Serum
5. impaired glucose tolerance. lipase activity is normally less than 87 IU/I (Table
17.15). The fractional secretion of amylase (FEarn) is
Diabetes mellitus is rare in horses; it is most com-
calculated by the following formula
monly associated with insulin resistance induced by
pituitary adenomas. Only insulin-dependent diabetes urine amylase serum creatinine
mellitus will be considered further here. X X 100 = FEarn
serum amylase urine creatinine

FEarn in normal horses is less than 1 per cent.

CHRONIC PANCREATIC DISEASE AND Interpretation of pancreatic enzyme activity in
INSULIN-DEPENDENT DIABETES horses can be difficult because the enzymes are not
MELLITUS exclusively of pancreatic origin, and may be released
from other tissues such as the gastrointestinal tract. In
Pancreatic exocrine insufficiencies are common causes
addition, renal disease may result in decreased excre-
of maldigestion in other species but they appear to be
rarely diagnosed in the horse. Insulin-dependent dia-
betes mellitus is very rare. However, adult horses and
ponies may develop signs of exocrine pancreatic insuffi-
ciency, with or without associated insulin-dependent
diabetes mellitus, following destruction of the pancreas
by diseases such as neoplasia (pancreatic adenocarci-
noma) and chronic pancreatic necrosis. Chronic
eosinophilic pancreatitis has been reported and is Serum Peritoneal flUid
assumed to be caused by parasite (Strongylus equinus and
S. edentatus) migration through the gland. The clinical
Amylase (lUll) 14-35 0-14
Lipase (lUll) 23-87 0-36
signs associated with chronic pancreatic disease may Glucose (mmolll) 4.0-5.6 4.9-6.4
include

349
17 COLIC
tion of amylase thus leading to elevated serum levels. In
the diagnosis of acute pancreatitis (see below) sec-
ondary damage to the pancreas from hypovolemia or
reflux of duodenal contents up the pancreatic duct can
result in release of pancreatic enzymes into the circula-
tion.
The diagnosis of insulin-dependent diabetes melli-
tus can be confirmed by performing either an oral glu-
cose tolerance test (see Chapter 2) or intravenous
glucose tolerance test. The intravenous glucose toler-
ance test is performed by administering intravenous
glucose (0.5 g/kg) as a bolus (e.g. 40 or 50%), and col-
lecting samples at times 0, 15, 30, 45, 60, 120, 180 and
240 minutes for glucose and insulin estimations.
Insulin-dependent diabetics will have high plasma glu-
cose concentrations, which fail to decrease as fast as
normal, with little increase in insulin levels.
Confirmation of chronic pancreatitis or pancreatic car-
cinoma is generally made either at exploratory laparo-
tomy or at post-mortem examination.
Owing to the difficulties in diagnosing chronic pan-
creatic disease in the horse, treatments have rarely
been attempted. Once the horse has developed
insulin-dependent diabetes mellitus due to destruction
of the islets of Langerhans, the only effective treatment
is the exogenous administration of insulin. The insulin
dosage should be assessed by monitoring the response
to small doses administered initially, and then gradu-
ally adjusting the dosage. In one report of diabetes
mellitus associated with pancreatitis in a pony, prota-
mine zinc insulin (0.5-1.0 IV/kg) was found to be
more effective in decreasing the hyperglycemia than
regular insulin.
HYPERINSULINEMIA
Hyperinsulinemia secondary to increased release of
insulin by a pancreatic tumor has been reported in a 12-
year-old pony. Hyperinsulinemia induces hypoglycemia,
which can also be seen following fraudulent or thera-
peutic injections ofinsulin. Clinical signs depend on the
degree of hypoglycemia, but may include
• trembling
• ataxia
• tachycardia
• tachypnea
• mydriasis
• nystagmus
• sweating
• unawareness of surroundings
• recumbency
• seizures
350
• coma
• death.
Signs may wax and wane depending on the animal's
diet.
ACUTE PANCREATITIS
Acute pancreatitis is a rare cause of severe abdominal
pain in horses. The cause is uncertain and ante-mortem
diagnosis is rarely made because the clinical signs
mimic other gastrointestinal diseases producing acute
colic (especially small intestinal strangulating obstruc-
tions and anterior enteritis). The pancreas is not easily
visualized during routine surgical exploration of the
abdomen, and may be overlooked at necropsy, espe-
cially if gastric rupture has occurred.
Acute pancreatitis can occur in association with ade-
novirus infection in Arabian foals affected by combined
immunodeficiency syndrome (CID). Infection of the
pancreatic duct by Cryptosporidium spp. may also occur
in foals affected by cm (see Chapter 26). Pancreatitis is
also sometimes found in association with hyperlipemia
(see Chapter 19). It has been speculated that excess
lipid is deposited in and around the pancreas in hyper-
lipemia. This lipid is subsequently hydrolyzed by pan-
creatic lipase and released as free fatty acids. Free
(unbound to albumin) fatty acids are cytotoxic and
when the albumin-binding capacity is exceeded then
pancreatic vascular injury occurs resulting in necrotiz-
ing pancreatitis.
The clinical signs of acute pancreatitis in adult
horses include
• severe abdominal pain
• hypovolemic shock
• tachycardia
• tachypnea
• pronged capillary refill time
• sweating
• cold extremities
• gastric distention and voluminous nasogastric
reflux.
Specific diagnostic features are not evident from the
clinical signs or clinical pathology findings. Abdominal
sounds are variable but are often reduced or absent. No
specific abnormalities are detected by rectal examina-
tion. Peritoneal fluid may be serosanguinous or frankly
hemorrhagic.
Most affected horses die within 24 hours. No spe-
cific therapy apart from symptomatic treatment for
abdominal pain and hypovolemic shock has been
described.

Causes of colic associated
with reproduction and the
reproductive tract in the
brood mare
eM Schweizer
GENERAL CONSIDERATIONS FOR
MARES DEMONSTRATING SIGNS OF
COLIC
Colic in the brood mare, as in any other equine patient,
represents both diagnostic and treatment challenges.
In addition to the more commonly encountered gas-
trointestinal compromises that result in abdominal
pain, the female equine is also susceptible to abdominal
pain that is either the direct result of a reproductive
abnormality or is secondary to a reproductive event that
has resulted in a compromise to the normal function of
another body system. Likewise certain conditions are
more likely, or they may only occur, in certain repro-
ductive classes of mares (i.e. open, pregnant, foaling,
and early postpartum). It is the responsibility of the
practitioner to accurately differentiate and identify the
source of the problem(s) and to take steps to correct
the situation.
In the event that the mare is pregnant, the practi-
tioner is faced with not one, but potentially two patients
simultaneously. The best course of treatment for one
may be in direct conflict with what is optimal for the
other. The potential value to the owner of the mare rel-
ative to the foal, and the chances of survival for each in
the given situation demands careful consideration by
the practitioner and a prioritization of treatment
options. In ideal circumstances both the mare and the
unborn foal can be saved. The goals of treating a colicky
pregnant mare therefore are
• to identify and correct whatever abnormality is
present as soon as possible
• to support placental function as needed to maintain
fetal viability throughout the insult to the mare and
throughout the remaining length of gestation.
The aim for the foal is to maintain an optimal envi-
ronment within the mare's womb for as long as possi-
ble, allowing the foal to mature and to be born with a
reasonable chance of survival outside the womb.
In general, where surgery is needed in the pregnant
mare, anesthesia of the dam presents little danger to
the unborn foal provided the anesthetic experience is
uncomplicated. Late gestation mares, however, repre-
OTHER CONDITIONS 17
sent more of a challenge. It has been reported that
approximately 18 per cent of all pregnant mares requir-
ing colic surgery abort their pregnancies postopera-
tively. Care must be taken therefore to quickly identify
the need for surgery and to proceed without delay
before the dam's condition can deteriorate further.
Throughout the surgery it is vital to make sure that arte-
rial oxygenation (> 80-100 mmHg) and blood pressure
are kept optimal for the duration of the anesthetic so
that adequate placental perfusion and exchange is
maintained. Beyond surgery a rapid full recovery by the
dam is optimal for both patients. Continued or
repeated stress to the mare may be detrimental to the
pregnancy. A great potential danger to the mainte-
nance of the unborn foal is the development of endo-
toxemia in the mare.
It is believed that endotoxemia in the pregnant mare
results in the release of prostaglandins, and may also
alter uteroplacental blood flow. Prostaglandins have
the potential effect of inducing abortion in pregnant
mares of less than 150 days gestation by causing luteoly-
sis of both the primary (ovulatory) corpus luteum and
secondary corpora lutea and therefore termination of
ovarian progesterone production when the pregnancy
is still dependent on an ovarian source of progesterone
for maintenance. In mares of more than 150 days gesta-
tion pregnancy maintenance is dependent on progesto-
gen production by the placenta and so is unaffected by
a loss of ovarian progesterone, however clinical evi-
dence suggests that chronic exposure of the gravid
uterus, at this point, to high levels of prostaglandins (as
is the case during endotoxemia) may perhaps be
responsible for inducing uterine contractions resulting
in abortion. Administration of intravenous fluid sup-
port and flunixin meglumine are beneficial in treating
the effects of endotoxemia, and in both instances (i.e.
gestation < 150 days and gestation >150 days) the timely
administration of supplemental progesterone has been
shown to prevent pregnancy loss in endotoxic mares.
At present there are only two available types of prog-
esterone supplementation proven to be effective in
achieving adequate blood levels of progesterone to
maintain pregnancy. They are
• injectable progesterone in oil (150-300 mg i.m,
s.i.d, in an average 450 kg (1000 Ib) mare)
• altrenogest (22-44 mg p.o. s.i.d. in an average
450 kg (1000 Ib) mare).
It is the author's preference to initiate supplemental
progesterone therapy to a pregnant mare as soon as
possible after the onset of severe colic or repeated colic
episodes that are occurring over a short span of time in
the event that endotoxemia is just around the corner.
The thought is also to give the pregnancy some addi-
351
17 COLIC

tional support during a time of severe or chronic stress monly known as mittelschmerz. In the author's experi-
in general. Again, it is the author's preference to initi- ence sensitive mares of this type will demonstrate inap-
ate progesterone therapy in a time of crisis using the petance and acute mild to moderate colic signs similar
injectable progesterone (loading dose of 300 mg i.m.). to those demonstrated by horses with acute, short-lived
Follow-up daily oral supplementation may be used in 'gas colic'. These mares typically respond well to a 250
those cases where there has not been severe intestinal mg i.v, dose of flunixin meglumine to control their dis-
damage that may interfere with absorption and/or comfort and laxatives (e.g. mineral oil) to lessen the
where the mare is not refluxing. Otherwise daily injec- possible discomfort associated with passage of feces
tions continue until either the mare can begin to take through the pelvic area and defecation at this time.
oral supplementation or the need for supplementation Usually the signs resolve immediately with medication
has ended. or within a few hours ifleft unmedicated. It is important
Once begun, therapy should be continued at least before this diagnosis is made to rule out any other pos-
until the mare has fully recovered and has returned to a sible cause of the abdominal pain, to ascertain that the
stress-free environment, and physiologically the mare is mare is indeed in estrus with a large follicle or recent
able to maintain the pregnancy on her own. In mares ovulation present on one or both ovaries at the time,
where the insult has occurred during the first 120 days and that the affected ovary is demonstrably painful to
of gestation the release of prostaglandins has likely palpation. Further credibility
resulted in the termination of ovarian progesterone
production, and therefore exogenous progesterone
supplementation must be provided until the placenta is
capable of maintaining the pregnancy on its own (i.e. at
> 150 days). If there is pressure to discontinue proges-
terone supplementation sooner in these early gesta-
tional mares, it is important to ascertain whether there
is enough remaining ovarian progesterone production
to support the pregnancy (i.e. blood progesterone lev-
e1s> 2 ng/ml and preferably> 5ng/ml) before therapy
is discontinued. If the mare is being supplemented with
injectable progesterone this will not be possible as the
progesterone assays will register an amount reflective of
both the exogenous and endogenous levels. If the mare
is being supplemented with the oral altrenogest then
measurement of blood levels of progesterone will only
reflect endogenous production. In mares where the
insult has occurred after the pregnancy is no longer
dependent on an ovarian source of progesterone (i.e.
>150 days) it should be safe to begin to discontinue the
progesterone supplementation as soon as the insult and
stress during recovery have ended. In both instances it
is the author's preference to 'wean' the mares off sup-
plementation gradually over 10-14 days, rather then
terminating progesterone supplementation abruptly.

REPRODUCTIVE-ASSOCIATED COLIC IN
THE NON-PREGNANT MARE

Colic during estrus

Occasionally the clinician will be presented with a mare
that demonstrates abdominal pain in association with
ovulation during estrus. This is probably similar to the
sensitivity and lower abdominal or back pain that some
women experience coinciding with ovulation, com-

352
 OTHER CONDITIONS 17
disposition by keeping the mare out of ovulatory estrus injury in general includes sexual rest (30-60 days),
with the use of altrenogest as described above. broad spectrum antibiotics, and a Caslick procedure to
prevent further peritoneal contamination via possible
Ovarian tumors pneumovagina. The rent in the vagina is usually small
and dorsal to the cervix and is left to heal on its own
Occasionally the presence of a large ovarian tumor
much as a colpotomy site would be. The mare should be
(most commonly a granulosa-theca cell tumor) may
prevented from lying down for the first several days fol-
result in the presentation of a mare with the primary
lowing the injury so as to further lessen the likelihood
complaint of intermittent colic especially associated
of secondary herniation of viscera. If the rent is in the
with exercise, with or without the more common com-
vaginal floor or if it is excessively large however, an
plaint of behavioral abnormalities. In the author's expe-
attempt to suture and close the deficit should be made.
rience, this history has accompanied the presentation
It is important to remember that the mare may have
of young race fillies or mares who have been referred
conceived as a result of the breeding so routine follow
for intermittent colic, reluctance to train, and/or poor
up rectal ultrasound examinations of the reproductive
performance who upon examination have been discov-
tract in order to check for pregnancy should be per-
ered to have an abnormally enlarged ovary. It is likely
formed 14-18 days post-ovulation.
that the pain associated with the enlarged ovary is the
result of the stretch on the broad ligaments as the
tumor bounces up and down with the mare's move-
ments. Treatment is surgical removal of the affected COLIC IN THE PREGNANT MARE
ovary.
Many pregnant mares show signs of abdominal pain at
Vaginal injuries during service one point or another during the course of their gesta-
tion. These episodes are typically very brief and mild. A
Colic signs may also occur secondary to natural service
mare may suddenly flank watch or kick at her belly for a
of an open, estrus mare. In situations where a stallion's
few moments and become agitated, or perhaps she may
penis is long relative to the mare's vagina, the stallion is
become quiet, inappetent, and even lay down for a little
forceful and vigorous during intromission and thrust-
while. No doubt some of these signs of discomfort may
ing, and/or the mare is restrained so she is unable to
be attributed to uncomfortable, vigorous movements of
move forward to protect herself from internal abuse,
the foal, mild stretching of the broad ligaments upon
during copulation the mare's vagina may be bruised
the movement of the mare or the foal, or mild digestive
and even torn to the degree where the stallion's penis
upsets. In most instances these signs resolve sponta-
penetrates into the peritoneal cavity through the cra-
neously on their own with little or no need for treat-
nial vaginal wall. Such injuries may be suspected any
ment. It is also worth mentioning that many
time there is fresh blood on the stallion's penis or com-
inexperienced owners may become alarmed upon find-
ing through the vulva of the mare immediately follow-
ing a late gestation mare who is lying down and groan-
ing dismount, and these findings warrant an immediate
ing and mistake it for a colic episode when in fact all she
manual vaginal examination of the mare to ascertain
is doing is trying to rest. The ever increasing size of the
the degree of injury. Immediate sexual rest of the mare
gravid uterus in these late-term mares presses the
is indicated to prevent further damage, as many times a
abdominal viscera up hard against the mare's
full vaginal rupture during copulation is preceded by a
diaphragm when she lies down making breathing diffi-
vaginal contusion that occurred during a previous cover
cult and causing her to groan. Upon rising these mares,
during the same cycle. This kind of injury may be pre-
however, are comfortable and go about their business
vented via AI breeding or by the judicious use of a
which usually entails looking for something to eat.
breeding roll where live cover breeding is mandated by
Fortunately the sort of episodes described above form
a breed registry and is unavoidable. Colic signs may be
the majority of colic cases reported in pregnant mares,
mild to severe immediately following the cover and are
however more serious conditions can and do occur.
sometimes accompanied by tenesmus, or the signs may
develop gradually over the next few days following the
Feed impactions
traumatic cover. A potentially severe peritonitis may
form after gross contamination of the peritoneal cavity Individual mares seem to be prone to developing feed
via direct contact with the stallion's penis, his ejaculate, impactions within their large colon and/or cecum as
or vaginal flora. Acute and severe colic signs may also pregnancy advances. The exact mechanism behind how
develop if a portion of the mare's viscera becomes this occurs is unknown, but in all likelihood the increas-
entrapped through the vaginal rent. Treatment for this ing size of the gravid uterus adversely effects bowel

353
17 COLIC
motility in these mares leading to an increase in the
transit time of the ingesta through the large colon. This
in turn leads to increased water resorption from the
slow-moving feed materials resulting in an impaction.
These mares usually present initially as low grade colic
with decreased manure production and mildly elevated
heart rates, but the longer standing the impaction the
more her clinical signs may deteriorate as gas builds up
behind the impaction. Direct palpation of the
impaction per rectum is often difficult due to the pres-
ence of the enlarged uterus and fetus which fill the cau-
dal abdomen obscuring the viscera. Treatment includes
aggressive overhydration with intravenous and or oral
fluids, and oral laxatives or mild cathartics such as (min-
eral oil, dioctyl sodium sulfosuccinate (DSS), and low
dose magnesium sulfate) to try to soften, lubricate, and
shift the mass of impacted ingesta. It is also important to
judiciously control the mare's pain with an analgesic
such as flunixin meglumine as needed to prevent her
from rolling, during the course of which she may inad-
vertently cause a torsion of her colon or gravid uterus.
Hand walking may also help to take her mind off her
discomfort, and help stimulate her gastrointestinal
tract, but be careful that an overzealous owner does not
exhaust the mare in their attempt to do something
helpful. Feed should be limited as much as possible
throughout the episode so as not to compound the sit-
uation, but in long-standing impactions the mare
should be supported parenterally as complete anorexia
may compromise the pregnancy. As in all things pre-
vention is the best route and care should be taken to
ensure that all pregnant mares have access to and are
consuming plenty of fresh, clean water and have plenty
of opportunity to move about freely. Laxative feeds
(grass and mashes) should be incorporated into the
mares' diets whenever possible. Individuals who have
demonstrated a tendency toward impactions in the past
may be preemptively administered mineral oil: either in
their feed on a regular basis if they will eat it or via naso-
gastric tube at the first sign of decreased or dry manure
production if they are not too stressed by the proce-
dure.
Dorsoretroflexion of the uterus
Cases of colic caused by dorsoretroflexion of the uterus
in gravid mares are extremely rare in the author's clini-
cal experience, but have been reported to occur.
Affected mares typically present sometime between 7.5
and 11 months of gestation with acute, moderate to
severe colic signs accompanied by abdominal straining,
constipation, and swelling of the vulva and perineal
region. Administration of analgesics is typically ineffec-
tive in controlling the mare's pain. Diagnosis of this
354
condition is made upon finding a tense uterus within
the pelvis with the fetal head and limbs in a normal
birth presentation overlying and obscuring palpation of
the mare's cervix. (It is important to differentiate the
presence of a tense uterine wall in this painful condi-
tion from the occasional incidental rectal finding in
late-gestation mares of a foal that is overlying the mare's
cervix dorsally but which is encased in a relaxed uterus
and causing no discomfort to the mare.) Vaginal exam-
ination is performed following the rectal examination
to differentiate between a mare with a dorsoretroflexed
uterus and a mare who is actively aborting. In the for-
mer case the cervix will be found to be closed in the cra-
nial extent of the vaginal canal and ventral to the fetus
which is palpable dorsal to the vagina through the vagi-
nal wall. This is in direct comparison to the aborting
mare whose cervix will be dilated and the fetus and its
membranes will be readily palpable within the vaginal
canal through the dilated cervix. Treatment of dor-
soretroflexion includes the administration of uterine
relaxants - 200 mg isoxsuprine i.m.: or 200 Ilg clen-
buterol slow i.v, or i.m, once, or repeatedly over 3-6
hour intervals for 1-2 days (van de Plassche 1987) - and
repelling the now relaxed uterus containing the fetus
back into the abdomen via careful rectal manipulation.
Resolution of colic signs usually occurs within 15 min-
utes of administration of the uterine relaxants, and it
has been reported that restricting the mare's food
intake and regular hand walking helps to return the
mare to normal within a few days. The cause of this
condition is unknown, but once the condition has been
corrected reported relapses are uncommon. Aborting
mares will occasionally exhibit colic signs preceding the
abortion.
Uterine torsion
Included in the differential for any third trimester mare
with signs of colic is uterine torsion. Uterine torsion in
mares has been reported to occur from 180-540
degrees in either direction, and unlike the cow, the site
of the twist is frequently cranial to the cervix within the
uterine body. This condition is rarer in mares than it is
in the bovine. The reason for this seems to be that the
dorsal attachments of the broad ligaments make the
equine uterus less prone to 'flipping over' along its long
axis. As in the bovine, however, the cause of uterine tor-
sion in the mare still seems likely to be the result of
inopportune fetal activity possibly combined with get-
ting up and down or rolling over by the dam. Affected
third trimester mares typically present pre-term with
signs of persistent/recurrent mild to moderate colic.
Except in cases where a segment of bowel has become
compromised as a result of the uterine twist, these

mares will typically continue to pass feces. The severity
of the pain sometimes .�et'Cms to be related to the degree
of torsion, and mares who also have bowel entrapped
along with the twisted uterus may demonstrate severe
pain. (kcasionally affected term mares will present at
parturition with a dystocia that is a result of the t\\lsted
uterine body ocduding normal delivery of the foaL
Diagnosis of uterine torsion is made typically by rec­
tal {�xaminaljon as the t\vist is usually cranial to the
cervix and therefore is not readily palpable per vagina
in the pre-term mare. Rect.al identification of the taut
hands of the stretched broad ligaments is the hallmark
of this condition. The broad ligament from one side of
the uterus is pulled over the top of the uterus past mid­
line toward the side of the direction of the uterine twist.
The other broad ligament is pulled ventrally under­
neath the uterus away Ii-om the side of the twist.
Therefore when viewed from the back of the marc a
countercloek\vise �ist to the marc's left will find the
right broad ligament pulled horiwntally over the top of
the uterus to the left and the left broad ligament will be
pulled ventrally underneath the marc's uterus to the
mare's right. Conversely a clockwise twist of the uterus
to th(" mare's right will find the left broad ligament
pnl!t'Cd horizonta!Iy over the top of the uterus to the
marc's right and the right broad ligament pulled ven­
trallv under the uterus to the mare's left. The practi­
ti(mer can often make an educated guess as to the
degree of the torsion based on the palpable tightness of
the broad ligament bands and the twist in the uterus
itself. Likewise an impression of the dt'Cgree of possible
uterine compromise may h� made based upon the feel
of the uterine wall (Le. either thick and taut or sti!!
somewhat pliable) and/or its appearance on rectal
ultrasound. Occasionally the small colon becomes con­
stricted as a result of the uterine twist and may obstruct
the examiner's ability to perform a filll rectal examina­
tion to determine the extent of the insult.
The fNllS will typically be displaced cranially in the
alx:!omen by the twist. in th� Illerine body and may be
out of reach of the practitioner per rectum. In this
instance, fetal viability may not be determinable via rec­
tal examination and instead may be determined by
detection of fetal cardiac motion or spontaneous fetal
movement via transabdominal ultrasound of the mare.
Depending on the degree of the twist and the duration
of the insult, the blood supply to the uterus may
become sufficiently compromised to (;ame fetal death.
The uterus likewise may become edematous and friable
and in some extreme cases even necrotic, and the risk
of uterine rupture and peritonitis becomes a real possi­
hilit\', It is therefore important to hoth the foal's and
'
the mare g continued well being that the presence of a
lltt'Crin(" torsion he r<tpidly identified after it occurs and
OTHER CONDITIONS 17
immediate steps taken to correct the torsion and return
the uterus to its normal position <tnd configuration.
Options for correcting the uterine torsion include
• rolling the mare
• standing flank surgery
• ventral midline celiotomy, and
• in the case of foaling mares who have an open
cen1x and a less than 270 degree t\vist (so that the
clinician, per vagina, can get an arm through the
t"'1St and alongsidt'C the foal) manual rotation of the
foal (and uterus) through th(" c("n1x to a normal
position may be possible.
Vl11en the marc is tractable and there are no indica­
tiollS that the twisted uterus has alrt'Cady ruptured, it is
the preference of this author and many others to correCt
the uterine torsion in a pre-term mare via a standing
flank laparotomy. An incision is made through the
mare's flank using a grid approach, and the incision is
preferably made on the side that the marc's uterus is
twisted to. The direction of the twist is (:onfirmed via
intra-abdominal palpation of the uterus and the broad
ligaments, and then the uterus is dctorsed by carefully
reaching underneath the uterus and gently rocking the
uterus to gd up enough momentum to lift the twisted
uterus up and pushing it over in the opposite direction
of the twist to return it to its normal position. If needed
the foal's limbs may somt'Ctimes be grasped through the
uterine wall to help the surgeon facilitate this maneuver,
but at all times care should be taken not to cause any
tears in the uterine wall. This may be especially chal­
lenging if the uterus has become friable. If the preg­
nancy is advanced enough it may require that a second
incision be made in the opposite flank and two surgeons
work simultaneously (one pushing and the other
pulling) to untv.,;ist the uterus and return it to its normal
position. Afkr the torsion has been corrected the sur­
geon then carefully palpates the dorsal smface of the
uterus and broad ligaments to confirm that the uterus is
no longer twisted. The surface of the uterus is also care­
htlly palpated for the presence of any tears (especially
where it was twisted) and an assessment of fetal viability
is made by trying to detect spontaneous fetal movement
or the presence of a heart beat in the foal's chest pal­
pated careh!!ly through the uterine wall. If the foal is
dead, once the torsion has been corrected the mare
should go on to abort naturally postoperatively, or deliv­
ery can he induced. The delivery of the dead fetus
should be supervised so any malpositiol1s may be quickly
corrected, and to assist the mare and minimize her
abdominal effort to rt'duce stu�ss on the surgical inci­
sion. If the foal is alive and has not heen compromised
too severely the pregnancy usually progresses unevent­
fully and successfully to term after surgical correction.
355
17 COLIC
Rather than surgery some pracuuoners prefer to
correct the less severely twisted and compromised uter-
ine torsions by administering general anesthesia to the
mare and rolling her to untwist the uterus. Two meth-
ods have been described. In both methods the mare is
placed in lateral recumbency on the same side that the
uterus is twisted to (i.e, if the mare's uterus is twisted to
her left side she is placed with her left side down). The
mare is then rolled from one side, up into a dorsal posi-
tion, and then over onto her opposite side and then up
into a sternal position. In the first method this maneu-
ver is done quickly so that the weight and inertia of the
heavily gravid uterus will hold the uterus still while the
mare is quickly rolled around it. In the second method,
a plank is positioned on the mare's flank and weighted
down by a person sitting or standing on it, the mare is
then slowly rolled over as described above. The
weighted plank is used to hold the gravid uterus still as
the mare is rolled carefully around it, effectively untwist-
ing the uterus. Care must be taken to identity the direc-
tion of the uterine twist correctly in the first place so
that the mare is positioned on the proper side, other-
wise these maneuvers may tighten the twist further if
the mare is rolled in the wrong direction. Once the
maneuver has been completed the mare is re-examined
rectally to ascertain whether the uterus has been
untwisted. If the uterus is still torsed additional rolling
attempts may be made. If the torsion is judged to have
been corrected then the mare is permitted to wake up
and care is taken to ensure she gets to her feet without
rolling around during recovery and possibly retorsing
her uterus. The 'plank in the flank' technique in the
author's experience is particularly successful in correct-
ing uncomplicated bovine uterine torsions, but the
same degree of success is not typical in the mare. This
may be a result of the fact that the mare's flank is much
shorter and more tightly muscled than a cow's thereby
making it more difficult to effectively place the plank to
hold the mare's gravid uterus in place while she is
rolled. It has also been the reported experience of some
practitioners that use of these rolling techniques results
in a higher risk of complications after successful correc-
tion of the twist. For these reasons therefore it is not the
author's first choice for attempting to correct uterine
torsion in a mare.
In the foaling mare, it may be possible to correct a
uterine torsion per vagina provided the twist is less than
270 degrees and the cervix is dilated enough to permit
the clinician to reach the foal and place his or her arm
ventrolaterally along the foal's body. The foal is then
grasped and manipulated so as to rock it side to side
progressively in the opposite direction of the twist until
enough momentum is achieved to flip the foal up and
over taking the uterus with it to resolve the twist. Once
356
the twist has been fully corrected and the foal posi-
tioned as needed to achieve a normal presentation then
the foal may be delivered. This maneuver requires some
finesse and upper body strength to accomplish, but can
be quite successful. The use of an epidural to control
straining, and positioning the mare in a standing posi-
tion with the hind end slightly elevated to provide the
maximum room to maneuver within her will also maxi-
mize the chances for success. (The abdominal viscera as
well as the foal will be pushed backwards into the pelvis
when the mare is recumbent, effectively decreasing the
available space in which to work.) The use of a detor-
sion rod in an awake mare is not recommended. It
should also be remembered that it is contraindicated to
anesthetize a dystocia mare to facilitate correction with-
out being able to elevate or hoist her hind end up at the
same time to provide room to work inside her.
A ventral midline celiotomy is indicated to correct
uterine torsion in the mare in those cases where the
uterus is already believed to be severely compromised,
or where the gastrointestinal tract has become entan-
gled in and compromised by the torsed uterus. This
approach permits better access to the abdominal viscera
and uterus which can then be more fully examined and
repaired than could be accomplished with a flank
surgery. In the case of very late pre-term mares it may
also permit easier manipulation to effect the untwisting
of the large, gravid uterus. This approach is also indi-
cated when other correction techniques have failed,
and there is the advantage that a c-section can also be
performed during the course of the procedure to facili-
tate delivery of the foal if needed. The risk of incisional
complications following this procedure in a heavily
gravid and subsequently foaling mare must be recog-
nized, and therefore this technique should be reserved
for those situations where it is absolutely indicated.
Potential complications that may follow resolution
of the uterine torsion using any of these described tech-
niques include
• tearing of the uterus and resultant peritonitis in the
mare
• premature placental separation and subsequent
death and abortion of the foal.
Prognosis for the mare in general is good provided
there has been no severe uterine damage or peritonitis.
Prognosis for the live foal is also good provided the
degree or duration of the torsion has not been severe
and is expediently corrected.
Other conditions during pregnancy
Other pregnancy related conditions that may cause
signs of abdominal pain in a pregnant mare include

pending prepubic tendon or other abdominal wall rup-
tures and imminent uterine rupture. Rupture of the
prepubic tendon or other abdominal wall musculature
is most commonly seen secondary to trauma or to the
stress of the weight of excessive ventral edema or an
abnormal pregnancy (hydrops or twins). The pain
demonstrated by the affected mare is a direct result of
the tearing of the abdominal support structures and/or
the possible herniation and strangulation of bowel
through the rents. Uterine rupture may also occur sec-
ondary to trauma or to a uterine torsion, placental
hydrops, or twin pregnancy. In the event of uterine rup-
ture the mare typically shows signs of colic just prior to
the rupture itself. Once the uterus ruptures there is typ-
ically an immediate respite in the colic signs because
the tension is relieved. The mare's signs however will go
on to deteriorate as secondary hemorrhage occurs
and/or peritonitis develops. In both scenarios, signs of
colic may not be the classic sign of the disorder but may
well be what the owner recognizes and reports. In each
presented case of colic the clinician is therefore
reminded to be as thorough as possible during the
examination and work up of a pregnant mare in order
to correctly identify the source of the pain.
COLIC IN THE PARTURIENT MARE
In the normal course of foaling, stage III labor (passage
of the placenta) normally causes some degree of dis-
comfort and pain to the mare. The signs associated with
the uterine contractions that are normally occurring at
this time range from mild discomfort (occasional kick-
ing at belly, stretching out and posturing as if to urinate,
laying down quietly in a sternal position, and flank
watching) to semi-dramatic bouts of pain (agitation, fre-
quently getting up and down, rolling, etc.). The major-
ity of mares seem to pass their placentas within 30-60
minutes of the foal's delivery (> 3 hours = retained). It
is not unusual for signs of discomfort to persist (usually
for no more than an additional hour) after passage of
the placenta, since uterine contractions continue as the
mare begins to involute and oxytocin release is stimu-
lated by the foal's initial nursing. More extreme demon-
strations of discomfort associated with these 'after
cramps' seems to occur more frequently in maiden
mares than in experienced multiparous mares. If the
mare is distracted enough by this pain that she is negli-
gent of her foal she may be successfully managed with a
single administration of low dose flunixin meglumine
(0.5 mg/kg i.v. is usually adequate) and hand walking
(if needed) to provide her with relief and distraction
from her discomfort. Typically throughout these
episodes a mare's vital signs are stable (± mild elevation
OTHER CONDITIONS 17
in heart and respiratory rates), and the mare recovers
quickly with little or no recurrence past the initial
episode. She remains bright and comfortable, with a
good appetite and interest in her foal and maternal
duties. This is in stark contrast to the parturient mare
whose pain is caused by serious parturition-related
pathologies.
Arterial rupture
Rupture of the middle uterine artery (most commonly),
utero-ovarian artery, or the external ileac artery at or
around the time of foaling is a significant cause of colic
and death in older (> 11 years) foaling mares. Rupture
of the middle uterine artery or utero-ovarian artery may
result in the formation of a large, painful hematoma in
the ipsilateral broad ligament that may dissect below
the serosal uterine surface if the hemorrhage is con-
tained within these structures. Pain results from the
stretching of, and pulling on, these structures as the
hematoma forms. Formation of this clot and the associ-
ated drop in arterial blood pressure due to blood loss
stops active hemorrhage. If the broad ligament or
serosa subsequently rupture and hemorrhage is no
longer contained then the mare will rapidly bleed out
into her abdominal cavity. Rupture of the external ileac
artery, because of its anatomic location, results in the
mare directly and fatally bleeding into her abdomen.
Fatal bleeds are most common in aged mares (> 18
years), and unfortunately the first occurrence of this
disorder is often a fatal one.
Age-related degeneration of the arterial structures
themselves has been theorized as a predisposing cause.
One study (Stowe 1968) has looked at copper levels in
older and affected mares and found that at the time of
foaling copper levels are significantly lower in older
mares than in younger mares, and that levels in affected
mares were lower than those in age-matched unaffected
mares. Copper has been associated with helping to
maintain vessel elasticity, so it is plausible that
decreased levels may predispose a mare to arterial rup-
ture at the time of foaling or during pregnancy when
arterial structures are under increased stress.
During pregnancy the uterine arteries increase in
diameter and tortuosity, and there is increased stress
within these structures due to concurrent increases in
blood flow, stretching of the broad ligaments, and fetal
movements. Parturition places additional stress on
these structures because of increased mean arterial
pressure during the foaling process and direct pressure
on these vessels as the foal is pressed through the pelvic
canal. The right middle uterine artery has been
reported to be the most frequently affected of these sus-
ceptible vessels. One theory as to why this occurs is that
357

fact that volume re-expansion will lead to an increase in
the mare's blood pressure which may renew or worsen
blood loss with disastrous results. The use of crystalloid
fluids to effect volume re-expansion may also dilute
blood coagulation factors and decrease blood viscosity
at a time when both are needed to promote hemostasis.
As a direct result of this therapeutic challenge, there are
two approaches to managing affected mares that survive
the initial stages of the hemorrhage - one conservative,
the other more aggressive. Regardless of the therapeu-
tic course chosen the single most important measure
that must be taken is to keep the mare as quiet as possi-
ble so as to cause no increases in her mean arterial pres-
sure (MAP).
The conservative approach to treatment primarily
involves minimizing stress or excitement of the affected
mare. The mare is kept in a quiet, darkened stall with or
without her foal (depending on which is least stressful
to the mare, and which is safest for a valuable foal).
Transportation of the mare is contraindicated, and
must be balanced against what can be accomplished
therapeutically on the mare's home farm. Tranquilizers
are used judiciously to help keep the mare calm, and, in
the case of acepromazine, to help reduce MAP directly.
Naloxone (8-32 mg/500 kg i.v., Le Blanc 1997) has
been anecdotally reported to be helpful in some mares.
Naloxone treatment promoted death in rabbits with
experimental hemorrhagic shock (Sherman 1998).
Analgesics (butorphanol 0.01-0.04 mg/kg i.m., Vivrette
1997) are also used as needed to control the mare's
pain. Attempts at volume re-expansion with fluids or
whole blood transfusions are indicated to preserve car-
diac output and perfusion but may increase MAP and
disturb any present hemostasis.
The more aggressive therapeutic approach involves
utilizing all of the above treatments as well as the care-
ful application of subtotal volume re-expansion with
crystalloid fluids to support tissue perfusion and whole
blood transfusions or synthetic oxygen-earrying fluids
(oxyglobin) as indicated to support tissue oxygenation.
Extreme care must be taken to keep MAP below normal
levels. It is also important to remember that anemia in
general is well tolerated provided blood volume is main-
tained, and that autotransfusion of about two-thirds of
the red blood cells lost into the abdominal cavity will
occur over time. For this reason whole blood transfu-
sion of affected mares is not advocated by many until
the mare's pev is less than 20 per cent. A further sig-
nificant consideration is that all mares must be carefully
cross matched with donor blood to avoid sensitization to
incompatible blood types and possibly causing neonatal
isoerythrolysis in future foals. In this regard the use of
synthetic oxygen-carrying fluids (oxyglobin 7.5-10
ml/kg, Sprayberry 1999) may have a distinct advantage
OTHER CONDITIONS 17
over whole blood transfusion as they are non-reactive in
terms of blood compatibility, and high volume expan-
sion is not required so support with minimal increases
to MAP is possible. When evaluating each mare for the
possibility of using more aggressive attempts at support
it is important to consider carefully what will be most
beneficial to the eventual outcome - a low hypotensive
state or the utilization of a low level of support for per-
fusion and oxygenation. At the time of this writing,
there are presently no survival comparisons for the two
approaches and the clinician can only use his or her
best judgment.
Additional agents and therapeutic measures have
been used or suggested for treatment of mares with
uterine artery rupture and may be beneficial. These
include simple supportive measures such as nasal oxy-
gen (if tolerated well by the mare) and applying exter-
nal pressure to the mare's abdomen via a belly wrap.
Hemostatic promoting agents such as aminocaproic
acid (10-20 mg/kg slow i.v.), intravenous 10% formalin
(anecdotal), and conjugated estrogens have also been
used. Anti-inflammatory agents (flunixin meglumine
and glucocorticoids) as well as antioxidant drugs (vita-
min E) may give support. Pentoxifylline (7.5 mg/kg
p.o., Britt and Byars 1997) is purported to increase red
blood cell deformability and may increase oxygen deliv-
ery to ischemic tissues, and therefore may be of benefit.
Finally, careful use of broad spectrum antibiotics ('care-
ful use' because affected mares have volume depletion
so some potential toxic effects of antibiotics may be
amplified) may also be indicated to protect against
infections that may occur secondary to ischemic dam-
age to the mare's bowel.
As discussed the prognosis for mares with uterine
artery ruptures is guarded. For those that survive the
acute episode, it is imperative that they be kept quiet for
several weeks as the clot resolves and the vessels slowly
repair as increases again in MAP during this period can
cause renewed bleeding. Final resolution of the
hematoma may take months depending on its initial
size. Mares that have survived their first episode ofuter-
ine artery rupture have a high likelihood of recurrence
with subsequent pregnancies and foalings. It is there-
fore recommended that affected mares are not re-bred.
If the mare has no other value than as a producer, and
must be re-bred it is recommended that the hematoma
be fully resolved prior to re-breeding and that the
mare's managers have a nurse mare lined up in case the
dam is lost on the next foaling. Prevention includes
keeping the pregnancy as stress free as possible (avoid
heavy exercise, stressful procedures, long transporta-
tion, etc.), and limiting roughage intake toward the end
of gestation so as to minimize cecal distention at the
time of foaling.
359
17 COLIC
Gastrointestinal complications of parturition
Gastrointestinal complications occur in parturient
mares as both a direct and an indirect result of the foal-
ing process. Portions of bowel may become entrapped
between the mare's pelvis and the gravid uterus during
the course of labor and become damaged. The small
colon is the structure most commonly traumatized in
this manner, resulting in bruising, ischemic compro-
mise from mesenteric tears, and even rupture and
extravasation of fecal material into the peritoneum.
Where small colon bruising has occurred mares experi-
ence compromised function and may present as consti-
pated immediately post-foaling, and by 48 hours
post-foaling they may begin to demonstrate signs of
colic with or without an elevation in temperature. By 72
hours if damage has been severe enough, the compro-
mised bowel may become leaky and peritonitis may
result. Diagnosis is made via rectal examination with the
identification of impacted small colon or a sausage-
shaped mass (the damaged segment) somewhere along
the length of small colon. Abdominocentesis will also
confirm the presence ofleaky, compromised bowel and
peritonitis in extreme cases. Surgical resection of the
damaged bowel may be indicated.
The tremendous increase in abdominal pressure
that occurs during the course of active expulsion of the
foal (stage II labor) may result in the rupture of a full or
gas-dilated viscus. The cecum in particular seems prone
to this kind of trauma with many ruptures occurring
near its base. The immediate effect is a disastrous peri-
tonitis due to contamination of the abdominal cavity
with the cecal contents that ultimately is fatal. Mares
rapidly demonstrate signs of severe shock immediately
post-foaling if there is a ruptured bowel, and diagnosis
can be confirmed via direct palpation of 'gritty' conta-
minated visceral surfaces or abdominocentesis reflect-
ing the gross fecal contamination. Mares experiencing
this kind of injury are doomed, and immediate
euthanasia once the diagnosis has been verified is the
kindest course. Limiting consumption oflarge amounts
of hay in late pregnancy immediately preceding foaling
may help prevent this sort of rupture by decreasing dis-
tention of the bowel with ingesta.
Perineal injuries
Mares who experience perineal damage (Ist, 2nd, and
"3rd degree perineal lacerations, vestibular bruising,
hematomas, excessive vulvar stretching, etc.) at foaling,
or who are especially sensitive to the pain of the nor-
mally postpartum swollen and inflamed perineal tissues
may experience a reluctance to defecate and secondary
constipation. Anti-inflammatory drugs (phenylbuta-
zone or flunixin meglumine) as well as local treatment
360
with topical anti-inflammatory ointments are indicated
to relieve pain and swelling of tissues. Administration of
oral laxatives (mineral oil) and laxative feeds (bran
mashes, grass, etc.) may help to soften the feces and
make their passage less painful to the mare so that she
is more willing to defecate.
Large colon displacements and tcrslon
For some as yet unknown reason, brood mares are
especially susceptible to large colon displacements and
torsions especially during the first 100 days post-foal-
ing. The combination of the sudden increase in avail-
able abdominal space post-foaling and changes in
exercise and metabolism in the postpartum mare has
been theorized as predisposing the brood mare's
colon, on its long mesentery to wandering from its
normal position. Vital signs and the degree of colic in
an affected mare are reflective of the severity of the
colonic disorder, i.e. a large colon volvulus will pre-
sent as a violently painful colic with a very high heart
rate (60-100 bpm) whereas a simple colonic displace-
ment may present with mild to moderate signs of colic
with a relatively normal heart rate. Diagnosis is once
again made by identification on rectal examination of
an abnormally positioned, gas-distended colon, and in
cases of torsion with bowel compromise analysis of
abdominal fluid will be reflective. Surgical correction
is required.
Uterine rupture
Rupture of the uterus at or near foaling can cause peri-
tonitis and/or abdominal pain. Diagnosis is made by
rectal and ultrasound examination in addition to
abdominocentesis and ventral midline celiotomy when
needed for both diagnosis and repair. If the tear is small
and dorsal postpartum, conservative treatment with
antimicrobials, crystalloids, colloids, peritoneal
drainage, and NSAIDs may be successful. There should
be no infusions made into a torn uterus. If there is gross
peritoneal contamination the prognosis is poor.
Inversion of the uterine horn
Lastly, though rare in horses, inversion of a uterine
horn post-foaling frequently results in acute pain within
the first few hours of foaling that is unresponsive to low-
dose analgesics. Pain is the result of the ovary and tip of
one horn becoming inverted and entrapped within the
uterine lumen. The myometrium proceeds to spasm
resulting in an intussuscepted ring. In response many
mares will begin to strain and the condition may
progress to a complete prolapse of the uterus through
the vulvar lips if left uncorrected. In the author's expe-

rience, invagination of a uterine horn has most com-
monly occurred in conjunction with a retained pla-
cen tao It may be caused by
• the weight of the placenta pulling on the horn in
which it is retained
• sudden pulling during attempts at manual removal
of the placenta
• sudden pulling if the mare steps on portions of
expelled placenta left to drag behind her.
Dystocia has also been reported as having a predis-
posing association with uterine prolapse.
Diagnosis of an inverted uterine horn is made
based on the finding per rectum of a blunted uterine
horn with a tense mesovarium disappearing into the
center of the blunted tip. In minor intussusceptions,
the ovary may not yet be entrapped (this is not as
painful to the mare) and is still palpable at the very tip
of the blunted horn. Palpation of this area is often
painful to the mare and sedation is recommended.
The inverted horn may also be felt per vagina, within
the lumen of the uterus.
In cases where there is a retained placenta it is best
to gently remove the portion of attached placenta if it
will come away readily so as to decrease the tension on
the horn. In cases where the placenta cannot be
detached the author prefers to cut off the majority of
the exteriorized hanging placenta at a level just below
the vulva to decrease the strain on the invaginating
horn and hopefully prevent progression to a full uter-
ine prolapse. Direct treatment and correction of the
invaginated uterine horn includes controlling the
mare's straining and pain (sedation, epidural), manual
reduction of the inverted horn per vagina (may
require the use of uterine relaxants (aceprornazine,
clenbuterol), or even general anesthesia (halothane)
to relieve the encircling spasm in the myometrium),
and full replacement of the previously invaginated
horn and ovary to their normal position (manually if
they can be reached, or use intrauterine sterile saline
to fully dilate the uterine horns thus ensuring that the
previously entrapped horn is fully expanded).
Supportive therapy in the form of intravenous fluids,
NSAIDs, antibiotics, tetanus prophylaxis, etc., may also
be indicated (especially in cases complicated by
retained placenta). Careful use of low dose oxytocin
(10-20 IV i.m.), once the horn has been returned fully
to its normal position, may also aid in rapid normal
involution and prevention of a recurrence. The author
has also seen two mares with inverted uterine horns
secondary to retained placentas who also had low ion-
ized calcium levels at presentation. Correction of low
calcium levels to normal may also help restore normal
uterine tone.
OTHER CONDITIONS 17
BIBLIOGRAPHY
Abdominal distention in the adult horse
Distention colic
Ducharme N G, Fubini S S (1983) Gastrointestinal
complications associated with the use of atropine in
horses.] Am. Vet. Med. Assoc. 182:229-31.
Messer N T (1987) Distention colic. In Current Therapy in
Equine Medicine 2nd edn, N E Robinson (ed.). W B
Saunders, Philadelphia, pp. 68-70.
RobertsonJ T (1990) Diseases of the stomach. In The Equine
Acute Abdomen, N A White (ed.). Lea and Febiger,
Philadelphia, pp. 338-46.
Whi te N A (1990) Diseases of the caecum. In The Equine Acute
Abdomen, N A White (ed.). Lea and Febiger, Philadelphia,
pp.369-74.
Uroperitoneum
Beck C, DartAJ, McClintock S A and Hodgson D R (1996)
Traumatic rupture of the urinary bladder in a horse. Aust.
Vet.] 73:154-5.
Gibson K T, Trotter G Wand Gustafson S B (1992)
Conservative management ofuroperitoneum in a gelding.
] Am. Vet. Med. Assoc. 200:1692-94.
Jones P A, Sertich P S andJohnstonJ K (1996)
Uroperitoneum associated with ruptured urinary bladder
in a postpartum mare. Aust. Vet.] 74:354-8.
Fetal hydrops
Frazer G S, Embertson R and Perkins N R (1997)
Complications of late gestation in the mare. Equine Vet.
Educ. 9:306--11.
Van de Plassche M (1987) Prepartum complications and
dystocia. In Current Therapy in Equine Medicine 2nd edn.,
N.E. Robinson (ed.). W.B. Saunders, Philadelphia,
pp.537-40.
Van de Plassche M, Bouters R, Spincemaille J and Bonte P
(1976) Dropsy of the foetal sacs in mares. Vet. Rec. 99:67-9.
Ventral body wall hernias and prepubic
tendon rupture
Frazer G S, Embertson R and Perkins N R (1997)
Complications oflate gestation in the mare. Equine Vet.
Educ. 9:306--11.
Hanson R and Todhunter R (1986) Herniation of the
abdominal wall in pregnant mares.] Am. Vet. Med. Assoc.
189:790-3.
Perkins N and Frazer G (1994) Reproductive emergencies in
the mare. Vet. Clin. N. Am. Equine Pract. 10:643-70.
Cushing's disease
Hillyer M H, Taylor F G R, Mair T S, Murphy D, Watson
T D G and Love S (1992) Diagnosis of
hyperadrenocorticism in the horse. Equine Vet. Educ.
4:131-4.
KolkJ H van der (1998) Diseases of the pituitary gland,
including hyperadrenocorticism. In Metabolic and
Endocrine Problemsof the Horse,. T D G Watson (ed.).
W.B. Saunders, London, pp. 41-59.
361
17 COLIC

Kolk] H van der, Kalsbeek H C, Garderen Evan, Wensing T

and Breukink H] (1993) Equine pituitary neoplasia: a
clinical report of21 cases (1990-1992). Vet. Rec.
133:594-7.
Love S (1993) Equine Cushing's disease. Br. Vet.].

Pancreatic diseases
Argenzio R A (1990) Physiology of digestive, secretory and
absorptive processes. In: TheEquineAcuteAbdomen.
N A White (ed.). Lea and Febiger, Philadelphia, pp. 25-35.
Bulgin M S and Anderson B C (1983) Verminous arteritis and
pancreatic necrosis with diabetes mellitus in a pony. Compo
Cont. Educ. Pract. Vet. 5:S482-S485.
Byars T D (1990) Pancreatitis. In: TheEquine Acute Abdomen.
N A White (ed.). Lea and Febiger, Philadelphia, p. 408.
Hamir A N (1987) Verminous pancreatitis in a horse. Vet. Rec.
121:301-2.
Lilley C Wand Beeman G M (1981) Gastric dilatation
associated with acute necrotizing pancreatitis. Equine Pract.
3:8-15.
Mair T S, Freestone], Hillyer M H, Love S and Watson E D
(1995) The pancreas. In The Equine Manual, A] Higgins
and I M Wright (eds). W.B. Saunders, London,
pp.560-63.
McClure JJ (1987) Acute pancreatitis. In: Current Therapy in
EquineMedicine2nd edn, N E Robinson (ed.). W.B.
Saunders, Philadelphia, pp. 46-7.
Parry B Wand Crisman M V (1991) Serum and peritoneal
fluid amylase and lipase reference values in horses. Equine
va.]. 23:390-1.
Ross M W, Lowe] E, Cooper B], Reimers T] and Froscher
B A (1983) Hypoglycemic seizures in a Shetland pony.
Cornell Vet. 73:151-69.
Reproductive-associated causes of colic in the
brood mare
Asbury A C (1993) Care of the mare after foaling. In: Equine
Reproduction, A 0 McKinnon and] L Voss (eds). Lea and
Febiger, Philadelphia, pp. 976-80.
Ball B A and Daels P F (1997) Early pregnancy loss in mares:
applications for progestin therapy. In: Current Therapy in
EquineMedicine 4th edn, N E Robinson (ed.). W.B.
Saunders, Philadelphia, pp. 531-3.
Blanchard T L, Varner D D and Schumacher] (1998) Manual
ofEquine Reproduction. Mosby, St Louis.
Bosu W T K and Smith C A. Ovarian abnormalities. In: Equine
Reproduction. A 0 McKinnon and] L Voss (eds). Lea and
Febiger, Philadelphia, pp. 397-403.
Britt B and Byars T D (1997) Hagyard-Davidson-McGee
Formulary. In: Proceedings from theAnnual Conventionof the
AmericanAssociation ofEquine Practitioners. AAEP,
Lexington, KY, pp. 170-7.
Frazer G S (1998) Periparturient problems and dystocia. In:
Proceedings from the Bluegrass Equine Reproductive Symposium,
October 18-21, Hagyard-Davidson-McGee Associates, PSG
Immegart H M (1997) Abnormalities of pregnancy. In: Current
Therapy in LargeAnimal Theriogenology, R.S. Youngquist
(ed.). W.B. Saunders, Philadelphia pp. II 3-29.
Immegart H M and Threlfal W R (1998) Accidents of
OTHER CONDITIONS 17
breeding. In: Equine Internal Medicine, S.M. Reed and W.M.
Bayly (eds). W.B. Saunders, Philadelphia, p. 800.
Le Blanc M M (1997) Immediate care of the postpartum
mare and foal. In: CurrentTherapy in LargeAnimal
Theriogenology, R SYoungquist (ed.). W.B. Saunders,
Philadelphia, pp. 157-60.
Lofstedt R M (1993) Miscellaneous diseases of pregnancy and
parturition. In: Equine Reproduction, A 0 McKinnon and
] L Voss (eds). Lea and Febiger, Philadelphia, pp.
596-603.
Maxson A D, Giger U, Sweeney C R et al. (1993) Use of bovine
hemoglobin preparation in the treatment of cyclic ovarian
hemorrhage in a miniature horse.] Am. Vet. Med. Assoc.
203:1308-11.
Parente E] (1999) Colic in the peripartum mare. In:
Proceedings from the Comprehensive Preventative Medicinefor the
Mare and FoalHighlighting Nutritional Management and
Developmental Orthopedic Disease Seminar, March 13-14,
Hilltop Farm.
Plumb D C (1995) Veterinary Drug Handbook 2nd edn. Iowa
State University Press, Ames, IA.
Santschi E (1997) Prepartum conditions. In: Current Therapy
in Equine Medicine4th edn, N E Robinson (ed.). W.B.
Saunders, Philadelphia, pp. 541-6.
Sherman D M and Lafarenko V A (1998) The mechanism of
the action of opiate receptor antagonists in acute shock-
induced blood loss. Eksp. Klin. Farnakol. 61(1):25-9.
Sprayberry K A (1999) Hemorrhage and hemorrhagic shock.
In: Proceedings from the Bluegrass Equine Medicineand Critical
Care Symposium, October 24-27. Hagyard-Davidson-McGee
Associates, PSG
Stowe H D (1968) Effects of age and impending parturition
upon serum copper of Thoroughbred mares.] Nutrition
95:179.
Trotter G W (1992) Surgical diseases of the caudal
reproductive tract. In: Equine Surgery,] A Auer (ed.). W.B.
Saunders, Philadelphia, pp. 730-50.
Vaala W E (1999) Periparturient problems in mares. In:
Proceedings from the Comprehensive Preventative Medicinefor the
Mare and FoalHighlighting Nutritional Management and
Developmental Orthopedic Disease Seminar, March 13-14,
Hilltop Farm.
van de Plassche M (1987) Prepartum complications and
dystocia. In: CurrentTherapy in Equine Medicine2nd edn,
N E Robinson (ed). W.B. Saunders, Philadelphia, pp.
537-42.
Vasey] R (1993) Uterine torsion. In: Equine Reproduction, A 0
McKinnon and] L Voss (eds). Lea and Febiger,
Philadelphia, pp. 456-60.
Vivrette S (1997) Parturition and postpartum complications.
In: CurrentTherapy in Equine Medicine4th edn, N E
Robinson (ed.). W.B. Saunders, Philadelphia pp. 547-51.
Zent W W (1987). Postpartum complications. In: Current
Therapy in Equine Medicine2nd edn. N E Robinson (ed.).
W.B. Saunders, Philadelphia, pp. 544-7.
363
 18
Chronic weight loss

T Mair

Differential diagnosis and It is sometimes easy to determine whether a horse is

losing weight from the physical findings and an accu­
evaluation of chronic rate history. However, in many cases, establishing
whether a problem exists or not, and its severity, can be
weight loss very difficult. In general, chronic weight loss should be
investigated if a horse has noticeably lost weight, and
fails to regain it, for no obvious reason.
Chronic weight loss (or wasting) is not a disease, nor
INTRODUCTION is it a diagnosis, but simply a state of affairs. Discerning
the cause of weight loss can vary from a straightforward
The maintenance of a normal and constant body weight
to a highly complex evaluation of the patient since
is a balance between input and output (Figure 18.1).
numerous management, environmental, and animal
factors can impact on a horse's ability to maintain
/I Nutrients OUT � Feces, adequate body condition.
Nutrients IN � HORSE urine, sweat A horse that is losing weight for no obvious reason
� Metabolic consumption usually falls into one of three categories

Figure 18.1 Balance between input and output necessary
to maintain body weight
Nutrients in the diet are the input. The output is the
sum of nutrients used in metabolism and exercise, and
nutrients lost or excreted in feces, urine, and sweat.
Weight loss occurs when the output of nutrients
exceeds the input of nutrients.
DEFINITION OF CHRONIC WEIGHT LOSS
1. the horse is healthy, but affected by some form of
imposed environmental stress or deprivation
2. the horse is affected by a disease that is causing the
weight loss with no other overt clinical signs
3. the horse is geriatric.
The first decision the veterinarian must make is
whether the case is a thin well horse or a thin ill horse?
Although this sounds very basic, it is very important,
and every effort should be made at the outset to deter­
mine which category a particular horse fits into.

Weight loss is a common problem that can affect horses
of all ages; there are numerous potential causes.
However, there is no precise definition of weight loss,
and individual owners and veterinarians often vary
enormously in their opinions about 'normal' body
condition and in their concern about weight loss.
ASSESSMENT OF BODY CONDITION
The body condition of an individual horse can be
assessed by documenting the fat:lean ratio or body con­
dition score. Estimating and recording the body condi­
tion score may be important for legal reasons. If a horse

367
18 CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
is being examined over a period of time, then regular
recording of body weight is helpful in monitoring the
course of weight loss or a disease, and for assessing the
response to therapy. A number of different systems for
assessing body condition have been described. One
such system is shown in Table lS.I.
Usual goals for body condition scores are about 4-5
for performance and sport, and 5-6 for reproduction.
Body condition Definition
score
Extreme emaciation. No fatty
tissue. Wasted muscles especially
noticeable over bones. Flat shelf
over transverse processes
2 Emaciation. Slight fat cover.
Prominent bones. Wasted
muscles
3 Thin. Fat covers transverse
processes and half-way up
spinous processes. Tailhead
prominent but individual
vertebrae not seen. Ribs seen
sharply
4 Moderate ly thin. Slight back
ridge. Ribs barely discernable
5 Moderate. Back is flat (no crease
or ridge). Ribs easily felt but not
seen
6 Modera tely fleshy. Fat feels
spongy over ribs and around
tailhead. Back crease slight or
absent
7 Fleshy. Back crease definite. Ribs
covered but individual ribs can
be palpated. Fat is palpable in
neck and rump
8 Fat. Back creased. Neck thick.
Fat along withers, behind
shoulders and inside thighs
9 Too fat. Back crease is deep. Fat
bulging on neck, along withers,
behind shoulders, around
tailhead and inside thighs
368
POTENTIAL CAUSES OF CHRONIC
WEIGHT LOSS
Chronic weight loss may occur in the following situa­
tions
• lack of food, water, or both
• poor quality of food or water
• failure to eat or swallow food
• failure to digest or absorb food
• increased or abnormal loss of nutrients once
absorbed
• increased utilization of nutrients once absorbed
• neuromuscular disease.
ASSESSMENT OF ENVIRONMENTAL
AND MANAGEMENTAL FACTORS
Managemental and environmental factors leading to
weight loss may be multifactorial and other horses on
the premises should be examined for assessment of
body condition. If other animals are also demonstrating
evidence of weight loss, then a management problem
becomes more likely. The most likely environmental
causes include
• insufficient food
• insufficient grass
• the wrong sort of food
• insufficient water
• excessive work
• irregular severe work in an unfit horse.
If environmental or managemental factors are
thought to be important in causing chronic weight loss,
then the attending veterinarian must examine these fac­
tors carefully him/herself. Information and history sup­
plied by the owner or manager cannot be relied upon
to be truthful. Owners often give misleading or inaccu­
rate replies to questions about a horse's management or
feeding because they are embarrassed and concerned
that they may appear negligent. Likewise, managers or
trainers may try to mislead or to conceal information.
Wherever possible, the attending veterinarian should
spend some time at the owner's premises assessing the
general management and feeding, and observing the
horse in its own environment.
Assessment of nutrition
A careful assessment of the nutritional status is essential
in the evaluation of chronic weight loss, it is worth
remembering also that documentation of body condi­
tion can be important in humane and legal actions. The
following questions should be addressed

1. Is enough food being offered?
2. Is the food of adequate quality?
3. Is the horse allowed to eat?
4. Is the food palatable?
If possible the veterinarian should make a direct
assessment of what the horse is being fed by asking the
owner to show him or her exactly what is fed and in
exactly what quantities. If the horse is pastured, a direct
assessment of the quality of the pasture and the stock­
ing density should be made. An average 450 kg horse at
rest will obtain adequate intake of energy from 8- 10 kg
of hay and 2-4 kg of grain per day. Some individual
horses will require more than this to maintain a con­
stant body weight, and some will require less. Increased
energy requirements occur if the horse is in work, or is
pregnant or lactating.
Many inexperienced horse owners are unaware of
the dietary needs of their horses, especially in relation
to increased work levels. Although they may provide
adequate quantities of food to meet the requirements
for maintenance and light work in the winter months,
they often fail to adjust the ration in the summer
when the horse is exercised more vigorously. Other
owners fail to feed adequate amounts of food during
cold winter weather. Another common cause of weight
loss is the reliance of inexperienced horse owners on
supplements and products advertised to improve
digestion and metabolism. This often leads to under­
feeding especially in the winter when pasture quality
has declined.
Some horses always lose weight when kept in full
work especially during the winter time. Many breeding
stallions lose weight during the breeding season. Such
horses are not considered abnormal if they regain
weight when rested or, in the case of breeding stal­
lions, when the breeding season ends. Late pregnancy
and lactation impose increased demands for energy
and nutrients. A mare in late pregnancy may require
20 per cent more nutrients than for normal mainte­
nance, and at peak lactation may require up to 50 per
cent more.
Competition for available food may be important in
groups of horses. This may be particularly important
with respect to new introductions to a group of horses,
or 'slow eaters'. A horse that is low in the pecking order
in a group may be unable to eat because it cannot
approach the food without other horses bullying it and
chasing it away.
Poor palatability of the food may become a problem,
especially when it has become spoiled or contaminated
by some substance. This is likely to affect the whole
batch of feed, and several or all horses exposed to that
batch are likely to be affected.
CHRONIC WEIGHT LOSS 18
Availability of water
Horses require free access to clean water. If water is
restricted then weight loss will result, partly due to an
associated decrease in voluntary food intake. An average
horse requires 20-30 liters of fresh water per day when
doing light work in a temperate climate. Increased
demands for water occur with increased work load,
lactation, and increased environmental temperature.
Assessment of general management
An assessment of the general management and preven­
tive medicine practices is helpful at this stage. Careful
questioning of the owner is carried out to assess in
particular:
• internal parasite control (see Chapter 4)
• routine dental care (see Chapter 6).
ASSESSMENT OF WEIGHT LOSS
ASSOCIATED WITH DISEASE
If environmental and managemental factors have been
ruled out as the cause of chronic weight loss, or if
disease is suspected but the associated clinical signs are
obscure, then the horse requires careful observation
and examination, often over a protracted period of
time. It may be preferable to hospitalize the horse for
several days so that its behavior, locomotion, eating,
and drinking can be monitored constantly. Thorough
and systematic clinical examinations should be per­
formed and repeated regularly until, hopefully, some
indication of a specific disease or a diseased body system
is identified. Routine hematological, serum biochemi­
cal, and parasitological profiles should be undertaken
at this time. Further clinicopathological examinations
may be performed as deemed necessary (e.g. abdomi­
nal paracentesis, rectal biopsy, oral glucose tolerance
test, urinalysis, etc.). Further clinical procedures, such
as diagnostic ultrasonography, radiography, laparo­
scopy, etc., may also be performed if appropriate.
CLINICAL PATHOLOGY
Over reliance on laboratory tests to diagnose the cause
of chronic weight loss must be avoided. However,
clinicopathological investigations can be an important
aid in the diagnosis of certain diseases.
Hematology
Hematology tests may reveal
• leukocytosis and neutrophilia - these are indicative
of chronic inflammation, and may be observed in
369
18 CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
infectious diseases (e.g. peritonitis, internal
abscesses) or neoplasia
• anemia - this occurs in chronic inflammatory
diseases or neoplasia
• dyserythropoiesis - this can be confirmed by bone
marrow aspirate or biopsy
• immune-mediated hemolytic anemia and/or
thrombocytopenia - these conditions are
sometimes associated with neoplasia
• hyperfibrinogenemia - this is another sensitive
indicator of inflammation and may be seen in both
infectious and neoplastic conditions.
Serum biochemistry
Decreased serum or plasma total protein or albumin
concentration is evidence of hypoproteinemia, which is
suggestive of one of the following conditions
• severe malnutrition
• protein-losing enteropathy (e.g. parasitism, colitis,
inflammatory and neoplastic bowel diseases)
• glomerular disease
• chronic liver disease
• peritonitis or pleuritis.
In chronic liver conditions, the total protein con­
centration is often normal, but albumin concentration
may be sub-normal and globulin concentration raised
(decreased albumin:globulin ratio).
Increased serum or plasma total protein (hyperpro­
teinemia) and total globulin (hyperglobulinemia) may
occur in inflammatory processes, infections, parasitism,
liver disease, and neoplasia. Raised gamma globulins
are suggestive of infection, whereas raised beta globu­
lins are suggestive of parasitism.
Urea concentration may be raised for a number of
different reasons
• increased tissue catabolism and protein turnover
associated with disease
• high protein diet
• dehydration
• renal failure.
In practice, increased urea concentration is rarely
identified as a direct result of increased tissue catabo­
lism or high protein diet. If renal failure is suspected,
further laboratory analyses should be performed
including serum creatinine, electrolytes, urinalysis, and
acid-base estimations.
Increases in the concentrations of acute and chronic
liver enzymes suggest an active liver problem. Serum
enzymes can be helpful in assessing liver disease (see
Chapter 19), these include
370
• gamma glutamyl transferase (GGT)
• aspartate aminotransferase (AST)
• alkaline phosphatase (AP)
• glutamate dehydrogenase (GLDH)
• iditol dehydrogenase ( IDH)
• arginase (ARG).
Further laboratory tests of liver disease and liver
function include
• bilirubin
• serum bile acids
• serum proteins
• blood ammonia.
Fecal examinations
A fecal egg count reflects the presence of adult egg­
laying strongyles (or other nematode parasites) in the
intestine. The fecal egg count gives no indication of the
burden of immature larval stages of parasites, and is
therefore of little use in the diagnosis of larval cyatho­
stomosis (see Chapter 2 1). Direct microscopy of a wet
preparation of feces may be helpful in identifying the
presence of cyathostome larvae.
Fecal occult blood may be positive with gastrointesti­
nal ulceration or neoplasia, but the presence of para­
sites or a recent rectal examination may also cause a
positive test result. This test is more likely to be positive
in cases where bleeding has occurred in the distal
intestinal tract than in cases where bleeding has
occurred in the proximal gastrointestinal tract.
Peritoneal fluid analysis
Total nucleated cell count and total protein should be
measured to differentiate between transudates and
exudates (see Chapter 17). Cytology may occasionally
document the presence of neoplastic cells due to intra­
abdominal neoplasia.
Both aerobic and anaerobic cultures of peritoneal
fluid should be performed if intra-abdominal infection
is suspected (see Chapter 17).
CAUSES OF CHRONIC WEIGHT LOSS
The common diseases associated with obscure chronic
weight loss include
1. conditions interfering with prehension of food,
and/or swallowing
2. persistent low-grade pain
3. conditions interfering with digestion and intestinal
absorption
4. protein-losing enteropathies

5. chronic liver disease
6. chronic kidney disease
7. chronic low-grade infection
8. neoplasia
9. chronic heart disease
10. chronic pulmonary disease.
Conditions interfering with prehension of
food and/or swallowing
Prehension, mastication, and swallowing are integrated
functions and abnormalities in one or more phases of
eating and swallowing can lead to reduced food (and
water) intake and, as a result, weight loss. Secondary
inhalation pneumonia is a common sequel to severe
dysphagia, in which case weight loss will become accel­
erated (with the development of additional clinical
signs). The causes and investigation of dysphagia are
described in detail in Chapter 5.
It is helpful to observe the horse eat and drink, and
to examine the stall for evidence of partially chewed
food. Signs indicative of dysphagia may be subtle or
obvious (depending on the severity of the disease), and
include
• an unwillingness to eat or a protracted time taken
to eat food
• dropping semi-masticated food from the mouth
while eating ('quidding')
• the accumulation and 'balling-up' of food in the
mouth
• halitosis
• nasal return of saliva, food, and water
• gulping, but not swallowing, water
• dipping and splashing the muzzle in water
• productive coughing.
Particular attention should be paid to the oral cavity
and teeth if there appears to be quidding of food or
painful mastication (see Chapters 5 and 6). The ability
of the horse to flex its neck and to eat and drink from
the ground should also be assessed.
Important causes of dysphagia include
• facial paralysis (see Chapter 5)
• lip lesions (see Chapter 5)
• temporomandibular joint and hyoid lesions (see
Chapter 5)
• dental disorders (see Chapter 6)
• lingual trauma and abnormalities (see Chapter 5)
• congenital and acquired palatal defects (see
Chapters 5 and 6)
• pharyngeal paralysis (see Chapter 5)
• pharyngeal compression (see Chapter 5)
• pharyngeal and palatal cysts (see Chapter 5)
• epiglottal lesions (see Chapter 5)
CHRONIC WEIGHT LOSS 18
• 4th branchial arch defects (see Chapter 5)
• megaesophagus (see Chapters 5 and 7)
• esophageal obstruction (see Chapters 5 and 7)
• esophageal strictures/stenosis (see Chapters 5 and
7)
• grass sickness (especially in the UK) (see Chapters 5
and 17).
Persistent low-grade pain
Persistent low-grade pain affects the animal's well­
being, reduces its appetite, and may affect its willing­
ness to move about and graze. Common causes of
low-grade pain and weight loss include chronic colic,
chronic lameness, and neoplasia.
Chronic colic is discussed fully in Chapter 17.
Common causes of chronic low-grade colic include
• diffuse or localized peritonitis (see Chapter 17)
• chronic grass sickness (especially in the UK) (see
Chapter 17)
• chronic inflammatory bowel disease (see
Malabsorption syndromes)
• Right dorsal colitis (see Chapter 2 1)
• neoplastic bowel infiltrates (see below and Chapter
17)
• abdominal neoplasia (see Chapter 17)
• gastric ulceration (see Chapter 12)
• ileal hypertrophy (see Chapter 13)
• chronic intussusceptions (see Chapter 13)
• sand irritation (see Chapter 15)
• enteroliths (see Chapter 15)
• cholelithiasis (see Chapter 19)
• cystic calculi.
Chronic lameness includes conditions such as
laminitis, navicular syndrome, and degenerative joint
disease. These conditions may be associated with
chronic weight loss, but signs directly referable to the
underlying disease are usually also present.
Conditions interfering with digestion and
intestinal absorption
If a horse with weight loss has been observed to eat
adequate quantities of an appropriate diet, then
decreased feed digestion or absorption should be
considered as a possible cause of the weight loss. In sim­
plistic terms, dietary proteins, fats, and non-cellulose
carbohydrates are digested and absorbed in the equine
small intestine. Undigested and unabsorbed nutrients
pass into the large intestine where they are broken
down by cecal and colonic microorganisms, and the
breakdown products are absorbed predominantly as
volatile fatty acids. Undigested material, chiefly fiber, is
lost via the feces.
371
18 CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
Conditions causing maldigestion in the adult horse
are very poorly understood. Pancreatic disease and
dysfunction appear to be very rare (see Chapter 17).
Specific brush-border enzyme deficiencies have not
been described in adult horses. However, maldigestion
probably occurs in conjunction with diseases that affect
intestinal absorption such as inflammatory bowel dis­
ease (see Malabsorption syndromes).
In general, enteropathies of the adult horse that
affect the hind-gut, or both the fore- and hind-gut, are
associated with diarrhea (see Chapters 20 and 2 1). If
fore-gut dysfunction is the only problem, then diarrhea
commonly does not occur, and the clinical presentation
will be characterized by progressive weight loss due to
malabsorption (and maldigestion). However, if small
intestinal function is very severe, then diarrhea may also
occur in the absence of any apparent large intestinal
lesions.
Small intestinal maldigestion and
malabsorption
A malabsorption syndrome can be produced by several
diseases of the small intestine, including
• diffuse alimentary lymphosarcoma
• granulomatous enteritis
• eosinophilic enteritis
• lymphocytic-plasmacytic enteritis
• mycobacterial enteritis
• parasitism.
These diseases are discussed in greater detail in
Malabsorption syndromes.
Typically, horses with malabsorption syndromes
present with progressive weight loss despite a normal
or even increased appetite. Affected animals are often
bright and alert in the early stages of the disease.
However, in the later and advanced stages of malab­
sorption syndromes, there may be debility, depression,
and inappetence.
The cause of small intestinal malabsorption cannot
be determined by clinical examination or routine
laboratory evaluations. Rectal examination sometimes
reveals evidence of bowel-wall thickening, and this may
be further evaluated by diagnostic ultrasonography.
Enlargement of mesenteric lymph nodes may also be
appreciable on rectal examination.
Hypoalbuminemia in a wasting horse is strongly
suggestive of malabsorption and/or protein-losing
enteropathy; other important causes include renal and
liver disease (see below). Occasionally serum globulin
levels may be elevated in chronic inflammatory bowel
disease, resulting in a normal total protein level and
decreased albumin:globulin ratio. Serum protein elec-
372
trophoresis can be helpful in determining the nature of
any hyperglobulinemia. Elevations in both alpha and
beta globulin fractions are frequently found in chronic
inflammatory bowel disease. An elevation of predomi­
nantly the beta-globulin fraction may be suggestive of
significant parasitic larval migration. Lymphosarcoma
is occasionally accompanied by low or undetectable
serum IgM levels. Lymphocytic-plasmacytic enteritis is
often associated with an increased serum IgA concen­
tration.
Chronic enteropathies may sometimes, but not
always, be associated with raised serum concentrations
of alkaline phosphatase, in particular the intestinal
isoenzyme of alkaline phosphatase.
Peritoneal fluid is frequently normal in horses with
chronic infiltrative bowel disease. The fluid is usually
normal even in horses with intestinal lymphosarcoma.
Occasionally, increased eosinophil numbers will be
found in the peritoneal fluid of horses with eosinophilic
bowel infiltrates.
Assessment of small intestinal absorptive capacity
should be performed by a monosaccharide absorption
test (such as the oral glucose tolerance test or the xylose
absorption test) (see Chapter 2) in all horses where mal­
absorption is suspected. Although the results of these
tests may be suggestive of a malabsorption syndrome,
they cannot provide definitive proof or diagnose the
underlying cause. Rectal biopsy may be helpful if the
inflammatory or neoplastic infiltrate extends to that part
of the intestinal tract. However, in most cases of small
intestinal malabsorption, the results of histological
examinations of rectal biopsies will be unremarkable.
Exploratory laparotomy and multiple full-thickness
bowel wall biopsies may be the only way to obtain a defin­
itive diagnosis in the living horse. However malabsorb­
ing horses are usually thin or debilitated, and are not
good surgical candidates and some will suffer wound
complications following surgery. Standing laparoscopy
is associated with much lower morbidity and may permit
biopsy of mesenteric lymph nodes which could provide
useful diagnostic information.
Large intestinal maldigestion and
malabsorption
Inflammatory and neoplastic infiltrates may affect the
large intestine as well as the small intestine. Severe infil­
trative and inflammatory large bowel diseases com­
monly result in progressive weight loss with diarrhea
(see Malabsorption syndrome and Chapter 2 1).
Parasitism affecting the large intestine can also result in
chronic weight loss. Larval cyathostomosis is typically
associated with a severe protein-losing enteropathy and
sudden onset diarrhea in young adult horses during the

winter time (see Chapter 21). However, in a small num­
ber of cases larval cyathostomosis may cause progressive
and rapid weight loss and subcutaneous edema (associ­
ated with hypoproteinemia) in the absence of diarrhea.
Cyathostome larvae may be found in the feces of such
cases (although fecal egg count is frequently negative),
and laboratory abnormalities typical of larval cyathosto­
mosis will also be present (leukocytosis, neutrophilia,
hypoalbuminemia, hyper-betaglobulinemia, elevated
intestinal alkaline phosphatase). Cyathostome infec­
tions have also been reported to cause a seasonal
malaise syndrome in adult horses during the autumn
and winter, characterized by vague signs of inappetence
and ill-thrift.
Protein-losing enteropathies
Protein-losing enteropathies comprise a group of dis­
eases where there is lumenal loss of fluid, electrolytes,
plasma proteins, and nutrients. Protein-losing
enteropathies can affect both the small and large
intestines. Common causes include
• inflammatory bowel disease (see Malabsorption
syndromes)
• right dorsal colitis (see Chapter 21)
• intestinal neoplasia (see Malabsorption
syndromes)
• gastrointestinal ulceration (such as N SAID toxicity)
(see Chapters 12, 20, and 21)
• larval cyathostomosis (see Chapter 21)
• severe parasitism (see Chapter 4).
These diseases result in continual loss of plasma pro­
teins into the gut lumen. Many of the diseases result in
maldigestion and malabsorption as well. Clinico­
pathological abnormalities are non-specific but include
anemia, leukocytosis, and hypoalbuminemia.
Hypoalbuminemia may result in ventral and limb
edema in these cases.
Chronic liver disease
Chronic liver diseases such as pyrrolizidine tOXICIty,
chronic active hepatitis, cholelithiasis, cholangio­
hepatitis, and cirrhosis can be associated with chronic
weight loss in the absence of overt clinical signs of
hepatic failure. These diseases result in weight loss
due to inappetence, maldigestion (due to inadequate
bile acid production), and inadequate or improper
processing of amino acids into nomlal plasma pro­
teins in the liver. The diagnosis is usually achieved by
estimation of serum proteins, liver enzynle and bile
acid concentrations, and biopsy. Liver disease is dis­
cussed in detail in Chapter 19.
CHRONIC WEIGHT LOSS 18
Chronic kidney disease
Chronic renal failure is an uncommon but important
cause of chronic weight loss. The potential causes
include
• chronic glomerulonephritis
• tubulointerstitial disease
• chronic septic pyelonephritis
• bilateral renal hypoplasia or dysplasia
• chronic oxalate nephrosis
• polycystic renal disease.
Congenital renal diseases such as renal hypoplasia,
dysplasia, or polycystic renal disease should be sus­
pected in young horses (less than 5 years of age) that
present with evidence of chronic renal failure.
Acquired renal diseases are usually insidious in onset,
and the initial renal injury may have occurred months
or years prior to the onset of clinical signs. IdentifYing
the precise cause of chronic renal failure may be very
difficult because many horses have evidence of
advanced glomerular and tubular disease, or 'end-stage
kidney disease' by the time clinical signs of chronic
renal failure become apparent.
Chronic weight loss is the most common presenting
clinical sign in horses with chronic renal failure. Other
signs that may be noted include
• inappetence
• ventral edema
• polyuria/polydipsia
• rough hair coat
• lethargy
• exercise intolerance
• uremic odor and halitosis
• excessive dental tartar.
Weight loss occurs for several different reasons in
horses with chronic renal failure. An increase in the
concentrations of nitrogenous wastes in the blood has a
central appetite-suppressant effect. Also azotemia can
cause oral ulceration and gingivitis, reducing appetite,
and in the gastrointestinal tract excess urea and
ammonia can lead to ulceration and protein-losing
enteropathy.
The diagnosis of chronic renal failure is made by
identifYing persistent isosthenuria (urine specific
gravity 1.008-1.01 4) in combination with azotemia
(increased serum urea and creatinine concentrations)
and typical clinical signs. Additional clinicopathological
abnormalities may include
• anemia
• hypoalbuminemia
• hyponatremia
• hyperkalemia
373
18 CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
• hypochloremia
• hypercalcemia
• hypophosphatemia
• metabolic acidosis or alkalosis.
Diagnostic ultrasonography and renal biopsy can
provide additional information.
Chronic low-grade infection
Chronic low-grade infection, either localized or sys­
temic, may result in chronic weight loss with few other
overt clinical signs. Vague signs such as depression
and inappetance may be present. Diseases which may
present in this way include
• chronic internal abscesses (see Chapter 17)
• chronic pneumonia or lung abscesses
• endocarditis
• localized peritonitis (see Chapter 17)
• cholangiohepatitis (see Chapter 19)
• equine infectious anemia ( E IA)
• leptospirosis
• brucellosis
• mycobacterial infections.
Persistent or intermittent pyrexia may be present,
and this may give an important clue as to the possibility
of a chronic infectious (or inflammatory) process.
Hematology and plasma fibrinogen estimation may
indicate a chronic septic process (leukocytosis, neutro­
philia, hyperfibrinogenemia). Increased serum globu­
lin levels (primarily gamma globulins) may be present
due to chronic antigenic stimulation. Abdominal para­
centesis may be helpful in the diagnosis of localized
peritonitis or intra-abdominal abscesses (see Chapter
17). Nuclear scintigraphy using radio-labeled white
blood cells might be useful to localize focal septic
lesions such as internal abscesses. Specific serological
tests are necessary to diagnose EIA, leptospirosis, and
brucellosis. Biopsy and/or culture are necessary to
diagnose mycobacterial infections. Horses with chronic
immune mediated disorders may also have intermittent
or persistent fever and weight loss.
Neoplasia
Cancer cachexia is an important paraneoplastic syn­
drome that is recognized in all species, including the
horse. It is characterized by a state of malnutrition and
wasting despite adequate nutritional intake, and is
believed to be caused by complex alterations in carbo­
hydrate, lipid, and protein metabolism. In addition to
weight loss, cancer cachexia may result in an increase in
infections due to an impairment of the immune system,
and decreased wound healing.
374
Weight loss may also occur in association with neo­
plastic disease as a result of
• low-grade pain (see above)
• physical obstruction (causing dysphagia or chronic
colic)
• small intestinal malabsorption (see above)
• reduced appetite.
Apart from weight loss, the clinical features of inter­
nal neoplasia are variable, and depend on the nature of
the neoplasm, its size, the presence or absence of other
paraneoplastic syndromes, and the mass effects of the
neoplasm on organs and tissues.
The major types of abdominal and thoracic neo­
plasia are listed in Table 18.2. Abdominal neoplasia is
considered further in Chapter 17.
Lymphosarcoma (lymphoma) is the most frequently
encountered malignant neoplasm in the horse. It
accounts for 1-3 per cent of all equine tumors. This
neoplasm is most common in mature horses, but may
occur at any age (it has been recognized in an equine
fetus). Four clinical categories of lymphosarcoma are
recognized
1. generalized/multicentric lymphosarcoma
2. alimentary/intestinal lymphosarcoma
3. mediastinal/thoracic lymphosarcoma
4. cutaneous lymphosarcoma.
Considerable overlap between these categories can
occur.
The clinical manifestations of lymphosarcoma vary
depending on the degree of organ involvement and the
specific organs involved in an individual patient. The
typical clinical signs associated with the different forms
of lymphosarcoma are summarized below.
1. Generalized/multicentric form
• depression
• weight loss
• lymphadenopathy
• intermittent fever
• ventral and limb edema
• chronic, intermittent colic
• thickened eyelids.
2. Alimentary/intestinal form
• depression
• weight loss
• ventral edema
• chronic, intermittent colic
• intermittent fever
• diarrhea
• ascites.
3. Mediastinal/thoracic form
• depression
• inappetence
 CHRONIC WEIGHT LOSS 18

• weight loss
• exercise intolerance Liver
• ventral thoracic and pectoral edema Lymphosarcoma
• tachypnea Hepatocellular carcinoma
• respiratory distress Biliary carcinomal cholangiocellular
• bilateral firm masses at the base of the jugular carcinoma
grooves Hemangiosarcoma
Adrenal gland
• intermittent fever.
Pheochromocytoma
4. Cutaneous form
Stomach
• solitary or multiple dermal or subcutaneous
Squamous cell carcinoma
masses Gastric polyp
• later development of visceral neoplasia (this may Leiomyoma and leiomyosarcoma
take months to years). Gastric adenocarcinoma
Small intestine
Lymphosarcoma
Leiomyoma and leiomyosarcoma
Adenocarcinoma
Lipoma
Cecum, large and small colons
Lymphosarcoma
Adenocarcinoma
Thoracic neoplasia Intestinal myxosarcoma
Primary lung tumors Lipoma and lipomatosis
Pulmonary granular cell tumor Rectum
Pulmonary adenocarcinoma Lipoma
Anaplastic bronchogenic carcinoma Lymphosarcoma
Pulmonary carcinoma Polyps
Bronchogenic squamous cell carcinoma Leiomyosarcoma
Pulmonary chondrosarcoma Melanoma
Bronchial myxoma Peritoneum
Pleural neoplasia Disseminated leiomyosarcomatosis
Mesothelioma Omental fibrosarcoma
Mediastinal and thymic tumors Mesothelioma
Thymoma Kidney
Lymphosarcoma Renal cell carcinoma
Metastatic and secondary thoracic neoplasia Adenoma
Hemangiosarcoma Transitional cell carcinoma
Squamous cell carcinoma Embryoma
Adenocarcinoma Squamous cell carcinoma
Renal carcinoma Ovary
Rhabdomyosarcoma Cystadenoma
Malignant melanoma Teratoma
Fibrosarcoma Dysgerminoma
Hepatoblastoma Granulosa cell tumor
Chond rosarcoma
Neuroendocrine tumor
Lymphosarcoma

Undifferentiated sarcoma and carcinoma

Chronic heart disease
Abdominal neoplasia Heart failure may result in weight loss due to ineffi­
Pancreas
ciency of the circulation of nutrients and oxygen to
Pancreatic adenoma and adenocarcinoma
peripheral tissues. Other clinical features of congestive
Spleen
heart failure include exercise intolerance, depression,
Lymphosarcoma
Melanoma
venous distention, edema, tachypnea and coughing.
Hemangiosarcoma Diagnosis is made by auscultation, ECG, and cardiac
ultrasound examinations.

375
18 CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
Chronic pulmonary disease
Horses affected by chronic obstructive pulmonary
disease (COPD) commonly maintain normal body
condition, but severe and long-standing disease may be
associated with weight loss. Other signs indicative of this
condition will be present (chronic cough, tachypnea
and dyspnea, nasal discharge, exercise intolerance,
wheezing and crepitant lung sounds).
Thoracic neoplasia (see above) may produce weight
loss before other signs indicative of the primary condi­
tion become evident. Likewise, chronic interstitial pul­
monary inflammatory disease and fibrosis may present
with weight loss as one of the earliest clinical signs.
Diagnosis of these conditions is aided by careful
thoracic auscultation, radiography, tracheal aspiration
or bronchoalveolar lavage, diagnostic ultrasonography,
and biopsy.
Figure 18.2 Marked asymmetric gluteal atrophy in a
horse affected by polyneuritis equi
376
NEUROLOGICAL AND
NEUROMUSCULAR DISEASE
�_���_lMiiWiI';'J!. a _""�
Muscle atrophy and weight loss may occur as a result of
local or generalized neurological or neuromuscular
disease. Pronounced symmetrical muscle atrophy (most
severe in the triceps, scapula, quadriceps, lumbar,
sacral, and neck muscles) is seen in equine motor
neuron disease. Other signs are expected in this disease
including trembling, lying down more often than nor­
mal, shifting weight on the rear legs, and holding all
four legs closer together than normal. Asymmetric
muscle atrophy affecting the gluteal musculature is
common in other neurological conditions such as
polyneuritis equi (Figure 18.2) and equine protozoal
myeloencephalitis. Chronic weight loss is also a com­
mon presenting sign in horses affected by chronic grass
sickness (see Chapter 17).
Malabsorption syndromes
_I WIiIUIlllliA 11._001IIS [
INTRODUCTION
Malabsorption syndrome refers to the group of diseases
that results in the impairment of digestive and/or
absorptive processes arising from structural or func­
tional disorders of the small intestinal tract and its asso­
ciated organs (including the pancreas and liver). In the
adult horse, such diseases that are confined to the small
intestine usually result in chronic weight loss, whereas
chronic diseases of the large intestine result in diarrhea
and protein-losing enteropathy (see Chapter 21).
However, small intestinal diseases may result in sec­
ondary large intestinal dysfunction due to abnormal
amounts of carbohydrates, fats, and amino acids enter­
ing the large bowel from the ileum. In addition, many
of the chronic infiltrative diseases that result in small
intestinal malabsorption can affect the large bowel con­
currently. Thus, in clinical cases there is often a combi­
nation of both small intestinal and large intestinal
malfunction.
The primary clinical sign associated with malabsorp­
tion syndromes in adult horses is chronic weight loss. If
the disease process is limited to the small intestine, then
weight loss may be the only clinical sign, and it becomes
important to rule out other causes of weight loss (see
Differential diagnosis and evaluation of chronic weight
loss). Although malabsorption syndromes will affect the
digestion and absorption of carbohydrates, protein,

and fat, diagnostic tests in the horse usually concentrate
on dysfunction of carbohydrate digestion/absorption.
Inadequate fat absorption is of limited importance in
the horse, although malabsorption of fat soluble vita­
mins may result in clinical conditions, such as dermati­
tis, neurological diseases, and retinal dysfunction.
Increased protein loss from the intestine (protein-los­
ing enteropathy) is more commonly associated with
large intestinal disease due to the larger surface area of
the equine large intestine. However, concurrent small
intestinal malabsorption and significant protein-losing
enteropathy is likely to cause severe and rapid weight
loss.
CAUSES OF MALABSORPTION
SYNDROME
The common causes of malabsorption syndrome in the
adult horse are listed in Table 18.3.
Table 18,3 �01N!'1OAQUSU of malablorpiton
syndrome in tI'/f.•ultholM
Extensive small intestinal resection
Chronic inflammatory bowel diseases
granulomatous enteritis
eosinophilic gastroenteritis
multisystemic eosinophilic epitheliotrophic
disease
Iymphocytic-plasmacytic enterocolitis
Alimentary lymphosarcoma
Enteric infections
mycobacterial infection
enteric fungal infections
Idiopathic villous atrophy
Congestive heart failure
Intestinal ischemia
Parasitism
Extensive small intestinal resection
Insufficient absorptive area is a common cause of
small intestinal malabsorption. This can be caused by
extensive!excessive small intestinal resection following
surgery for small intestinal strangulations. The greater
the amount of small intestine resected, the greater the
risk of malabsorption. Small sections of resected bowel
have no untoward long-term effects, but extensive
CHRONIC WEIGHT LOSS 18
resections may result in the horse becoming a 'digestive
cripple'. The precise amount of small intestine that can
safely be resected appears to vary from horse to horse,
and the residual bowel is probably capable of compen­
sation for the loss of the resected portion over time.
One study suggested that no more than 60 per cent of
the small intestine could be safely resected, but other
studies suggest that up to 70 per cent can be removed
without causing subsequent malabsorption. Other
problems that are sometimes observed following
extensive small intestine resection in horses and ponies
include anorexia and liver disease.
Chronic inflammatory bowel disease
Chronic inflammatory bowel disease ( C I BD) is the col­
lective term for the group of infiltrative bowel diseases
that produce similar clinical signs to one another (pri­
marily chronic weight loss). These diseases are not as
well defined in the horse as they are in other species,
and their etiology is generally unknown. Both the small
and large intestines, the regional lymph nodes, and
sometimes other abdominal organs, may be involved
(Plate 18.1). The cellular infiltrate may consist of a
mixed cellular population or there may be a predomi­
nance of specific cell types such that CIBD may be
classified into a number of different disease types.
Differentiation between these diseases usually relies
upon histopathological examination.
Granulomatous enteritis is characterized by diffuse
granulomatous lesions, predominantly in the small
intestine, with lymphoid and macrophage infiltration of
the lamina propria, and variable numbers of plasma
cells and giant cells. There is marked villous atrophy
and an absence of lesions attributable to other forms of
granulomatous change (such as mycobacterial and fun­
gal infections). No etiological agent has been identified
in granulomatous enteritis, although it has been pro­
posed that the disease may result from an abnormal
host inflammatory reaction to intestinal bacteria, or
dietary components. The pathology of the condition
has similarities to that of Johne's disease in cattle and
Crohn's disease in man. Chronic mycobacterial infec­
tion of the intestine has similar histopathological
lesions, however, acid-fast organisms can be identified
in Ziehl-Neelson stained sections.
Granulomatous enteritis can occur in any age or
breed, or either sex, although it appears to be most com­
mon in young adult horses ( 1-5 years of age). It has also
been most commonly reported in the Standardbred. A
familial predisposition to the disease has been sug­
gested, and one report documented the occurrence of
the condition in three sibling Standardbred horses.
Chronic eosinophilic infiltrates may take the form of
377
18 CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
diffuse inflammatory cell infiltration of the small intesti­
nal mucosa with eosinophils and lymphocytes, or an
eosinophilic granulomatous infiltrate. Mucosal ulcera­
tion, enlargement of ileal Peyer's patches, and mesen­
teric lymphadenopathy are frequently present. The
etiology of the condition is unknown, but the nature of
the inflammatory infiltrate has led to the suggestion
that it represents an immune-mediated response to
parasites. The condition of multisystemic eosinophilic
epitheliotrophic disease has gastrointestinal as well as
cutaneous, hepatic, and pancreatic lesions.
Lymphocytic-plasmacytic enteritis is characterized
by mucosal infiltration by lymphocytes and plasma cells
in the absence of granulomatous change.
Alimentary lymphosarcoma
Alimentary lymphosarcoma may be a primary neoplas­
tic disease, or it may represent part of a multicentric
disease or a metastatic spread from a primary focus
somewhere else in the body. The disease may take the
form of discrete focal tumor masses in the bowel wall
(usually associated with chronic or recurrent colics; see
Chapter 17) or a diffuse intestinal infiltrate of neo­
plastic cells that may cause malabsorption. Both small
and/or large intestines may be affected, and mesenteric
lymph nodes are also commonly infiltrated by malig­
nant cells. Villous atrophy is commonly present in asso­
ciation with small intestinal infiltrates. Mucosal ulcers
are also commonly present, and these can contribute to
serum protein leakage and hypoproteinemia. Lumenal
bleeding can result in a blood-loss anemia in addition
to the typical anemia of chronic inflammation/
neoplasia. Lesions may also be present in other organs
throughout the body, and these may give rise to addi­
tional clinical signs and abnormalities of clinical pathol­
ogy. Although lymphosarcoma can affect horses of any
age, the disease is more commonly seen in horses over
5 years old.
Enteric infections
Mycobacterial granulomatous enterocolitis is rare, and
is usually associated with avian strains of Mycobacterium
tuberculosis or M. intracellulare. There are also rare
reports of enteric fungal infections due to Aspergillus
fumigatus or Histoplasma capsulatum. It has been sug­
gested that fungal infections may be most likely in
horses undergoing chronic antibiotic or corticosteroid
treatments.
CLINICAL SIGNS
The clinical signs associated with chronic infiltrative
small intestinal diseases are generally similar regardless
378
of the pathological lesion (apart from horses affected
by alimentary lymphosarcoma and multisystemic
eosinophilic epitheliotropic disease which may have
signs related to involvement of other body systems).
The clinical presentation is characterized by chronic
weight loss. Other signs are variable and may include
• diarrhea
• intermittent or chronic colic
• variable appetite - increased appetite, normal
appetite, inappetence, or anorexia
• depression
• lethargy
• peripheral and dependent edema (Plate 18.2)
• pyrexia
• skin lesions.
Skin lesions occurring in horses with malabsorption
include thin hair coat, patchy alopecia, and focal areas
of scaling and crusting (Plate 18.3). Severe, and often
highly pruritic, skin lesions may be present in horses
affected by multisystemic eosinophilic epitheliotrophic
disease ( Plate 18.4).
DIAGNOSIS
The general approach to evaluation of horses present­
ing with signs of chronic weight loss is described in
detail above (see Differential diagnosis and evaluation
of chronic weight loss). Clinicopathological findings
are non-specific, but may include
• hypoalbuminemia
• hyperglobulinemia or hypoglobulinemia
• neutrophilia (occasionally neutropenia)
• anemia
• hyperfibrinogenemia
• raised serum alkaline phosphatase
• reduced glucose absorption during oral glucose
absorption test
• reduced xylose absorption during D (+)-xylose
absorption test
• elevated serum IgA concentration
• depressed serum IgM concentration
(lymphosarcoma) .
Enlarged mesenteric lymph nodes may be palpable
per rectum in some cases (especially in cases of alimen­
tary lymphosarcoma). Abnormally thickened bowel wall
may occasionally be palpated per rectum, and this
can sometimes be confirmed using ultrasonography.
Abdominal paracentesis frequently yields normal peri­
toneal fluid. Neoplastic cells are rarely present in the
peritoneal fluid of horses with alimentary lymphosar­
coma. Elevated numbers of eosinophils may sometimes

be observed in horses with eosinophilic infiltrative
disease,
Rectal biopsy may yield a histopathological diag­
nosis in a small proportion of cases, but only if the
inf-iltrative lesion extends back to this level of the
intestinal tract.
A diagnosis of small intestinal malabsorption is
made using- a carbohydrate absorption test such as the
oral glucose absorption test or the D (+ )-xylose absorp­
tion !est (see Chapter 2). The oral glucose absorption
test is more commonly employed because of the ease of
analyzing plasma glucose levels. Horses can be divided
into three groups on the basis of the results of the oral
glucose absorption test
�onnal absorption - the glucose levels at 50 and
120 minutes are within the normal range as defined
by the mean ± 2 SD of the result_� of Roberts and
Hill (1973), and the glucose level at 120 minutes
shu\\'S a greater than 85 per cent increase over the
rCHing level.
2, Partial malabsorption - the glucose levels at 60 and
120 minutes arc below the normal range as defined
hy the mean :t 2 SD of the results of Roberts and
HilI ( 1 973), and the glucose level at 120 minutes
shows a less than 85 per cent but greater than
1 5 per cent increase over the resting level.
:-I. Total malabsorption - the glucose levels at 50 and
120 minutes are below the normal range as defined
by the mean ± 2 SD of the results of Roberts and
Hill (1973), and the glucose level at 120 minutes
shows a less than 15 per cent increase over the
resting level.
I Iorses with ' total malahsorption' are likely to have a
diffuse infiltrative small intestinal disease. Horses with
'normal absorption' are likely to have a histologicalIy
normal small intestine. Horses with a 'partial malab­
sorption' re.�ult may have evidence of an inflammatory
infiltrate or villous atrophy, hut they may also have
histologically normal intestine, and further diagnostic
tesl.� should be carried out.
Confirmation of r.he diagnosis of infiltrative small
intestinal diseases and villous atroph} is made by histo­
logical examination of sections of slllall intestin(\ Full
thickness bowel \,;al1 hiopsies may be obtained at
exploratory laparotomy for thi.� purpose, although
horses with malabsorption state.� are often not good
(·andidates for m'ljor exploratory surgery, and vmund
complicatiolls arc common in the postoperative period
because of hypoproteinemia and the (�atabolic state. If
surge!)' is to be performed, biopsies should be taken
from any grossly abnormal section of bowel, but. if the
bowel appears grossly normal then at least three small
intestinal biopsies should be taken from the proximal,
CHRONIC WEIGHT LOSS 18
mid- and distal small intestine, Biopsies should also be
obtained from the ceCUlIl and large colon at the same
time. Biopsies of mesemeric lymph nodes often reveal
similar pathological change to small illlcstinal infil­
trates, and at least one lymph node should be biopsied
at the same time as the bowel wal! biopsies are taken,
Bowel wall and lymph node: biopsies can also be suc­
cessfully obtained via a flank laparotomy that can be
performed in the standing horse utilizing local anesthe­
sia. This approach greatly reduces the complications
associated with ventral midline wound healing.
Alternatively, mesenteric lymph node biopsies may he
taken �ia laparoscopic techniques in the standing
patient, thereby eliminating the necessity for general
anesthesia and significantly reducing the risk of wound
complications. However, the sensitivity of this approach
for the diagnosis of small intestinal infiltrative disease
has not yet been assessed.
TREATMENT
The prognosis for horses affected by malabsorption syn­
dromes is generally guarded to very poor. By the time
that the precise diagnosis is reached, the disease is fre­
quently well-advanced. Horses affected by diffuse ali­
mentary lymphosarcoma have a hopeless prognosis and
should be humanely destroyed, although chemother­
apy may prolong survival for 6-1 2 months. Treatment
of fimg'<l1 enterocolitis with systemic antifungals is
usually unrewarding.
Some horses with CIBD !nay henefit from heing fed
highly digestible feeds. Provision of a palatable, easily
assimilated high energy and protein source is indicated.
Supplementing the diet with electrolytes, minerals, and
vitamins is also useful. Feeds with high quality fiber con­
tent may also contribute to body weight g'<lin in that they
may be more extensively converted from cellulose to
volatile free fatty acids in the cecum; this type of diet is
especially beneficial tn horses affected by CIBD without
diarrhea. Feeding more fh�quent meals in smaller
amounts may also aid in better digestion and absorp­
tion. l<:nteral feeding through an indwelling nasogastric
tube is rarely indicated in view of the poor long-term
prognosis. There i.� no justification in tf)ing to sustain a
severely debilitated horse when the progllosis is so poor.
Corticosteroid therapy is often ineffective in treating
CIBD, although some cases of eosinophilic infiltrates
and lymphocytic-plasmacytic enterocolitis appear to be
responsive to corticosteroids. Parenterally administered
dexamethasone is likely to he more effective than oral
corticoMeroids, and prolonged courses are required.
Surgical resection of limited areas of affected bowel
may produce some short term benefiL�, but the diffuse
379
18 CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
nature of the lesions usually precludes this therapeutic
option.
BIBLIOGRAPHY
Differential diagnosis and evaluation of
chronic weight loss
Brown C M ( 1 989) Chronic weight loss. In Problems in Equine
Medicine, C M Brown (ed. ) . Lea and Febiger, Philadelphia,
pp. 6-22.
Divers TJ, Mohammed H 0, CummingsJ F ( 1 998) Equine
motor neuron disease. In Current Therapy in Equine
Medicine, 4th edn, N E Robinson (ed. ) . W B Saunders,
Philadelphia, pp. 321-2.
East L M, Savage C J ( 1 998) Abdominal neoplasia (excluding
urogenital tract) . Vet. Clin. N. Am. Equine Pract. 14: 475-93.
ForemanJ H ( 1 998) Changes in body weight. In Equine
Internal Medicine, S M Read and W M Bayly (eds ) . W B
Saunders, Philadelphia, pp 1 35-9.
Kronfeld D S ( 1993) Starvation and malnutrition of horses:
recognition and treatment. ]. Equine Sci. 1 3: 298-304.
Kronfeld D S ( 1 998) Clinical assessment of nutritional status
of the horse. In Metabolic and Endocrine Problems of the Horse,
T D G Wat�on (ed. ) . W.B. Saunders, London,
1 84-217.
Mair T S, Hillyer M H ( 1 99 1 ) Clinical features of
lymphosarcoma in the horse: 77 cases. Equine Vet. Educ.
4:108-13.
Rebhun W C, Bertone A ( 1984) Equine lymphosarcoma.
]. Am. Vet. Med. Assoc. 1 84:720-1.
Savage CJ ( 1 998) Lymphoproliferative and
380
myeloproliferative disorders. Vet. Clin. N. Am. Equine Pract.
1 4:563-78.
Scarratt W K, Crisman M V ( 1998) Neoplasia of the
respiratory tract. Vet. Clin. N. Am. Equine Pract. 1 4:45 1-73.
Taylor F G R ( 1 997) Chronic wasting. In Diagnostic Techniques
in Equine Medicine, F G R Taylor and M H Hilyer (eds) .
W B Saunders., London, 65-70.
Malabsorption syndromes
Cohen N D, Loy j K, Lay j C, Craig T M, McMullan W C
( 1 992) Eosinophilic gastroenteritis with encapsulated
nematodes in a horse. ]. Am. Vet. Med. Assoc.
200: 1 5 1 8-20.
Duryea j H, Ainsworth D M, Maudlin E A, Cooper B j,
Edwards R B ( 1997) Clinical remission of
granulomatous enteritis in a Standardbred gelding
following long term dexamethasone administration.
Equine Vet.]. 29: 1 64-7
Kemper D L, Perkins G A, Schumacher j, EdwardsJ F,
Valentine B A, Divers T j, Cohen N D ( 1 999) Equine
Iyrnphocytic-plasmacytic enterocolitis: a retrospective
study of 14 cases. Equine Vet. ].
MacAllister C G, Mosier D, Qualls C W, Cowell R L ( 1 990)
Lymphocytic/plasmacytic enteritis in two horses. ]. Am.
Vet. Med. Assoc. 196: 1 995-8.
Mair T S, Hillyer M H, Taylor F G R, Pearson GR ( 1 991 )
Small intestinal malabsorption i n the horse: an assessment
of the specificity of the oral glucose tolerance test. Equine
Vet.]. 23:344-6.
Roberts M C ( 1 985) Malabsorption syndromes in the horse.
Compo Cont. Educ. Pract. Vet. 7:S637-S646.
Roberts M C, Hill F W G ( 1973) The oral glucose tolerance
test in the horse. Equine Vet.]. 5: 1 71-3.
 19
Hepatic and biliary tract diseases
Acute hepatic disease with
failure
TJ Divers
There are a large number of equine disorders that may
cause hepatic disease but few ever result in hepatic fail­
ure. For example, horses with strangulating or inflam­
matory intestinal diseases frequently have evidence of
liver disease (elevated hepatic enzymes in the serum)
caused by portal hypoxia and/or increased concentra­
tion of endotoxin in the portal circulation, but these
conditions rarely progress to liver failure.
Many disorders that cause chronic liver disease, e.g.
pyrrolizidine alkaloid toxicosis, may present with acute
signs of hepatic failure. Those disorders that cause
chronic liver disease are covered elsewhere in this text
(see Pyrrolizidine alkaloid intoxication and Chronic
liver disease ) .
In ponies and miniature horses, the most common
cause of acute hepatic disease and failure is hepatic lipi­
dosis (see Hyperlipemia) . In adult horses, the most
common syndrome causing acute hepatic disease with
failure is Theiler's disease.
Theiler's disease is a subacute hepatic necrosis often
resulting in hepatic failure and acute encephalopathy
in horses. It has been termed 'serum hepatitis' because
often there is a history of the affected horses receiving
tetanus antitoxin 4-10 weeks prior to the onset of
clinical signs. In some cases, the affected horses may not
have received tetanus antitoxin, but may have been in
contact with another horse that had received tetanus
antitoxin. In other cases, there is no history of equine
origin biological products being administered. The
disease appears to be more common in late summer or
early fall. This apparent seasonal pattern could suggest
a vector spread of the disease, or could simply reflect
the fact that many foaling mares may receive tetanus
antitoxin in the spring of the year along with their new­
born foal. Most commonly, only one horse on a farm is
affected, although outbreaks are reported and other
horses on the farm may have evidence of liver disease,
e.g. elevated enzymes, without clinical signs of hepatic
failure. A specific tetanus antitoxin product and/or
the same batch and lot number, may be found to be
responsible for a high number of cases. A nearly
identical clinical and pathological syndrome has been
described in pastured horses in France.
Clinical signs
The clinical signs of Theiler's disease, or any severe
hepatic necrosis, are attributable to the rapid loss of
hepatocyte function and collapse of the liver
parenchyma. The most common clinical signs seen with
Theiler's disease are
• signs of central nervous system (CNS) disorder
• jaundice
• discolored urine.
The CNS signs are variable and may range from
acute depression to maniacal behavior. Blindness may
be present and the affected horses may be ataxic. Icteric
381
19 CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
membranes can be noted in most cases, although in
peracute cases this may not be pronounced. The urine
may be abnormally dark indicating bilirubinuria and,
in a few cases, red if there is a concurrent microangio­
pathic hemolytic process.
Neurologic signs are frequently observed with acute
hepatic failure and are referred to as hepatoencephalo­
pathy. Hepatoencephalopathy is a metabolically induced,
potentially reversible, functional disorder of the brain.
Neurologic signs are the most pronounced and clini­
cally troublesome signs in most cases of equine hepatic
failure. Signs of hepatoencephalopathy may vary from
depression to bizarre maniacal behavior. Common
signs include
• apparent blindness
• ataxia
• head pressing
• propulsive circling
• frequent yawning.
The pathophysiologic mechanism of hepatoencephalo­
pathy is undoubtedly complex but is mostly due to
abnormal hepatic protein metabolism. The failing liver
may be unable to sufficiently convert colonic-derived
ammonia to urea via urea cycle enzymes located in the
hepatocyte. The effect of excessive ammonia on the
central nervous system (CNS) may include one or more
of the following
• enhancement of neurotransmitters
• interference with normal neurotransmission
• structural changes in the blood-brain barrier
• changes in cerebral blood flow
• interference with biochemical or
electrophysiological pathways in the brain.
Cerebral edema with development of Alzheimer type
II cells are characteristic of high CNS ammonia.
Alzheimer type II cells may result from hepatic failure,
primary hyperammonemia or severe uremia. In rare
cases, the cerebral edema may be so severe that hernia­
tion occurs. Additionally, there may be decreased
hepatic extraction of gut synthesized y-aminobutyric
acid (GABA) which may additionally serve as a potent
inhibitory neurotransmitter. The GABA-ergic neuro­
transmission is also closely linked to an increase
in natural benzodiazepines. Furthermore, abnormal
accumulation of glutamate may serve as excitatory
neurotoxins. Complex interactions of these neurotoxins
may determine if the horse with hepatoencephalopathy
is depressed or maniacal. The movement of GABA into
the CNS may be aided by an increased aromatic to
branched chain amino acids ratio in the plasma, and by
increased concentrations of plasma bile acids. Increased
amounts of aromatic amino acids, which are normally
382
metabolized by the liver, may also serve as false neuro­
transmitters. In adult horses with hepatic failure, the
CNS signs of severe depression are rarely caused by
inadequate hepatic gluconeogenesis and hypoglycemia.
Horses with acute hepatic failure and/or Theiler's
disease generally have increases in both conjugated and
unconjugated bilirubin, with the increase in unconju­
gated being the most pronounced in all acute diseases
except biliary obstruction. The unconjugated portion
becomes elevated because of lost hepatocellular
function with reduced uptake and conjugation of the
bilirubin.
Intravascular hemolysis and red discoloration of the
urine may be seen occasionally with equine hepatic
failure. This occurs most frequently with acute hepatic
necrosis, e.g. Theiler's disease, and is often, but not
always, a terminal event. The cause of the hemolysis
may be a microangiopathic hemolytic anemia caused
by the physical damage to the red cells as they pass
through the necrotic liver.
Severe bleeding problems are not commonly
observed in horses with acute liver failure. When bleed­
ing occurs, it is generally prolonged bleeding associated
with hepatoencephalopathy and self-inflicted physical
trauma. Hemorrhage in horses with liver failure is gen­
erally a result of failure in both the extrinsic and intrin­
sic pathways of coagulation causing prolongation of
both prothrombin and partial thromboplastin times.
These occur because of decreased hepatic production
of clotting factors. Factor VII has the shortest half-life,
so prothrombin time (PT) should be prolonged prior
to prolongation of partial thromboplastin time (PTT)
with liver failure. In some horses with liver failure, the
PTT may sometimes be prolonged beyond the normal
range prior to the PT being prolonged. The reason for
this is unknown. Disseminated intravascular coagula­
tion (DIC) may be present in some horses with acute
severe liver failure. The cause of this is often multifacto­
rial and may include decreased hepatic production of
antithrombin III, plasminogen, and high molecular
weight proteins that inhibit excessive coagulation.
Additionally, overwhelming hepatic tissue damage
and/or increased circulating endotoxin may stimulate
release of soluble proteins that affect coagulation.
Fibrin degradation products (FDPs ) are often abnor­
mally high in horses with liver failure since the liver is
the organ responsible for clearance of circulating FDPs.
An increase in FDPs, PT and PIT would be expected in
horses with liver failure and these findings should not
be overinterpreted as being diagnostic for DIC. If a liver
biopsy is required, this can generally be performed
safely in spite of the prolongation in PT and PTT, since
platelet counts generally remain normal in horses with
liver failure.

Diagnosis
The diagnosis is based on
• history
• clinical findings
• laboratory confirmation of hepatic disease and
hepatic failure.
Hepatic disease can be detected most easily by measur­
ing serum or plasma activity of liver-derived enzymes
including
• gamma glutamyl transferase (GGT)
• aspartate aminotransferase (AST)
• sorbitol dehydrogenase (SDH)
• glutamic dehydrogenase (GD)
• lactate dehydrogenase (LDH-5) .
Gamma glutamyl transaminopeptidase will be elevated
in all cases of Theiler's disease and is most often in the
range of 1 00-300 IV/I. Aspartate aminotransferase
should be measured because it may provide an indica­
tion of prognosis, i.e. those horses having values
greater than 4000 IV/1 have a poor prognosis. The
repeated measurement of AST may also be used to
measure recovery as the AST would be expected to
decrease within 3-5 days if the horse is going to
recover. Gamma glutamyl transaminopeptidase, on the
other hand, will frequently elevate further during the
first 3 days of the illness in spite of clinical improve­
ment and eventual recovery in an affected horse. A
decrease in SDH in the serum would be expected to
occur more rapidly in improving horses than a
decrease in AST, because of its shorter half-life, and
measuring SDH can provide prognostic information
more quickly than measuring AST.
Total serum bile acids may also be used to detect
liver disease. In horses with Theiler's disease, the
measurement of serum or plasma bile acids rarely adds
further information than that provided by the measure­
ment of hepatic enzymes. Virtually all horses clinically
affected with Theiler's disease will have total serum
bilirubin values greater than those commonly observed
with anorexia. Total bilirubin in horses showing clinical
signs caused by Theiler's disease is generally in the
range of 12-20 mg/dl (205-340 flmol/I) . The percent­
age of bilirubin in the unconjugated form is almost
always greater than 70 per cent, although there is some
increase in conjugated bilirubin in affected horses. The
conjugated bilirubin values are generally 1.5-5.0 mg/dl
(25.5-85.5 J.lmol/I). The PT and PTT times are gener­
ally abnormally high in comparison to a control sample,
but rarely offer information not already gathered from
the measurement of direct and indirect bilirubin, bile
acids, and hepatic enzyme activity in the serum or
HEPATIC AND B ILIARY TRACT DISEASES 19
plasma. Other laboratory findings that are frequently
abnormal in Theiler's disease include
• moderate to severe acidosis
• hypokalemia
• polycythemia
• increased plasma aromatic amino acids
• hyperammonemia
A more definitive diagnosis of Theiler's disease can
only be made by liver biopsy. If the history, clinical
findings, and laboratory findings are characteristic of
Theiler's disease, a biopsy is not imperative, and in
many cases, may not be easy to perform since the liver is
often shrunken and may be difficult to visualize with
ultrasound examination. Microscopic examination gen­
erally reveals marked hepatocellular necrosis involving
the entire lobule, most severe in the central and mid­
zonal hepatocytes. There is some fatty change and a
very mild-to-moderate accumulation of lymphocytes
and a few neutrophils. The degree of bile duct prolifer­
ation is often positively correlated with the duration of
the disease. On necropsy examination, the liver is
usually smaller than normal, tan in color, and may
have markedly congestive centrilobular patterns. The
borders of the liver are sharp.
Therapy
There is no specific therapy for Theiler's disease
although supportive therapy is often successful. The
affected horse should not be stressed if at all possible .
Stressful situations such as moving the animal to
another facility or weaning the mare's foal often exac­
erbate the clinical signs of the hepatoencephalopathy.
Sedation should be used only when necessary to control
fulminant hepatic encephalopathy causing propulsive
behavior. Xylazine (0.2-0.4 mg/kg) can be used to
control bizarre behavior in order to prevent injury of
the animal and to allow catheter placement. Doses of
xylazine that cause lowering of the head should be
avoided if possible as low-head position and hypoventi­
lation may worsen cerebral edema. Phenobarbital can
be used but diazepam should be avoided since it may
worsen hepatoencephalopathy. The benzodiazepine
receptor antagonist, flumazinil (0.2 mg/kg given slowly
intravenously) may be administered for uncontrolled
hepatic encephalopathy, but its efficacy in both horses
and humans is unproven.
Intravenous fluids are probably the most important
component of treatment for hepatic encephalopathy in
horses! The intravenous fluids should consist of a
balanced electrolyte solution, preferably without lac­
tate, and should be supplemented with potassium
20-40 mEq/l, and 5-10 g dextrose per 100 ml. Sodium
383
19 CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
bicarbonate should be given only if blood pH is less
than 7.1 and/or bicarbonate is less than 1 4 mEq/1.
Additional potassium may be given as potassium
chloride mixed in molasses and administered per os via
a dose syringe. Fresh frozen plasma may be used but
hetastarch or stored whole blood should be avoided.
Supplemental vitamins can be administered but are not
necessary in the treatment.
An effort should be made to decrease ammonia pro­
duction in the bowel and this can be done by adminis­
tering neomycin 5.0 mg/kg p.o. q. 8 h by dose syringe
for 2 days. With fulminant hepatic encephalopathy in
the horse, I prefer not to pass a nasogastric tube since
nasal bleeding could occur. Nasal bleeding could exac­
erbate the hepatic encephalopathy if the blood is swal­
lowed and because of insufficient clotting proteins the
bleeding may be prolonged. Lactulose 0.2-0.5 ml/kg q.
8-12 h may also decrease ammonia production in the
bowel and can be used concurrently with neomycin.
Both lactulose and neomycin may cause diarrhea if
given in excessive dosages or for prolonged periods.
Vinegar (acetic acid) may also be effective in decreasing
blood ammonia when it is administered per os at 8 oz
(240 ml)/450 kg horse. Affected animals should be fed
high carbohydrate, high branch chain amino acid
(BCAA) feeds, with moderate to low total protein
content. Sorghum and/or cracked corn mixed with
molasses or commercially prepared BCAA paste are
ideal. Carbohydrates should be fed in frequent small
amounts. A moderate protein grass hay should be fed
rather than alfalfa hay or spring-cut grass hay. Affected
animals should be protected from sunlight in order to
prevent photosensitization.
Anti-oxidant, anti-inflammatory and anti-edema
therapy is indicated in acute hepatic failure. The anti­
oxidant, anti-edema treatments include dimethylsulfox­
ide, acetyicysteine and mannitol given intravenously
and vitamin E given intramuscularly. Anti-inflammatory
therapy should include flunixin meglumine and
pentoxifylline.
Cases of fulminant hepatic necrosis that do not
respond quickly to medical therapy are generally hope­
less. In the future extracorporeal liver support might be
helpful in managing some horses.
Prognosis
Horses with Theiler's disease that can be maintained
for 3-5 days without deterioration and that continue to
eat often recover. A decline in the SDH and PT, along
with improvement in appetite, are the best positive pre­
dictive laboratory and clinical indicators of recovery.
Horses that have fulminant encephalopathy that cannot
be easily controlled with sedatives have a very poor
384
prognosis, although some will recover. The degree of
hyperbilirubinemia is a less powerful prognosticator
than encephalopathy. Those animals that continue to
eat during the first 3 days of the illness generally have a
good prognosis. If the affected horse recovers, which
many do within 5-10 days, its long-term prognosis is
excellent. There is no evidence that severe hepatic
fibrosis and/or neoplasia occur following Theiler's
disease in the horse.
MISCELLANEOUS CAUSES OF ACUTE
HEPATIC DISEASE AND FAILURE
There are only scattered reports of other causes of
acute hepatic disease and failure in adult horses.
Mycotoxicosis or other hepatotoxins make up the bulk
of these reports. Fusarium moniliforme toxins, especially
fumonisin B, may cause hepatic disease and rarely
hepatic failure in horses eating the fungi-contaminated
corn. Leukoencephalomalacia is the most common
disease and clinical syndrome caused by this toxin.
Aspergillus flavus and aflatoxins B" B2 and Mj contami­
nation of grain may cause hepatic necrosis and fulmi­
nate hepatic failure in horses. Fortunately aflatoxicosis
is rare in horses in most parts of the world. Pyrrolizidine
alkaloid-containing plants may also cause acute hepatic
disease and failure, although chronic disease with acute
failure is most common (see Pyrrolizidine alkaloid
intoxication ). Septic portal vein thrombosis is rare in
horses but should be considered in adult horses with
acute hepatic encephalopathy.
Primary hyperammonemia
SF Peek
INTRODUCTION
Primary hyperammonemia in the absence of significant
hepatic disease is an uncommon cause of encephalopa­
thy in horses. The reports of primary hyperammonemia
in adult horses are limited to a single case report from
the United Kingdom and a series of cases from the
north eastern United States. In addition, a potentially
inherited condition of Morgan horses causing primary
hyperammonemia and clinical disease in weanlings has
also been reported in the United States. Experimentally
hyperammonemia can be induced by the ingestion of
urea but there are no clinical reports of spontaneous
urea poisoning in horses. By comparison with rumi-

nants horses are considered to be fairly resistant to the
toxic effects of urea.
ETIOLOGY
The etiology of primary hyperammonemia in adult
horses is unknown. The association between primary
hyperammonemia and antecedent or concurrent signs
of gastrointestinal disease, without biochemical evi­
dence of liver disease, raises suspicion that excessive
ammonia production within the large intestine is a
possible etiology.
CLINICAL SIGNS
The clinical signs associated with primary hyper­
ammonemia in adult horses include acute encephalo­
pathy, blindness, and gastrointestinal signs that can vary
from colic to acute diarrhea. The clinical signs relating
to gastrointestinal dysfunction typically precede the
development of encephalopathy.
CLINICAL PATHOLOGY
Consistent abnormal laboratory findings identified in
adult horses with primary hyperammonemia include
evidence of dehydration, severe hyperglycemia (> 275
mg/dl or IS mmol/I), and metabolic acidosis (venous
pH < 7 . 15 ) . A blood ammonia concentration of greater
than 150 mg/ml in the absence of clinical and bio­
chemical evidence of liver disease is considered diag­
nostic, but clinical cases of primary hyperammonemia
frequently have blood ammonia concentrations in
excess of 250 mg/ml prior to treatment. Accurate mea­
surement of blood ammonia concentration requires
rapid and careful sample handling. Ideally a control
sample should be obtained from a normal, healthy
horse and quantitated simultaneously for comparative
purposes. Individuals with primary hyperammonemia
that present with acute diarrhea may also develop
severe electrolyte abnormalities and life-threatening
hypoproteinemia.
TREATMENT
Treatment of primary hyperammonemia is predomi­
nantly supportive but should include administration of
products per os to decrease the production and intesti­
nal absorption of ammonia. Recovery is possible if
horses can be supported during the acute encephalo-
H E PATIC AND B ILIARY TRACT DISEASES 19
pathic stage and any concurrent intestinal disease does
not become a life-threatening problem. Intravenous
fluid therapy is important to maintain tissue perfusion
and to correct specific electrolyte and acid-base abnor­
malities. Dextrose-containing fluids should be avoided
due to the severe hyperglycemia that accompanies this
condition. Individual horses with primary hyperam­
monemia may survive following intensive intravenous
fluid therapy with balanced polyionic fluids. In cases
where hypoproteinemia becomes a complicating factor,
fresh blood, plasma, or plasma expanders should be
considered. The addition of bicarbonate to intravenous
fluids should be considered when systemic pH falls
below 7. 10. The acidifying agent lactulose (90- 120 ml
p.o. q.i.d.) can be used to decrease ammonia absorp­
tion from the large intestine by increasing the conver­
sion of ammonia to ammonium ions, which are not
absorbed from the lumen. In addition oral antibiotics
such as neomycin (20-30 mg/kg q.i.d. ), or metronida­
zole ( l 0-15 mg/kg q.i.d.) may be administered to
decrease ammonia-producing bacteria within the large
intestine.
POST·MORTEM FINDINGS
Histologic abnormalities in the brain of horses that
have died or been euthanized due to primary hyperam­
monemia include edema and frequent Alzheimer type
II cells. Alzheimer type II cells are diagnostic for hyper­
ammonemia and will therefore also be seen in horses
that exhibit hepatic encephalopathy ante mortem due
to either acute or chronic liver failure. Cases of primary
hyperammonemia that demonstrate diarrhea ante
mortem may also have moderate to severe inflamma­
tory changes in the large colon and cecum, although no
specific infectious etiologic agent has so far been
associated with the condition.
HYPERAMMONEMIA IN MORGANS
Etiology
Persistent hyperammonemia has been documented in
two related Morgan weanlings. The same stallion sired
the affected horses and their dams were sisters. Based
upon the familial relationship and the demonstration
of abnormal serum and urine amino acid con­
centrations it is suggested that this condition may be an
inherited disorder that is analogous to the hyperor­
nithinemia, hyperammonemia, and homocitmllinemia
(HHH) syndrome in man. HHH syndrome is a rare
autosomal recessive disorder that results from
385
19 CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
abnormal ornithine transport into mitochondria with
subsequent ornithine accumulation and a reduced
ability to clear ammonia through the urea cycle.
Clinical signs
The affected foals were clinically normal until approxi­
mately 2 weeks post-weaning when they began exhibit­
ing generalized unthriftiness and abnormal behavior.
The neurologic status of both individuals deteriorated
and they were euthanized at approximately 7 months of
age. Seizure activity was reported in one foal, but both
demonstrated other signs of encephalopathy including
severe depression, propulsive circling, teeth grinding,
and dementia.
Clinical pathology
Unlike primary hyperammonemia of adults, where no
biochemical evidence of hepatic dysfunction has been
documented, one of the weanlings did have enzymatic
evidence of hepatocellular disease while the other had
a prolonged bromosulfthalein (BSP ) retention time.
Severe hyperammonemia (200-500 mg/ml ) was docu­
mented on several separate occasions in both indivi­
duals. Serum ornithine and glutamate concentrations
were elevated in both weanlings compared to controls.
Urinary orotic acid concentration was measured in one
of the two foals and was found to be significantly
elevated.
Treatment
Although supportive therapy including intravenous
fluids, oral lactulose, and the provision of a low protein
diet was instituted, both horses were euthanized due to
a progressive deterioration in neurologic status.
Post-mortem findings
Necropsy findings were not specific but included
plasmacytic/lymphocytic hepatitis as well as histologic
changes in the central nervous system consistent with
hyperammonemia.
Biliary tract disease
SF Peek
INTRODUCTION
Cholangiohepatitis is the most commonly encountered,
clinically significant form of biliary tract disease in
386
horses. Other forms of true biliary disease appear to be
very uncommon in horses, but biochemical evidence of
hepatobiliary injury and dysfunction, including eleva­
tions in serum bilirubin, gamma glutamyl transferase
(GGT) , alkaline phosphatase (AP), bile acids, and
prolonged exogenous dye excretion tests frequently
accompany both acute and chronic hepatic diseases
such as Theiler's disease, Tyzzer's disease, hepatic
lipidosis, and pyrrolizidine alkaloid toxicity. Rarely, bio­
chemical and clinical evidence of biliary tract disease
may occur in association with the so-called 'chronic
active hepatitis', abscesses, granulomas, or infiltrative or
obstructive neoplastic conditions, such as primary
cholangiocarcinoma, hepatic adenocarcinoma, or
metastatic hepatic tumors.
CHOLANGIOHEPATITIS
Although this condition probably begins as a cholangi­
tis, the term cholangiohepatitis is appropriate because
clinically significant inflammatory biliary disease in
horses is extremely rare without extension into the peri­
portal region of the liver. It is probable that many mild
cases of cholangitis/cholangiohepatitis are undiag­
nosed because horses are asymptomatic, but the condi­
tion predisposes horses to chronic, active, inflammatory
hepatobiliary disease and the formation of biliary
calculi. Chronic cholangiohepatitis may frequently be
associated with significant intrahepatic or extrahepatic
calculus formation. Discrete calculi can often be visual­
ized ultrasonographically or at post mortem examina­
tion, but some horses with cholangiohepatitis develop a
more sonolucent 'sludge-like' material within the bil­
iary tract. With severe suppurative cholangiohepatitis,
particularly if the condition is long standing, significant
periportal and bridging fibrosis can occur. Clinically
significant hepatobiliary disease appears to be more
common in middle-aged to older horses. Due to the
absence of a gall bladder, the nomenclature surround­
ing biliary calculi in the horse has been confusing. The
term cholelithiasis broadly refers to calculi anywhere
within the biliary tract, but in man it has come to be syn­
onymous with calculi within the gall bladder. It is per­
haps more appropriate in horses to refer to intrahepatic
calculi as hepatoliths and extrahepatic calculi, usually
located within the common bile duct, as choledocho­
liths (Plate 19. 1 ) .
Etiopathogenesis
The etiopathogenesis of cholangiohepatitis in adult
horses is presumed to be ascending bacterial infection
from the proximal small intestine. Evidence for this

comes from retrospective studies documenting the iso­
laticm of predominantly gram-negative, enteric bacteria
such as Escherichia coli, Enterobacter spp. and Citrobacter
spp. from clinical cases. The ascending infection is
believed to predispose to calculus formation by creating
a nidus around which the calculus forms. The composi­
tion of calculi in horses is predominantly calcium bili­
rubinate and calcium phosphate, analogous to brown
pigment stones in man.
Clinical signs and diagnosis
Cases of cholangiohepatitis commonly present with the
non-specific clinical signs of fever, icterus, colic, weight
loss, and encephalopathy.
Careful history taking will often reveal recurrent
bouts of mild-to-moderate colic coincident with fever
in the preceding days to weeks. Significant weight
loss will commonly accompany more chronic cases.
Occasionally signs of hyperammonemic hepatic
encephalopathy can be seen when complete calculus
obstruction to biliary outflow occurs or the disease
process has progressed to fulminant hepatic failure.
Serum biochemical abnormalities include large
increases in the hepatobiliary enzymes GGT and AP,
alongside moderate increases in the hepatocellular
enzymes aspartate transaminase (AST) and sorbitol
dehydrogenase (SDH). Total serum bilirubin is ele­
vated, frequently well above the levels typically seen with
anorexia alone, with the direct reacting or conjugated
fraction representing more than 25 per cent of the
total. The ratio of direct to indirect bilirubin is a very
helpful parameter in the diagnosis of cholangiohepati­
tis because the proportionate increase in the direct
reacting fraction is fairly specific to this condition in
horses. Bilirubinuria may also be observed. Serum bile
acids will be elevated in many cases of cholangiohepati­
tis, and can reach very high levels (> 1 00 mmol/l ) in
cases with significant biliary obstruction. Horses with
either maniacal or depressive hepatic encephalopathy
in association with complete calculous obs truction or
severe, chronic cholangiohepatitis will have elevated
blood ammonia levels. Typically hematologic changes
are consistent with chronic, active inflammation and
include neutrophilia and hyperfibrinogenemia. If the
condition is more than 2-3 weeks in duration hyper­
globulinemia may also be documented.
Although clinical and laboratory findings can be
highly suggestive of the condition, a definitive diagnosis
of cholangiohepatitis requires liver biopsy. It is recom­
mended that in vitro measurements of clotting function,
specifically the prothrombin time and activated partial
thromboplastin time, be made prior to hepatic biopsy.
Frequently these indices are normal but they may be
HEPATIC AND BILIARY TRACT DISEASES 19
prolonged if the biosynthetic capacity of the liver
has diminished in association with advanced post­
inflammatory fibrosis. The biopsy procedure is best
performed under light sedation and ultrasonographic
guidance using a 1 4-gauge biopsy needle. Sufficient
biopsy material should be obtained for aerobic and
anaerobic culture as well as for routine histopathology.
Visualization of the liver via ultrasound lessens the risk
of inadvertent colonic, diaphragmatic, or pulmonary
i�ury, that can occur when the procedure is per­
formed blind using traditional anatomic landmarks.
Histologically the liver tissue should be evaluated for
both the severity of inflammation and the presence
and extent of any periportal and bridging fibrosis.
Advanced bridging fibrosis should carry a more
guarded prognosis, particularly when it is accompanied
by biochemical evidence of liver failure such as hypo­
albuminemia, hypoglycemia, and altered clotting times.
Bile duct hyperplasia is invariably reported but repre­
sents a non-specific response to liver injury.
In normal horses the liver can best be visualized
between the 1 1th and 1 6th intercostal spaces on the
right side, and the 9th and 1 1 th spaces on the left side.
In cases of cholangiohepatitis the liver image can fre­
quently be visualized over a much greater area due to
hepatomegaly. The degree of hepatomegaly, bile duct
dilation, and the presence of significant hepatoliths
should be evaluated ultrasonographically. It is not
Figure 19.1 Sonogram from a 14-year-old Thoroughbred
mare with chola n giohepatitis and hepatolithiasis. Ultra­
sonographically there is an obvious dilated bile duct with
an intraluminal hepatolith (white arrow). Note the vari­
ably hyperechoic appearance of the hepatic parenchyma
(dark arrows). The image was obtained with a 3.5 MHz
sector scanner
387
19 CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
possible to visualize bile ducts via ultrasound in the nor­
mal horse. However, significant bile duct dilation and
discrete calculi may be detected in many clinical cases
(Figure 19.1 ). The echogenicity of calculi and degree of
acoustic shadowing will vary with the extent of mineral­
ization. With experience it may be possible to charac­
terize the hepatic parenchyma as being diffusely more
echogenic than normal, particularly in cases where
significant hepatic fibrosis has occurred.
Medical management
Long term antimicrobial therapy is essential in the suc­
cessful treatment of cholangiohepatitis and choledo­
cholithiasis/hepatolithiasis in adult horses. In certain
situations where biliary obstruction is complete, or the
horse is in uncontrollable abdominal pain, surgery
may be considered (see below) . The choice of specific
antibiotics should be ideally based upon both aerobic
and anaerobic cultures of liver biopsy material. If biopsy
culture results are either unavailable or negative, then
broad spectrum antibiotics such as potentiated sulfon­
amides, cephalosporins, or fluoroquinolones would be
appropriate choices. Although the spectrum of activity
of the aminoglycosides is limited to aerobic, gram-nega­
tive bacteria, a good clinical response to this family of
antibiotics is often observed. The duration of anti­
microbial therapy will vary on a case by case basis but
experience suggests that weeks to months of therapy are
necessary. Treatment failure can commonly be associ­
ated with premature antibiotic withdrawal, and it is
worth considering that both clinical and biochemical
resolution should be confirmed before treatment is
stopped. Many horses will show substantial clinical
improvement in terms of appetite, absence of fever, and
weight gain while still demonstrating significant bio­
chemical evidence of hepatobiliary disease. It is recom­
mended that antibiotic treatment be continued until
serum GGT and AP levels have been normal for 2-4
weeks . Repeated ultrasonographic evaluation of the
liver during the course of therapy can be useful in
assessing improvements in hepatomegaly, bile duct
dilatation, and the resolution of any identifiable calculi.
Intravenous polyionic fluid therapy can be a very useful
adjunct to antimicrobial therapy both in cases of acute
cholangiohepatitis and during long-term therapy when
an individual horse clinically deteriorates.
Individuals that present with hyperammonemic
hepatic encephalopathy may be treated with products
to reduce both the production and absorption of
ammonia in the large intestine. The oral administration
of either neomycin (20-30 mg/kg q.i.d.) or metronida­
zole ( 10-1 5 mg/kg q.i.d.) has been recommended to
alter cecal and colonic bacterial flora and thereby
388
reduce ammonia production. Lactulose (90- 120 ml
p.o. q.i.d. ) can be given as an acidifying agent to alter
lumenal pH and increase the conversion of ammonia to
non-absorbable ammonium ions. Adult horses with
hepatic encephalopathy can vary from somnolent to
violent and maniacal and will often require chemical
restraint for both their own protection and that of
people around them. If the hepatic encephalopathy
accompanies fulminant liver failure the prognosis
should be extremely guarded. Intensive intravenous
fluid therapy to correct and maintain hydration, elec­
trolyte and acid-base status are essential parts of the
therapy of cases of cholangiohepatitis that present with
concurrent fulminant liver failure.
Specific bile salt therapy with compounds such as
ursodeoxycholic and chenodeoxycholic acid is contra­
indicated in horses, not only because cholesterol rich
calculi are extremely rare but also because these com­
pounds have been shown to be metabolized to pro­
inflammatory hepatotoxic compounds in other hind
gut fermenters such as rabbits. There is however,
specific evidence to support the use of intravenous
dimethylsulfoxide (DMSO) in the medical manage­
ment of brown pigment stones in man, and by analogy
its use is justifiable in cases of equine choledocholithia­
sis and hepatolithiasis. DMSO can be given intra­
venously at a dose of 1 g/kg s.i.d. for 5-7 days, diluted to
a 5% solution in fluids.
Surgical management
Surgical management of cholangiohepatitis and biliary
calculi should probably be reserved for cases of com­
plete biliary obstruction with severe, unrelenting
abdominal pain that is unresponsive to conventional
analgesics. Cases of complete obstruction often present
with hyperammonemic encephalopathy and will there­
fore benefit from intensive supportive medical manage­
ment as well as surgical relief of the obstruction.
Anecdotal and published reports of successful surgical
management by either manual lithotripsy or choledo­
cholithomy do exist but bile peritonitis carries such a
grave prognosis that great care should be taken when
attempting to either remove, or 'milk' calculi into the
proximal small intestine at laparotomy. Recurrent
obstruction is likely because most cases will have addi­
tional intrahepatic calculi that are inaccessible to the
surgeon, and these may continue to partially or com­
pletely obstruct biliary outflow post-surgically.
OTHER CONDITIONS
Hepatic abscesses, neoplasia, and parasitic granulomas
are documented, but rare causes of obstructive hepato-

biliary disease in horses. Cholangiocarcinoma is the
commonest form of primary hepatic neopla�m bnt liver
metastases may be seen in association with primary
tumors such as !ymphosarcoma, squamous cell carci­
noma, and melanoma, However, clinical and biochemi­
cal evidence of biliary tract disease is often absent, even
with significant parenchymal infiltration, unless there is
obstruction to biliary drainage. This is most commonly
associated with space occupying lnasses that impede
extrahepatic biliary flow through the right and left
hepatic ducts and the common bile duel.
Occasiona!!y elevations in GGT, AP, and bilirubin
arc .�een in association with colonic (espedaUy 180"
rotations of the large colon) and proximal small intesti­
nal disease in adult horses and foals. Foals with severe
gastroduodenal ulcnation that progresses to signifICant
stricture fOrmation close 10 the duodenal papilla may
haw elevations in [hese enzymes due to compromised
hiliary outflow. Furthermore, horses with colonic dis­
placement or torsion may have elevations in the
hepatobiliary enzymes probably because of abnormal
extrahepatic biliary drainage rather than true hepat(}­
biliary disease. It is worth remembering that donkeys,
mules. and asses have a higher (up to 3 times) normal
lerel of GGT compared to horses.
Pyrrolizidine alkaloid
intoxication
GP Carlson
INTRODUCTION
PyrroliLidine alkaloid intoxication is the most common
came of chronic liver failure in horses in the western
C nited States and toxicity has been recogni7.ed in many
("()untries around the world. Pyrrolb:irline alkaloid-<:on­
taining toxic plants (Table 19.1) tend 10 be unpalatable
and are generally ",'oided by horses. Poor pasture con­
ditions or over grazing may contribute to consumptioll
of these plants, however intoxication is more likely to
occur folIo"l'oing the feeding of contaminated hay.
Pelleted or (:ubed hay may pose a particular risk since
t.he presence of poison()LL� planL� can not be seen. For
some plants, such as Amsinckia intermedia, toxic alkaloids
are concentrated in the seeds that may be found in
srret'nings of grain harvested from contaminated fields.
Such screenings are highly toxic and feeding relatively
modest amounts can lead to massive liver damage and
functional failure within days.
HEPATIC AND BILIARY TRACT DISEASES 19
T.b1.1�1 . �ltidiM1I1k.1OickD''ita1nl",p'lnts
Botanical name Common name
Amsinckia intermedia Fid dleneck fireweed,
,
or t a rweed
Senecio vulga ris Common groundsel
Senecio fideJli Woolly groundsel or
Ridell's groundsel
Senecio jacobaea Tansy or common
ragwort. ragwort, or
stinking Willie
Crota/aria spp. Rattle box
Heliotropium europaeum Common heliotrope or
potato weed
Cynog/ossum officinale Hounds tongue
Horses generally present with depression, anorexia,
and weight loss for variable periods of time. Horses with
areas of unpigmented skin may develop photosensitiv­
ity. Thc clinical course may vary from several days to
several months but when sufficient livcr damage has
occurred to produce functional failure, there may be an
abrupt onset of profound clinical signs and in many
cases death. The appart'lll aC!l11' onset of clinical i11nt'.�s
generally represents the end stage of a chronic, pn)­
gressive disease process. Clinical signs and death may
occur up to a year after the contaminated feed was
eaten. Since all horses with access to a contaminated
feed sourn� are at risk, a history of other animals with
progressive depression, weight loss, icterus, anrl death
should alert the clinician to a possible common cause.
ETIOLOGY
Pyrrolilidinc alkaloid toxicity is largely determined by
the total dose of the pyrrolizidine alkaloid ingested.
Toxi{: cffecL� are cumulative and tend to be progressive;
thus, ingestion of relatively small quantities over a long
periorl of time may produce similar effects to those
ohsel\led folIov.'ing ingestion of larger quantities for a
shorter time period. Pyrrolizidine alkaloids are proxi­
mate toxins which are metabolized in the liver to highly
reactive, unstable metabolites (the dehydroalhloids)
which are potent alkylating agents. These compounds
arc responsible for much of the direct hepatocellular
389
19 CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
damage. Hydrolysis of the dehydroalkaloid yields the
dehydroaminolcohol, which can be both antimitotic
and carcinogenic . These toxic metabolites are thought
to be responsible for the production of the megalo­
cytes, which are a characteristic, histopathologic feature
of this disease.
Experimental feeding studies indicate several stages in
the development of pyrrolizidine alkaloid toxicity.
Initially modest characteristic liver lesions may develop
along with associated biochemical evidence of liver
damage without producing overt clinical signs. In a
report of racing horses fed Senecio-contaminated
alfalfa hay, poor performance was one of the earlier
indicators of disease. Later, progressive liver damage
results in compromised hepatic function, and at this
stage clinical signs become evident with progressive
development of
• depression
• anorexia
• weight loss
• variable icterus.
The final phase of the disease process occurs with the
onset of failure of function and terminal hepatic
decompensation. The onset of severe clinical signs may
occur quite suddenly and represent the end stage of a
disease process that may have been developing for an
extended period of time. Vital signs (temperature,
pulse, and respiratory rate) are often within normal
limits unless the horse has become agitated or convul­
sive. Clinically detectable icterus can be quite variable
until the final stages of the disease process when
icterus may be moderate to severe. Central neurologic
signs range from moderate depression to compulsive
walking, excessive yawning, ataxia, apparent blindness,
and head pressing, to maniacal behavior, convulsions,
coma, and death. Self-inflicted trauma may occur in
horses that become oblivious to their surroundings.
Intravascular hemolysis may occur in the terminal
stages of the disease with resultant hemoglobinuria.
Photosensitivity may be noted in non-pigmented areas
of the skin. Although laryngeal paresis, edema, ascites,
and diarrhea have been reported they are not com­
mon features in horses with pyrrolizidine alkaloid
intoxication.
A history of exposure to pyrrolizidine alkaloid-con­
taining plants and clinical signs compatible with pro­
gressive liver failure would allow a tentative diagnosis of
pyrrolizidine alkaloid intoxication. This is particularly
true if there had been previously confirmed cases from
390
the same property or from other animals on the same
feed.
CLINICAL PATHOLOGY
Elevation of liver-derived serum enzyme activities (SDH
and AST) is associated with active liver damage, but
activities may decrease toward normal until the later
stages of the disease process when marked elevation
may again be noted. Elevation of GGT and AP activities
reflects the focus of the pathologic process in the peri­
portal regions and the biliary system. Sustained moder­
ate to marked elevation in these enzymes provides an
early and persistent indication of liver involvement. The
bromosulfthalein (BSP) clearance half time and the
serum bile acid concentration are generally increased.
Serum bilirubin concentrations may remain within nor­
mal limits until the horse reaches a state of functional
failure. Total serum bilirubin generally remains less
than 10 mg/dl (170 mmol/l) and the direct-reacting
bilirubin rarely accounts for more than 25 per cent of
the total. The blood urea nitrogen (BUN) is generally
below normal in horses with functional failure.
Foodstuffs can be tested for the presence of
pyrrolizidine alkaloids.
PATHOLOGY
Demonstration of typical liver lesions on biopsy or at
necropsy is necessary for confirmation of the diagnosis.
The liver is often small and firm and nodules of regen­
erating liver tissue may be noted in some long-standing
cases. Typical lesions of pyrrolizidine alkaloid intoxica­
tion are megalocytosis, periportal fibrosis, biliary hyper­
plasia, and occlusion of the central veins. Liver lesions
tend to be progressive and as normal hepatic architec­
ture is damaged and replaced by fibrous tissue, the
prognosis becomes less favorable. Well-developed
lesions of veno-occlusion are also considered an
unfavorable indication. Exposure to massive doses of
pyrrolizidine alkaloids may produce acute centrilobular
necrosis, as has been documented experimentally in a
number of species.
TREATMENT AND PROGNOSIS
There are no specific recommendations for treatment
of the damage produced by these toxic plants other
than removal of the contaminated feed source.
Complications associated with photosensitivity can be
reduced if the horses are housed out of direct sunlight,

and retention of appetite and maintenance of body
weight are the most useful prognostic indicators. Even
horses with moderate histologic evidence of liver dam­
age may survive if they maintain a normal appetite. It is
often recommended that horses with liver disease be
put on a low protein diet. This recommendation may
not always be appropriate, it may be better to feed
something that the horses will eat, alfalfa hay for exam­
ple, than to offer a lower protein feed source that the
horses refuse to eat. It is critical to provide adequate
caloric intake of a nutritionally balanced diet of grain
and forage or hay. Some horses with extensive liver
damage survive, but remain unthrifty and may not be
able to handle the stress of active athletic training.
Vigorous supportive care may be unrewarding in a
horse with clinical signs of advanced liver failure and
histologic evidence of generalized fibrosis with loss of
normal hepatic architecture.
Chronic active hepatitis
GP Carlson
INTRODUCTION
Chronic active hepatitis is not a specific disease entity,
but is a descriptive term for a group of conditions
characterized by active, progressive, inflammatory liver
disease of some duration. The history is often one of
depression, weight loss, and variable icterus. Signs are
often intermittent and may be associated with fever.
Some horses have a history of previous or active intra­
abdominal disease. There has, thus far, been no clear
evidence of association with advancing age, viral dis­
ease, or drug administration. The disease can progress
to the point of liver failure with major central nervous
system involvement and death. Unusual cutaneous
manifestations such as moist lesions at the coronary
bands may be present. Liver lesions lend to be located
in the periportal region and the histopathologic
diagnosis is often cholangiohepatitis.
Clinical signs vary with the degree of liver damage and
the presence any underlying disease process. Horses
often present with anorexia, weight loss, variable
icterus, and moderate to marked depression.
Neurologic signs may progress to convulsions, coma,
and death. Some horses have elevated rectal tempera-
H E PATIC AND B ILIARY TRACT DISEASES 19
ture, pulse, and respiratory rates. The moderate to high
fever noted in some horses with chronic active hepatitis
is not a common feature of many of the other causes of
liver failure, unless there have been complications.
Petechial or ecchymotic hemorrhages may be noted in
the visible mucous membranes. Intra-abdominal prob­
lems such as an enlarged anterior mesenteric artery,
thickened bowel, or mass lesion may be noted. Some
horses develop a moist exfoliative dermatitis at the
coronary bands and in some cases this may be the
presenting complaint.
CLINICAL PATHOLOGY
Laboratory evaluation provides evidence of liver
damage and allows an assessment of the degree of
functional failure. Initially liver-derived serum enzyme
activities may be slightly to moderately elevated. Later
in the disease process substantial elevation of liver­
derived serum enzyme activities and marked elevation
of the enzymes that reflect biliary damage, GGT and
AP, will be noted. Serum bilirubin may be markedly ele­
vated with direct-reacting bilirubin comprising up to 40
per cent of the total. The urine is strongly positive for
bilirubin and serum bile acids are greatly elevated. The
BUN is often low and hypoglycemia will be noted in
some horses. The hemogram may show evidence of an
inflammatory response with a leukocytosis, left shift,
and monocytosis. Total plasma protein concentration is
generally elevated, largely because of an increase in
globulins. Culture of liver biopsy specimens may be
rewarding since bacterial agents may contribute to
hepatitis or cholangitis.
PATHOLOGY
Histopathologic lesions are most prominent in the peri­
portal region with hepatocyte damage and loss, variable
fibrosis and an inflammatory infiltrate. The cellular
component of this infiltrate tends to be mononuclear
cells, except those cases with suppurative hepatitis that
may have a marked neutrophilic response. There is
often evidence of cholangitis with biliary hyperplasia
and bile stasis. Bacteria may colonize the liver during
bacteremia, via the portal drainage from damaged
bowel, or as an ascending process from the common
bile duct. Viral agents or idiosyncratic reactions to
drugs are thought to be major factors in the develop­
ment of chronic active hepatitis in other species. The
pathogenesis of the skin lesions is unclear, but these
lesions appear to represent an immune-mediated
vasculitis associated with liver disease.
391
19 CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
TREATMENT
intensive supportive care is indicated until horses
regain their appetite. A fairly consistent favorable
response to corticosteroids can he anticipated. Initial
!Tf"atlllcnt should consist. of 20-40 mg of dexametha­
sone given hy injection. This dose rate is maintained for
�)...5
. days {depending upon the response), and is then
gradually decreased o\"cr the next 7-1O days. At this
lime the horse may be placed on onll prednisone at
40/l-6QO mg/day. Treatment may be necessary for 4-6
weeks or longer with careful monitoring of clinical signs
and biochemical parameters. R;I(:lI'rial infection may
play a role. especially in horses with fever and a
neutrophilic intlamlllatory infiltrate on liver biopsy,
and systemic antibiotics arc indicated, Improvement in
attilllde and appetite are among the earliest and most
consiMelll indicators of response to therapy,
Chronic liver disease
GP Carlson
Horses with chronic: liver disease may present with a his­
tory of clnonic progressively developing clinical signs or
they may pn�st'nt with recently recognized and fi.!lmi­
\lant clinical signs at the end stage of function<ll failure,
Several of the more .�pecific and common causes for
chronic liver failure have been discussed in other sec­
tions {pyrro!izidine alkaloid !oxicosi�, chrnnic active
hepatitis, biliary (ract disease, and hyperlipemia). This
St'rliOll will address chronic liver failure of undeter­
mined cause as well as some of the less common causes
of liver disease such as hepatic neoplasia.
CHRONIC LIVER FAILURE OF
UNDETERMINED CAUSE
The history, clinical signs, and dinical patholob'Y data
fOr these cases may essentially be the same a� described
for horses with pyrrolizidine allwloid intoxication
except perhaps for the absence of a history of exposure
to toxic plants. Most horses I-I-ith chronic liver failure
prese!H with chronic. weight loss, depression, variable
icterus, and progressive neurologic signs terminally.
Clinical signs arc generally non-specific and laboratory
indications of liver damage such as serum enzyme
auivities (SDH, AST, <lnd I.OH) may be only mod{'�tIy
elevated if the process of hepatocyte destruction is no
longer \'('1)' active, while GGT and AP tend to be elevated
in disease processes that involve the biliary system.
392
Indicators of compromised livt�r function such as bile
acids, total and direct bilirubin, BU:-I, blood ammonia.
blood glucose, and the ratio of plasma branched
chain to aromatic amino acids may only be abnomJ<lI
during the termimll stage of the disease process.
Hypoproteinemia and hypoalbuminemia are not COIll­
mon features of chronic liver failure in the horse, bUlan
increase in globulins is a frequent finding. Po\ycythemiil
Illay be noted in some horses with chronic liver failure.
\-1casures of liver function such as BSP or indocyanine
green clearance would probably indicate altered liver
funnion. However, the routine application of these
diagnostic procedures is limited by the lact that sterile
pn�parations of BSP are no longer commercially avail­
able in the United States and indocyanine green is
expensive. Imaging of the liver using ultrasound pro­
vides a non-invasive means to evaluate liver location,
size, and texture. This information can be most helpful
in determining the most appropriate site for liver
biopsy. It is possihle in some instances to identify masses,
abscesses, enlarged bile ducts, and bile stones using
these techniques. The most useful diagnostic tool in the
animal manifesting clinical and biochemical evidence
ofliver failure is the liver biopsy. It is possible with ultra­
sound-guided liver biopsy to obtain tissue samples from
areas with focal liver lesions. However, most horses with
chronic liver failurt have ilwolvement of over 80 per
cent of the liver and liver biop�ies generally provide
representative samples for histological evaluation.
The liver has a great capacity for regeneration and
repair following injury. Chronic liver failure generally
result� from processes in which there has been damage
to hepatocytes, hepatocyte loss, inflammation, and pro­
gressive replacement of hepatic parenchyma by fibrosis.
Potential causes or factors that may contribute to the
development of chronic liver failure include
• recurrent bacterial or viral infections
• immunological reactions
• parasitism
• exposure to toxic chemicals or pharmaceutical
agenL�
• poisonous plants
• mycotoxins
• chronic hypoxia
• dietary imbalances
• iron overload
• trauma
• amyloidosis.
In many instances at the end stage of liver failure it is
not po.�sible to determine the specific cause or causes of
the liver injury and subsequent fibrosis, a� over time
many factors may have contributed to progressive
damage and loss of function.

KLEIN GRASS (PAN/CUM COLORA TUM)
� i •
Chronic liver disease has been reported from Texas in
horses grazing pasture planted to Klein grass as well as
horses fed Klein-grass hay. Icterus, anorexia, and pro­
gressive weight loss were the principal signs with some
horses developing colic signs. Elevated GGT activity,
total and direct bilirubin, blood ammonia, and BSP
clearance times were noted. Typical liver lesions
included bridging hepatic fibrosis, cholangitis, and
hepatocellular regeneration. The toxic principal is
thought to be a saponin. Although death losses were
reported in horses with advanced liver lesions, most
horses recovered after Klein grass was removed from
the diet. The sporadic nature of the disease suggests
individual susceptibility, variability in the amount of
feed ingested and perhaps seasonal or maturational
variation in the content of the toxic principal.
ALSIKE CLOVER
Horses grazing alsike clover may develop signs of liver
failure, especially photosensitization, anorexia, and
icterus. Several horses on a farm may be affected at one
time. Generally these horses are on a clay soil pasture
containing large amounts of alsike clover. The disease
appears to have yearly fluctuations in areas where alsike
clover is common (eastern USA and Canada) suggest­
ing that environmental factors contribute to either the
toxicity of the plant or growth of a hepatotoxin on the
plant. Removal of affected horses from the pasture and
supportive care treatments result in complete recovery
of most cases. If the horses are not removed from
the alsike clover, the disease may progress to hepatic
fibrosis, fulminant hepatic failure, and death.
HEPATIC NEOPLASIA
Primary liver tumors are relatively rare in horses.
Cholangiocarcinoma occurs mainly in older horses,
which may present with anorexia, weight loss, icterus,
edema, and abdominal distention. This tumor tends to
produce multiple masses within the liver. Extrahepatic
metastasis may occur with involvement of the peritoneal
and pleural cavities, intestine, spleen, and lung.
Cholangiocarcinoma has been reported in combination
with hepatocellular carcinoma in one horse and in
another horse with concurrent septic cholangiohepatitis.
Hepatocellular carcinoma has been reported pri­
marily in young horses less than 3 years of age. These
tumors are often solitary and may be multilobulated.
Clinical signs include depression, anorexia, weight loss,
H E PATIC AND B ILIARY TRACT DISEASES 19
abdominal distention, intermittent diarrhea, and
hyperemic mucous membranes. Modest elevation of
liver enzyme activity may be observed. Polycythemia or
erythrocytosis as indicated by marked elevation in the
hematocrit has been noted in these patients, this may
be due to secretion of an erythropoietin-like substance
by the tumor. In one patient hepatocellular carcinoma
was associated with an increase in serum alpha feta­
protein, a globulin normally produced by fetal liver
cells. However, it is not proven that this protein is a con­
sistent indicator of hepatocellular carcinoma in horses.
The liver is frequently involved with metastatic
lesions from primary tumors arising from other sites.
These tumors include lymphosarcoma, mammary carci­
noma, bronchogenic carcinoma, squamous cell carci­
noma, granulosa cell tumor, and Sertoli cell tumor. In
most instances these lesions do not result in massive or
generalized liver damage and the only biochemical
indication in some horses may be modest elevation of
liver-derived serum enzyme activities. Most horses do
not manifest clinical or biochemical evidence of liver
failure although depression, anorexia, weight loss, and
edema may be features of an invasive and generalized
neoplastic process. Ultrasonic evaluation of the liver
may provide evidence of focal neoplastic lesions within
the liver parenchyma.
IRON OVERLOAD,
HEMOCHROMATOSIS
Iron is a highly reactive element that plays an essential
role in oxidation-reduction reactions. Iron balance is
largely regulated by intestinal absorption as there is no
mechanism for excretion of excessive iron stores.
Newborn foals given an oral intestinal inoculum con­
taining ferrous fumarate during the first day or two of
life developed acute liver failure due to iron overload.
This was probably associated with an inability of the
newborn animal to effectively regulate intestinal
absorption of iron. Additionally, newborn foals nor­
mally have high serum iron and high per cent transfer­
rin saturation at birth, rendering them less able to
deal with a sudden massive iron intake. Clinical signs
developed within a few days with rapid progression of
anorexia, depression, icterus, collapse, and death.
Liver lesions included massive necrosis, bile ductule
proliferation, inflammatory infiltrate, and bile stasis.
Deficiencies of vitamin E and selenium may play a
permissive role in the tissue damage of iron toxicity.
Vitamin E and selenium are thought to exert protective
effects due to their anti-oxidant properties. Acute iron
overload with liver damage has also been reported in a
few adult horses given iron supplements orally.
393
19 CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
Iron overload or hemochromatosis associated with
chronic hepatic cirrhosis has been reported in adult
horses. Clinical signs in these horses included depres­
sion, anorexia, weight loss, icterus, ventral edema,
and terminal hepatic encephalopathy. Liver-derived
enzyme activities and serum bilirubin were increased.
Histologic lesions included disruption of hepatic archi­
tecture, bridging fibrosis, and bile duct hyperplasia.
Iron accumulation was noted within hepatocytes,
macrophages, and Kupffer's cells as indicated by
Prussian blue staining. Liver iron concentrations, mea­
sured in two horses, were very high (6700 and 18 437
ppm wet weight ), some 20-1 00 times that found in the
liver of control horses. Iron accumulation was not
noted in other tissues in these horses. Serum iron was
high in one of these horses and within the normal
range in the other. Interestingly, none of the reported
horses with confirmed hemochromatosis had a dietary
history suggestive of excessive iron intake, and only one
horse had been fed a vitamin and mineral supplement
that contained iron.
This condition in horses has some similarities with
familial idiopathic hemochromatosis, an inherited dis­
order of humans, in which excessive intestinal absorp­
tion of iron leads to hepatic cirrhosis associated with
iron accumulation in the liver and other tissues. This
disorder of humans is associated with high serum iron
and nearly complete saturation of transferrin. The few
published reports in horses suggest a sporadic occur­
rence although multiple cases of liver failure in horses
with high serum iron may occur on given properties.
There is at present no evidence that the disorder in
horses is inherited. Since excessive dietary iron has not
been a consistent feature in these horses, it has been
suggested that for unknown reasons excessive intestinal
iron absorption occurs with resultant accumulation of
iron in the liver. We have noted high serum iron in
some horses with chronic liver failure, although a causal
relationship to liver damage could not be established. It
is possible that the accumulation of iron in the liver is
the result of liver failure, and may not be the cause of
liver failure. Secondary iron overload occurs in humans
with alcoholic cirrhosis.
RIGHT HEPATIC LOBE ATROPHY
Atrophy of the right hepatic lobe is a rare and often
unnoticed condition of horses. The condition has been
reported in adult horses with colic due to major
gastrointestinal abnormalities, and is also an incidental
finding at necropsy. Although the pathophysiology of
this condition is unresolved it has been suggested that
this condition may result from compression of the liver
394
associated with chronic distention of the right dorsal
colon. High grain, low fiber diets may contribute to this
condition.
Hyperlipemia
T Mair
INTRODUCTION
Hyperlipemia is a disorder of lipid metabolism charac­
terized by hypertriglyceridemia and fatty infiltration of
body organs. The disease is most common in ponies,
miniature horses, and donkeys, although it occasionally
affects larger horses. The condition is usually precipi­
tated by periods of anorexia, malnutrition, stress, and
other diseases, and occurs most commonly in the winter
months. The clinical signs are often vague initially, but
the condition progresses rapidly and is frequently fatal
unless early and aggressive therapy is instituted.
EPIDEMIOLOGY
Hyperlipemia is most commonly seen in small pony
breeds, such as Shetland ponies and Welsh Mountain
ponies, and in donkeys. Two retrospective studies from
equine referral hospitals in the USA reported an
incidence of hyperlipemia of 1 1 per cent in miniature
ponies and 1 8 per cent in donkeys presented to these
hospitals. The condition is relatively rare in larger horse
breeds, but is occasionally identified in horses affected
by other diseases including renal disease, lympho­
sarcoma and pituitary adenoma (Cushing's disease or
hyperadrenocorticism) .
The incidence of hyperlipemia is higher in mares
than in stallions and geldings. This predisposition is
partly explained by the fact that hyperlipemia is com­
mon in pregnant and lactating mares. However, there
also appears to be an inherently higher risk in females
that is independent of the reproductive status.
Hyperlipemia can be seen in horses and donkeys of
all ages, although it is uncommon in animals less than
18 months of age, with older animals being at greater
risk (possibly due to an age-related decrease in insulin
sensitivity). It is occasionally diagnosed in ill foals and
has been seen as a congenital condition in foals born to
hyperlipemic dams.
Hyperlipemia is often seen as a complication of
other diseases, especially gastrointestinal diseases.
Some of the more common diseases identified in asso-

Intestinal parasitism
Colitis
Colonic impaction
Gastric i mpaction
Dysphagia and dental disorders
Esophageal obstruction
Esophageal ulceration
Lymphosarcoma.
Hyperadrenocorticism (Cushing's disease)
Peritonitis
Metritis
Laminitis
Renal failure
Liver disease
Septicemia
Hypocalcemic tetany
Post-injection abscess
Sub-solar abscess
C1atlon with hyperlipemia are summarized in Table
1 9.2. Many of these diseases are thought to predispose
to hyperlipemia by causing inappetence or anorexia. In
addition to disease, hyperlipemia may be induced by
periods of enforced malnutrition, such as inadequate
availability of pasture or competition for food. Pregnant
mares, especially in the last trimester, and lactating
mares have increased nutritional requirements and are,
therefore, at greater risk of developing hyperlipemia.
Obesity and stress are other important risk factors for
the development of the disease . Stress factors that have
been implicated include transportation, change of
environment or diet, inclement weather, and the
stress of pregnancy, lactation, and disease.
PATHOGENESIS
Hyperlipemia represents an excessively rapid mobiliza­
tion of the body's fat reserves (Figure 1 9 . 2 ) in response
to stress or failure to maintain energy homeostasis. In
response to negative energy balance and after depletion
of glycogen reserves, non-esterified fatty acid (NEFAs )
H E PATIC AND B ILIARY TRACT DISEASES 19
Figure 1 9.2 Schematic representation of the metabolic
fate of non-esterified fatty acids mobilized from adipose
tissue (NEFA non-esterified fatty acids; TG triglycerides;
= =
VLDL = very low density l i poproteins; LPL=lipoprotein
lipase) (adapted from Watson 1 998)
are mobilized from fat stores and released into the cir­
culation (Figure 1 9.2). The majority of NEFAs are taken
up by the liver where they may overwhelm the oxidative,
gluconeogenic, and ketogenic pathways and are esteri­
fied to form triglycerides. Triglycerides then accumu­
late in the liver and are exported in the circulation in
the form of very low density lipoproteins (VLDLs)
(Figure 19.3). This process occurs at such a fast rate that
the VLDLs cannot be utilized by peripheral tissues, and
plasma levels become excessive. VLDLs are also taken
up by cells of the reticuloendothelial system resulting in
fatty infiltration of many organs .
Adipose tissues represent energy stores that form as
a result of esterification of free fatty acids to produce
triglyceride. This esterification is promoted by the
action of insulin and glucose. In the presence of nega­
tive energy balance, lipolysis takes place in adipose tis­
sues, mediated by glucagon which activates the enzyme
hormone sensitive lipase (HSL) . HSL is normally inhib­
ited by insulin and glucose, but with reduced insulin
and glucose levels (which occur in negative energy bal­
ance), and enhanced glucagon activity HSL is activated.
HSL can also be activated by hormones released in
response to stress (such as adrenocorticotrophic hor­
mone - ACTH, glucocorticoids, and catecholamines)
and by hormones released in pregnancy and lactation
(progesterone and growth hormone) .
The lipolysis induced by HSL results in the release of
NEFAs into the circulation. NEFAs may be used by
tissues for oxidation as a source of energy. However,
most NEFAs are taken up by the liver where they can be
used for ketogenesis or gluconeogenesis, or they are
395
19 CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER D ISEASE

Adipose tissue

Plasma N E FA transport to the liver

Normal ponies 8.2 ± S.2 mmol/h
Hyperlipemic ponies 148.2 8.4 mmollh

Figure 1 9.3 Schematic representation

Normal ponies
6.6 ± 4.4 mmol/h
Hyperlipemic ponies
1 90.6 3.9 mmollh
of non-esterified fatty acid (N EFA) and
very low density lipoprotein (VLDL)
metabolism in ponies with hyper­
lipemia. Kinetic data are shown for
NEFA transport to the liver, hepatic
VLDL-triglyceride (TG) synthesis, and
VLDL-triglyceride fractional catabolic
rate in normal and hyperlipemic ponies
(adapted from Watson 1 998)

esterified to form triglycerides. The horse has a poor CLINICAL SIGNS

capacity for ketogenesis, and most NEFAs are used to
produce triglycerides. These triglycerides are exported
from the liver in the form of VLDLs that can be utilized
as a source of energy in peripheral tissues or re-stored
in adipose tissue. In the presence of food deprivation,
plasma VLDL levels rise excessively and triglycerides
accumulate in the liver.
The clearance of VLDL triglycerides from the circu­
lation is promoted by lipoprotein lipase (LPL), and it
has been suggested that raised plasma triglyceride levels
in hyperlipemia may be caused by reduced clearance of
VLDLs due to inhibition of the action of LPL. LPL
activity may be inhibited by azotemia and endotoxemia.
However, studies of ponies with hyperlipemia suggest
that the activity of LPL is increased rather than
reduced.
Insulin resistance probably plays an important role
in the pathogenesis of hyperlipemia. Tissue resistance
to insulin results in a diminished ability to regulate
HSL. Thus, when the enzyme is activated in response to
a negative energy balance , or as a result of stress or
concurrent disease, lipolysis progresses in an excessive,
uncontrolled way. NEFAs are released in excessive
amounts that overwhelm the liver's oxidative, gluco­
neogenic, and ketogenic capacity, such that triglyc­
erides are produced resulting in hypertriglyceridemia
and hyperlipemia. Insulin resistance is common in
ponies and donkeys, and is exacerbated by obesity and
pregnancy/lactation.
Clinical signs of hyperlipemia will be compounded by
the signs relating to the underlying disease or cause,
such as diarrhea or dysphagia . In addition, fatty infiltra­
tion of the liver and kidneys may produce signs of
hepatic and renal failure. The initial signs of hyper­
lipemia are often vague and include anorexia, lethargy,
and weakness (Table 19.3) . Rapid progression of the
disease is common, with the development of ataxia,
muscle fasciculations, head pressing, profound depres­
sion, recumbency, convulsions, coma, and death.
Sudden death occasionally occurs as a result of hepatic
rupture. Dysphagia is observed in some cases, and may
result from encephalopathy or myopathy involving the
muscles of mastication; alternatively dysphagia may be
caused by an underlying primary esophageal disease
such as choke . Pregnant mares may abort sponta­
neously or undergo premature labor.
Some animals demonstrate a period of rapid weight
loss and development of ventral edema at the onset of
the disease. This may reflect the primary underlying dis­
ease or may develop as a consequence of subcutaneous
thrombosis caused by the hyperlipemia. Edema might
also develop as a result of rapid fatty infiltration of the
liver, partial obstruction of the portal circulation, and
increased hydrostatic pressure in subcutaneous abdom­
inal veins . Likewise, mild intermittent abdominal pain
(restlessness, flank watching, and rolling) may be caused
by a primary gastrointestinal disease, or may occur as a

396
 H E PATIC AND BILIARY TRACT DISEASES 19

sitive method of diagnosis, especially in animals

with mild degrees of hyperlipemia and animals with
hyperlipidemia (see below) . Accurate measurements of
Anorexia plasma triglyceride levels are recommended to assess
Lethargy the degree of hyperlipemia and to monitor the course
of the disease during treatment.
Weakness
Plasma triglyceride levels of greater than 5 mmol/l
Ataxia (500 mg/ml) in ponies with clinical signs of hyper­
Muscle fasciculations lipemia are diagnostic. Triglyceride concentrations of
Dysphagia 1-5 mmol/l ( l 00-500 mg/ml) can be present in ponies
without clinical or pathological evidence of hyper­
Sham drinking
lipemia; this has been classified as hyperlipidemia, and
Profound depression may sometimes progress to hyperlipemia if adequate
Head pressing nutritional support is not provided. However, triglyc­
eride levels in this range can sometimes be present in
Circling
clinically normal pony mares during pregnancy.
Recumbency Normal plasma triglyceride levels in donkeys are
Seizures higher than in ponies. Healthy, non-pregnant donkeys
Nystagmus may have levels as high as 3.5 mmol/l (350 mg/ml).
Triglyceride levels in suckling foals are also higher than
Weight IOS5
in adults because of the relatively high daily fat intake.
Ventral edema Plasma concentrations of other lipids, such as chol­
Ascites esterol, phospholipids, and NEFAs, are also raised in
Abdominal pain hyperlipemia. However, increases in concentrations of
these lipids are not as great as triglycerides, and they are
Reduced intestinal motility and fecal output
not routinely assessed for diagnosis. Identification of
Pyrexia fatty infiltration of liver biopsies is diagnostic but has
Tachycardia no advantage over simple measurements of plasma
triglycerides.
Tachypnea
Congested mucous membranes
Clinical chemistry
Icterus
Halitosis Monitoring of serum or plasma biochemistry panels can
help to
Abortion
Sudden death • detect the presence and severity of organ failure in
hyperlipemia
• determine appropriate supportive therapies
• monitor the course of treatment, and
result of hepatomegaly and stretching of the liver • detect underlying primary conditions.
capsule. Intestinal motility and fecal output are often
Table 19.4 lists an appropriate chemistry panel for
reduced, and this may predispose to colonic impaction.
this purpose.
The clinical course of hyperlipemia is rapid in most
Biochemical measurements of some substances may
cases. The average interval between the onset of clinical
be complicated due to interference by high triglyceride
signs and death or euthanasia is 6- 10 days. In a few
levels. This can be overcome by clearing the plasma or
cases a more protracted clinical course may occur.
serum of lipids prior to analysis by ultracentrifugation
or chemical precipitation.
Blood glucose concentrations may be normal, low,
DIAGNOSIS
or elevated, depending on the duration of anorexia,
previous glucose therapy, and the presence or absence
Plasma triglycerides
of Cushing 's disease. Metabolic acidosis is often
Gross lipemia in blood samples centrifuged or left to present, as shown by decreased arterial pH, decreased
stand is the simplest way to diagnose hyperlipemia in PC02, decreased bicarbonate levels, and a base deficit
practice (Plate 19.2 ) . However, this is a relatively insen- of 0-24 mEq/1.

397
19 CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE

fissured, or there may be capsular rupture and associ­

T__ ".4 IIocIWtlNstry IMnt' for Invtltigltinv ated hemorrhage. Fatty infiltration of other organs
and monltDrlng hyptrilpemli In liqUids (from including adrenals, skeletal muscle, and myocardium
WttiQn 1_ may be evident. Necrotizing pancreatitis is present in
some cases (see Chapter 17). Vascular thrombosis can
Metabolic status occur secondary to hyperlipemia and fat embolism, and
• triglycerides
can result in focal hemorrhages, myocardial infarction,
• glucose
and renal infarction.
• hydration status - albumin
PCV
• electrolytes - No·
K·
TREATMENT
".
Ca2•
The treatment of hyperlipemia has nve different objec­
• add-base status - pH
HCO)- tives
peol
1 . treatment of underlying or concurrent disease
2. correction of dehydration, electrolyte and
Liver damage and function
acid/ba�e imbalances
• gamma glutamyl transferase (GGn
• alkaline phosphatase (AP) 3. symptomatic therapies
• bile acids 4. nutritional support
• ammonia 5. normalization of lipid metabolism

Rena! function Treatment of underlying or concurrent

• ammonia
• urea nitrogen
• creatinine
Fan)' inlHtration of the liver result..'; in elevations of
liver·derived emymes, including GGT, AP, LDH, and
SDH. Liver funelion may be impaired, as asscs.�ed by
elevations of bilirubin, hile acids, and ammonia. Fatty
infiltration of the kidneys can result in impaired renal
li.mction, and elevation of plasma concentrations of
urea and creatinine. These metabolites may also he
increased as a result of dehydration, and reassessment
following rehydration is required to a')sess the degree of
renal failure.
P!a.�ma albumin concentrations may be normal, or
e1evat.ed (associated with dehydration), or reduced
(associated with chronic hepatopathy, a primary
gastrointestinal lesion, or parasitism). Serum protein
electrophoresis can he helpful in as.'iessing underlying
conditions such as intestinal parasitism.
PATHOLOGY
T}pica! pathological findings in ponies and donkeys
am'eled hy hyperlipemia include fatty infiltration of the
tissues, espedaJIy the liver and kidneys (Plate 19.3). The
liver and kidneys are enlarged, yellow, friable, and
greasy. In severe cases, the surface of the liver may be
disease
Intestinal parasitism is a common cause of hyperlip­
emia in ponies and donkeys, therefore appropriate
anthelmintic therapy is required in all cases "'�th con­
firmed parasitic burdens, and should be administered
to all other cases where no obvious cause of the hyper­
lipemia is identified. Other treatments for underlying
diseases should he administered as appropriate, such as
pergolide therapy for Cushing's disease.
Correction of dehydration, electrolyte, and
acid-base disturbances
Correction of dehydration, electrolyte and acid-base
abnormalities is essential. Intravenous fluid and c1ectf(}­
lyte therapy is generally required, the principles of
which are discussed in Chapter 9. Correction of severe
acidosis in the presence of liver failure may require the
administration of intravenous bicarbonate. Blood gas
analysis should be used when available to monitor the
response to bicarhonate therapy, since too rapid an
increase in blood pH may exacerbate signs of hepatic
encephalopathy, and overdosing of bicarbonate can
lead to persistent metabolic alkalosis and respiratory
depression.
Dextrose should be added to the intravenous
polyionic fluids or <ldministered as 5% dextrose solu­
tions in animals with hypoglycemia. ""hen 5% dextrose
solutions are being administered, monitoring of serum
electrolytes should be undertaken, and potassium chlo­
ride or calcium g!uconate administered as necessa!)'.

398
 HEPATIC AND BILIARY TRACT DISEASES 19

Care must be taken to avoid overdosing with dextrose,
since this can result in transient or prolonged periods
of hyperglycemia with associated diuresis, dehydration,
and hyponatremia.
Symptomatic therapies
Symptomatic therapies include the use of analgesia,
non-steroidal anti-inflammatory drugs, and anti-ulcer
treatments. These are used as necessary on an individ­
ual basis. Therapies for hepatic encephalopathy (see
above) may also be beneficial. Plasma transfusions have
been used in hyperlipemic patients with hypoprotein­
emia, endotoxemia, and in foals with failure of passive
transfer of immunity.
Nutritional support
Nutritional support is an essential component of
therapy of hyperlipemia in all cases. Mfected animals
should be maintained in positive energy balance in
order to limit the mobilization of NEFAs from adipose
tissues.
In animals that are still eating, fresh and highly palat­
able foods, such as grass, leafy hay, rolled grains, and
high energy feeds with added molasses, should be fed.
In animals that are inappetent or anorexic, enteral
feeding via a nasogastric tube should be undertaken.
Even in animals that are still eating voluntarily, supple­
mentation by enteral feeding should be considered
if the plasma triglyceride levels exceed 5 mmol/l
(500 mg/ml). Glucose and electrolyte solutions, com­
mercial enteral formulations, and slurries made from
hay or pelleted feeds can all be administered by naso­
gastric tube.
Glucose in the form of dextrose can be administered
orally at a dose of approximately 1 00 g once or twice a
day for miniature horses and small ponies. Plasma glu­
cose levels should be monitored on a daily basis during
the period of treatment. Excessive glucose administra­
tion might exacerbate lactic acidosis : to reduce this risk
it has been suggested that 1 00 g of galactose is substi­
tuted for the glucose on alternate days, galactose is
slowly converted to glucose thus minimizing the pro­
duction of lactic acid.
Nutritionally complete formulations are preferred
to simple glucose solutions for enteral administration.
Commercially available formulations for use in horses
can be used, or recipes of formulations incorporating
water, dextrose, casein or dehydrated cottage cheese,
dehydrated grass meal, and electrolyte/mineral mix­
tures can be used (Table 1 9 .5 ) . Commercial enteral for­
mulations for use in humans have also been successfully
used in ponies and donkeys with hyperlipemia.
The daily ration of enteral feeding should be calcu­
lated and divided into 4-1 2 small feeds so that the total
volume of each feed should not exceed 3 liters for
miniature horses, 5 liters for small ponies and 7 liters
for larger ponies and horses. The daily basal require­
ment for digestible energy (DE ) input can be calculated
from the following formula
DE (Mcal/day ) = 0.975 + 0.021 x body weight in kg
The daily DE requirement may be multiplied by a
'stress factor ' of 1 .2-2.0 to compensate for the
increased metabolic rate associated with stress and hos­
pitalization. One suggested protocol for enteral feeding
of hyperlipemic ponies based on calculation of basal
and 'stress-adjusted' DE requirements is as follows
• day 1 75% of basal DE requirement
• day 2 1 00% of basal DE requirement

Parameter Day
1 2 3 4 5 6 7

Water (I) 8 8 8 8 8 8 8

Dextrose (g) 1 20 1 60 200 240 320 320 360

Casein or dehydrated cottage

cheese (g) 1 20 1 20 1 80 240 240 300 360

Dehydrated lucerne meal (g) 600 600 600 700 700 800 800

Electrolyte and vitamin

mixture (9) 80 80 80 80 80 80 80

399
19 CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
• day 3 75% of 'stress-adjusted' DE
requirement
• day 4 and 1 00% of 'stress-acljusted' DE
subsequent days requirement.
This procedure of increasing the plane of nutrition
allows the gastrointestinal tract to become tolerant to
the regime.
In affected animals with compromised gastrointesti­
nal function, such as ileus and diarrhea, intravenous
nutrition is required. In most cases, the constant intra­
venous administration of 5% dextrose at 1-2 ml kg-I hrl
is used. Although this will not fully meet the animal's
total nutritional requirements, it has proved effective in
clinical cases. Overdosing with glucose must be avoided
since it can result in diuresis, dehydration, hypona­
tremia, and enhancement of hepatic lipidosis. Amino
acid solutions can also be administered intravenously,
but this significantly increases the cost of treatment.
Plasma glucose levels should be monitored regularly,
and electrolytes added as necessary. Human parenteral
nutrition formulations can also be used, but these
preparations are expensive and careful monitoring is
required.
Anabolic steroids and multivitamin preparations are
commonly administered to hyperlipemic patients to
assist hepatic function. Corticosteroids should be
avoided since they stimulate HSL and may induce
laminitis.
The induction of abortion or premature foaling in
pregnant mares has been recommended, since this
significantly reduces the demands for energy. However,
prematurely delivered foals have a high mortality rate
because of the immaturity of body systems and suscepti­
bility to infectious disease. There is also a risk of
retained placenta and laminitis in the mare. Lactating
mares that develop hyperlipemia should have their
foals weaned if possible.
Normalization of lipid metabolism
Two approaches to modifying lipid metabolism in
hyperlipemic patients are possible
1. reducing the net release of NEFAs from adipose
tissues
2. accelerating the removal of triglycerides from
plasma VLDLs to adipose tissues and skeletal
muscle.
The release of NEFAs from adipose tissue is promoted
by the action of HSL. Reducing the stimulus for lipoly­
sis may be achieved by
• providing a positive energy balance
• removing stress factors
400
• removing the hormonal influences of pregnancy
and lactation.
The activity of HSL is inhibited by the action of insulin,
and thus exogenous insulin therapy has been recom­
mended in the treatment of hyperlipemia. Protamine
zinc insulin has been used most frequently, at dosages
of 30-80 IU ( 0. 1 -0.3 IU/kg) by intramuscular injection
once or twice a day. Insulin in combination with glucose
and galactose administration also promote the re-ester­
ification of NEFAs. The efficacy of insulin therapy has
been questioned in view of the fact that most hyper­
lipemic ponies and donkeys are insulin resistant: how­
ever, this treatment is unlikely to be harmful so long as
the patients are normoglycemic and are receiving oral
or intravenous glucose. The following regimen has
been suggested for treatment of a 200 kg pony
• day 1 30 IU protamine zinc insulin i.m. and
1 00 g glucose p.o., both b.i.d.
• day 2 1 5 IU protamine zinc insulin i.m. b.i.d.
and 1 00 g galactose p.o. s.i.d.
• day 3 as for day 1
• day 4 as for day 2.
Stimulation of LPL in order to increase the clearance
of triglycerides from the plasma has been attempted
by means of heparin therapy; 100-200 IU /kg of
heparin may be administered intravenously twice a
day. However, the rationale for this therapy has been
questioned because the activity of LPL in affected
ponies has been shown to be at its physiological maxi­
mum. There is also a risk of hemorrhage with heparin
therapy.
PROGNOSIS
The prognosis for animals with hyperlipemia is poor.
The reported mortality rate for the disease (including
animals that are euthanased) ranges from 57-85 per
cent. In individual patients, the nature and severity of
the underlying disease has an important impact on the
prognosis. The degree of measured lipemia does not
appear to influence the prognosis, although animals
with hyperlipidemia (triglycerides < 5 mmol/l) have a
much better prognosis than those with hyperlipemia
(triglycerides > 5 mmol/l).
Plasma triglycerides and blood biochemistry (see
above) should be monitored during treatment, and
these results can be helpful in assessing the prognosis.
In animals that recover, plasma triglycerides usually
return to normal values within 3-10 days. Early diagno­
sis and prompt initiation of therapy result in the best
chances for survival.
 HEPATIC AND BILIARY TRACT DISEASES 19

PREVENTION (1994) DMSO as a direct so!uhilizer of <aki",n

:.;:.::
= :.:..:.
:.:.:..
.:.; _
- --" ..__ .. _. - ,.
bilirubinate stones. Hrj>fJlog",lrlJlml
l'Tnl"f;J' 41 ( I ) :65-9.
Johnston J K, Divers T.l, Reef V B, Acland H (191l9)
Risk factors for hyperlipemia in susceptible classes of Cholelithiasis in horses: Ten cases (1982-1986) J. Am. V�l.
equids include AI�d. A.I.mr. 194:40;;-9.
Ram...,,,,,, t\ W (1990) J)i'ea.'''.' of the li\""... F�I. �in. N. Am.
• obesity f:quinF Prado 2:105-1 14.
• stress R"dV B,Johnston] K, Divers T.l, Acland H (1990)
• malnutrition Cltrasonographic filldings in horses with cholelithiasis:
Eight (as("s (1985-191l7) .f. Am. litl. Med. Assoc.
• pregnancy and lac tation
196: IH36-1 I.
• parasitism Schneider [) A (l!N7) Choiestasis and biliary calculi in
horse<. (;omj" Coni. Fdllf P,.,ul. V�t. 19(fi):744-il3.
Avoiding these factors will therefore help in prevent­
ing this disea�e. Particular emphasis should be placed
Pyrrolizidine alkaloid intoxication, Chronic
on providing adequate nutrition to susceptible
active hepatitis, Chronic liver disease
animals without allowing them to become obese, and
Barton M H, :\1orris, D D (199il) Diseases ofth" l.iver. In
providing good routine parasite con trol measures.
F.quinli Intl'17!{1[ A1�dirinf, S M R"ed and W M gayly (cds).
Food intake and general demeanor should be care­
W B Saund"rs, l'hila(klphia, PI" 707-3H.
fully monitored following periods of enforced s tress Carlson (; P ( 1 992) Icterus in the Horse. In lielmllal)
such as disease, transportation, inclement weather, G(l.\lromlat>/o,;y (2nd "dn), :\ V Anderson, (cd.). Lea &

change of environment, etc. Exercise regimes may be
helpful in reducing insulin in sensitivi ty. Plasma triglyc­
eride levels may abo be measured at times of stress
and during pregnancy and lactation. The early identi­
fication and treatment of hyperiipt'mia is far more
like ly to result in recovery than identification laler in
the course of the disease.
BIBLIOGRAPHY
Acute hepatic disease with failure
Diwrs T] (1996) The Liver. In Mrlnbo/ir Disnms oj Horsfs, T
Watson (cd). W B Saunders, UK
Guglick M A, MacAllister C G, Ely R W, Edwards W C (1995)
.
Hepatic disease a\Sociated with administration of tetanus
antitoxin in eight hor:ses.]' Am. Vtl. Mtd. A.HOC.
206(1 1) : 1 737-40.
\bonder R, Haliburton], Stubblefield R, �I a! (1991) Aspflgillu.1
flam.., and aflatoxins B" B" and M, in (Om associated with
equine death. Arch. Environ. Cm,lam. TOl.lcol. 20( 1 ):151-3.
Zienlara S, Trap D. Fontaine]], e/ al. (1994) SUn'cy of ",!uine
hepatic encephalopathy in France in 1992. .."fl. /Ur.
1 34{ I ) : 1R--19.
Primary hyperammonemia
Mair T S.Jones R D ( I 99;;) Acme enccphalopathy and
h;perammonaemia in a hONI, without evi'knce of liver
disease. Vtl. /U,. 137:642-3.
McConnico R S , Duckett W M, ",rood P A (1997) Persistellt
hyperammonemia in two related Morgan weanlings. j. V�I.
Inl. Mrd. I I (4):264--6.
Peek S F, DiveN T],]ackson C] (1997) Hj-pcrammonaemia
as.�()cia!ed with encephalopathy and abdominal pain
without evidence of liver disea.�e in four mature horses.
Equin� V�I. J 29(1) :70--4.
Biliary tract disease
i'iimi II, A.�akawa S, Tamura R, Yamamoto Y, Shimura H
Febigcr: Philadelphia, pp. fiHH-702.
Cornick] L, Carln G K, Bridges C H ( 1 9RR) Kkin gra," ,.
a"ociated hepatotoxicosis in horst'S. j. /"m. \·'�I. M�d. A'.loc.
193:932-5.
]akov.-;ki R M (1994) Right l"'pati(" lobe mrophy ill hor�es: 17
cases ( 1 9R:'.-1993) J Am. 1',1. l\1ni. A.\.Wf. 204,]()?i7-6 1 .
Lavoie] 1', T""ser",,. E ( 1993) ),1;,,,i,,e iron overload and liver
fibrosis n'",,"biing haerno<;hrolllatosis in a racing POllY.
!-."quiw. lel.j. 2�:552-4.
I.cS<ard P, Wilson W D, Olander H.l, Rogers Q R, �1endel V E
( 1 9Hfi) ClinicopaThologic study of horses slIn'iving
pyrrolizidilW alkaloid (Sm�ri() vulgaris) toxicosi<. Am. j. Iftl.
Rn 17:1776-80.
Mendel V E, Wilt �l R, Gilchdl B S, �I (II. ( 1 9HIl) Pvrroliljdinl'
alkaloid-induced liver dis�asc in hors,'s: an "arly diagnosis.
Am.I \,,1. Re.'. 49:572--8.
Mullaney T P, Bwwn C M (19H!I) Iron toxicity in "eonatal
foals. Equin' V,I. .f. 20:1 1 9-21.
Pearson E G, Hed."nlm 0 R. l'op[wng-d R H (1991) llel'''';'
cirrhosis and h"mochromatosis ill three horses. .
J Am. V�I.
Med. AmY., 201,1053--fi.
Hyperlipemia
Burkholder Wj, Thatcher. c: D (1992) Emera! nutritiollal
support of sick horses. In Curr
en! 7'ht>mjl)' in f:quint
Mfdici7lt (3rd edn), l\ E Rohinson (cd.) \-\' B Saunders,
Philadelphia, PI" 727-31
Golenz �1 R. Knight D A, YmrdlUk St] (1992) l'se of a
human en[('ral r"eding preparatioll for treatment "r
hyperlipemia and nutriti"nal support during h"aling ofan
oesophageal lacera!.ion in a miniature hor.'l" j. Am. litl.
M�d. A",,,," 200:951-3.
Harris P A, Frape D L,Jdlcolt l B. l.lIe,"s D M, Meyer H,
Savage C] (199.';) ;o.Jutritional aspt'cL� of metabolic
diseases. Hyp"rlipaemia. In T"� Equillt Manual. AJ
Higgins and 1 M \'\'right ("ds) \\' B Saunder<. l.ondon,
pp. 181-3.
Jeffcott L B. Field] R ( 1 985) Epidemiologkal a�pcct"' of
hyperlipaemia in poni"s ill southeastern Amtralia. Amlr.
llel. J. 62:110-1.
Mogg T D, Palmer,,) E ( 1 995) Ilyperlipidemia, hyplTlipemia.
and hepatic lipidosi, in American miniature hors"" 23
cast'.• (Hl90-1991).j. Am. l'eI. J\"ffd. AlSll{. 207:(i01-7.

401
19 CHRONIC WEIGHT LOSS, MALABSORPTION SYNDROMES, AND LIVER DISEASE
Moore B R, Abood S K, Hinchcliff K W ( 1 994) Hyperlipaemia
in 9 miniature horses and miniature donkeys . ). Vet. Intern.
Med. 8:376--8 1 .
Naylor j M, Kronfeld D S , Acland H ( 1980) Hyperlipemia in
horses: effects of undernutrition and disease. Am.). Vet.
Res. 41 :899-905.
Reid S W j, Mohammed H 0 ( 1996) Survival analysis
approach to risk factors associated with hyperlipaemia in
donkeys . ] Am. Vet. Med. Assoc. 209:1 449-52.
Watson T D G ( 1 998) Equine hyperlipaemia. In Metabolic and
402
Endocrine Problems of the Horse, T Watson (ed. ) . W B
Saunders, London pp 23-40.
Watson T D G, Love S ( 1994) Equine hyperlipaemia. Compo
Cont. Educ. Pract. Vet. 1 6:89-97.
Watson T D G, Murphy D, Love S ( 1 992) Equine
hyperlipaemia in the United Kingdom. Clinical features
and blood biochemistry of 1 8 cases. Vet. Rec. 1 3 1 : 48-5 1 .
Wensing T H , Schotman Aj, Kronemanj ( 1974) Effect of
treatment with glucose, galactose, and insulin in
hyperlipemia in ponies. Tijdschr. Dierfeneesk 99:919.
20
Acute diarrhea
General principles of
treatment of acute diarrhea
in adult horses
, ____________________
_"l1'"&
TJ Divers
The most important treatment for horses with severe
diarrhea is to give intravenous fluids to correct extracel­
lular fluid deficits (especially intravascular volume
deficits) , and any electrolyte and acid-base abnormali­
ties. A balanced polyionic crystalloid, with or without
hypertonic saline, is the preferred intravenous fluid.
Hypertonic saline may be used if there is extremely
poor perfusion and shock is apparent, but this must be
followed by appropriate and generally large volumes of
polyionic crystalloids. The long-term use of sodium
chloride will result in acidosis. Once the patient is seen
to urinate, potassium should be added (20-40 mEq/l)
to the crystalloids. Potassium should be used in all cases
unless there is oliguric renal failure, the horse has the
hyperkalemic periodic paralysis (HYPP) gene, or the
serum potassium is abnormally high. Although the
amount of potassium lost in diarrhea is not as great as
sodium, anorexia and continual loss of potassium in
urine generally cause a severe total body potassium
deficit.
The rate of fluid administration depends upon the
severity of dehydration. Clinically this can be crudely
determined by examining
• dryness of mucous membranes
• skin turgor
• speed of distension of the jugular vein when
compressed.
Packed cell volume (PCV) and degree of azotemia
provide laboratory evidence of the degree of dehydra­
tion, although PCV is quite variable, and blood urea
nitrogen (BUN) and creatinine can be affected by
intrinsic renal factors in addition to pre-renal influ­
ences (dehydration). Fluid replacement should include
• volume replacement (per cent dehydration x body
weight in kg liters needed)
=
• maintenance needs (60-100 ml kg- I day- I )
• ongoing losses, these are variable depending upon
the degree of dehydration.
The initial volume deficit should ideally be replaced
within 6-12 hours or less, depending on cardiopul­
monary status, evidence of edema formation, plasma
protein concentration remaining greater than 4.5 gl dl
(45 gil) , and urine output. If urination is oliguric and
there is minimal or no decline in the degree of
azotemia in spite of rapid fluid therapy for several
hours, intrinsic renal failure should be considered.
If colloids are also being administered, fluid deficits
can be replaced much faster. Because of the loss of albu­
min and decreased oncotic pressure in most horses with
acute colitis, it becomes increasingly difficult to main­
tain the crystalloid fluids in the intravenous space, thus
promoting organ dysfunction (e.g. kidney, lung, �nd
.
heart) and edema in all interstitial spaces, both vlSlble
and occult, including the colon and feet. Therefore,
treatment with a colloid fluid such as plasma or het­
astarch is generally indicated if economics permit. The
amount administered is generally controlled by eco­
nomics, but 2-1 0 liters of plasma or 1 0 ml/kg het­
astarch are generally used as the initial treatment.
Supplemental calcium should be added ( 1 1 g cal­
cium borogluconate per 500 kg horse) to 5 liters fluids
405
20 ACUTE AND CHRONIC DIARRHEA
if there are obvious signs of hypocalcemia, e.g.
diaphragmatic flutter. If the ionized calcium is low
« l.2 mmol/I) but there are no clinical signs, the same
amount of calcium borogluconate can be added to 20
liters of crystalloid fluids. Repeated calcium treatment
should be performed only when the ionized calcium
remains low.
In cold weather, fluids should be given at nearly
body temperature. They are ideally administered
through an over-the-wire polyurethane catheter since
horses with colitis have the highest rate of jugular
thrombosis of any equine patient.
Oral fluids should be provided free choice unless the
patient is colicky and has gastric reflux after passage of
a nasogastric tube. These fluids should include both
clean freely available water, and water with electrolytes.
Electrolyte supplements containing sodium chloride
(30 g), sodium bicarbonate ( 1 2 g ) , dextrose (20 g ) , and
potassium chloride (5 g) per gallon of water is a fre­
quently used mixture that is only slightly hypertonic.
Glutamine could be added to the fluid mixture since it
is thought to support enterocyte function, and decrease
endotoxin absorption and bacterial translocation. This
would considerably affect cost, and the benefits are
unproven in equine colitis. If the patient has a meta­
bolic acidosis and normal anion gap, the amount of
chloride in the solution should be decreased by substi­
tuting potassium bicarbonate (5-10 g) for 5-1 0 g of the
sodium chloride.
ORAL REHYDRATION WITHOUT
INTRAVENOUS FLUIDS
Some horses with mild diarrhea can be adequately rehy­
drated using oral fluids. If there is no gastric reflux, flu­
ids can be given via an indwelling 'capped' nasogastric
tube. A 500 kg horse may be given 4 liters of a solution
(l5g sodium chloride, 5 g sodium bicarbonate, 4 g dex­
trose, 10 g potassium bicarbonate, and 1 0 g potassium
chloride) every 30 minutes so long as signs of abdomi­
nal pain are absent. Larger volumes may result in
abdominal pain and too rapid transit time. Higher
concentrations of sodium chloride may cause metabolic
acidosis.
Treatment to help negate the effects of
endotoxin/ cytokine/systemic inflammatory response
should be routinely provided for all colitis cases. This
would include flunixin meglumine (0.3 mg/kg q. 8 h ) ,
and plasma with antibody against core lipopolysaccha­
ride. Polymyxin B in combination with dextran 70 is
sometimes used in the hope of binding endotoxin.
406
Over the years, a variety of drugs have been used to
try to 'slow ' the intestines or promote development of a
more formed stool. Loperamide (0.04-l.6 mg/kg p.o.)
may be used in non-infectious diarrheal conditions. Its
primary benefit could be an antisecretory effect.
Phenoxyben zamine has an antisecretory effect but
should not be used because of its hypotensive effect.
Bismuth subsalicylate (up to 4 1/500 kg q. 12 h) may
have antidiarrheal, antibacterial, and anti-inflammatory
properties but historically has had little effect on severe
infectious diarrhea in the adult horse, other than mak­
ing the feces block. It is often effective in treating non­
infectious diarrhea in adult horses and some infectious
diarrheal conditions in foals. Kaolin and pectin should
not be used in severe diarrhea as they may worsen mal­
absorption and increase ion loss during diarrhea.
Activated charcoal has been used (0.5 kg/500 kg) in
acute equine colitis. Early treatment may decrease
intestinal endotoxin absorption while other therapies
are being employed. Recently, a compound containing
naturally occurring macro-and micro-minerals was
reported to prevent many of the clinical findings of tox­
emia in a lincomycin model of equine colitis. Further
research on this product as a treatment for equine coli­
tis is needed before any recommendations can be
made.
The use of products that contain Lactobacillus spp.
are frequently recommended in the treatment of
equine colitis. Although they probably cause no harm
they are also of no proven benefit.
Additional treatment in the hope of preventing
laminitis, an all-too-frequent occurrence in acute diar­
rhea, includes nitroglycerin patches applied over the
digital arteries for 1 2 hours each day, for up to 3 days
during the greatest risk period. Support wraps on the
limbs can help prevent leg edema. The tail should be
protected by covering it with a plastic obstetric sleeve
loosely taped with elastic bandage at its base. The per­
ineum should be cleaned as needed to prevent contact
dermatitis and/or scalding. Silver sulfadiazine oint­
ment should be applied topically if dermatitis develops.
Prevention and/ or early treatment of irritant dermatitis
is especially important in stallions.
Salmonellosis
TJ Divers
ETIOPATHOLOGY
Salmonella spp. are gram-negative bacteria that belong
to the Enterobacteriaceae family. Salmonella spp. are

divided into serogroups (A through I) based upon their
common 0 antigens. All Salmonella spp. are considered
pathogenic, although a few serotypes are responsible
for the majority of serious infections in horses;
Salmonella typhimurium (a serotype in serogroup B)
being the most serious. Other Salmonella spp. reported
to cause mild to serious diarrhea in horses are S. agona
and S. anatum (both group B ) , S. newport (group C) and
S. krefeld (group E) . Virulence genes on plasm ids and in
chromosomes are important in the establishment of
infection and disease. Salmonella abortosuis, a cause of
equine abortion often without diarrhea, is found in
Europe but not North America.
A low « 1 %) percentage of normal horses shed
enough Salmonella spp. in the stool to permit a positive
fecal culture. The percentage of positive cultures is
higher (approximately 5 % ) if polymerase chain reac­
tion (PCR) methods are used. Horses with abdominal
pain have increased shedding (5% via culture and up to
40% via PCR) suggesting Salmonella spp. are common
inhabitants of the gastrointestinal tract, but are gener­
ally shed in low numbers in the stool unless there is an
abdominal disorder. Changes in intestinal motility and
volatile fatty acids production by normal flora may
increase the ability of Salmonella spp. to attach to the
intestinal mucosa and to proliferate. The increased
shedding of Salmonella spp . in horses with abdominal
pain does not significantly affect mortality, but is un­
desirable because of the potential for colitis and
increased environmental shedding.
Salmonella spp. have numerous virulence factors that
enhance their toxicity
• adhesion fimbriae that permit attachment to
intestinal epithelial cells
• gene products which activate macropinocytosis
• cytotoxins that either directly, or indirectly via
cytokines, cause epithelial cell damage
• enterotoxins that cause increased secretion of
extracellular fluid and electrolytes into the
intestinal lumen.
Intestinal epithelial cell damage is a result of
cytokine activation, leukocytic enzymes and reactive
oxygen species production. The loss of intestinal bar­
rier permits endotoxin absorption which, along with
inflammatory mediators, is responsible for systemic
effect. Intestinal attachment and invasion is thought to
be most common in the distal small intestine, cecum,
and colon, initially via specialized enterocytes called M
cells. Highly virulent Salmonella spp. contain genes
(type III secretory) that promote secretion of virulent
proteins. Salmonella organisms are invasive facultative
anaerobes that survive and multiply within
macrophages in the intestinal lamina propria and
ACUTE DIARRHEA 20
mesenteric lymph nodes. Virulence proteins of
Salmonella spp. may interfere with macrophage activity
allowing the organism to proliferate within
macrophages. Proliferation within the epithelial cells
and/ or intestinal macrophages is necessary for progres­
sion to enterocolitis. Bacteremia is believed to be rare
in adult horses but is common in foals. In adult horses,
bacteremia must occasionally occur because hepatic,
renal, and mesenteric lymph node abscesses have been
reported caused by Salmonella spp.
RISK FACTORS FOR SALMONELLOSIS
AND EPIDEMIOLOGY
There are at least three major risk factors that deter­
mine whether exposed horses have clinical disease.
These include
• virulence of the salmonella strain
• inoculation dose
• host defenses.
Host defenses include both humoral and cell-medi­
ated immunity, along with enteric protection facilitated
by normal enteric flora and low gastric pH.
Horses may become infected by several means
including environmental salmonella or Salmonella spp.
shed by birds, rodents, i!nd other animals, including
contact with other horses. Birds may pose a special risk
since they often congregate around horse feeds where
infected dropping may contaminate the feed.
Risk factors for infection include
• any change in intestinal motility
• abdominal pain
• change in intestinal flora that may occur with
antibiotic administration and anorexia
• innate stress factors that may affect the horse's
immune response.
Horses with impaction colic are particularly at risk.
Outbreaks tend to be more common in tertiary-care
hospitals where these factors are common, on brood
mare farms with a high-density population of mares and
foals, or on farms where horses have been fed feed con­
taminated with Salmonella spp. Hot weather, increasing
numbers of horses and foals on a farm, and wet flooring
in barns or hospitals all seem to increase infection rates.
CLINICAL SIGNS AND LABORATORY
DIAGNOSIS
The clinical signs are variable (Table 20. 1 ) and include
fever, mild abdominal pain, anorexia, and depression
407
20 ACUTE AND CHRONIC DIARRHEA
Table 20.1 Clinical signsas_'eted WIth
ilalmoneJlo. . . . j . , .. :.. .
Adult horses Fever
Inappetence or anorexia
Depression
Abdominal pain
Diarrhea - varying from nil to
severe and watery
Small colon impaction
Foals Fever
Depression
Anorexia
Hemorrhagic diarrhea
Pneumonia
Meningitis
Septic arthritisiphysitis
without diarrhea in some horses, but most horses that
are clinically affected have moderate to severe, watery
diarrhea. Foals may develop hemorrhagic diarrhea
(rarely seen in adult horses) , pneumonia, meningitis,
and lameness due to either septic arthritis or physitis.
Small colon impactions in adult horses frequently have
associated salmonellosis.
Most clinically affected horses have neutropenia,
vacuolated neutrophils (toxic changes ) , hypo­
chloremia, hyponatremia, elevated PCV, and azotemia.
Acidosis will be present if the anion gap (lactate) is
increased. Hypoproteinemia generally occurs within a
couple of days even in those horses without diarrhea. A
rebound neutrophilia may occur after the initial neu­
tropenia. Importantly, coagulation abnormalities such
as thrombocytopenia and low antithrombin III may
occur in more severe cases resulting in colonic, pul­
monary, and limb thrombosis. Elevations in sorbitol
dehydrogenase are expected, but liver disease is rarely
of clinical significance.
The organism can be cultured from feces, mesen­
teric lymph nodes, and cecum or colonic mucosa of
infected horses. If the feces are very watery, negative
culture results are often reported; as the fecal consis­
tency becomes more formed, repeat cultures should be
positive if the horse has salmonellosis. Feces can be
plated directly onto brilliant green agar and/or can be
placed in selenite broth (40°C) overnight for enrich­
ment. PCR testing is more sensitive than fecal culture
and may be performed on watery fecal samples. A posi­
tive PCR does not confirm that a Salmonella sp. is the
cause of the diarrhea and occasionally false negatives
occur. Appropriate history (see above) , clinical find­
ings, eliminating other causes of diarrhea, and a heavy
408
growth of Salmonella spp. from feces is the most appro­
priate route to reach an ante-mortem definitive diagno­
sis. PCR may be too sensitive for practical use since 45
per cent of horses with abdominal pain are positive.
In foals complete blood count (CBC ) , electrolyte,
clinical chemistry, and coagulation markers are similar
to those in the adult horses, although the number of
bands are often greater, and electrolyte abnormalities
are generally more severe. Blood cultures, joint fluid,
cerebrospinal fluid, or tracheal aspirates may be salmo­
nella positive in infected foals.
TREATMENT
Antibiotic therapy is imperative in nursing foals but
probably has little or no positive effect in adult horses.
The antibiotic(s) of choice for foals should be ones that
have historically been effective in vitro and in vivo
against Salmonella spp. (e.g. amikacin or a group-3
cephalosporin) and are likely to be effective against
translocation of other enteric bacteria. Once the sensi­
tivity is known, a less toxic antibiotic with better intra­
cellular penetration may be added or substituted. In
adult horses, bacteriocidal antibiotic usage might be
justified based upon severe leukopenia, compromised
immune system, skin wounds, invasive procedures (e.g.
abdominocentesis) or in the hope of preventing bacter­
ial translocation. Enrofloxacin (5 mg/kg i.v. s.i.d.) can
be used in adult horses if antibiotics are deemed neces­
sary. Prolonged use of broad-spectrum antibiotics
should be avoided or fungal colitis and pneumonia may
develop.
Fluid therapy is the most important treatment in
adult horses, this should consist of crystalloids and
plasma. The initial crystalloid could be hypertonic
saline if perfusion appears abnormal. Early treatment
with plasma is important in both adults and foals.
Plasma provides oncotic properties that improve the
crystalloid treatments by helping to maintain the crys­
talloid fluid in the intravascular compartment for a
longer time. Plasma also has anti-thrombotic properties
such as anti-thrombin III and protein C, which may
help prevent colonic vessel thrombosis. Thrombosis of
colonic vessels is a frequent post-mortem finding in
Salmonellosis cases that die. Commercial plasma con­
tains an antibody against endotoxin but this property is
probably not as important as albumin, anti-thrombin
III, fibronectin, and other proteins. The preferred iso­
tonic fluids are those that have a slightly alkalinizing
effect. Isotonic sodium chloride given in large volumes
over several days causes an acidosis. The crystalloids
should be provided at a sufficient volume to maintain
urine output, return the blood urea and creatinine to

normal, and normalize PCV and electrolytes.
Additional potassium chloride (20-40 mEq/l) is usually
required to maintain normal potassium concentrations.
Isotonic bicarbonate (l.25%) is sometimes needed if
the horse or foal has plasma bicarbonate of less than 16
mEq/1 and a normal anion gap. If isotonic bicarbonate
is administered, it should contain 40 mEq/1 potassium
chloride.
Additional treatments should be provided to combat
the effects of endotoxemia or endotoxin-induced
cytokines or prostanoids. Of these, flunixin meglumine
(0.3 mg/kg q. 8 h) appears to be the most valuable,
although its use should be limited in a sick foal (only
one or a few treatments ) . Foals should be treated with
appropriate gastric protectan ts and/or prostaglandin
EI (misoprostol, 2-4 Ilg/kg p.o. q. 12-24 h) if non­
steroidal anti-inflammatory drug therapy is needed for
more than 2 days. Additional therapies in the early
stages of the disease intended to combat the effects of
endotoxin and pro-inflammatory cytokines include
polymyxin B (6000 IU/kg i.v.) and dimethylsulfoxide
(DMSO ) . DMSO (0.05-0.1 g/kg i.v. q. 12-24 h) may be
administered in the intravenous fluids during the initial
48 hours of treatment in the hope of diminishing oxida­
tive injury to the colon. Nitroglycerine cream (2%) is
often applied over the digital arteries every 12 hours
during the first 3 days in the hope of maintaining more
normal perfusion to the feet.
Most orally administered intestinal protectants seem
to have minimal benefit. Activated charcoal (l g/kg)
given early in the course of the disease may help bind
lumenal endotoxin. The horse should be fed palatable
grass hay ad lib. during the early stages of the disease if
there is no abdominal pain. As the toxemia resolves the
affected horse should also be fed small amounts of
grain. Both free water and electrolyte-enriched water
(30g sodium chloride, 1 09 sodium bicarbonate, 5g
potassium chloride, 109 of dextrose/gallon of water)
should be provided.
PROGNOSIS
If early and aggressive therapy is provided the survival
rate is high. Laminitis, severe thrombocytopenia with
infarction of the bowel, and oliguric renal failure are
poor prognostic findings in the adult horse. Meningitis,
pneumonia, septic physitis, or septic arthritis worsen
the prognosis in foals. Other complications include
venous thrombosis, uveitis, cellulitis (often associated
with severe limb or scrotal edema) , fungal pneumonia
(caused by severe ulceration of the bowel, antibiotic
administration, and fungal overgrowth) , rectal pro­
lapse , and iatrogenic necrosis of the tail caused by a
ACUTE DIARRHEA 20
tight tail wrap. Although considerable body weight is
lost during the disease process, the weight will generally
return to normal upon resolution of the diarrhea when
the plasma protein concentration returns to normal.
The majority of adult horses that survive salmonellosis
have formed manure within 2 weeks after the initial
episode of diarrhea. A low percentage (probably < 5%)
of cases may have more chronic diarrhea, persistent
hyporoteinemia and failure to gain weight.
Horses with salmonellosis can be expected to shed
the organism in significant numbers (easy to culture)
for 1-2 months. After that time, the shedding numbers
generally decrease so that most samples are culture-neg­
ative by standard methods. When the horse is shedding
heavily, it should be isolated from other horses or put in
a large pasture with non-stressed, healthy adult horses.
Although macrophages and neutrophils are involved in
the pathogenesis of Salmonellosis, they are also inti­
mately responsible for prevention of disease in other­
wise healthy but exposed horses.
CONTROL AND PREVENTION
All infected horses in a hospital environment should be
isolated, and all attendants should wear examination
gloves when handling the horse and disposable boots
when in the stall. Any rodent or bird movement from
that stall should be prevented. The contaminated stall
should be cleaned of organic debris by scrubbing the
stall with a suitable disinfectant-detergent (I-stroke env­
iron, Calgon Vestal Laboratories Inc., St Louis, MO)
and then treated with 10% hypochlorite for at least 1 5
minutes prior to rinsing with tap water. Complete dry­
ing should then be permitted and environmental sam­
pling should indicate the absence of Salmonella spp.
before another horse is allowed to enter the stall. Stalls
that have wooden walls are more difficult to disinfect
than stalls constructed from other materials, but water
sealants applied to the wood might be helpful.
Horses and foals at increased risk of contracting
Salmonella spp. should be given special protection. Gas­
sterilized stomach tubes should be used for all such
horses, especially those being evaluated for abdominal
pain. Foals should be housed apart from horses with
abdominal pain. Prophylactic administration of probi­
otics to postoperative horses had no effect on the shed­
ding of Salmonella spp. or on the prevalence of diarrhea
in one large study. Stalls should be kept as dry as possi­
ble. Cultures and sensitivity should be performed on all
sick horses admitted to a hospital to keep track of the
source of infection and drug resistance patterns. Sick
horses should not be housed in the same wards as sick
cattle since cattle may shed the organisms in greater
409
20 ACUTE AND CHRONIC DIARRHEA
numbers. Molecular techniques may be required to
determine the origin of the initial infection during an
outbreak. All people, especially children, the elderly,
and immunosuppressed individuals should be pre­
vented from having contact with infected horses, their
housing, or bedding. Salmonella typhimurium DT 1 04
(resistant to ampicillin, chloramphenicol, sulfon­
amides, and tetracycline) has been isolated from horses
and appears to be particularly virulent in people.
Clostridial diarrhea in adult
horses
TJ Divers
Clostridial diarrhea in adult horses may result from
infections with toxigenic strains of Clostridium difficile or
C. perJringens. C. perJringens type A with enterotoxin has
been frequently incriminated as a cause of adult horse
diarrhea, but has been difficult to document. An unclas­
sified type of C. perJringens that produces a beta2 toxin
has been recently reported as a cause of diarrhea in
adult horses. Toxigenic C. difficile has been well docu­
mented in adult horses and much is known about the
etiopathogenesis of this disease. In many intensive care
veterinary hospitals, C. difficile is a more common cause
of diarrhea in adult horses than are Salmonella spp.
ETIOPATHOLOGY
Clostridium perJringens is thought to cause diarrhea by
elaboration of either an enterotoxin or a newly
described beta2 toxin. C. perfringens is considered to be
normal flora of the equine intestinal contents, and it is
often cultured in low numbers ( 1 0 CFU/g) from the
feces of normal horses. The numbers of C. perfringens in
the stool may increase in horses with diarrhea, even
when another organism is thought to be responsible for
the diarrhea. A low percentage of C. perfringens strains
(type A) produce an enterotoxin which has the poten­
tial to cause intense fluid secretion into the lumen of
the bowel. Production of the enterotoxin and gastroin­
testinal attachment and absorption are necessary to
develop diarrhea. The diarrhea is likely to be a result of
a combination of hypersecretion effects and tissue dam­
age. Enterotoxins stimulate guanylyl cyclase and cause
accumulation of intracellular cyclic guanosine
monophosphate (GMP) , which opens the chloride
channels triggering intestinal secretion. C. perfringens
enterotoxin may also induce a pro-inflammatory
cytokine response with production of interferon
410
gamma, interleukin-l and 6. In humans, enterotoxi­
genic C. perfringens is usually associated with food poi­
soning, and much less commonly with antibiotic
administration or other factors that disrupt intestinal
flora or motility. Enterotoxin can rarely be found in the
feces of healthy horses, but may be found in normal
feces of horses with colic.
The incidence and etiopathogenesis of a recently
described C. perfringens producing a beta2 toxin is
unknown. The type of C. perJringens producing this
toxin is not described. Affected horses were all adults
and most had a hemorrhagic diarrhea, suggesting that
if this toxin was the cause of the diarrhea, then it has the
ability to cause severe intestinal necrosis. The toxin can
also be found in the feces of horses with intestinal dis­
orders other than colitis, similar to the findings for C.
perfringens type A and enterotoxin.
The etiopathology of C. difficile is well described in
both horses and other species. Pathogenic strains of C.
difficile produce either toxin A or B or both in the
intestinal track. Toxin A is an enterotoxin which causes
both hypersecretion and cytotoxicity similar to that pre­
viously described for C. perfringens enterotoxin. Tumor
necrosis factor (TNF) and other cytokines are undoubt­
edly involved in the cytotoxicity of toxin A. Toxin B (a
cytotoxin) causes severe intestinal inflammation and
necrosis. C. difficilll-induced inflammatory changes to
the intestinal mucosa and disturbances of the intestinal
microflora may permit translocation of other intestinal
bacteria into the blood and other organs.
There are several circumstances that either predis­
pose to or are necessary for the development of C. diffi­
cile. Exposure to a toxigenic strain of the bacteria is a
prerequisite. Clostridium difficile is rarely found in nor­
mal equine feces. A great source of hospital and occa­
sionally farm environmental contamination may be
antibiotic-treated foals which may shed the toxigenic C.
difficile in normal feces. Foals with diarrhea, regardless
of its etiology, may be another source of environmental
contamination as toxigenic C. difficile can frequently be
found in the feces of diarrheic foals, although cause
and effect in the foals is more difficult to prove.
In the majority of adult horses with C. difficile diar­
rhea, prior and recent antimicrobial therapy is almost
always in the history, suggesting that some disruption of
normal flora is required in order for the C. difficile to
proliferate in the colon. Antimicrobials that most com­
monly predispose to C. difficile colitis include
• erythromycin
• trimethoprim/ sulfonamides
• beta-lac tam antibiotics.
Although antimicrobials given per os and reaching a
high concentration in the colon are most likely to pre-

dispose to diarrhea, antimicrobials given by the par­
enteral route may also predispose to C. difficile colitis.
Foals treated with erythromycin per os actually increase
the risk of C. difficile colitis in their dams. This is espe­
cially true if the mare and foal have been to a veterinary
hospital or farm where the C. difficile is more likely to be
in the environment. Presumably the erythromycin­
treated foals have enough erythromycin in their feces to
contaminate the mare's feed and/or water predispos­
ing the mare to the C. difficile colitis.
Foals less than 4 months of age treated with ery­
thromycin rarely develop severe diarrhea. The risk of C.
dilficile diarrhea in horses treated with
trimethoprim/sulfonamide is much less than with ery­
thromycin. Other antibiotics, even injectable ones such
as ceftiofur, may occasionally predispose to C. difficile
diarrhea.
Another predisposing risk factor is withholding
roughage, a common occurrence both for most surgical
procedures requiring general anesthesia and in ill
anorexic horses. Volatile fatty acids produced by nor­
mal fiber fermentation in the colon are protective
against the overgrowth of C. difficile. Intestinal stasis
associated with many cases of abdominal pain also pre­
disposes to overgrowth of the organism.
CLINICAL SIGNS AND CLINICAL
PATHOLOGICAL FINDINGS
The clinical signs and clinical pathological findings of
Clostridium spp. diarrhea in adult horses are not very dif­
ferent from salmonellosis and monocytic ehrlichiosis.
Colic and signs of severe toxemia accompany a large
number of cases, although the severily of C. difficile diar­
rhea can vary similarly to Salmonella spp. or Ehrlichia ris­
ticii. The most severe cases of C. difficile diarrhea show
the following signs
• tympanitic abdominal distension
• passage of scant liquid feces
• bowel necrosis and death.
The tympanitic gas distension may be more common
with C. difficile colitis than with other infectious diar­
rheal diseases in adult horses. Other cases have only
slightly liquid feces and few signs of toxemia. Fever is
present early in the course of the disease in most cases.
In more advanced cases, the temperature may be sub­
normal but the heart rate remains high, extremities are
cold and membranes are discolored. A hyponatremia
and hypochloremia are present in most infectious
equine diarrheal diseases. Azotemia may be pro­
nounced with toxemia. The neutrophil count is often
low early in the course of the disease and immature
ACUTE DIARRHEA 20
neutrophils and toxic changes may be noted, but these
findings are not different from other infectious causes
of diarrhea in adult horses.
DIAGNOSIS
The diagnosis of Clostridium perfringens as a cause of diar­
rhea in horses is difficult. There is usually no common
predisposing event as in humans, i.e. outbreak of food
poisoning or prior antibiotic administration as with C.
difficile. Furthermore, the organism is frequently pre­
sent in the manure of normal horses, and both the
organism and enterotoxin can be found in horses with
abdominal disorders, i.e. colic without diarrhea. If C.
perfringens is to be blamed as the cause of colitis, there
should be
• large numbers of organisms (> lOs/ml feces) in the
stool
• some evidence of sporulation
• presence of enterotoxin in the feces
and other causes of the diarrhea should be ruled out.
The presumptive diagnosis of beta2 toxigenic C. per­
fringens would be based upon clinical signs (most often
hemorrhagic diarrhea) and detection of the beta2 gene
by PCR. All other causes of diarrhea should be ruled out
until more information becomes available on the inci­
dence and pathogenesis of this organism.
The diagnosis of C. difficile is the most straightfor­
ward of the three clostridial organisms associated with
diarrhea.
• In adult horses, there is almost always a history of
antibiotic administration that precedes the diarrhea
for 1-6 days.
• It should be considered more strongly in horses
that have been or are housed in veterinary hospitals
or farms with foals that are being treated with
antibiotics, and/or foals with diarrhea.
• A gram stain of the feces may reveal large numbers
of C. difficile-Iike organisms.
• Toxin A or B, or both, should be found in a fecal
sample. The toxin assay ( ELISA) can be performed
within 1 hour. The fecal sample should be taken
immediately to the laboratory or frozen for the
fecal toxin assay. Detection of the toxin in the feces
is faster and more practical than isolation of the
organism and cytotoxicity assay.
• PCR assays are now available that can, within a few
hours, detect the C. difficile toxin gene in the
feces.
Feces with C. difficile are generally colored green to
brown and are less commonly hemorrhagic.
411
20 ACUTE AND CHRONIC DIARRHEA

Hemorrhagic diarrhea was reported to be common in sonne I and isolation of infectious horses and foals
horses that had the novel beta2 toxin in the feces. should be performed. Housing high risk adult horses in
stalls not previously occupied by antibiotic-treated foals
might be ideal, but is often not practical. Feeding a fer­
TREATMENT mentable fiber as soon as feasible after abdominal
surgery might be helpful by increasing the normal bac­
Treatment of clostridial diarrhea in horses can be terial metabolic products in the colon that are known to
divided into two categories inhibit C. difficile growth. The use of narrow spectrum
antibiotics (as narrow spectrum as possible) and cau­
1 . general supportive treatment (see General
tion in using orally administered antibiotics other than
principles of treatment of acute diarrhea in adult
metronidazole and chloramphenicol in high risk horses
horses) including
could be helpful in decreasing the incidence of C. diffi­
• fluids (crystalloids and colloids)
cile colitis. Mares with foals being treated with ery­
• anti-inflammatory drugs
thromycin should be fed from a container raised off the
• intestinal protectants
ground to decrease exposure to the foal's feces con­
2. antimicrobial therapy.
taining erythromycin and possibly toxigenic C. difficile.
The antimicrobials of choice are metronidazole or Foals should not be allowed to drink water from a
chloramphenicol. Metronidazole would be the first shared water bucket immediately after being dosed with
choice since most (but not all) C. difficile organisms are erythromycin.
very sensitive to the drug, and it has been used success­
fully for a decade in treating this condition. However
there have been several horses at one facility in the US
that had metronidazole-resistant strains of C. difficile. Potomac horse fever
One advantage of chloramphenicol, although not as
JM Bartol
sensitive against most C. difficile organisms, is it is less
readily absorbed by the intestine than metronidazole,
Potomac Horse Fever (PHF) is the common name
and would therefore be expected to have a higher con­
given to the equine infectious enterocolitis caused by
centration in the colonic ingesta. Oral antimicrobial
Ehrlichia risticii. It is also known as equine monocytic
treatment should be continued for at least 7 days.
ehrlichiosis (EME) because of E. risticii's predilection
Relapses may occur when the treatment is discontin­
for peripheral monocytes and macrophages. The dis­
ued, but subsequent clinical episodes are usually
ease was first reported along the Potomac River in
milder. Most horses with C. difficile diarrhea have a clin­
Maryland in 1979, but presently has been confirmed
ical response to the above treatment within 2-3 days if
throughout the United States, Canada, and in Europe.
the diagnosis is correct. All other oral antimicrobial
Several surveys have identified 16-33 per cent of
treatments should be discontinued. If there is fear of
clinically normal horses to be seropositive, many of
bacterial translocation of other enteric bacteria, sys­
which have had no history of illness. Previous studies
temic aminoglycosides may be used if renal function is
have indicated that the majority of disease caused by
normal and monitored. Synthetic bismuth and diocta­
PHF is subclinical. There is also evidence that many
hedral smectite have a favorable in vitro effect against C.
horses with relatively low immunofluorescence assay
difficile and these should be evaluated further in the
(IFA) titers « 1:320) may have not been infected but
horse.
have false positive titers influenced by administration of
If Clostridium perfringens is believed to be the cause of
other equine vaccines. It predominantly causes diar­
the diarrhea, oral metronidazole and/or intravenously
rhea in adui t horses and yearlings, but not in foals.
administered penicillin may be used.
Currently there is evidence for the involvement of E. ris ­
ticii in brood mare reproductive problems and abor­
tions.
PREVENTION
The clinical syndrome may be characterized by one
or more of the following clinical signs
Prevention of Clostridium difficile infection may be diffi­
cult in intensive care hospitals with large numbers of • fever
foals and adult horses receiving broad-spectrum antibi­ • depression
otics. C. difficile forms heat-resistant spores but surface • anorexia
disinfection with hypochlorite may be successful in • dehydration
destroying most cells. Routine hand washing by all per- • diarrhea

412

• colic
• laminitis.
Many cases manifest signs of colitis in varying
degrees. The onset of clinical signs usually occurs 7-14
days after infection, and following a transient fever 2-4
days post-infection with E. risticii. Diarrhea develops in
less than 60 per cent of cases of PHF even though it is
thought to be a primary clinical sign. More often
affected horses are depressed, anorexic, febrile, and
toxemic, and have complete blood count (CBC) and
chemistry findings suggestive of colitis. Laminitis is a
serious sequela to PHF and is seen in 5-30 per cent of
cases. The apparent increased incidence of laminitis
associated with PHF compared to other enteric disor­
ders might be explained by the presence of E. risticii in
circulating mononuclear cells and the resulting release
of proinflammatory cytokines.
EPIDEMIOLOGY
PHF has a seasonal occurrence and is frequently
reported to be associated with close geographical prox­
imity to a river although this is not a prerequisite. It is
infectious and minimally contagious. Epidemiological
studies have supported the infectious nature of the dis­
ease supporting a helminth vector. Until recently no
arthropod vectors had been identified. Studies investi­
gating the role of several species of ticks, flies, and non­
equine mammals in the transmission of Ehrlichia risticii
have been unsuccessful in implicating any of them as
the vector. Currently, investigators are examining the
role of aquatic insects as intermediate hosts.
Experimental oral infection of horses via nasogastric
administration of feces from infected horses has been
successful in transmitting the disease. Large numbers of
E. risticii are shed into the lumen of the colon in exfoli­
ated colonic epithelial cells at the time of the diarrhea
and for 4-8 days after it has begun. However, casual
contact with infected horses and contaminated feces
does not generally provide a high enough level of expo­
sure to result in natural infection. Polymerase chain
reaction (PCR) testing has determined that large num­
bers of E. risticii are present in the blood on day 1 after
experimental intravascular infection, and for nearly 2
weeks after if untreated. At the time of the diarrhea and
for 4-8 days after it has begun, casual contact with
infected horses and contaminated feces does not gener­
ally provide a high enough level of exposure to result in
natural infection.
Indirect oral transmission through concentration of
E. risticii in a helminth or coprophagus arthropod, and
inadvertent ingestion by a horse is likely. Neorickettsia
ACUTE DIARRHEA 20
spp., also in the family Ehrlichieae, are transmitted
through ingestion of infected helminths. Similarities in
DNA structure between E. risticii and Neorickettsia
helminthoeca, the etiologic agent of salmon poisoning in
dogs transmitted by a fluke, raised the question of
helminth transmission in the horse. A rickettsial
pathogen parasitizing fish in japan, also transmitted by
flukes, was isolated and found to share 99 per cent DNA
homology with E. risticii. Thus, more evidence is pro­
vided for the potential of helminth transmission in the
horse. Similarly, E. risticii may be concentrated in
coprophagous insects which are unknowingly ingested
by the horse. Tenebrio beetle species have been identi­
fied in large numbers on PHF endemic farms. They are
known to be intermediate hosts of nematodes, as well as
Ehrlichia sennetsu, an ehrlichial pathogen of humans
closely related to other ehrlichial organisms. The
involvement of an arthropod or helminth would be con­
sistent with the seasonality of the disease. More recently
E. risticii, or a nearly identical organism, has been found
in freshwater stream operculate snails (Pleuroceridae:
Juga spp.) and in cercariae released in their secretions.
Water environments make up the natural habitat of
these snail species. The possibility of snails being a
potential vector is supported by evidence that PHF is
associated with close proximity to water (rivers, ponds,
streams) and that horses on dry pastures in endemic
areas usually do not develop the clinical disease.
Environmental stress factors are not associated with risk
of the disease.
The paricular virgulate cercariae of fresh water snails
in which E. risticiiwas isolated are associated with trema­
todes of the family Lecithodendriiae, common parasites
of bats in North America which use freshwater snails
and aquatic insects as intermediate hosts. Using PCR
testing, E. risticii positive metacerariae were identified
in immature and adult caddisflies, mayflies, damselflies,
dragonflies, and stoneflies. In additon E. risticii PCR
posItIve adult trematodes in the family
Lecithodendriiae were found in the intestines of bats.
The gene sequences of the metacercariae and adult
trematodes were found to be essentially identical to the
1 6S rRNA gene sequences of E. risticii from horses and
snails in northeren California. This new information
indicates that there is a broad range of intermediate
hosts for trematodes that act as vectors for E. risticii.
Therefore, aquatic insects are likely to play an impor­
tant role in the epidemiology of PHF. Horses may acci­
dentally ingest aquatic flies in addition to snails carrying
the E. risitcii infected metacercariea. Aquatic insects as a
potential vector is also supported by evidence that PHF
is associated with close proximity to water.
Different strains of E. risticii, as compared to the
1984 isolate, were isolated from clinically sick horses in
413
20 ACUTE AND CHRONIC DIARRHEA
the early 1990s. It is known that PHF is caused by diver­
gent strains. Multiple strains may account for incom­
plete vaccine efficacy since commercial vaccines are
made of the single 1984 isolate. Divergent strains may
also account for difficulties in interpretation of diag­
nostic tests in horses with clinical signs consistent
with PHF. False negative results or lower titers may
occur if diagnostic tests identify only a single type strain
of E. risticii.
E. risticii may also cause abortion. Abortions in the
seventh month of gestation have been seen with both
experimental E. risticii infection and natural infection.
Abortion was accompanied by placentitis and retained
placenta in mares that had fully recovered from the
enterocolitis while 3-6 months pregnant. E. risticii was
cultured from the fetal tissues. Gross and histologic evi­
dence of enterocolitis, hepatitis, and lymphoid hyper­
plasia were present. The frequency of PHF-associated
abortion is unknown but it seems more likely that it
would occur in endemic areas. E. risticii, as an agent of
abortion, must be taken into consideration in cases of
late-term abortions on endemic farms with confirmed
cases of PHF. Since a large proportion of disease due to
E. risticii is subclinical, and therefore undetected, it
should be considered in cases of late-term abortions in
herds without history of illness.
CLINICAL SIGNS
The disease is characterized by one or more clinical
signs including
• fever
• depression
• anorexia
• dehydration
• diarrhea
• colic
• laminitis.
Physical examination and laboratory test results are
consistent with enterocolitis and endotoxemia. The
onset of clinical signs occurs 7-1 4 days post-infection
following a transient, often subclinical fever 2-4 days
post-infection. The initial fever spike may be accompa­
nied by partial anorexia. Diarrhea only occurs in a
small percentage of infected horses « 60%) but when
it does occur it can be severe and accompanied by
abdominal pain and/or laminitis. Fever is generally
present at the time of the diarrhea which occurs 7-1 0
days after infection. Fever and laminitis may occur
without diarrhea. The complete blood count and
chemistry panel are characterized by hemoconcentra­
tion (often severe), leukopenia, occasional monocyto-
414
sis, pre-renal and/or renal azotemia, hypoproteinemia
(often severe), hyponatremia, hypochloremia, and
hypokalemia. It is common to see a marked leukocyto­
sis after leukopenia in clinical PHF. Because these find­
ings are similar to those found in acute endotoxemia,
diarrhea caused by Salmonella spp. is the primary differ­
ential diagnoses.
DIAGNOSIS
At the time of writing, accurate practical diagnosis of
PHF is complicated. Cell culture from infected blood
would be the most sensitive and accurate means of
diagnosis, but is not rapid enough to be of practical
use. The PCR uses genomic amplification to identify a
unique genomic sequence of Ehrlichia risticii, the par­
tial 1 6S rRNA sequence. A combination of PCR and
indirect immunofluoresence assay (lFA) is employed
to increase diagnostic accuracy and decrease time for
test results. A whole blood, EDTA sample is submitted
for PCR and E. risticii organisms are identified in the
buffy coat component of the sample. The PCR is a sen­
sitive and specific test that does not seem to be influ­
enced by vaccination. It also aids in interpretation of
low IFA titers in clinically sick horses. Even a titer as
low as 1:80 with a positive PCR test is indicative of
probable infection given clinical signs and time of
year. One disadvantage of PCR is possible sample cont­
amination. Positive and negative controls are included
during testing to limit false negative and false positive
results. The genes that PCR detects may exhibit minor
sequence divergence among strains of individual
species, and so may be useful for detection of variant
strains of a single species as occur in E. risticii or may
make definitive diagnosis complicated if the PCR does
not detect all possible divergent strains.
The diagnosis of PHF can also be made by detecting
seroconversion of consecutive serum samples. Five to
seven days after the first titer is sufficient time to collect
the second sample. A four-fold or greater change in IFA
titer is diagnostically significant in rickettsial disease as
stated by the Center for Disease Control. However fail­
ure to seroconvert does not rule out infection because
the onset of clinical signs can be delayed as long as 1 4
days, and the horse may have already seroconverted by
the time the first sample was obtained. Another compli­
cating factor is the ability of horses in endemic areas to
maintain very high titers for prolonged periods of time
without clinical disease. The bottom line in accurate
diagnosis of PHF is best made by considering the over­
all picture, including clinical signs, geographic loca­
tion, and season of year, and using this information to
interpret test results.

TREATMENT AND PREVENTION
Treatment considerations for PHF are similar to those
for any acute colitis in the horse
1. addressing hydration status, acid-base deficits, and
electrolyte abnormalities with intravascular fluids is
the basis of supportive therapy in acute colitis
2. signs of endotoxemia warrant the use of low anti­
endotoxic doses of NSAIDs like flunixin meglumine
3. a plasma transfusion of at least 3-6 liters is
beneficial in severe hypoproteinemia by providing
albumin to increase plasma oncotic pressure as well
as in endotoxemia by providing anti-thrombin III,
coagulation inhibitors, and plasma proteins.
Specific treatment of PHF includes administration
of oxytetracycline at 6.6 mg/kg Lv. q. 12-24 h for 3-5
days. If the diagnosis is correct, a favorable response to
therapy is usually seen within 1 2-24 hours, manifested
by resolution of fever, depression, and anorexia.
Diarrhea typically resolves within 3-4 days or fails to
develop if treatment is instituted prior to onset.
Although it has been discussed extensively among prac­
titioners, it is unlikely that oxytetracycline will exacer­
bate or cause disease by organisms such as Salmonella
spp. or Clostridium spp. The high risk of laminitis, a
sometimes f atal sequela, often outweighs the risks of
oxytetracycline when there is a high index of suspicion
of PHF and diagnosis is still pending.
Laminitis is a frequent complication of PHF with a
5-30 per cent rate of occurrence. Because of the high
risk involved, it is prudent to take preventative measures
against laminitis in patients with suspected PHF.
Unfortunately, efficacy of any one prophylactic treat­
ment for laminitis is difficult to assess , therefore there
are many options and combinations
1. Lily pads, NSAIDs (phenylbutazone, flunixin
meglumine, aspirin) , and DMSO are frequently used.
2. More recently topical application of nitroglycerine
ointment to the digital arteries has been
recommended for vasodilatory effects and clinical
observations seem to be consistent with some success.
3. The use of pentoxifylline, a methylxanthine
derivative has become a popular therapy as well. It
may increase blood flow to hypoxic tissues by
improving the flexibility of red blood cells,
reducing blood viscosity, and inhibiting thrombus
formation. Experimentally it has been shown to
inhibit tissue-damaging inflammatory mechanisms
including inhibition of tumor necrosis factor. These
effects may deem it efficacious in laminitis
prevention but it has not been proven. Currently
studies are being performed to evaluate the efficacy
ACUTE DIARRHEA 20
of pentoxifylline in the treatment of endotoxemia
in horses.
Presently vaccination efficacy is questionable. There
are numerous cases of clinical PHF in vaccinated
horses. A possible explanation is the identification of
new disease-causing strains of Ehrlichia risticii. Studies
on vaccine efficacy have shown that annual immuniza­
tion is inadequate, with only 50 per cent of vaccinates
being fully protected 6 months after vaccination. Based
on this evidence, recommendations for vaccination are
that horses in endemic areas be vaccinated every 3-4
months from July to November (peak incidence) after
an initial vaccination protocol of 2 doses, 3 weeks apart,
initiated in April. This protocol increases the likelihood
of more complete protection. Even if complete protec­
tion is not achieved, vaccination may lessen the severity
of disease and is therefore strongly recommended.
Possible explanations for the marginal nature of the
vaccines include deficiencies in the antibody response
of the horse from the inactivated vaccine and the anti­
genic variation of divergent strains of the organism. No
serious adverse vaccine reactions have been reported
and the vaccine has not been proven unsafe for preg­
nant mares. Vaccination is probably unnecessary for 2
years after natural disease because of the long-lived
immunity evidenced by clinical resistance to re-infec­
tion for 20 months.
Non-steroidal anti­
inflammatory drug toxicity
ND Cohen
INTRODUCTION
Non-steroidal anti-inflammatory drugs (NSAIDs) are
frequently administered to horses with colic, endotox­
emia, musculoskeletal disorders, and other medical
problems because of the antipyretic, analgesic, and anti­
inflammatory properties of the drugs. In addition to
these therapeutic properties , NSAIDs also exhibit toxic
properties. The mechanisms, clinical signs, clinical
pathology, diagnosis, treatment, and prevention of
NSAID toxicity are reviewed in this section.
MECHANISMS OF TOXICITY
The major toxicities related to NSAIDs include
• gastrointestinal tract damage
• renal damage.
415
20 ACUTE AND CHRONIC DIARRHEA
Gastrointestinal tract abnormalities are the most
common manifestations of NSAlD toxicity. Gastric
ulceration is the condition most commonly detected,
and it can develop anywhere in the gastrointestinal tract
(from the mouth to the rectum) . Renal toxicosis also
may develop. The primary mechanism of both thera­
peutic and toxic effects of NSAlDs is related to inhibi­
tion of the cyclooxygenase enzymes. Two isoforms of
the cyclooxygenase enzyme have been identified
• cyclooxygenase-l (COX- I )
• cyclooxygenase-2 (COX-2 ) .
COX-l i s produced constitutively and thought to
play an important role in maintaining physiologic
homeostasis; it is found in such tissues as the stomach
and kidney, and in the endothelium and platelets. In
contrast, COX-2 is an inducible enzyme thought to be
associated with inflammation, and is produced by a vari­
ety of cells including monocytes, fibroblasts, synovio­
cytes, and chondrocytes. It has been postulated that
drugs which inhibit COX-l more than COX-2 will have
greater toxic potential because they inhibit physiologic
functions to a greater extent. Evidence exists that the
ulcerogenicity of the following drugs decreases in
sequential order:
• phenylbutazone
• flunixin meglumine
• ketoprofen.
The differing toxicity may relate to varying affinities
of these agents for the COX-l and COX-2 isoforms.
Inhibition of cyclooxygenase results in inhibition of
prostanoid synthesis. In the stomach, inhibition of
cyclooxygenase can increase acid secretion, decrease
output of mucus and bicarbonate, impair vasodilation,
and diminish epithelial restitution, cell division, and
angiogenesis. Inhibition of cyclooxygenase also
increases the severity and impairs the healing of existing
ulcers. In the kidney, prostaglandin E2 (PGE) and
prostacyclin (PGI) produce vasodilation in the autoreg­
ulatory response of renal blood flow to hypoperfusion;
consequently, hypovolemia, hemorrhage, or renal dis­
ease will increase the risk of renal NSAlD toxicosis.
Damage is greatest at the renal crest (papilla) and pap­
illary crest necrosis may be associated with subsequent
nephro- or ureterolithiasis and chronic renal failure.
Not all of the adverse effects of NSAIDs are attribut­
able to cyclooxygenase inhibition. The NSAIDs also
cause injury from a variety of mechanisms, including
microvascular damage, increased intracellular concen­
tration of reactive oxygen and other free radicals, direct
local injury (particularly with ion trapping in the stom­
ach ) , inhibition of cell division, and reduced hydropho­
bicity of the gastric mucus coat.
41 6
Although the toxicity of NSAIDs is dose-related, pre­
disposing factors such as dehydration or sepsis con­
tribute to the development of NSAlD toxicity. Some
horses may have an idiosyncratic predisposition and,
experimentally, arthritic animals may be more suscepti­
ble to NSAlD-induced gastropathy than healthy animals.
The latter finding is important because NSAlDs are
often administered to chronically lame horses. In some
areas, concurrent use of two or more NSAlDs is com­
mon. Combination of two NSAlDs will prolong their
pharmacologic effect and increase the risk of toxicity.
CLINICAL SIGNS
Clinical signs of NSAlD toxicosis are usually referable to
the gastrointestinal tract and include inappetance or
anorexia, lethargy, and occasionally fever. Oral or lin­
gual ulceration may also lead to difficulty in prehension
and mastication. Esophageal ulceration may result in
signs of apparent pain (stretching of the neck, groan­
ing) during swallowing, and ptyalism. Gastric ulceration
may result in inappetance, particularly for grain by some
horses. Horses that have gastric outflow obstruction
associated with gastroduodenal ulceration may exhibit
ptyalism, reflux esophagitis, and, in severe cases, spon­
taneous nasogastric reflux. Horses with ulceration any­
where in their gastrointestinal tract may exhibit signs of
colic which may be intermittent and varying in severity.
Horses with colonic ulceration may have unformed
stools or diarrhea, and edema of the ventrum. Intestinal
damage caused by NSAIDs can disrupt the mucosal bar­
rier of the intestinal tract, resulting in endotoxemia.
Clinical signs of endotoxemia (e.g. altered appearance
of mucous membranes, fever, and dehydration) may be
seen in some horses with NSAlD enteropathy.
CLINICAL PATHOLOGY
The most consistent clinicopathologic abnormality in
horses with NSAlD toxicosis is hypoproteinemia and
hypoalbuminemia, presumably from loss and microbial
digestion in the intestinal tract. These findings are
more commonly observed with involvement of the dis­
tal portions of the intestinal tract, and are unreliable as
a diagnostic tool for horses with NSAlD gastropathy.
Some horses will have decreased concentration of cal­
cium, attributable in part to intestinal loss of protein­
bound calcium.
In chronic cases, horses may be anemic from inflam­
mation or intestinal blood loss. Occult blood may be
found in the feces of horses with more distal enteric
involvement, but these tests often lack sensitivity and

false positive results may be expected for up to 24 hours
after rectal palpation.
The concentration of leukocytes is usually within the
reference range, although leukocytosis and hyperfib­
rinogenemia, associated with inflammation , and
leukopenia and neutropenia, presumably caused by
endotoxemia, can be seen in some horses with NSAID
toxicosis. Results of peritoneal fluid analysis are often
within reference ranges, but increased concentration of
nucleated white blood cells, total protein, and fibrino­
gen may be seen. When abnormal, cytologic examina­
tion of peritoneal fluid is more consistent with
non-septic than septic inflammation.
Pre-renal or renal azotemia may be observed in some
horses with NSAID toxicosis. Pre-renal azotemia may be
associated with dehydration. Renal azotemia is not
often found clinically and is generally observed late in
the course of disease. Other urinary indices of renal
damage are generally insensitive; urinalysis may reveal
hematuria. Serum concentration of phosphorous may
be increased but this also is an insensitive indicator of
renal NSAID toxicosis.
DIAGNOSIS
Diagnosis is usually made on the basis of history of
NSAID use, clinicopathologic findings, and clinical
signs. Endoscopy can be useful to visualize the location
and extent of esophageal, gastric, and, when possible,
duodenal lesions. Gastric lesions are more common in
the glandular epithelium, although non-glandular
lesions can be observed. In some cases, contrast radiog­
raphy or scintigraphy may be useful to document
delayed gastric emptying. Lesions of the jejunum,
ileum, cecum, and colon can be difficult to identifY
without celiotomy and enterotomy. It has been sug­
gested that isotope-labeled white blood cell scinti­
graphic scans may identifY colonic ulceration; the
sensitivity and availability of the procedure is probably
quite limited. Ultrasonographically horses with renal
crest necrosis may have increased echogenicity of the
renal crest and echogenic debris in the renal pelvis.
TREATMENT
In all cases treatment should include discontinuation of
NSAIDs. In horses with acute overdose (e.g. inadvertent
administration of a full 12-g tube of phenylbutazone
paste), gastric lavage and administration of 4.5 liters ( 1
gallon) per 450 kg of mineral oil via a nasogastric tube
may be of benefit to reduce the absorption of the
ingested NSAID. Treatment for gastric ulceration with a
proton-pump inhibitor (e.g. omeprazole) , an Hz-blocker
ACUTE DIARRHEA 20
(e.g. ranitidine) , or sucralfate should be implemented
for horses with gastric ulceration. Regardless of the site
of NSAID toxicity, administration of misoprostol, a syn­
thetic analog of prostaglandin E ' may be of benefit
I
because it has been demonstrated to prevent phenylbu­
tazone-induced gastrointestinal lesions in horses. The
drug can be administered orally (5 Ilg/kg q. 12 h or 2
Ilg/kg q. 6 h ) . Some clinicians avoid use of this drug
because gastrointestinal side effects have been described
in people and anecdotally among horses. For manage­
ment of colonic lesions, the reader is referred to Chapter
2 1 , Right dorsal colitis. Horses with strictures of the
pylorus, duodenum, jejunum, or colon may require
surgical management.
PREVENTION
Prevention of NSAID toxicosis can be achieved in many
horses by avoiding the use of NSAIDs or by limiting the
dose and duration of treatment to the minimum that is
required to control the problem, however some horses
may experience NSAID enteropathy. Use and develop­
ment of less ulcerogenic agents (e.g. ketoprofen or
agents that are more COX-2 selective) could prevent
NSAID toxicosis in some horses. Limiting the extent of
predisposing factors such as dehydration should
decrease the risk of NSAID toxicosis. Some clinicians
administer anti-ulcer medications to prevent gastric
ulceration in horses treated with NSAIDs. As described
above, administration of misoprostol can prevent or
limit the severity of NSAID-induced enteropathy.
Toxic colitides
ND Cohen
INTRODUCTION
Various toxic causes of enteritis and colitis have been
reported. In this section a discussion of cantharidin tox­
icosis is presented, along with a brief review of other
toxic causes of colitis. Non-steroidal anti-inflammatory
drug toxicity and right dorsal colitis are discussed else­
where in this book (see Chapters 20 and 2 1 ) .
Cause
Cantharidin is a toxic principle found in many of the
'blister' beetles (Epicauta spp. ) (Figure 20.1) that cause
417
20 ACUTE AND CHRONIC DIARRHEA
Figure 20.1 Beetle, Epicauta sp., associated with blister
beetle toxicosis (photograph courtesy of Dr DG Schmitz)
blistering of mucosal surfaces. Cantharidin toxicosis
results from ingestion of dead blister beetles in alfalfa
hay or, very rarely, other alfalfa products. Male beetles
produce the toxin and pass it to females during mating;
concentration of cantharidin is highest in the
hemolymph and genitalia of the beetles.
Some species of blister beetles feed and mate in
large groups. The modern forage harvesting technique
of simultaneously cutting and crimping forage can
result in entrapping these swarms of beetles, resulting
in a large number of insects in a small number of bales
or flakes of forage. Ingestion of as little as 4-6 grams of
dried beetles (about 100 beetles) can be lethal to a
horse, although lethal doses have a wide range, proba­
bly because of such factors as predominate gender
ingested and inter- and intra-species variation among
beetles in the production of toxin.
The toxin rapidly causes hypovolemic shock and
pain because of the extensive necrosis and sloughing of
the mucosal lining of the proximal gastrointestinal
tract. In the urinary tract, cantharidin causes ulceration
and hemorrhage of the bladder mucosa, ureters, and
renal pelvis; variable amounts of renal tubular damage
may occur. Cardiac toxicity is less common, abnormali­
ties include ventricular myocardial necrosis and peri­
cardial effusion.
Clinical Signs (Table 20.2)
Onset and duration of clinical signs of cantharidin toxi­
cosis vary from hours to days. Horses often sweat pro­
fusely and have elevation in rectal temperature, heart
rate, and respiratory rate. Mucous membranes are gen­
erally congested and may have a bright, brick red color;
the capillary refill time will be prolonged. Signs of colic
418
Inappetance
Depression
Playing with water
Salivation
Pollakidipsia
Pollakiuria
Sweating
Pyrexia
Tachycardia
Tachypnea
Congested mucous membranes
Colic
Diarrhea
Hematuria or hemoglobinuria
Synchronous diaphragmatic flutter
Muscle fasciculations
Stiff gait
Sudden death
of variable severity are commonly observed. Affected
horses are usually inappetant or anorectic and
depressed. Often they will submerge their muzzles in
water and appear to be playing in it. Pollakidipsia and
pollakiuria are frequently observed, the latter being
particularly common if the horses survive longer than
6-8 hours. Hematuria can be seen, usually later in the
course of the disease. Because hypocalcemia often
develops in horses with cantharidin toxicosis, some
horses may demonstrate synchronous diaphragmatic
flutter, muscle fasciculations, a stiff gait, or other less
common signs of hypocalcemia (including abnormal
facial expressions - the so-called sardonic grin, cardiac
arrhythmias, hindlimb ataxia, laryngospasm, and dys­
phagia) . The course of disease can be very acute and
sudden death may occur.
Diagnosis
Although the clinical signs described are non-specific,
together they may be strongly suggestive of cantharidin
toxicosis. A history of eating alfalfa hay (or possibly
other alfalfa products) and finding blister beetles in the
hay supports the diagnosis - however beetles may not be
found because they often appear only in a small portion
of a bale that has already been consumed. Occasionally,
blister beetle body parts can be identified macro- or
microscopically in the gastrointestinal contents or feces
of affected horses. Clinicopathologic findings often
include hypocalcemia, hypomagnesemia, hypopro­
teinemia, and elevated creatine phosphokinase.

The toxin can be identified in urine or gastric con­
tents using high pressure liquid chromatography or gas
chromatography and mass spectrometry. The earlier in
the disease that a sample is collected, the higher the
probability of finding the toxin; cantharidin in urine is
essentially non-detectable by 3-4 days after intoxica­
tion. For analysis at least 500 ml (a little more than 1
pint) of fresh urine should be submitted; or at least 200
g (about 7 ounces) of solid stomach contents. Serum
samples (at least 24 ml) can also be submitted, although
the test is much less sensitive using serum.
Treatment (Table 20.3)
Appropriate treatment is symptomatic and should be
administered promptly. Activated charcoal ( 1 -3 g/kg
p.o.) may adsorb cantharidin. Administration of min­
eral oil will help to evacuate intestinal contents, includ­
ing toxins, from the gastrointestinal tract, and may bind
some of the lipid-soluble cantharidin. Because the oil
can interfere with the adsorptive activity of charcoal,
these two substances probably should not be adminis­
tered concurrently. Fluids should be administered
intravascularly to combat dehydration and, once rehy­
drated, to promote diuresis, unless contraindicated for
physiologic reasons (e.g. marked hypoproteinemia or
myocardial disease) . Diuresis with furosemide should
be avoided because it may exacerbate hypocalcemia.
Calcium borogluconate (24 mg calcium/kg body
weight) and/or magnesium sulfate (6 mg/kg body
weight) often need to be supplied in intravascular flu­
ids. Diluted calcium solutions should be given slowly
intravascularly and should not be administered through
the same line as bicarbonate solutions.
Intestinal protectants, particularly sucralfate (20
mg/kg p.o. q. 6 to 8 h ) , should be of benefit in treating
the gastritis. Analgesics are often required to manage
pain. Adequate pain relief may not be possible with
.. \ . .
: .
Mineral oil
Activated charcoal
Intravenous fluid therapy
Calcium borogluconate
Magnesium sulfate
Analgesics
xylazine
detomidine
romifidine
butorphanol tartrate
flunixin meglumine
Antibiotics
ACUTE DIARRHEA 20
flunixin meglumine, so xylazine, detomidine, or romifi­
dine, alone or in combination with butorphanol tar­
trate should be considered, although these drugs
markedly suppress colonic motility. Furthermore,
affected horses may be more susceptible to the ulcero­
genic effects of NSAlDs because of dehydration and
concurrent intestinal damage. Broad - spectrum antimi­
crobials are usually administered because of damage to
the intestinal mucosal barrier. If used, the potential for
nephrotoxicity must be considered.
Currently there is no antidote for cantharidin toxi­
cosis. Prognosis is often poor but varies based upon the
amount of toxin ingested, the stage of disease when
treatment is implemented, and the quality of intensive
care provided. Prognosis can likely be reflected by the
severity of clinical signs and time from exposure to ini­
tiating treatment.
Prevention
Many species of blister beetles prefer the perimeter of
fields. Because they do not migrate far, avoiding simul­
taneous cutting and crimping of forage from the
perimeter of fields may help prevent cases. Cutting hay
when adult beetles are less active (early and late cuttings)
should decrease the risk of intoxication. Pesticides are
available that facilitate control of blister beetles. If a case
is diagnosed, it is advisable to either discontinue feeding
the implicated batch of alfalfa hay or to inspect each
flake for evidence of blister beetles. The beetles can be
recognized by a prothorax that is narrower than the
head and abdomen (Figure 20. 1 ) , and it should be
remembered that not all toxic beetles are striped.
OTHER TOXINS
A variety of plants (Table 20.4) and other chemical
compounds (Table 20.5) can be toxic to horses. Acorns
and the blossoms, buds, leaves, and stems of oak
( Quercus spp.) may be toxic to horses. Clinical signs in
horses may be peracute or acute, including colic, hem­
orrhagic diarrhea, and sudden death. Renal toxicity can
also occur. Rarely, ingestion of acorns can cause gastric
impaction. Diagnosis is based on history of exposure,
finding acorns in the intestinal tract, detecting high uri­
nary phenolic content, and necropsy.
Some species of blue-green algae found in stagnant
pond water can cause hemorrhagic diarrhea and signs
of liver disease (including photosensitization) when
ingested. Diagnosis is generally presumptive on the
basis of clinical signs and apparent exposure. Avocado
toxicity may cause diarrhea, colic, and edema of the
lips, tongue, head, and neck.
419
20 ACUTE AND CHRONIC DIARRHEA

Products containing arsenic are used as herbicides,

Table JGAPlal'lu ���_,��"�:i�b'�. insecticides, moluskicides, rodenticides, and defoliants.
Acorn/oak
Horses may become intoxicated from ingesting shrubs
Algae or grass contaminated by arsenicals, or when their for­
Avocado age is contaminated. Arsenicals vary in their potency
Castor bean (e.g. sodium arsenite and arsenic trioxide are both her­
Oleander bicides used to kill weeds and bush but trioxide is about
Selenium-accumulating plants (e.g. Astra/agulus 1 0 times less toxic on a weight basis) . Peracute or acute
spp.) toxicosis can result in diarrhea which may be hemor­
Heath (Erica spp.)
rhagic. Specific treatment for arsenic intoxication
Japanese yew
includes sodium thiosulfate ( 20-30 g diluted in 300 ml
Potato
water p.o.) or dimercaprol (BAL) . The latter com­
St John's wort (Klamath weed)
pound is administered intramuscularly as an antidote
for trivalent arsenical intoxication (3 mg/kg) , and its
efficacy is questionable. Concentrations of arsenic in
�r,:,:'��:::ko.�r��'''�' the liver or kidneys that are greater than 1 0 ppm are
considered diagnostic.
, " �
' ;'

Raw linseed oil is occasionally used as a laxative in

Amitraz
Arsenic
Linseed oil
Mercury
Mycotoxins
Organophosphates
Propylene glycol
Salt
Reserpine
Selenium
Siaframine
Seeds of the castor bean plant (Ricinus communis)
can cause severe colitis and diarrhea in horses. The
plan t is found predominately in southern regions of the
United States. Diagnosis is based on finding seeds in the
feed, history of ingestion, or necropsy. Castor oil (oil
derived from this plant) has been used experimentally
to produce colitis in horses.
Oleander is often grown as an ornamental hedge in
the southern and western United States. Although the
toxic element is a cardiac glycoside, horses that ingest
oleander may develop profuse watery or hemorrhagic
diarrhea.
Selenium may accumulate in some plants grown in
areas where there is a high selenium content in the soil,
for example Astragulus spp. Acute toxicosis may result in
diarrhea, respiratory distress, and abnormal posture or
gait, the serum concentration of selenium may be useful
diagnostically. Chronic forms of intoxication (e.g. alkali
disease) appear to be more common than acute forms.
Amitraz is an acaricide for cattle that is not approved
for use in horses because these animals are more sensi­
tive to its effects. Although colonic impaction is the
more common side effect, some affected horses will
develop diarrhea.
horses, it is increasingly being recommended as a feed
additive as a source of linolenic acid. Linseed oil is par­
tially saponified by gastrointestinal secretions to form
soap and glycerine, both of which act as irritants to the
intestinal mucosa. Administration of linseed oil (2.5
ml/kg twice at an interval of 12 hours) can cause diar­
rhea, inappetance, lethargy, and colic in healthy horses.
Conceivably, a lower dose could cause similar signs in a
horse with pre-existing mucosal irritation .
Ingestion o f mercury-treated seed grains o r applica­
tion of mercuric blisters can result in toxicity to the ali­
mentary tract and kidneys. Because treatment of grains
with mercuric fungicides is no longer practiced, inges­
tion (licking) of mercuric blisters is the most common
route of exposure. Diagnosis can be made by history of
exposure, clinical signs, and increased tissue concentra­
tions of mercury.
Various mycotoxins (toxins produced by fungi) can
result in diarrhea in horses, including aflatoxins, tri­
chothecenes, and slaframine. The latter mycotoxin is
produced by Rhizoctonia leguminicola on red clover grass
and hay, it also causes excessive salivation. However
diarrhea is rare with mycotoxins. Diagnosis can be
made on the basis of clinical signs, identifying the toxin
in grains or hay, or increased concentrations of toxins
or their metabolites in tissues.
Organophosphates used as pesticides can cause diar­
rhea in horses. Signs of urination, lacrimation, and sali­
vation also may be observed. Diagnosis can be made on
the basis of clinical signs and determination of
cholinesterase activity in the blood or brain. Treatment
for organophosphate toxicosis should include adminis­
tration of activated charcoal (0.5-1 kg/500 kg) by naso­
gastric tube and atropine (0.25-0.5 mg/kg; 1 /4 of the
dose given Lv. and the remainder given i.m. ) . If
detected within 24 hours of intoxication, the oxime

420
 ACUTE DIARRHEA 20

2]AM can be used (20 mg/kg i.v. q. 1 2 h or 1 0-15
mg/kg s.c. as needed) .
Propylene glycol is used by large animal veterinarians
to treat cattle with ketosis and is present in so-called 'safe'
motor vehicle antifreezes. Because propylene glycol
physically resembles mineral oil, it can be inadvertently
administered to horses. Clinical signs usually develop
within 30 minutes of administration, can include diar­
rhea, and may be fatal. If the error is detected promptly,
efforts to evacuate the stomach by siphoning and admin­
istration of sodium bicarbonate intravenously to combat
probable acidemia may be of benefit.
Intoxication with salt can result in diarrhea. History
of access or ingestion of salt without access to water and
serum (or CSF) concentration of sodium can support a
diagnosis. Administration or ingestion of hypotonic flu­
ids or 5% dextrose to such horses is contraindicated
and may exacerbate neurological signs.
development of diarrhea to death resulting from a rup­
tured stomach. Laminitis developing as a result of the
overingestion of soluble carbohydrates is a well-docu­
mented occurrence. Indeed, the ability of soluble car­
bohydrates to induce laminitis has been used as a
standard method for the scientific study of that disease.
The signs of symptomatic grain overload may
include
• colic
• abdominal distension
• lameness caused by laminitis
• trembling
• sweating
• diarrhea.
Clinical examination findings relate to endotoxic
and hypovolemic shock, gastritis, and ileus, and may
include

• hyperemic to purple mucous membranes

• tachycardia
Grain overload • tachypnea, (endotoxic and/or hypovolemic shock)
• gastric reflux
MA Ball • colonic distension
• gas 'pings' and decreased motility on abdominal
INTRODUCTION auscultation .

Clinical findings are variable depending o n the indi­

Despite widespread awareness among horse owners vidual case.
about the seriousness of the condition, grain overload is
still recognized as a relatively common disease. To some
degree it is more related to a sudden change in the MANAGEMENT
amount of concentrate, as many performance horses
are fed a considerable volume of concentrates as part of Treatment options for grain overload are summarized
their daily ration, but they have become accustomed to in Table 20.6.
it. That particular horse may require a greater amount The most immediate concern following the
of inadvertent ingestion of concentrate than the horse overingestion of soluble carbohydrates is gastritis and
that has never been fed concentrates before. In addi­
tion, it is the amount of soluble carbohydrate in the
concentrate that is the predator, so the corn/maize­
containing products are generally a greater danger
than a grain product such as oats. Although horses are Nasogastric intubation
rarely fed barley, this grain can be extremely high in sol­ Activated charcoal
uble carbohydrates. Many cases of grain overload are Mineral oil
Magnesium sulfate
related to the excessive feeding of corn during the win­
Flunixin meglumine
ter months under the false pretense that this practice
Aspirin
will increase heat production and aid the horse in keep­
Antihistamines - doxylamine or diphenhydramine
ing warm. Actually, the fermentation of fiber in the Intravenous polyionic fluids - lactated Ringer's
cecum and large intestine generates a greater amount solution
of heat than the digestion of concentrates. hypertonic saline
sodium bicarbonate
Plasma
Pentoxifylline
Frog supports
There are several sequelae to the sudden ingestion of Glyceryl trinitrate
soluble carbohydrates ranging from mild colic and the

42 1
20 ACUTE AND CHRONIC DIARRHEA
subsequent overdistension of the stomach. In such
cases, the horse typically shows signs of colic, and the
passage of a nasogastric tube is essential to prevent
stomach rupture. There is the possibility of continued
fluid production and accumulation in the stomach, so
the nasogastric tube may be left in place or the horse
carefully monitored for the recurrence of stomach dis­
tension.
If the horse is not (or has stopped) refluxing, the
administration of activated charcoal (0.5 kg or l ib) or
mineral oil (4 liters or 1 gal) is thought to be helpful in
reducing toxin absorption from the gastrointestinal
system. The administration of 0.5 kg ( l Ib) of magne­
sium sulfate (Epsom salts) per os with 4 liters ( 1 gal) of
water is indicated if evaluating a horse suspected to
have grain overload, before clinical signs develop, in
order to speed the evacuation of the gastrointestinal
system.
Systemic therapy may include flunixin meglumine at
the 0.25 mg/kg dose for its 'anti-endotoxic' properties
or at a higher dose for the anti-inflammatory effects
should laminitis be developing. In addition, the admin­
istration of aspirin ( 1 0 mg/kg p.o. or i.v. s.i.d.) may be
of benefit in maintaining digital perfusion; if the horse
is still refluxing, aspirin can be administered per rec­
tum. Although aspirin has not been proven to inhibit
equine platelets after endotoxin stimulation, it will
increase bleeding time in normal horses. Other sys­
temic therapy may include an antihistamine (doxy­
lamine 0.5 mg/kg S.c. q.i.d. or diphenhydramine 1
mg/kg i.m. b.i.d.) for the first 24 hours.
Many of these horses are also moderately to severely
dehydrated, this can be determined by physical exami­
nation and further characterized by measurement of
plasma total protein and packed cell volume. There can
also be a variable degree of acidosis presen t (both lactic
acidosis from decreased perfusion and an increase in
organic acids from the grain digestion) , so lactated
Ringers is a good choice of fluids. In severe cases, the
administration of bicarbonate may be necessary to cor­
rect the acid-base disturbance. If the horse is experi­
encing severe hypovolemic shock, the administration of
hypertonic saline (7% sodium chloride) can be of sig­
nificant benefit as the initial fluid, but must be followed
within several hours by a volume replacement quantity
of normotonic polyionic fluids. Many of these horses
may require the additional supplementation of calcium
. and potassium. Also, if the signs of endotoxemia are
severe, the administration of plasma (especially hyper­
immune endotoxin plasma) can be of benefit as well as
the administration of pentoxirylline (8.4 tng/kg p.o.
t.i.d. ) .
A� a potential prophylaxis against laminitis treat­
ment should focus on maintaining laminar circulation.
422
First and foremost is the volume replacement fluid ther­
apy. Frog supports (rubber pads or other suitable mate­
rial) should be placed on the feet, and the stall bedding
made deep and soft. The application of glyceryl trini­
trate cream ( nitroglycerine) to the coronary area has
been shown to increase digital blood flow in both nor­
mal and laminitic feet; a thin coating of a 2% cream of
nitroglycerine in a band 2.5 cm wide around the limb
can be applied once or twice daily to an area of skin
starting at the coronary band. In recent studies, the use
of isoxsuprine has not been shown to have a clinical
effect because of low bioavailability and therefore is no
longer recommended. If laminitis has developed, the
treatment must be aggressive and instituted without
delay (see Chapter 1 1 ) .
Acute diarrhea i n adult
horses - other causes
TJ Divers
There are many causes of acute diarrhea in adult horses
other than salmonellosis, clostridiosis, ehrlichiosis, can­
tharidin toxicosis, cyathostomosis (see Chapter 2 1 ) ,
and non-steroidal anti-inflammatory toxicity. A review
of a computer generated (Consultant*) list of all
reported causes of diarrhea in adult horses revealed
more than 30 causes. The great majority of these are
rare and will not be discussed here but can be found on
Consultant.
TOXICITIES
Toxic causes of acute diarrhea include excessive salt
ingestion, accidental administration of propylene gly­
col, excessive administration of linseed oil (> 1 ml/kg)
or even mineral oil, nicotine ingestion and organophos­
phate toxicity. Toxins that more commonly cause other
organ system failure and/ or acute death, but which may
cause diarrhea, include monensin, foxglove, heavy
metal, or castor bean toxicosis. Toxins that may cause
diarrhea in grazing horses are found in tall fescue grass
(Festuca arundinacea) contaminated with endophytic
fungus (Acremonium coenophialum) and slaframine toxin
(Rhizoctonia leguminicola) , most commonly found as
*Consultant on-line database, White, M E, College of
Veterinary Medicine, Cornell University, Ithaca, NY:
www.vet.Comell.edulconsultant

black mold on clover. Both of these toxins are more
commonly associated with clinical signs other than diar­
rhea - fescue fungus is associated with agalactia and
clover fungus with excessive salivation.
Hoary alyssum (Berteroa incana) , a member of the
mustard family, may cause diarrhea, fever, and limb
edema in horses either grazing the plant or consuming
alfalfa hay contaminated with large amounts of the mus­
tard plant. Berteroa incana is most commonly found in
the northern United States and southern Canada.
Horses will rarely ingest acorns, oak leaves, or oak buds
but if ingested, diarrhea and subcutaneous edema may
occur. Acute renal failure is uncommon in horses after
acorn ingestion. Other dietary causes of acute diarrhea
include sand, rapid changes in forage, especially lush
grass or green hay, and ingestion of large amounts of
highly fermentable carbohydrates. Diarrhea and oral
ulcers have also been reported in horses ingesting
Quassia amara (Simarubaceae) wood chips.
DRUGS
Drug administration may be another cause of acute
diarrhea in adult horses. Antibiotics may occasionally
calise diarrhea without causing c1ostridiosis, although
this is rare in the adult horse. This may occur from the
disruption of normal flora which may cause abnormal
colonic fermentation and changes in volatile fatty acid
concentrations and/or osmolality of the colonic
ingesta. Neomycin may cause intestinal mucosal dam­
age when given in sufficient quantities or for prolonged
periods. Misoprostol and chenodeoxycholic acid are
secretagogues causing active secretion of chlorine and
bicarbonate ions and passive efflux of sodium, potas­
sitlm, and water into the intestinal lumen, and which
may cause diarrhea. Any hypertonic drug given per os
has the potential to cause diarrhea via either osmotic
laxative effect or activation of the gastric/colic reflux.
Dioctyl sodium sulfosuccinate (DSS) may produce diar­
rhea via several mechanisms, including intestinal
mucosal damage.
DERANGED INTESTINAL MOTILITY
Acute diarrhea may also occur in association with
deranged motility. This may be the result of peritonitis
(see Chapter 1 7 ) , gastric ulcers, colonic displacement,
drug administration, or organophosphate toxicity.
Gastric ulcers are infrequently associated with diar­
rhea in adult horses. In these cases the mechanism to
explain the diarrhea is unknown, but it may involve a
gastrocolic or gastroenteric reflex causing increased
ACUTE DIARRHEA 20
fluid secretion into the large colon. This reflux is medi­
ated by afferent neural receptors in the gastroduodenal
mucosa. Proximal duodenitis/jejunitis and gastric
administration of hypertonic fluids (e.g. magnesium
sulfate) are other conditions or treatments that may
cause diarrhea by stimulating this reflex.
Colonic displacements generally cause abdominal
pain and abdominal distension, but in a rare case, may
present with acute or subacute diarrhea. Some horses
develop acute diarrhea almost immediately after receiv­
ing intravenous antibiotics. These include ery­
thromycin, which is thought to stimulate motilin
receptors and intravenous penicillin (idiosyncratic) .
Tapeworm infections, Anoplocephala spp. are known to
affect ileocecal motility and may cause colic and/ or pas­
sage of loose stool. Massive exposure of the immuno­
logically naive horse to large strongyles may cause colic
and diarrhea, although this is more common in foals
(acute strongyle syndrome ) .
BACTERIAL INFECTIONS
Additional bacterial, fungal, and viral agents that may
cause diarrhea include Aeromonas spp., Mycobacterium
avium, Aspergillus spp., and rarely Histoplasma spp.
Aeromonas spp. have recently been incriminated as a
cause of acute diarrhea in horses. In a relatively large
study, the organism was found in the feces of 55 per
cent (22 of 40) horses with diarrhea and was not iso­
lated from any of the 34 control horses. Salmonella spp.
were found in some of the aeromonas-positive horses,
and c1ostridiosis was not evaluated, making it only spec­
ulation that the Aeromonaswas the cause of the diarrhea.
Aeromonas spp., a gram-negative rod, commonly found
in the water and soil, may be a primary cause of acute
diarrhea in horses or it may just be more frequently iso­
lated in equine diarrheic feces. Aeromonas spp. have
been incriminated as a cause of diarrhea in humans.
Strains producing virulence-associated adhesions, cyto­
toxin, enterotoxin, or with invasive properties are
believed to be potential pathogens. Gastroenteritis asso­
ciated with Aeromonas spp. is reported to be most com­
mon in humans and horses in the summer months, and
it has been suggested that the infection may occur from
contaminated drinking water. Aeromonas spp. are gener­
ally susceptible to enrofloxacin, gentamicin, and
amikacin.
Mycobacterium avium has been infrequently docu­
mented as a cause of diarrhea in horses. Chronic weight
loss and chronic diarrhea are the most common pre­
senting signs with M. avium. Granulomatous enterocol­
itis and hepatitis with mesenteric lymphadenopathy are
the characteristic lesions.
423
20 ACUTE AND CHRONIC DIARRHEA
ASPERGILLOSIS
Aspergillus colitis is well documented in horses. In vir­
tually all cases, the Aspergillus sp. is a secondary invader,
following a toxic or infectious colitis and broad-spec­
trum antibiotic administration. When fungal colitis
occurs, it will often disseminate to the lungs or other
organs and the prognosis is extremely grave.
BIBLIOGRAPHY
General principles of treatment of acute
diarrhea in adult horses
Brooks H W, Hall G A, Wagstafls A], Mitchell A R ( 1 998)
Detrimental effect� on villus form during conventional
oral rehydration therapy for diarrhea in calves; alleviation
by a nutrient oral rehydration solution containing
glutamine. Vet.J 155 ( 3 ) : 263-74.
Ecke P, Hodgson D R, Rose R] ( 1 998) Induced diarrhea in
horses Part 2: Response to administration of oral
rehydration solution. VetJ 1 55 : 1 6 1-70.
Salmonellosis
Cohen N D, Martin L], Simpson R B ( 1 996) Comparison of
polymerase chain reaction and microbial culture for
detection of salmonella in equine feces and
environmental samples. Am. J Vet. Res. 57(6) : 780-786.
Hartmann F A, Callan R], McGuirk S M, West S E H ( 1 996)
Control of an outbreak of Salmonellosis caused by drug­
resistant Salmonella anatum in horses at a veterinary
hospital and measures to prevent future infections.J Am.
Vet. Med. Assoc. 209 ( 3 ) : 629-31 .
Parraga M E, Spier S], Thurmond M , Hirsh D ( 1 997) A
clinical trial of probiotic administration for prevention of
Salmonella shedding in the postoperative period in horses
with colic. J Vet. Intern. Med. 1 1 ( 1 ) :36-4 1 .
Spier S .I ( 1 993) Salmonellosis. Vet. Clin. N. Am. J<-'quine Pract.
9 ( 2 ) : 385-94.
Clostridial diarrhea in adult horses
Baverud V, Franklin A, Gunnarsson A, et al. ( 1 998) Clostridial
difficile associated with acute colitis in mares when foals are
treated with erythromycin and rifampicin for Rhodococcus
equi pneumonia. Equine Vet. J 30(6) :482-8.
Donaldson M T, Palmer.I E ( 1 999) Prevalence of Clostridium
perfringens enterotoxin and Clostridium difflcile toxin A in
feces of horses with diarrhea and colic. J Am. Vet. Med.
Assoc. 2 1 5 (3) :358-61 .
Herholz C , Miserez R, Nicolet], et al. ( 1 999) Prevalence of
beta-2 toxigenic Clostridium perfringens in horses with
intestinal disorders. J Clin. Microbiol. 37( 2 ) : 358-6 1 .
.lang S S, Hansen L M , Breher.I E, e t al. ( 1 997) Antimicrobial
susceptibilities of equine isolates of Clostridium difficile and
molecular characterization of metronidazole-resistant
strains. CZin. Infect. Dis. Sep. 25 supp!. 2:S266-7.
Potomac horse fever
Barlough.l E, Reubel G H, Madigan] E, et al. ( 1 998)
Detection of Ehrlichia risticii, the agent of Potomac horse
424
fever, in freshwater stream snails ( Pleuroceridae: Juga
spp.) from northern California. Appl. Environ. Microbial.
64:8.
Biswas B, Mukherjee D, Mattingly-Napier B L, et al. ( 199 1 )
Diagnostic application of polymerase chain reaction for
detection of Ehrlichia risticii in equine monocytic
ehrlichiosis ( Potomac horse fever) . J Clin. Microbial. 29: 10 .
Dutta S K, Vemulapalli R , Biswas B ( 1 998) Association of
deficiency in antibody response to vaccine and
heterogeneity of Ehrlichia risticii strains with Potomac
horse fever vaccine failure in horses. J Clin. Microbial. 36:2.
Long M T, Goetz T E, Whiteley H E, et al. ( 1 995)
Identification of Ehrlichia risticii as the causative agent of
two equine abortions following natural maternal infection.
J Vet. Diagn. Invest. 7:201-5.
Palmer .l E ( 1 993) Potomac horse fever. Vet. Clin. N. Am.
Equine Pract. 9:2.
Pusterla N, Chase .l S, ]ohnson E, et al (2000) Potomac horse
fever: discovery of the ontermediate and definitive host of
the helminithic vector of Ehrlichia risticii. Proc 1 8th Annual
ACVlM Forum
Pusterla N, Leutenegger C M, Sigrist B, et al (2000) Detection
and quatification of Ehrlichia risticii genomic DNA in infected
horses and snails by real-time PCR. Vet. Parasitol. 90:1-2
Pusterla N, Madigan] E, Chae ] S, et al (2000) Helminthic
transmission and isolation of Ehrlichia risticii, the causative
agent of Potomac horse fever, by using trematode stages
from freshwater stream snails . . f. Clin. Microbiol. 38:3.
Reubel G H, Bariough] E, Madigan] E ( 1 998) Production
and characterization of Ehrlichia risticii, the agent of
Potomac horse fever, from snails ( Pleuroceridae: Juga
spp.) in aquarium culture and genetic comparison to
equine strains. J Clin. Microbiol. 36:6.
Wen B, Rikihisa Y, Yamamoto S, et al. ( 1 996) Characterization
of the SF agent, an Ehrlichia sp. isolated from the fluke
Stellantchasmusfalcatus, by 1 6S rRNA base sequence,
serological, and morphological analyses. Int. J Syst.
Bacteriol. 46: 1 .
Non-steroidal anti-inflammatory drug toxicity
Griswold D E, Adams] L ( 1 996) Constitutive cyclooxygenase
(COX- I ) and inducible cyclooxygenase (COX-2) : rational
for selective inhibition and progress to date. Medicinal Res.
Rev. 1 6 (2) : 1 81-206.
Johnston S A, Fox S M ( 1 997) Mechanisms of action of anu­
inflammatory medications used for treatment of
osteoarthritis.J Am. Vet. Med. Assoc. 2 1 0 ( 1 0) : 1 486-- 1 492.
MacKay R.I, French T W, Nguyen H T, Mayhew I G ( 1 983)
Effects of large doses of phenylbutazone administration to
horses. Am. .f. Vet. Res. 44 (5) :774-780.
McCarthy D M ( 1995) Mechanisms of mucosal injury and
healing: the role of non-steroidal anti-inflammatory drugs.
Scand. J Gastroenterol. 30 supp!. 208: 24-29.
Snow D H, Douglas T A, Thompson H, Parkins.l ], Holmes P
H ( 1 98 1 ) Phenylbutazone toxicosis in equidae: a
biochemical and pathophysiological study. Am . .f. Vet. Res.
42 ( 1 0) : 1 754-1759 .
Toxic colitides
Helman R G, Edwards W C ( 1 997) Clinical features of blister
beetle poisoning in equids: 70 cases ( 1983-1996) . J Am.
Vet. Med. Assoc. 2 1 1 : 1 0 1 8-2 1 .
Schmitz D G ( 1 989) Cantharidin toxicosis in horses . .f. Vet. Int.
Med. 3:208-15.

Smith B P (ed) ( 1990 and 1996) Large Animal Intemal Medicine
( 1 st and 2nd edns) . C V Mosby, St Louis.
Acute d iarrhea in adult horses - other causes
Dave B , Rubin W ( 1 999) Inhibition of gastric secretion
relieves diarrhea and postprandial urgency associated with
irritable bowel syndrome or functional diarrhea. Dig. Dis.
Sci. 44(9 ) : 1 893-8.
ACUTE DIARRHEA 20
Freeman D E , Ferrante P L, Palmer] E ( 1 992)
Comparisons of the effects of intragastric infusions of
equal volume of water, dioctyl sodium sulfosuccinate,
and magnesium sulfate on fecal composition and
output in clinically normal horses. A m. ]. Vet. Res.
53(8) : 1 347-53.
Hathcock T L, Schumacher], Wright], Stringfellow] ( 1999)
The prevalence of Aeromonas species in feces of horses
with diarrhea. ]. Vet. Int. Med. 1 3:357-60.
42 5
 21
Chronic diarrhea
Differential diagnosis and
evaluation of chronic
diarrhea in the adult horse
T Mair
INTRODUCTION
Chronic diarrhea occurs sporadically in horses and is a
relatively uncommon clinical syndrome. In the adult
horse, chronic diarrhea is almost invariably associated
with large intestinal (cecal and colonic) disease, caused
either by physical damage to the colonic wall or physio­
logical disturbances of colonic function. Unfortunately,
from a diagnostic viewpoint, most of the different
diseases that can result in chronic diarrhea can present
with very similar clinical and clinicopathological find­
ings. In addition, many of the causes and mechanisms
of chronic diarrhea are poorly understood. For these
reasons, horses affected by chronic diarrhea are often
diagnostic and therapeutic challenges. A definitive
diagnosis of the cause of chronic diarrhea will be
achieved in only 60-70 per cent of cases, and in many of
these the diagnosis will only become apparent following
post-mortem examination.
The clinical signs associated with diseases causing
chronic diarrhea are summarized in Table 21.1.
diarrhea - variable consistency
- persistent or recurrent
pyrexia
inappetence
depression
weight loss
subcutaneous edema
colic (chronic or recurrent)
To be considered 'chronic' diarrhea will have been
present for at least 7-14 days. In many cases the diarrhea
will persist for weeks or months. The nature of diarrhea
varies from case to case and may vary over time in indi­
vidual cases. Some diseases causing chronic diarrhea will
present with recurrent bouts of diarrhea separated by
periods of relatively normal fecal consistency. Feces may
vary from soft 'cowflop' or 'cowpat' consistency to watery
diarrhea. Fiber content of feces is variable.
Rectal temperature, heart rate, and respiratory rate
are frequently normal. However, pyrexia (persistent or
intermittent) may be present in some inflammatory
diseases such as larval cyathostomosis, peritonitis, sand
enteropathy, and some cases of gastrointestinal neopla­
sia. Other signs of systemic illness such as depression and
427
21 ACUTE AND CHRONIC DIARRHEA

inappetence may also accompany these diseases. Weight

loss may occur in many of the diseases, but may be absent
in some, especially those caused by motility abnormali­
Clinical history
ties or other physiological disturbances of colonic func­
tion. Peripheral subcutaneous edema (especially ventral
Management, nutrition, parasite control
abdominal) is commonly present due to hypoprotein­
emia caused by protein-losing enteropathy. Signalment

Physical examination
DIFFERENTIAL DIAGNOSIS
Hematology and plasma fibrinogen
The more common causes of chronic diarrhea are
listed in Table 2l.2. Serum biochemistry

Serum protein electrophoresis

Abdominocentesis

Fecal examinations - worm egg count

Cyathostomosis
examination for larvae
other parasitological
Mixed strongyle infections
examinations
white blood cells
Peritonitis
bacteriology

Alimentary lymphosarcoma
Sugar absorption tests

Inflammatory bowel - granulomatous enteritis/

Rectal biopsy
diseases colitis
- Iymphocytic-plasmacytic
Ultrasonography
enteritis/colitis
- eosinophilic enteritis/colitis
Exploratory surgery and bowel wall/colonic lymph
node biopsies
NSAID toxicity

Salmonellosis

Chronic liver disease*

chronic diarrhea, but even after exhaustive tests the
clinician and owner of an affected horse should be
Sand enteropathy
aware that a definitive diagnosis may not be attainable.
Chronic non-specific colitis Some of the important components of the examination
of affected horses are summarized in Table 2l.3. As a
Idiopathic colonic dysfunction general rule, horses with chronic diarrhea but with no
weight loss, normal plasma albumin levels, and no other
Giardiasis** overt clinical signs, are likely to have no pathological
lesions identifiable (even at post-mortem examination).
*chronic diarrhea Is a rare manifestation of chronic liver
disease
**giardiasis is of questionable significance as a cause of Clinical history, management, nutrition, and
diarrhea parasite control

A full clinical history and evaluation of management

EVALUATION OF CHRONIC DIARRHEA
Thorough and repeated clinical and laboratory evalua­
tions are often required to diagnose the cause of
and nutrition are important. These aspects are dis­
cussed more fully in Chapter 18, Differential diagnosis
and evaluation of chronic weight loss. The history relat­
ing to routine parasite control measures applied to the
horse (and other in-contact horses) should also be
assessed (see Chapter 4), bearing in mind the tendency

428

of many owners to answer questions about parasite con­
trol in terms of what they believe should be done rather
than what is actually done!
Signalment
Age can be useful in assessing the likelihood of a partic­
ular disease being present. For example, larval cyatho­
stomosis is most common in horses less than 5 years of
age, whereas chronic inflammatory bowel diseases and
intestinal neoplasia are most common in older horses
(over 10 years of age).
Physical examination
Although there are virtually no characteristic physical
findings of individual diseases causing chronic diar­
rhea, a full and detailed physical examination should
always be undertaken. Physical examination of the large
intestine is restricted to abdominal auscultation and
percussion, transabdominal ballottement, and trans­
rectal palpation. Borborygmi may be heard more fre­
quently than normal as a result of increased motility of
the large bowel caused by irritation or inflammation.
Sand in the large intestine can sometimes be detected
by auscultation behind the xiphoid.
The rectal examination is the most useful physical
examination technique for assessing the large intestine
(see Chapter 1). The primary objective of the rectal
examination is to assess the size, consistency, and posi­
tion of segments of the large intestine. Evaluation of the
wall thickness and texture, the mesenteric structures
(blood and lymphatic vessels, and lymph nodes), and
other organs (such as the spleen) may also be helpful in
diagnosing the cause of chronic diarrhea.
Hematology and plasma fibrinogen
Hematological changes occurring in diseases of the large
intestine are frequently non-specific, but are helpful
all the same in evaluating cases of chronic diarrhea.
Neutrophilic leukocytosis, with or without hyperfibrino­
genemia, is commonly seen in chronic inflammatory and
neoplastic conditions of the large intestine. Neutrophilia
is also frequently seen in cases of larval cyathostomosis.
Anemia may be present in chronic inflammatory and
neoplastic conditions. Hemoconcentration, with an
increase in packed cell volume (PCV) may occur if the
horse is dehydrated, but this is less likely in chronic as
compared with acute diarrhea.
Serum biochemistry and serum protein
electrophoresis
Electrolyte losses (especially sodium, potassium, cal­
cium, and bicarbonate) may occur as a result of severe
CHRONIC DIARRHEA 21
diarrhea, but are less likely in chronic diarrhea than in
acute colitis. Plasma protein levels vary depending on
the degree of gastrointestinal loss of albumin and
globulin. Hypoproteinemia and hypoalbuminemia are
common in chronic enteropathies, and may be accom­
panied by reduced, normal, or elevated globulin levels.
Serum protein electrophoresis is sometimes useful for
differentiation of parasitic colitides from other
enteropathies. Serum alkaline phosphatase (in particu­
lar the intestinal isoenzyme of alkaline phosphatase)
may become elevated in chronic enteropathies. The
degree of abnormality in the levels of total protein,
albumin, and alkaline phosphatase relate to the severity
of the chronic enteropathy, and can be helpful, to a
limited extent, in predicting prognosis. Elevated liver
enzymes are indicative of liver damage which can some­
times cause chronic diarrhea; further assessment of
liver function (e.g. bile acids) and liver biopsy should be
considered to more fully evaluate the nature of the
disease in such cases (see Chapter 19).
Abdominocentesis
Examination of peritoneal fluid is most useful in diag­
nosing peritonitis and some cases of intestinal neoplasia
(see Chapters 2 and 17).
Fecal examination
Gross examination of the feces can provide informa­
tion about digestion and transit time in the large
intestine. Increased fecal particle size, especially the
presence of large fiber particles, with loose or watery
stool is suggestive of poor mastication, poor colonic
digestion or decreased colonic transit time. Feces con­
taining sand or gravel are not necessarily abnormal,
but a large amount of sand implies that significant
quantities of sand may be present in the colon. The
presence of blood in the feces implies hemorrhage
into the distal colon, this may occur with some inflam­
matory conditions involving the small colon or rectum;
frank hemorrhage observed following rectal examina­
tion should alert the clinician to the possibility of a
rectal tear (see Chapter 16). Cyathostome larvae may
be identified by the naked eye in the feces of horses
affected by larval cyathostomosis, especially if the lar­
vae are alive and moving. In other cases, microscopical
examination of a wet smear of feces may be required
to identifY larvae.
Cytological examinations are used mainly for para­
sitological evaluation (see Chapter 4). Examination
for cyathostome larvae, and eggs of small and large
strongyles, tapeworms, and roundworms is helpful if a
parasite-associated disease is suspected. Coccidia and
429
21 ACUTE AND CHRONIC DIARRHEA

Cryptosporidia spp. are occasionally observed, but in

most cases are not considered to be pathogenic.
General principles of
Tests for occult blood are used to detect mucosal treatment of chronic
inflammation. These tests detect not only occult blood
but also degraded blood. A positive test indicates sig­ diarrhea in adult horses
nificant hemorrhage into the gastrointestinal tract, but
the source and amount of hemorrhage within the tract T Mair
cannot be determined. However, the test can prove
negative even in the presence of significant hemor­
rhage into the proximal gastrointestinal tract because INTRODUCTION
of extensive degradation of the blood in the lower
intestinal tract. As in acute colitis and diarrhea, chronic diarrhea can
Examination for fecal inflammatory cells (white result in significant lumenal loss of fluid, electrolytes, and
blood cells) has been used to assess the presence of protein. Since the precise causes of chronic diarrhea are
inflammatory lesions in the bowel. This test is more frequently difficult to establish, specific treatments are
likely to be positive in horses with acute enterocolitis often not possible. Horses with chronic diarrhea often lose
than in chronic enteropathies. However, the presence weight as a result of chronic protein loss, and euthanasia
of large numbers of fecal white blood cells is indicative may become necessary on humanitarian grounds.
of an inflammatory lesion, and suggests that the lesion
is located in the distal gastrointestinal tract.
FLUID AND ELECTROLYTE THERAPY
Fecal cultures are important in the evaluation of
horses with acute colitis but are less important in
The rate of fluid administration depends upon the
chronic diarrhea. Salmonella spp. may be cultured from
severity of dehydration. This can be determined by
horses affected by chronic diarrhea, but there is likely
examining the
to be another underlying cause of the diarrhea.
• dryness of mucous membranes
Ultrasonography • skin turgor
• speed of distention of the jugular vein when
Ultrasonography is complementary to rectal examina­
compressed
tion and can be helpful in the evaluation of chronic
• PCV
diarrhea. Abnormalities that may be identified in
• blood urea nitrogen (BUN).
horses affected by chronic diarrhea using transcuta­
neous and/or transrectal ultrasonographic examina­ Fluid replacement should include
tions, include peritoneal effusion, masses and abscesses,
• volume replacement (percent dehydration x body
and increased bowel wall thickness (see Chapter 2).
weight in kg liters needed)
=

• maintenance needs (60-100 ml kg-I dayl)

Biopsy and exploratory surgery
• ongoing losses that are variable, depending upon
Rectal mucosal biopsies are easily and safely obtained the degree of dehydration.
(see Chapter 2) and are sometimes diagnostic in cases
The principles of fluid and electrolyte therapy are
of chronic enteropathy. However, for a diagnostic yield
discussed in greater detail in Chapter 20.
from this procedure, the pathological lesions must
Dehydration is often not a major problem in animals
extend to the rectum, and in most cases of chronic
affected by chronic diarrhea, and these horses may
enteropathy the rectum is not affected; diagnostically
compensate for persistent increased fecal fluid loss by
useful information can be expected in only about one­
increased water consumption. Nevertheless, free access
third of cases of chronic enteropathy. Full-thickness
to water and electrolyte solutions should be available.
bowel wall biopsies of the cecum and large colon, and
Intravenous or oral fluid therapy, and treatment of
associated lymph nodes, are more likely to be diagnosti­
acid-base disturbances should be administered as
cally useful, but attaining such biopsies is only possible
necessary (see Chapter 20).
via a surgical approach (flank or ventral midline
approach). Laparoscopy offers a safer and easier tech­
nique for observing the dorsal surfaces of the cecum PLASMA THERAPY
and large colon in a standing patient, and direct biopsy
of abnormal masses and colonic lymph nodes can be Intestinal diseases that cause chronic diarrhea com­
achieved by this method. monly involve loss of plasma proteins into the intesti-

430

nal lumen with resulting hypoproteinemia and hypo­
albuminemia. These horses may benefit from plasma
transfusions. Plasma or colloid infusions are particu­
larly important in horses that are dehydrated and are
receiving intravenous fluid therapy (see Chapter 20),
since the low oncotic pressure caused by hypoprotein­
emia may result in sequestration of administered fluid
into tissue spaces, thereby worsening tissue edema and
predisposing to multi-organ failure. Plasma transfu­
sions are indicated when the total plasma protein con­
centration falls to 50 gil (5.0 g/dl) or less, or the
plasma albumin concentration is 15 gil (1.5 g/dl) or
less. Initially 5-10 liters of either commercially avail­
able plasma or cross-matched plasma from a donor
should be administered intravenously. The effect of a
single intravenous dose of plasma is short-lived and
multiple transfusions (in combination with other treat­
ments) are likely to be necessary to result in a sus­
tained increase in the measured total plasma protein
and albumin concentrations.
ANTHELMINTICS
Anthelmintics are indicated in all cases where a para­
sitic etiology is suspected. Even in horses with chronic
diarrhea where no specific diagnosis is reached,
anthelmintic therapy should be considered. Larvicidal
doses of anthelmintics suitable for the treatment of
confirmed or suspected cases of strongyle-associated
disease include
• ivermectin 0.2 mglkg p.o.
• moxidectin 0.4 mg/kg p.o.
• fenbendazole 7.5 mglkg p.o. for 5 consecutive
days
• oxfendazole 10-50 mg/kg p.o.
ANTIBIOTICS
Oral antibiotics are generally contraindicated in cases
of chronic diarrhea since they may either cause or
worsen a colonic microflora imbalance, thereby wors­
ening the diarrhea. Salmonella spp. are not considered a
m,yor cause of chronic diarrhea and, even in cases
where they are isolated, another underlying cause of
diarrhea may be present. However, a small percentage
of horses with chronic diarrhea do appear to improve
with antibacterial therapy using potentiated sulfon­
amides or metronidazole (the reason for this is uncer­
tain). Antibiotics are indicated in horses with chronic
diarrhea due to peritonitis (see Chapter 17).
CHRONIC DIARRHEA 21
TRANSFAUNATION
Transfaunation using cecal contents or fresh feces from
a normal horse has been used as a treatment of horses
with chronic diarrhea in an attempt to replace some of
the normal bacterial flora in the colon. Unfortunately
there are no controlled studies of the technique and
reports of its successful use are anecdotal only.
Transfaunation can be achieved by introducing the
material via stomach tube or directly into the cecum via
laparotomy. Fecal slurry should be obtained from a nor­
mal horse that is negative for Salmonella spp. on culture.
Fresh cecal contents obtained at euthanasia provide
higher numbers of bacteria. The suggested dose is 5-6
liters of fluid repeated for 2 or 3 treatments.
PROBIOTICS
The use of products that contain Lactobacillus spp. is
frequently recommended in the treatment of chronic
diarrhea in adult horses. Although they probably cause
no harm they are also of no proven benefit.
MOTILITY MODIFYING AGENTS AND
ANTISECRETORY DRUGS
A variety of drugs have been suggested to try to 'slow'
the intestines or promote development of a more
formed stool
• codeine phosphate (1-3 mg/kg p.o. once or twice a
day to effect) has proven useful as a non-specific
treatment of chronic diarrhea in adult horses
• loperamide (0.04-1.6 mg/kg p.o.) may be used in
non-infectious diarrheal conditions, its primary
benefit could be an antisecretory effect
• phenoxybenzamine has an anti-secretory effect but
should not be used because of its hypotensive
effect.
INTESTINAL PROTECTANTS AND
ADSORBENTS
Bismuth subsalicylate (up to 4 1/500 kg q. 12 h) may
have antidiarrheal, antibacterial and anti-inflammatory
properties but is relatively ineffective in diarrhea in the
adult horse. Kaolin and pectin should not be used in
severe diarrhea as they may worsen malabsorption and
increase ion loss during diarrhea. Activated charcoal
has been used (0.5 kg/500 kg) in acute equine colitis,
but is relatively ineffective in chronic diarrhea.
431
21 ACUTE AND CHRONIC DIARRHEA
OTHER TREATMENTS
Iodochlorohydroxyquin (5-10 g p.o. s.i.d.) is helpful in
a small number of horses with chronic diarrhea. The
mechanism of action of the drug is unknown, but it may
involve a change in the colonic microflora. The drug
may also have antiprotozoal activity but there is very lit­
tle evidence to suggest that this is important in relation
to the treatment of chronic diarrhea in the adult horse.
NUTRITIONAL SUPPORT
Horses with chronic diarrhea and protein-losing
enteropathy benefit from additional protein in the diet.
Often these horses are also in a state of energy, mineral,
and vitamin malnutrition. They should be fed alfalfa
hay ad lib., as well as a high protein-energy concentrate,
a mineral supplement providing calcium, magnesium,
zinc, copper, and iron, and fat and water-soluble vita­
mins. Some horses with chronic diarrhea benefit from
being turned out to grass; this may promote normaliza­
tion of gastrointestinal flora. Any change of diet should
be gradual. Gradual change from high roughage to low
roughage, or occasionally vice versa, may cause the stool
to normalize in a few horses with idiopathic chronic
diarrhea.
Larval cyathostomosis
0011111111
T Mair
INTRODUCTION
In recent years larval cyathostomosis has become an
increasingly common problem in many areas of the
world. The increasing prevalence of the disease is asso­
ciated with an increased prevalence of cyathostomes in
grazing horses. The cyathostomes are now ubiquitous
parasites, and virtually all grazing horses in temperate
areas are assumed to be infected by them. This
increased prevalence of cyathostomes has occurred
over the last 30 years since the introduction and wide­
spread use of interval treatment with broad-spectrum
anthelmintics such as benzimidazoles, pyrantel, and
ivermectin. Interval treatment using these drugs has
been highly effective at reducing the prevalence of
large strongyles such as Strongylus vulgaris, but it is rela­
tively ineffective at controlling the cyathostomes. Even
in well-managed horses, cyathostome infection is likely
432
and is probably responsible for subclinical production
losses that are difficult to quantify. When the parasite
burden becomes high, overt clinical disease is more
likely to be manifested, particularly in young horses.
The most clearly defined disease syndrome associ­
ated with cyathostome infection is the acute diarrheal
syndrome called larval cyathostomosis (previously
known as larval cyathostomiasis or acute larval cyatho­
stomiasis), that occurs most typically in young adult
horses in the winter. However, a number of other
clinical syndromes associated with these parasites have
been recognized, including the following
• recurrent diarrhea in older and aged horses and
ponies
• rapid weight loss and peripheral edema without
diarrhea
• chronic weight loss and ill-thrift
• seasonal (late autumn to spring) 'malaise
syndrome'
• non-specific colic
• cecocecal and cecocolic intussusceptions
• non-strangulating intestinal infarction
• weight loss with or without diarrhea in weanlings
during the autumn.
There may be some overlap between these different
clinical presentations in individual cases.
ETIOLOGY AND PATHOGENESIS
The cyathostomes (or small strongyles) comprise a
large group of eight genera and over 40 species of
nematode parasites (see Chapter 4). The potential role
of different species in causing different clinical mani­
festations is at present unclear. The parasites have a
direct life cycle, with adults laying eggs that pass out in
the feces and contaminate the pasture. In temperate cli­
mates (including the UK, most of continental Europe,
and the northern half of the US) the eggs hatch within
about I week during the summer, but hatching and
development are delayed during colder times of year.
In southern temperate zones (the southern half of the
US), hatching of larvae occurs rapidly all year round,
although the larvae do not survive long during hot dry
weather. Moisture and oxygen are essential for hatch­
ing and development, but levels of these are usually
adequate in the fecal pile. Infective third-stage larvae
cannot ingest nutrients so they survive on the pasture by
consuming limited, intracellular energy reserves. The
duration of their survival is inversely proportional to the
environmental temperature because they utilize their
energy reserves faster in hot weather. The environmen­
tal constraints on the cyathostome life cycle result in

Northern temperate areas
Development Persistence
Spring +++ +++
Summer ++ +
Autumn +++ +++
Winter +++
+++ excellent
++ good
+ fair
patterns of transmiSSIOn that are seasonal and pre­
dictable. These patterns of cyathostome development
and persistence on the pasture in different geographi­
cal locations are summarized in Table 21.4.
The pre-infective first stage larvae (Ll) develop in
the presence of warmth and moisture via second stage
larvae (L2) to infective third stage larvae (L3) that are
eaten by grazing horses. In the gut, the infective larvae
exsheath in the small intestine and invade the wall of
the cecum and large colon. Within the mucosa and sub­
mucosa the L3 become surrounded by a fibroblastic
cyst, and either develop into fourth stage larvae (L4) or
enter a state of arrested larval development (also called
hypobiosis or inhibited larval development). At some
stage, the encysted L4 break out of the cyst and migrate
back to the lumen of the cecum and colon where they
develop into fifth stage larvae (L5) and eventually egg­
laying adults. Early L3 undergoing arrested larval devel­
opment may remain in this state for a few months to
several years. The signal or stimulus for these larvae to
resume their development is unclear, although climatic
conditions seem to be important. In addition there is
evidence that anthelmintic therapy which removes the
population of adult cyathostomes from the lumen, and
stressful conditions (such as travelling or change of
premises, parturition, etc.) can also stimulate resump­
tion of development of these larvae and precipitate
clinical disease.
Cyathostome-associated diseases have traditionally
been attributed to the synchronous emergence of large
numbers of previously inhibited L3 and L4 stages from
the cecal and colonic walls, thereby leading to physical
disruption of the mucosa and resultant typhlitis and
CHRONIC DIARRHEA 21
Southern temperate areas
Development Persistence
++ ++
++ ++
+ +
colitis. Gross lesions in the wall of the cecum and large
colon are characterized by generalized inflammation,
mucosal edema, and ulceration. The inflammation
probably results in diarrhea as a result of increased
active and passive secretion of fluid, electrolytes, and
protein. Protein loss can be severe, resulting in pro­
found hypoproteinemia and hypoalbuminemia. Altera­
tions in intestinal motility may occur as a result of larval
migration, and this may also be important in the patho­
genesis of diarrhea and colic that can occur in cyathos­
tome infections. In addition, there is the possibility that
the larvae themselves may release substances or stimu­
late local host cells to release mediators that cause vaso­
constriction and mucosal edema, thereby adding to the
pathological effects.
The intensity of cyathostome infection may be an
important factor in determining the nature and severity
of the clinical disease. Thus, mild infections might be
more likely to produce clinical signs of 'malaise
syndrome', recurrent diarrhea, or non-specific colic,
whereas heavy infections may cause acute, severe diar­
rhea and rapid weight loss, or colic caused by cecal intus­
susceptions or non-strangulating intestinal infarction.
In addition to the pathological damage caused by
emerging larvae, mucosal larval penetration by infective
L3 may be important as a cause of disease. Reduced
weight gain, altered protein metabolism, and transient
neutrophilia have been recognized within the first 4-6
weeks of experimental 'trickle' cyathostome infections.
This disease process may be particularly important in
weanlings grazing contaminated pasture during the late
summer to autumn, when pasture larval counts may be
very high.
433
21 ACUTE AND CHRONIC DIARRHEA
EPIDEMIOLOGY
Diseases associated with acute larval cyathostomosis
typically occur in young adult horses (1-6 years of age)
during the winter to early spring (November to April in
northern temperate climates). The disease tends to be
sporadic, although multiple cases may occur in similarly
aged horses managed together. Factors that increase
the risk of high cyathostome burdens in horses include
• overstocking and use of permanent horse pastures
• poor parasite control methods applied to young
grazing horses
• failure to use routine larvicidal anthelmintics with
activity against arrested cyathostome larvae
• resistance by cyathostomes to anthelmintics.
Factors that have been associated with the onset of
clinical disease in individual cases include
• season, late winter to early spring
• recent administration of anthelmintics
• stressful situations such as travel, new environment,
parturition, etc.
• other diseases, e.g. alimentary lymphosarcoma.
The incidence of larval cyathostomosis is unknown, but
there are many anecdotal reports that suggest an
increasing prevalence in northern temperate zones. In
the UK surveys have shown that cyathostomosis is the
most common cause of chronic diarrhea in adult
horses.
CLINICAL SIGNS
The typical clinical signs of acute larval cyathostomosis
include
• sudden onset of profuse diarrhea that becomes
chronic
• diarrhea of variable nature ('cowpat' to watery)
• diarrhea that may be continuous or intermittent
• weight loss - this is often severe and rapid, and may
precede the onset of diarrhea by up to 48 hours
• weakness
• depression
• subcutaneous edema of the limbs, ventral
abdomen, and prepuce
• variable signs of colic
• abdominal distention due to cecal/colonic tympany
pyrexia.
The disease can affect horses of all ages, but is com­
monest in horses less than 6 years of age. The disease
tends to be most severe in the very young and the very
old. In many cases, signs of systemic illness (dehydra-
434
tion, signs of endotoxemia, anorexia, etc.) are not as
marked as in other acute coli tides in the adult horse.
However, in severe cases there may be evidence of
dehydration and acid-base imbalance, and in some
cases the disease may cause apparent 'sudden death'.
DIAGNOSIS
Diagnosis is usually achieved by a combination of some
or all of the following.
History and epidemiology
The history and epidemiology include a combination of
season, age, recent administration of anthelmintics
and the history of parasite control, recent stress, and
concurrent disease.
Fecal examination
Numerous cyathostome larvae may be observed by the
naked eye either in the feces or on the rectal glove fol­
lowing a rectal examination. Gently scraping the wall of
the rectum with the fingers during a rectal examination
may yield higher numbers of larvae. Larvae are variable
in their size and appearance depending on which species
are present, some appear white while others are red.
Microscopical examination of a wet preparation of
feces may be necessary to confirm the presence of L4
and L5. Larvae may be difficult to detect in the feces of
some cases, especially if the horse has recently been
treated with an anthelmintic.
Fecal worm egg counts are of little help diagnosti­
cally because the disease is caused by the larval stages
of the parasites. However, a high strongyle worm egg
count in either the affected animal or in-contact horses
suggests poor routine parasite control.
Fecal cultures sometimes yield Salmonella spp.
and/or Campylobacter spp.
Hematological examination
Routine hematological examination usually reveals
leukocytosis and neutrophilia. Some cases may also
show anemia and/or mild eosinophilia.
Serum biochemistry
Serum biochemistry usually reveals a profound hypo­
albuminemia. The total protein concentration may be
low, normal, or even elevated because of variable hyper­
globulinemia. Some cases show elevated serum alkaline
phosphatase levels.
Serum protein electrophoresis
This may show elevated beta-globulin levels and some­
times elevated alpha-globulin levels.

Histological examination
Histological examination of rectal biopsies is rarely
diagnostic. However, biopsies of the cecum and/or
large colon are likely to show characteristic pathological
changes including edema and eosinophilic inflamma­
tion, and possibly the presence of mucosal larvae.
Unfortunately cecal and colonic biopsies can only effec­
tively be obtained surgically via a laparotomy.
TREATMENT
Despite the fact that in many cases an accurate diagno­
sis of larval cyathostomosis is readily achieved (by
identification of numerous larvae in feces) the disease
carries a high death rate. Successful treatment can be
expected in little more than 40 per cent of severe cases.
Many affected horses appear to survive for several days
or weeks, but then show a rapid deterioration followed
by death. Mild cases treated early in the course of the
disease have a better prognosis.
Treatment consists of
• anthelmintics
• corticosteroids
• fluids and electrolytes
• plasma therapy
• antidiarrheal agents
• nutritional support.
In mild cases, especially if treatment is instituted early,
anthelmintics alone may be successful. However, in
severe cases intensive treatment with other agents will
be required. Even with intensive therapy many cases
die.
Anthelmintics
Fenbendazole, ivermectin, and moxidectin are active
against the mucosal stages of cyathostome larvae. These
agents are more effective against the maturing (as
opposed to inhibited) larvae. For this reason, repeated
doses of anthelmintics are recommended in order to
kill parasites as they develop from an arrested state.
Frequent anthelmintic dosing at 10-14 day intervals on
two to five occasions is advocated. The following larvici­
dal doses of these drugs are suggested
• fenbendazole 7.5-10.0 mg/kg p.o. s.i.d. for 5 days
• ivermectin 0.2 mg/kg p.o.
• moxidectin 0.4 mg/kg p.o.
The use of fenbendazole and either ivermectin or
moxidectin in individual cases (alternating treatments)
is used by many clinicians. However, increasing preva­
lence of benzimidazole resistance among populations
CHRONIC DIARRHEA 21
of cyathostomes may limit the effectiveness of fenben­
dazole in certain locations. Particular care should be
taken when calculating the dose of moxidectin because
of the increased risk of toxicity with this drug, especially
since many affected horses are in a catabolic state.
Corticosteroids
Corticosteroid therapy has proven beneficial in the
treatment of clinical cases. Dexamethasone (50 Ilg/kg)
administered by intravenous or intramuscular injection
can be given for 1-5 days, followed by oral prednisolone
(l mg/kg p.o.) until the diarrhea has resolved. The
prednisolone is then 'tailed off over the next 7-10 days.
Two potential mechanisms have been attributed to the
beneficial effects of steroids in this disease
1. their anti-inflammatory activity
2. the steroid-induced immunosuppression may
encourage resumption of larval development and
render the parasite more susceptible to the effects
of anthelmintics.
It is important that the potential side effects of corticos­
teroid (especially dexamethasone) therapy are recog­
nized.
Non-steroidal anti-inflammatory drugs are generally
ineffective in this disease. Their use should be under­
taken with extreme caution because of the increased
risk of toxic side effects due to concurrent hypo­
proteinemia and dehydration.
Fluid, electrolytes, and plasma therapy
Therapy with intravenous or oral fluids and electrolytes
are often beneficial, and are essential in cases with
clinical dehydration. Guidelines for these therapies are
given elsewhere (see General principles of treatment of
chronic diarrhea in adult horses and Chapter 20,
General principles of treatment of acute diarrhea in
adult horses). Plasma therapy is also beneficial even
though measured plasma albumin will remain elevated
for only a short time.
Antidiarrheal agents
Various antidiarrheal agents have been employed in the
treatment of larval cyathostomosis. Codeine phosphate
(3 mg/kg p.o. t.i.d., adjusted depending on fecal con­
sistency) is commonly used. This drug reduces gastro­
intestinal secretions and delays intestinal transit, and
has proved to be effective in the control of diarrhea in
adult horses Typically, an improvement in fecal consis­
tency is apparent within 48 hours of instituting codeine
therapy, and the dosage can be acljusted on an empiri­
cal basis thereafter. Side effects can be seen with higher
435
21 ACUTE AND CHRONIC DIARRHEA

doses of codeine phosphate, including sedation and weight loss, and subcutaneous edema, and cyathostome
predisposition to colonic impaction. larvae were identified in the feces.

PREVENTION
OTHER CLINICAL PRESENTATIONS
Prevention of larval cyathostomosis is dependent on
Recurrent diarrhea
effective parasite control measures, especially in the
Bouts of recurrent diarrhea associated with larval foal and young adult horse. The reader is referred to
cyathostomosis were first reported in aged ponies, Chapter 4 for more information concerning parasite
although the problem can also occur in other age control.
groups. Bouts of diarrhea may occur several times a
year, but are most common in the winter and spring.
They are associated with the presence of low numbers
of cyathostome larvae in the feces. In most cases, the Strongylosis
periods of diarrhea respond to anthelmintic therapy.
T Mair
Weight loss and edema
Equine strongylosis involves mixed infections of large
Rapid and severe weight loss with the development of
strongyles (subfamily Strongylinae) and small strongyles
subcutaneous edema associated with hypoalbuminemia
(subfamily Cyathostominae). The large strongyles have
may sometimes occur in larval cyathostomosis in the
a direct life cycle, with parasitic and free-living stages.
absence of diarrhea. In some of these cases, diarrhea
They have been recognized for many years as an impor­
will develop at a later stage (days to weeks after the
tant cause of colic. The small strongyles have increased
initial clinical signs). Cyathostome larvae are present in
in prevalence in recent years and are a major cause of
the feces.
diarrhea as well as being implicated in the cause of colic
(see Larval cyathostomosis).
Seasonal malaise syndrome
The pathogenicity of large and small strongyles is
A seasonal (late autumn to spring) malaise syndrome greatest in young horses. Nearly all grazing horses will
has been identified in adult horses in the UK, and is harbor mixed strongyle burdens. Clinical signs that can
believed to be caused by cyathostome infection. This be associated with these infections include
syndrome is characterized by reduced appetite,
• colic
lethargy, and weight loss with variable fecal consistency
• ill thrift
(from normal to mild diarrhea). Affected horses
• weight loss
respond to treatment with larvicidal doses of
• anorexia
anthelmintics.
• poor hair coat quality
• diarrhea
Non-specific colic
• episodes of pyrexia.
Cyathostome infection is being increasingly recognized
However, most infected horses show no overt clinical
as a cause of colic. In one epidemiological study the
signs.
effect of different anthelmintic programs on the inci­
Strongylus vulgaris is the most common of the large
dence of colic was compared. This study demonstrated
strongyles and is considered to be the most pathogenic.
a marked decrease in the incidence of colic on farms on
The pathogenesis of S. vulgaris is the result of thrombo­
which effective cyathostome control was achieved com­
embolic arteritis of the cranial mesenteric artery and its
pared with the incidence recorded on farms where
major branches. Within 2 weeks of infection infective
cyathostome control failed.
larvae penetrate the intestinal mucosa and cause arteri­
tis of submucosal and serosal arteries, and a marked
Cecocecal and cecocolic intussusceptions
inflammatory reaction. The larvae then migrate up the
A recent report has described four horses affected by intestinal arteries to the cranial mesenteric artery. The
cecal intussusceptions with clinical and/or pathological larvae continue to develop in these arteries and pene­
evidence of concurrent larval cyathostomosis. All four trate the intima, causing arteritis of the ileocolic and
horses demonstrated a variable number of other signs associated arteries. Agamous adults develop within 3-4
of larval cyathostomosis, such as diarrhea, pyrexia, months and are carried by the blood stream to the

436

cecum and large colon. Here they form cysts containing
the worms surrounded by necrotic debris and neutro­
phils adjacent to thrombosed terminal intestinal arter­
ies. The cysts eventually erode through the intestinal
wall to release the adult parasites into the lumen.
The importance of Strongylus vulgaris as a cause of
diarrhea in the horse is uncertain. Diarrhea could be
caused by thromboembolic damage to the bowel or dif­
fuse vasoconstriction in the intestinal wall, resulting in
inflammatory damage and motility changes.
Diagnosis of strongylosis may be difficult. Since clin­
ical disease is usually caused by the immature, migratory
larval stages of the parasites, the fecal worm egg count is
unreliable. However, a high strongyle fecal worm egg
count does suggest inadequate routine parasite control,
increasing the index of suspicion of strongylosis.
Hematological changes, such as anemia, leukocytosis,
neutrophilia, and eosinophilia, are non-specific and
unreliable indicators of strongyle larval migration.
Likewise, hypoalbuminemia and hyperbetaglobulin­
emia are inconsistent changes that may occur in horses
affected by diarrhea for other reasons.
Although clinical disease is most commonly associ­
ated with larval migration, heavy burdens of adult
strongyles can also cause disease characterized by
• ill thrift and weight loss
• poor performance
• anemia
• diarrhea
• colic.
In these cases the fecal strongyle worm egg count is
expected to be high.
Treatment of suspected strongylosis includes symp­
tomatic treatments (see General principles of treatment
of chronic diarrhea in adult horses) and larvicidal doses
of anthelmintics. Return to normal intestinal function
may be protracted and in some patients repeated
anthelmintic dosing may be required.
Chronic inflammatory bowel
disease and intestinal
neoplasia
T Mair
Chronic inflammatory and neoplastic diseases, such as
lymphosarcoma, granulomatous en teri tis/colitis, lym­
phocytic-plasmacytic enteritis/colitis, and eosinophilic
enteritis/colitis, primarily affect the small intestine and
CHRONIC DIARRHEA 21
are associated with malabsorption and chronic weight
loss (see Chapter 18). However, if the large intestine is
affected as well then diarrhea is likely. Chronic inflam­
mation of the large intestine results in hypersecretion
of fluid and electrolytes, reduced absorption of water,
and motility abnormalities.
Rectal examination findings in these cases may
include enlarged mesenteric lymph nodes and palpable
thickening of the bowel wall. The rectum itself may be
thickened and friable. Ultrasonography can be helpful
to confirm bowel wall thickening. Moderate to severe
hypoalbuminemia and mild to moderate hyperglobu­
linemia are often present. Elevated serum alkaline
phosphatase may be present. Non-specific hematologi­
cal abnormalities (anemia, leukocytosis, neutrophilia,
hyperfibrinogenemia) may also be identified. Diagnosis
of inflammatory or neoplastic bowel infiltrates usually
depends on histopathology of bowel wall biopsies.
Rectal biopsy may be diagnostic in some cases. The
diagnosis and treatment of these diseases are described
in more detail in Chapters 17 and 18.
Chronic idiopathic colitis was diagnosed as a com­
mon cause of diarrhea in one clinical review of horses
with chronic diarrhea. This disease was diagnosed only
by histopathological examinations (obtained at post­
mortem examination). The disease was characterized
by diffuse, non-specific inflammatory changes in the
lamina propria and/or submucosa, and some also
had mucosal ulceration. The cause of this syndrome
remains uncertain.
Sand enteropathy
T Mair
INTRODUCTION
Accumulation of large quantities of sand in the gastro­
intestinal tract is an uncommon cause of chronic diar­
rhea. Sand accumulation is more commonly associated
with impaction of the colon and colic (see Chapter
15). Light sandy soils, overstocking, poor pasture
management, inadequate nutritional supplementation,
drought conditions, and feeding horses in sand
schools can all result in horses consuming significant
quantities of sand. Sand accumulates within the cecum
and large colon where it probably irritates the mucosa
and disrupts normal motility patterns leading to diar­
rhea. Fine sand tends to accumulate in the ventral
colon, whereas coarse sand may accumulate in the
dorsal colon.
437
21 ACUTE AND CHRONIC DIARRHEA
CLINICAL SIGNS
Diarrhea associated with sand enteropathy is usually rel­
atively mild and is not associated with severe dehydra­
tion. The diarrhea may be persistent or intermittent.
There may be associated fever, decreased appetite,
weight loss, and episodes of colic. Complete obstruction
of the colon results in persistent colic (see Chapter 15).
Severe irritation and mucosal inflammation may result
in secondary peritonitis that may become septic if bowel
perforation occurs. In such cases, the horse will develop
signs of endotoxemia with tachycardia, congested
mucous membranes, prolonged capillary refill time,
and a toxic rim at the gum/incisor margin.
DIAGNOSIS
Sand may be identified in the feces in large quantities.
If a fecal solution is made by mixing feces and water
together, sand will sediment to the bottom of the con­
tainer when the solution is allowed to stand for a few
minutes. Frank or occult blood may be present in the
feces. Transrectal palpation may reveal an impacted
segment of colon (unless the transverse or right dorsal
colon is involved in which case they are not normally
palpable per rectum). Auscultation of the abdomen
may reveal decreased frequency of borborygmi, and a
characteristic sound of 'pouring sand' over the ventral
abdomen. This sound is only heard in association with
progressive contractions of the colons. Radiography
can also be used to identify radiodense sand in the
intestinal tract in the cranioventral abdomen, especially
in small horses and ponies.
Hematology is often normal, but in some cases there
may be evidence of hemoconcentration (pev 45-55%
and total protein 72-80 gil (7.2-8.0 g/dl». Plasma
fibrinogen may be normal or elevated.
Peritoneal fluid is usually normal, although there
may be an increased total protein concentration.
Increased nucleated cell counts and protein levels will
be found if peritonitis is present. Abdominocentesis
should be undertaken with caution in horses suspected
of sand impaction because of the increased risk of
enterocentesis. However, identification of sand particles
in the sample of peritoneal fluid is diagnostic when seen.
TREATMENT
Intravenous and/or oral fluid therapy should be admin­
istered as necessary. Psyllium hydrophilic mucilloid is a
bulk laxative that hydrates intestinal contents and stim­
ulates intestinal motility. By mixing with sand in the
438
colon, it promotes evacuation of the sand-psyllium
mucilloid mixture from the intestinal tract. A dose of
0.25-0.5 kg/500 kg body weight is mixed with 4-8 liters
of water and administered rapidly through a nasogastric
tube. In order to reduce the risk of the gel blocking the
nasogastric tube, some authors recommend administra­
tion by nasogastric tube of the powder mixed with 2
liters of mineral oil; this is followed by the administra­
tion of 4 liters of water through the tube. Magnesium
sulfate (Epsom salt) can be administered at the same
time. Once the clinical signs are relieved, prolonged
therapy is frequently necessary to remove the accumu­
lated sand. Dry psyllium (1 g/kg) can be added to the
feed daily for several weeks. This may be repeated after
3-4 months; continuous daily feeding of psyllium
mucilloid should not be continued more than a few
weeks at a time. The efficacy of this form of treatment
has recently been questioned and in one experimental
study psyllium mucilloid was found to be ineffective in
removing sand from the intestinal tract. High fiber
ingredients in the diet, such as wheat bran, may also be
helpful in removing accumulated sand from the colon.
Alternative bulk-forming laxatives can be used.
Ispaghula husk at 300-400 g/450 kg mixed with 4 liters
of water and administered immediately by nasogastric
tube has proved useful in some cases. The treatment
can be repeated at daily intervals for 4-5 days.
Surgical therapy is occasionally needed if there is com­
plete colonic obstruction (see Chapter 15). In horses
developing peritonitis secondary to sand enteropathy,
antibiotics and other therapies for peritonitis are
required (see Chapter 17, Peritonitis).
PREVENTION
Prevention of the disease is important and recurrence
of clinical signs in individual horses is common.
Feeding horses from elevated bins (with rubber mats
underneath) and allowing grazing only in fields with
adequate growth to prevent ingestion of sand are vital
to avoid this condition.
Equine right dorsal colitis
NO Cohen
INTRODUCTION
Right dorsal colitis has been clinically and experimen­
tally associated with administration of phenylbutazone

to horses. Clinical signs in horses with this condition
include inappetance, anorexia, weight loss, intermit­
tent or sporadic episodes of acute abdominal pain, and
diarrhea. Some horses with right dorsal colitis can be
managed medically. Early recognition of this condition
is likely to be important for successful medical manage­
ment. The purpose of this section is to describe
methods for the diagnosis and management of right
dorsal colitis.
CAUSE
Right dorsal colitis (RDC) has been associated with
administration of phenylbutazone. Although the condi­
tion may develop in horses given excessive amounts of
the drug, RDC may develop in horses that receive
recommended doses of phenylbutazone (4.4 mg/kg
p.o. b.i.d.) for periods as brief as 1 week. Other non­
steroidal anti-inflammatory drugs (e.g. flunixin meglu­
mine) can also cause RDC but they are less frequently
associated with the condition. Dehydration and physio­
logic stress associated with performance may increase
the risk of RDC. Idiosyncratic or genetic predisposition,
protein composition of the diet, or concurrently admin­
istered drugs may also contribute to development of
right dorsal colitis. Concurrent administration of
phenylbutazone and flunixin meglumine prolongs the
pharmacologic effects of these drugs. Young perfor­
mance horses, horses with chronic lameness, and
ponies may be more likely to develop RDC. It is
unknown why the right dorsal colon is affected in
particular.
Salmonella spp. have been isolated from the feces of
horses with right dorsal colitis. The clinical importance
of isolating Salmonella spp. is unclear because appar­
ently healthy horses may shed Salmonella spp. and
gastrointestinal disease predisposes to enteric
salmonellosis. Salmonellosis can cause diarrhea,
abdominal pain, and protein-losing enteropathy in
horses. Although these clinical signs are observed in
horses with RDC, Salmonella spp. are not likely to be
causally associated with RDC.
CLINICAL SIGNS
The clinical signs of right dorsal colitis are
• colic
• weight loss
• diarrhea
• inappetence
• icterus
• ventral edema.
CHRONIC DIARRHEA 21
Physical examination of horses with RDC may reveal
few abnormalities and clinical signs are non-specific.
Horses may have signs of acute abdominal pain (colic).
Often episodes of colic are recurrent and some horses
may be presented when they are apparently healthy
for evaluation of intermittent colic (see Chapter 17).
Although weight loss is seen in horses with RDC, some
horses may be in good body condition. Weight loss is
probably related to duration of the condition. Some
horses with RDC may have diarrhea but the feces usu­
ally have a normal consistency. When present diarrhea
is rarely profuse. Though rarely reached, the right dor­
sal colon may feel edematous and thickened when pal­
pated per rectum. Because of inappetance or anorexia,
some horses may have icteric mucous membranes.
Occasionally, horses with RDC will have edema of the
ventrum or limbs attributable to hypoproteinemia.
CLINICAL PATHOLOGY
Common hematologic abnormalities of horses with
RDC include anemia, hypoproteinemia, and hypoalbu­
minemia. Decreased PCV probably results from colonic
loss of blood and/or chronic inflammatory disease.
Occult blood can be found in the feces of affected
horses but the tests that are currently available are not
highly sensitive. False positive results can occur when
the test is performed on feces collected from a horse
within 24 hours following a rectal examination.
Hypoproteinemia is very common in horses with
RDC. Based on the results of the clinical history, physi­
cal findings, urinalysis, peritoneal fluid analysis, and
serum biochemistry, hypoproteinemia can be attrib­
uted to gastrointestinal loss in affected horses. Because
it is the most abundant protein in equine plasma and
has a lower molecular weight than globulins, albumin is
often decreased in horses with gastrointestinal inflam­
matory disease. Because of decreased intravascular
oncotic pressure, hypoproteinemia and hypoalbumin­
emia may exacerbate hypovolemia, further predisposing
to NSAID-induced intestinal damage. The hypoprotein­
emia is rarely severe enough to cause dependent
edema. The concentration of leukocytes is usually
within the reference range, although leukocytosis and
hyperfibrinogenemia, associated with inflammation,
and leukopenia and neutropenia, possibly caused by
endotoxemia, can be seen in some horses with RDC.
Hypocalcemia is frequently observed in horses with
RDC. Hypocalcemia may result from inadequate dietary
intake associated with abdominal pain, loss of protein­
bound calcium into the gastrointestinal tract, and
decreased protein-bound calcium associated with
hypoalbuminemia and hypoproteinemia. Because the
439
21 ACUTE AND CHRONIC DIARRHEA
ionized fraction of calcium is rarely decreased severely,
signs of tetany are not generally observed in horses with
RDC. Other serum biochemical abnormalities are not
consistently observed. Some horses may have prerenal
azotemia and hyperbilirubinemia associated with
decreased ingestion of water and feed. In dehydrated
horses that become hemoconcentrated, the decreased
PCV and hypoproteinemia may not be apparent until
they are rehydrated. Cytologic and biochemical analysis
of peritoneal fluid rarely reveals abnormalities. In some
horses an increased concentration in peritoneal fluid of
total protein, fibrinogen, and nucleated cells may be
observed. Grossly, the affected colon will appear thick­
ened, edematous, and reduced in cross-sectional diam­
eter. Varying degrees of nlceration may be observed if
the mucosal surface is inspected.
DIAGNOSIS
None of the clinical or clinicopathologic findings
observed is specific for RDC. Consequently diagnosis is
difficult. Localizing a problem to the right dorsal colon
exclusively can only be made anatomically by examin­
ing the gastrointestinal tract by celiotomy or necropsy
(Plate 2 1.1 ). Because celiotomy is invasive, it is often
desirable to recognize the condition and establish a
presumptive diagnosis accurately. This can be accom­
plished on the basis of interpreting findings of signal­
ment and history, clinical signs, and clinicopathologic
findings, particularly hypoalbuminemia.
The chief complaint is often non-specific and history
of recurrent episodes of anorexia, lethargy, and colic is
frequently described. History of administration of non­
steroidal anti-inflammatory drugs (NSAID) is of partic­
ular importance. The condition is frequently seen in
horses that have a history of use for competitive perfor­
mance. Such horses often receive NSAIDs, including
phenylbutazone, for management of musculoskeletal
pain. Moreover, such horses may be predisposed to
adverse effects of NSAIDs because of dehydration and
physiologic stress associated with strenuous exercise
and travelling. Ascertaining an accurate history of
NSAID administration can be difficult, particularly in
cases where blame may be an issue.
The amount and duration of NSAID administered
may be important. It is, however, important to recog­
nize that colonic inflammation or ulceration may develop in
horses receiving doses of phenylbutazone tolerated by many
other horses.
Findings of history and the aforementioned physi­
cal, clinical, and clinicopathologic attributes should
make a diagnosis of RDC likely. Similar findings, how­
ever, can be seen in horses with gastric and small intesti-
440
nal ulceration caused by administration of NSAIDs and
with other causes of chronic colic. If possible, gas­
troscopy (see Chapter 2) should be performed in all
horses with clinical signs suggestive of RDC. Clinical
signs of RDC are similar to those associated with gastric
ulceration. Because colonic inflammation and ulcera­
tion can occur independently of, or concurrently with,
gastric ulceration, it may be necessary to treat some
horses with colonic ulceration for gastric ulceration.
Definitive localization requires visualization of the right
dorsal colon, this is best achieved via celiotomy.
Ultrasonographic examination of the right dorsal colon
can provide a non-invasive method of identifYing
colonic mural thickening that might be associated with
right dorsal colitis. The sensitivity of this technique,
however, appears limited. It has been suggested that
isotope-labeled white blood cell scintigraphic scans may
identifY colonic ulceration; the sensitivity and availabil­
ity of the procedure is likely to be quite limited.
TREATMENT
Initially RDC was described as a condition requmng
surgical management and carrying a poor prognosis.
Surgical management entails bougienage, or either
bypassing or resecting the affected portion of the colon.
Many cases of RDC, however, can be managed medically.
The principal aims of medical management are to
• avoid treatment with NSAIDs
• minimize stress for the horse
• implement dietary management.
Certain drugs may also be of benefit in managing this
condition (see below).
Avoidance of NSAIDs
Because RDC has been induced in horses by adminis­
tration of phenylbutazone, NSAIDs should not be
administered to horses with this condition. Compliance
with this recommendation can be difficult because
some horses continue to have episodes of colic during
medical management and caretakers may be tempted
to treat these episodes with flunixin or other NSAIDs.
Also some horses may have a problem (e.g. chronic
lameness) that the owners want to continue to treat
with an NSAID because of availability, cost, and clinical
effectiveness for the problem. Nevertheless, these drugs
should be avoided because some horses may have an
idiosyncratic or other predisposition to RDC; the mag­
nitude of doses and the duration of administration of
phenylbutazone in horses with RDC are not necessarily
unusually high relative to recommended doses.

Minimizing stress for the horse
Physiologic stress and dehydration appear to increase
the risk of gastrointestinal ulceration induced by
NSAIDs. Minimizing physiologic stress and avoiding
dehydration may help decrease the risk of recurrence
and promote healing in horses with RDC. Examples
of management practices designed to decrease stress
include discontinuing or decreasing the frequency of
performance, strenuous exercise, and travelling. Horses
with RDC should be provided access to adequate
amounts of water. Efforts should be made to ensure or
enhance consumption of water
• provide salt in a block or as granules on the feed, or
• sweeten the water with flavored preparations (this
may be of particular benefit in horses that are being
transported for long periods or to environments
with water that is less palatable to the horse).
Implementing dietary management
Dietary management is directed toward providing a low­
hulk diet in the form of a pelleted concentrate, and
restricting or eliminating ingestion of roughage. These
changes aim to decrease the mechanical and physio­
logic load of the colon. A complete pelleted diet (i.e.
pellets containing both concentrate and adequate
dietary roughage) will decrease intestinal fill in the
colon, therehy decreasing the mechanical load of the
colon. A diet lower in fiber should decrease the physio­
logic load of the colon because the cecum and large
colon are the primary sites in horses of fiber digestion
and exchange of fluid and electrolytes. Concentrate
should be fed in smaller amounts and more frequently
(4-6 feedings per day), rather than twice daily. Some
horses will not eat complete pellets and some will eat
bedding or wood if roughage is withheld. Such horses
should be allowed to eat fresh grass in small amounts
(approximately 5-10 minutes of grazing 4-6 times
daily). Roughage should be eliminated or restricted to
small amounts of fresh grass for a period of 3-6 months.
The importance of and optimal duration for restriction
of roughage is unknown.
Drug therapy
Drugs used to treat right dorsal colitis are
• psyllium mucilloid
• misoprostol
• sucralfate
• metronidazole
• sulfasalazine
• linoleic acid
• intestinal protectants and adsorbents.
CH RONIC DIARRHEA 21
Psyllium mucilloid
Feeding psyllium mucilloid may promote colonic heal­
ing in horses with RDC. In other animal species, psyl­
lium mucilloid has been demonstrated to increase the
concentration of short-chain fatty acids of the large
bowel, and short-chain fatty acids can positively influ­
ence colonic mucosal repair. The amount and duration
of psyllium mucilloid administered orally that is
required to alter the colonic concentration of short­
chain fatty acids and the role of short-chain fatty acids in
repair of RDC in horses is unknown. Continuous feed­
ing according to manufacturers' recommendations for
3-6 months is suggested, or feeding 30-60 g (1-2 oz) of
psyllium mucilloid once or twice daily for the same dura­
tion may be considered. Horses should be returned to
their usual diet over a period of several days to decrease
the risk of inducing other digestive disorders.
Misoprostol
Specific chemotherapy for RDC remains speculative
because the pathophysiology is unknown. Because
misoprostol has been demonstrated to prevent
phenylbutazone-induced gastrointestinal ulceration in
horses, administration of this synthetic analog of
prostaglandin E) may be of benefit in horses with RDC.
The drug can be administered orally (2.5-5 J.1g/kg
q. 12 h or 2 J.1g/kg q. 6 h). The latter regimen may
better mimic constitutive production of prostanoids by
cyclooxygenase-l (COX-I), whose inhibition may be
associated with the toxic effects of NSAIDs. It is
unknown if misoprostol will improve colonic healing or
be cytoprotective for the colon; side-effects may include
colic. The author has not observed colic in horses
receiving misoprostol at a dose of 2 J.1g/kg q. 6 h.
Sucra/fa te
Because sucralfate has been demonstrated to diminish
intestinal discomfort and reduce intestinal disturbances
following radiotherapy for pelvic cancer in humans, it
has been suggested that sucralfate may promote healing
of colonic ulcers in horses. The extent to which sucral­
fate influences NSAID-induced colonic disease in
horses has not been determined. Because the drug is
relatively inexpensive and has few side effects, adminis­
tration of sucralfate (22 mg/kg p.o. q. 8-12 h) does not
appear to be contraindicated for treating RDC. Other
medications used routinely to treat gastric ulceration in
horses (antacids, proton-ion pump blockers such as
omeprazole, and H2-receptor antagonists such as raniti­
dine) would not be expected to be effective because
their principal mechanism of action is to decrease
gastric acidity.
441
21 ACUTE AND CHRONIC DIARRHEA
Metronidazole and sulfasalazine
In humans, NSAID-induced enteropathy has been
treated with sulfasalazine and metronidazole with vary­
ing success. These agents have not been evaluated for
the management of colonic lesions induced by NSAIDs
in horses. Metronidazole has anti-inflammatory effects
in the intestinal tract of other species, including models
of NSAID-enteropathy. Metronidazole can decrease the
neutrophilic adherence to intestinal mucosa in experi­
mental NSAID-induced enteropathy. Adherence of
neutrophils to vascular endothelium contributes to
NSAID-induced gastric mucosal injury, suggesting that
metronidazole may be of benefit in RDC. The author
has used metronidazole in the management of RDC in
horses at a dose of 1 0- 1 5 mg/kg p.o. b.i.d.
Linoleic acid
Oral administration of dietary linoleic acid may be
effective for managing NSAID-induced gastric ulcera­
tion because linoleic acid may result in modulation of
the profile of pro-inflammatory eicosanoids produced
during inflammation. Administration of corn oil has
been suggested, presumably because it has been
demonstrated to increase gastric prostaglandin E2 in an
experimental model of gastric ulceration in rats. In
addition corn oil can provide additional dietary calories
that will be absorbed principally by the distal small
intestine. The benefits of feeding omega-3+/omega to
fatty acid diets to prevent or help repair intestinal
mucosal injury are unknown in the horse.
Intestinal protectants and adsorbants
The benefit of intestinal protectants and adsorbants,
such as bismuth subsalicylate, mineral oil, and activated
charcoal, for treating RDC is unknown and cannot be
recommended. Although these agents generally do not
cause harm, it is unclear whether the salicylate liberated
from bismuth subsalicylate in the colon could potenti­
ate NSAID-induced colitis.
PROGRESSION AND PROGNOSIS
Owners should be advised that horses with RDC may
experience episodes of colic during medical manage­
ment, these episodes should follow a trend of decreas­
ing frequency and severity. If a colonic stricture
develops, the severity, duration, or frequency of
episodes may progress. Owners should be advised that
successful medical management is dependent upon
compliance to recommendations by the veterinarian.
Continued physiologic stress, administration of
NSAIDs, and feeding roughage may promote recur-
442
rence or exacerbate the condition and ultimately lead
to stricture of the right dorsal colon. Colonic stenosis
has been described in horses with chronic, severe RDC,
and stenosis or stricture of the colon generally requires
surgical management and entails a guarded to poor
prognosis. Early recognition of the problem prior to the
development of irreversible lesions and dietary man­
agement with elimination or restriction of roughage
may enable recovery in some horses, thereby obviating
the need for surgical intervention.
Several methods are available for monitoring the
progress of horses with this condition. Some horses will
have occasional episodes of mild abdominal pain prior
to resolution of signs. Such horses may require surgical
evaluation and management. Monitoring the PCV and
concentration of total protein is of benefit. These values
should increase with resolution of colonic inflamma­
tion, usually over a period of 2-8 weeks. If the right
dorsal colonic wall appears thickened sonographically,
repeated ultrasonographic examination may facilitate
assessment of relative changes.
Chronic diarrhea in adult
horses - other causes
T Mair
INTRODUCTION
A wide variety of diseases have been reported to result
in chronic diarrhea in horses. In some of these diseases,
diarrhea is a minor or unusual presenting sign of the
disease, for example, diarrhea is sometimes seen in
horses affected by the following conditions
• abdominal abscess (see Chapter 1 7)
• abdominal neoplasia (see Chapter 1 7)
• cecal impaction (see Chapter 1 4)
• chronic intussusceptions
• chronic renal failure
• congestive heart failure
• Cushing's disease
• enteroliths (see Chapter 1 5)
• grass sickness (see Chapter 17)
• hyperlipemia (see Chapter 19)
• intestinal diverticulae (see Chapter 13)
• malnutrition/starvation
• myeloproliferative leukemia
• non-strangulating intestinal infarction (see
Chapters 13 and 15)
 CHRONIC DIARRHEA 21

• pancreatic diseases (see Chapter 17) tion may persist for several months. Systemic antibiotics
• peritonitis (see Chapter 17). are of questionable value in these cases even when
sensitivity test results are followed. Affected animals are
Toxic causes of diarrhea are described in Chapter 20.
a potential health hazard to other animals and to
humans, and they should be isolated and treated symp­
tomatically until such time as shedding in the feces can
IDIOPATHIC CHRONIC DIARRHEA
no longer be detected.

Some horses with chronic diarrhea remain undiag­

nosed after exhaustive diagnostic testing, and even after
INTESTINAL TUBERCULOSIS
post-mortem examination. These horses are described
as being affected by idiopathic chronic diarrhea. In
Mycobacterium tuberculosis (usually avium) and
many cases, the horses are well in other respects, have
Mycobacterium paratuberculosis can rarely cause chronic
normal serum chemistries, and maintain normal body
granulomatous enteritis and colitis, presenting clini­
condition. The diarrhea is a nuisance and management
cally with chronic weight loss, inappetance, and chronic
problem, rather than a significant veterinary or welfare
diarrhea. Other signs relating to involvement of other
problem. It is assumed that many of these cases are
body systems (including the skin, lungs, and skeleton)
caused by physiological osmolality disturbances or
may also be present. The diarrhea may be intermittent
motility abnormalities affecting the cecum and large
or persistent. Ulceration of the mucosal surface of
colon.
the colon can occur in some affected horses.
Some h orses with idiopathic chronic diarrhea will
Histopathologically, acid-fast bacteria can be found in
respond to dietary modification. If the affected horse is
the gut wall and mesenteric or colonic lymph nodes. In
stabled, then turning it out to pasture and maintaining
some cases, acid-fast bacteria may be identified in rectal
it on a grass only diet may be helpful. Alternatively, a
biopsies. Culture of the organisms from feces takes
horse affected by idiopathic chronic diarrhea at pasture
several weeks and is frequently unsuccessful, although
may benefit from being stabled and maintained on a
acid-fast organisms can sometimes be found in fecal
dry hay diet. Fresh water as well as water spiked with
smears. The intradermal skin test is unreliable in horses
electrolytes should be available to these horses at all
because of the presence of many false positive reactions.
times.
There are no reports of attempts to treat affected
Other treatments that can be beneficial in the man­
horses, although isoniazid (5-20 mg kg-l dayl) and/or
agement of idiopathic diarrhea include the following
rifampin (10 mg/kg b.i.d.) might be considered.
(see also General principles of treatment of chronic
diarrhea in adult horses)

• iodochlorhydroxyquin NEOSPORA CANINUM

• metronidazole or poten tiated sulfonamides
• anthelmintics ( larvicidal doses) Neospora caninum has been diagnosed as a possible cause
• transfaunation of colitis in a middle aged horse that demonstrated
• probiotics signs of chronic diarrhea and anemia. At necropsy,
• codeine phosphate and other motility-modifYing tachyzoites of N. caninum were identified in sections of
drugs the colon and mesenteric lymph nodes.
• acetic acid (vinegar) .

HISTOPLASMOSIS
CHRONIC SALMONELLOSIS
Histoplasmosis has been identified in a small number of
Chronic salmonellosis appears to be a rare cause of horses affected by chronic diarrhea and weight loss.
chronic diarrhea in adult horses. Although Salmonella Although there are enzootic areas of histoplasmosis in
spp. can frequently be cultured from the feces of horses the USA, cases are rarely reported.
Histoplasma capsula­
with chronic diarrhea, other underlying causes of the tum has been diagnosed as a cause of granulomatous
diarrhea (such as cyathostomosis, lymphosarcoma, colitis, resulting in chronic diarrhea and protein-losing
inf1ammatory bowel disease, etc.) may be present. Some enteropathy. The organism can also cause peritonitis,
horses recovering from acute salmonellosis will be pulmonary infection, and abortion. Diagnosis is
affected by chronic or intermittent diarrhea and achieved by bowel wall biopsy. Skin tests are unreliable.
remain persistent shedders of Salmonella spp.; this situa- No attempts at treatment have been reported.

443
21 ACUTE AND CHRONIC DIARRHEA

GIARDIASIS PERITONITIS

Giardia equi infection has been described as a rare cause Diarrhea is an unusual presenting clinical sign associ­
of chronic diarrhea, decreased appetite, and abdominal ated with peritonitis. The disease is described in detail
pain in adult horses, but the significance of the proto­ in Chapter 1 7 .
zoal organism is uncertain; it can be detected in the
feces of some normal foals and adult horses. Diagnosis
of giardiasis should be based on the exclusion of other
causes of chronic diarrhea (this is difficult to achieve in INTESTINAL LYMPHANGECTASIA
many cases), the repeated detection of giardial cysts in
Lymphangectasia involves a disturbance of lymphatic
the feces (by zinc sulfate centrifugal flotation or
drainage of the intestine, resulting in loss of protein­
immunofluorescence), and response to treatment with
rich lymph into the intestinal lumen. This disease was
metronidazole.
diagnosed at post-mortem examination in one horse
that had a history of intermittent diarrhea and weight
loss. The affected horse had hypoproteinemia and an
TRICHOMONAS EQUI abnormal oral glucose absorption curve. No specific
" �W-'''' ,,", i''-�,h".' ,,' "'"' ,," ',' ",*""m"1)...,""�+,tI"C �,,, oii!> "'J,'"''''''',�",", """'" .,,¥ """
cause was identified, and no treatment was described.
Trichomonas equi is a common flagellate parasite of the
equine large intestine. Although the organism is com­
monly present in the feces of horses with chronic diar­
INTESTINAL FIBROSIS
rhea, it is unlikely to play any role in the pathogenesis of
diarrhea. Experimental infections with the organism Diarrhea has been recorded in horses and ponies
have failed to cause clinical disease. Chronic fluidity
affected by intestinal fibrosis. Affected animals usually
of the colonic contents in horses with diarrhea may
have a history of chronic weight loss and recurrent
encourage secondary proliferation of the organism.
colic. Thickening of the intestine may be palpable per
However, empirical treatment of horses affected by
rectum. Diagnosis is achieved by surgical examination
diarrhea where the organism is present might be con­
and biopsies that show submucosal fibrosis of the small
sidered if another cause cannot be identified. Diagnosis
intestine. The only reported treatment has been resec­
is achieved by identifYing the organism microscopically
tion of affected segments of bowel.
in wet fecal smears.

BIBLIOGRAPHY
EIMERIA LEUKARTI
Differential diagnosis and evaluation of
Eimeria leukarti is a protozoan parasite that is adapted to chronic diarrhea in the adult horse
the small intestine of horses, and has been associated
Love S, Mair T S, Hillyer M H ( 1 992) Chronic diarrhoea in
with mild, self-limiting diarrhea in juvenile horses. adult horses: a review of 5 1 referred cases. Vet. Rec.
Oocysts are commonly found in the feces of normal 1 30:2 1 7-19.
foals. Experimental infections with the organism have Mair T S, Cripps P ], Ricketts, S W ( 1 993) Diagnostic and
failed to cause clinical disease and it is unlikely that this prognostic value of serum protein electrophoresis in
horses with chronic diarrhoea. Equine Vet. ] 25:324-6.
organism is a significant cause of diarrhea in adult
Merritt A M ( 1 983) Chronic diarrhoea. In Current Therapy in
horses. Equine Medicine 1st edn, N E Robinson (ed. ) . W B
Saunders, Philadelphia, p. 2 1 6.
Morris D D , Whitlock R H , Palmer] E ( 1 983) Fecal leukocytes
and epithelial cells in horses with diarrhea. Cornell Vet. 73:
265-74.
HEPATIC DISEASE Pearson E G , Smith B B and McKim] M ( 1 987) Fecal blood
determinations and interpretation . Proe. Am. Assaf. Equine
Chronic hepatic disease is a rare cause of diarrhea. Praet. 33:77-8 1
Alterations in intestinal microflora, portal hyperten­ Ragle C A and Meagher D M ( 1987) Abdominal auscultation
as an aid to diagnosis of sand colic. Proc. Am. Assoc. Equine
sion, and deficiency of bile acids may be involved in the
Praet. 33:521-523
pathogenesis. The diagnosis and treatment of chronic Rantanen N W ( 1 986) Diseases of the abdomen. Vet. Clin. N.
hepatic diseases are discussed in Chapter I g . Am. Equine Praet. 2:67-88

444

General principles of treatment of chronic
diarrhea in adult horses
Hansen T 0 ( 1 994) Treatment of chronic diarrhoea in
horses. Camp. Cant. Educ. Pract. Vet. 1 6 : 1 490-2.
Harris P A, Frape D L, ]effcott L B , Lucas D M, Meyer H and
Savage C] ( 1 995) Nutritional aspects of me tabolic
diseases. In The Equine Manual, A] Higgins and I M
Wright (eds ) . W B Saunders, London, pp. 1 75-85.
Larval cyathostomosis
Giles C], Urquhart K A and Longstaffe ] A ( 1 985) Larval
cyathostomiasis (immature trichonema-induced
enteropathy) : a report of 1 5 clinical cases. Equine Vet. J
27:29-40
Love S, Mair T S and Hillyer M H ( 1 992) Chronic diarrhoea
in adult horses: a review of 51 referred cases. Vet. Rec.
1 30 : 2 1 7-2 1 9
Mair T S ( 1 993) Recurrent diarrhoea i n aged ponies
associated with larval cyathostomiasis. Equine Vet. J
25:1 61-1 63
Mair T S ( 1 994) Outbreak of larval cyathostomiasis among a
group of yearling and two-year-old horses. Vet. Rec.
1 35:598-600
Mair T S, Cripps P] and Ricketts S W ( 1 993) Diagnostic and
prognostic value of serum protein electrophoresis in
horses with chronic diarrhoea. Equine Vet. J 25:32-326
Mair T S and Pearson G R ( 1 995) Multifocal non­
strangulating intestinal infarction associated with larval
cyathostomiasis in a pony. Equine Vet.J 2 7 : 1 54-155
Mair T S, Sutton D G M and Love, S (2000) Caeco-caecal and
caeco-colic intussusceptions associated with larval
cyathostomosis in four young horses. Equine Vet. J
32:77-80
Paul] W ( 1 998) Equine larval cyathostomosis. Camp. Cant.
Educ. Pract. Vet. 20:509-5 1 4
Reid S W], Mail' T S , Hillyer M H and Love S ( 1 995)
Epidemiological risk factors associated with a diagnosis of
clinical cyathostomiasis in the horse. Equine Vet. J
27:1 27-130
Reilly G A C, CassidyJ P and Taylor S M ( 1 993) Two cases of
diarrhoea in horses associated with larvae of the small
strongyles. Vet. Rec. 1 32:267-268
Uhlinger C A ( 1 990) Effects of three anthelmintic schedules
on the incidence of colic in horses. Equine Vet. J
22:25 1-254
Uhlinger C A ( 1 99 1 ) Equine small strongyles: epidemiology,
pathology and control. Camp. Cant. Educ. Pract. Vet. 1 3:863
Xiao L H, Herd R P and Majewski G A ( 1 994) Comparative
efficacy of moxidectin and ivermectin aginst hypobiotic
and encysted cyathostomes and other equine parasites.
Vet. Parasitol. 53:83-90
Strongylosis
Austin S M ( 1 994) Large strongyles in horses. Camp. Cant.
Educ. Pract. Vet. 1 6:650-657
Greatorex ] C ( 1 977) Diagnosis and treatment of 'verminous
aneurism' formation in the horse. Vet. Rec. 1 0 1 : 1 84-187
Love S ( 1 992) Parasite-associated equine diarrhea. Camp.
Cant. Educ. Pract. Vet. 14:642-649
Wallace K D, Selcer B A and BechtJ L ( 1 989) Technique for
transrectal ultrasonography of the cranial mesenteric
artery of the horse. Am. J Vet. Res. 50: 1 695-1697
CHRONIC DIARRHEA 21
Wallace K D, Selcer B A, Tyler D E and Brown] ( 1 989)
Transrectal ultrasonography of the cranial meseneric
artery of the horse. Am. J Vet. Res. 50: 1 699-1703.
Chronic inflammatory bowel disease and
intestinal neoplasia
Love S, Mair T S and Hillyer M H ( 1 992) Chronic diarrhoea
in adult horses: a review of 5 1 referred cases. Vet. Rec.
1 30:2 1 7-219
Platt H ( 1 986) Chronic inflammatory and Iymphoproliferative
diseases of the equine small intestine. J Camp. Patho!.
96:671-684
Roberts M C ( 1985) Malabsorption syndromes in the horse.
Camp. Cant. Educ. Pract. Vet. 7:S637-S646
Scrutchfield L ( 1 987) Chronic diarrhea. In Current Therapy in
Equine Medicine 2nd edn, N E Robinson (ed. ) . W B
Saunders, Philadelphia, pp. 1 00-102
Sand enteropathy
Bertone ]], Traub-Dargatz ] L, Wrigley R W ( 1 988) . Diarrhea
associated with sand in the gastrointestinal tract of horses.
J Am. Vet. Med. Assoc. 1 93 : 1 409- 1 4 1 2
Denberg T ( 1 979) Equine colic associated with sand
impaction of the large colon. Can. Vet. J 20:269-272
Hammock P D, Freeman D E and Baker G ] ( 1998) Failure of
psyllium mucilloid to hasten evacuation of sand from the
equine large intestine. Vet. Surg. 27:547-554
Hansen T 0 ( 1 994) Treatment of chronic diarrhea in horses
Camp. Cant. Educ. Pract. Vet. 1 6: 1 490-1492
Jones S L, Snyder] R and Spier S] ( 1 998) Obstructive
conditions of the large intestine. In Equine Internal
Medicine, S M Reed and W M Bayly (eds ) . W B Saunders,
Philadelphia, pp. 682-694
Equine right dorsal colitis
Cohen N D , Carter G K, Mealey R H, Taylor T S ( 1 995)
Medical management of right dorsal colitis in 5 horses
( 1 987-1993 ) . J Vet. Int. Med. 9:272-276
Karcher L F, Dill S G, Anderson W I, et al ( 1 990) Right dorsal
colitis. J Vet. Int. Med. 4:247-253
Chronic diarrhea in adult horses - other
causes
Barker I K. and Remmler 0 ( 1 970) Experimental Eimeria
leuckarti infection in ponies. Vet. Rec. 86:448-449
Bennett S P and Franco D A ( 1 969) Equine protozoan
diarrhea (equine intestinal trichomoniasis) at Trinidad
racetracks. J Am. Vet. Med. Assoc. 154:58-60
Chineme C N, Tulpule S S and ]amdar M N ( 1979) Enteritis
associated with Eimeria leuckarti infetion in donkeys. Vet.
Rec. 1 05 : 1 26
Cline] M, Schlafer D W, Callihan D R, Vanderwall D and
Drazek F J ( 1 99 1 ) Abortion and granulomatous colitis due
to Mycobacterium avium complex infection in a horse. Vet.
Patho!. 28:89-9 1
Damron G W ( 1976) Gastrointestinal trichomonads in horses:
occurrence and identification. Am. J Vet. Res. 37:25-28
Goetz T E and Coffman] R ( 1984) Ulcerative colitis and
protein losing enteropathy associated with intestinal
salmonellosis and histoplasmosis in a horse. Equine Vet. J
1 6:439-441
445
21 ACUTE AND CHRONIC DIARRHEA
Gray M L, Harmon B G, Sales L and Dubey J P ( 1 996)
Visceral neosporosis in a 1 0-year-old horse.]. Vet. Diagn.
Invest. 8: 1 30-133
Johnson P J, Pace L W, Mrad D R, Turnquist S E, Moore L A
and Ganjam V K ( 1 997) Small intestinal fibrosis in two
horses . ]. Am. Vet. Med. Assoc. 2 1 1 : 1 0 1 3-- 1 0 1 7
Kirkptrick C E and Skand D L ( 1 989) Giardiasis i n a horse.
]. Am. Vet. Med. Assoc. 197: 1 63-164
Kirkptrick C E ( 1 989) Giardiasis in large animals. Compo Cont.
Educ. Pract. Vet. 1 1 :80-84
LofstedtJ andJakowski R M ( 1 989) Diagnosis of avian
tuberculosis n a horse by use of liver biopsy. ]. Am. Vet.
Med. Assoc. 194:260-262
Love S ( 1 992) Parasite-associated diarrhea. Compo Cont. Educ.
Pract. Vet. 1 4:642-649
Love S, Mair T S and Hillyer M H ( 1 992) Chronic diarrhoea
in adult horses: a review of 51 referred cases. Vet. Rec.
1 30:2 1 7-2 1 9
Lyons E T , DrudgeJ H and Tolliver S C ( 1 988) Natural
446
infection with Eimeria leuckarti: prevalence of oocysts in
feces of horse foals on several farms in Kentucky during
1986. Am. ]. Vet. Res. 49:96-98
Merritt, A.M. ( 1 994) Chronic diarrhoea in horses: a summary.
Vet. Med. 130: 2 1 7-219
Milne E M, Woodman M P, Rowland A C, Patrick CJ and
Arthur SJ ( 1 994) Intestinal lymphangectasia as cause of
chronic diarrhoea in a horse. Vet. Rec. 134:603-604
Platt H ( 1986) Chronic inflammatory and
lymphoproliferative diseases of the equine small intestine.
]. Compo Palhol. 96:671-684
Scrutchfield L ( 1 987) Chronic diarrhea. In Current Therapy in
E-quine Medicine 2nd edn, N E Robinson ( ed . ) . W B
Saunders, Philadelphia, pp. 100-102
Traub-DargatzJ L, Schultheiss P C, Kiper M L, et al. ( 1 992)
Intestinal fibrosis with partial obstruction in five horses
and two ponies. ]. Am. Vet. Med. Assoc. 201 603-607
Wheeldon E B and Greig W A ( 1977) Globidium leuckarti
infection in a horse with diarrhoea. Vet. Rec. 100: 1 02-103
22
Clinical evaluation of the foal
Evaluation of the foal with
colic
CS Cable
INTRODUCTION
Colic in the foal is commonly encountered in equine
practice and has numerous etiologies. Evaluation of the
foal with colic is a diagnostic challenge since the rectal
examination - one of the primary tools used in the eval­
uation of colic in the adult horse - cannot be used in foals.
Furthermore, foals tend to be less tolerant of abdominal
pain than adults, making it difficult to distinguish
between conditions requiring medical or surgical
therapy. A significant number of foals with enteritis will
be initially examined for abdominal pain. Evaluation of
the foal with colic should include a thorough history, sig­
nalment, physical examination, clinicopathologic data,
and other diagnostic aids such as ultrasound examina­
tion of the abdomen and/or radiographic study of the
abdomen (with or without contrast medium) . The infor­
mation obtained from these procedures can narrow the
list of differential diagnoses and help make the decision
as to whether medical or surgery therapy is warranted.
HISTORY
The historical events surrounding colic in the foal can
provide clues as to the true etiology of the colic episode.
Especially in the neonate, the peripartum events should
be discussed. Normal parameters for neonates are
•
•
gestational age - mean 341 days (range 3 1 5-365)
time to suckling reflex - normally suckles within 20
minutes
• time to standing - mean 57 minutes (range 1 5- 1 65)
• time to nursing from mare - mean III minutes
(range 35-420) .
In general, a foal that is not able to stand and nurse
by 2 hours of age should be considered potentially
abnormal.
Adequate intake and/or absorption of colostrum
should be evaluated by immunoglobulin (IgG) testing.
Inadequate immunoglobulin l evels can result from
m aternal disorders (premature lactation or agalactia) ,
or from illness in the foal. A foal with partial or com­
plete failure of passive transfer will be much more sus­
ceptible to infectious causes of colic (enteritis) , than
the foal with adequate passive transfer.
Other information that should be obtained includes
• age of the foal at the onset of colic
• specific signs, e.g. bruxism, milk or food
regurgitation (reflux), nursing behavior, passage of
meconium and/or character of feces, straining to
urinate or defecate, rolling and/ or lying on the
back
• drugs administered and their effect
• previous or current disease on the farm and its
treatment, e.g. diarrhea, respiratory infection (e.g.
Rhodococcus equi) .
Furthermore, previous or concurrent disease in the
affected foal such as septicemia or musculoskeletal
disorders m ay predispose to gastrointestinal ileus,
ulceration, and/or peritonitis. Neonates undergoing
intensive care, especially those with premature body
449
22 GASTROINTESTINAL DISEASE IN THE FOAL
systems are predisposed to functional obstruction of
the gastrointestinal tract resulting from ileus. Older
foals with a history of diarrhea and/or chronic colic
and failure to thrive are more likely to have intermit­
tent or chronic ileocecal intussusception or gastric
ulceration.
SIGNALMENT
Age at the onset of signs of colic can help form the dif­
ferential diagnosis in a foal with colic, especially for the
neonate. For example, foals with atresia coli, lethal
white syndrome ( ileocolonic aganglionosis) , or meco­
nium impactions usually present within 1 2-36 hours of
birth with a distended abdomen and failure to pass
meconium. Neonates with uroperitoneum usually pre­
sent at 3 days of age with depression, distended
abdomen, and/or abnormalities with urination.
The breed of the horse can also help indicate disease
processes, for example, miniature horse foals are quite
predisposed to small colon impaction due to fecaliths.
EVALUATION AND PHYSICAL
EXAMINATION
A complete physical examination is paramount in the
evaluation of the foal with colic, especially in the new­
born, as overlooking other congenital disorders not
associated with the cause of the abdominal pain can
lead to a disastrous end result, as well as needless waste
of money by the owners.
Observation from a distance
Examination of the foal should begin by observing the
foal in its environment without restraint. Valuable infor­
mation can be obtained by simply standing quietly at
the side of the stall. By observing the foal with the mare
in a stall or in a small paddock, the clinician can get a
better idea of the true severity of pain, as foals that are
being restrained often can not or will not display mild
to moderate signs of pain. The foal's nursing behavior
can also be observed, for example the foal that nurses
then detaches from the teat early and retreats to grind
it� teeth and salivate, might indicate possible gastric
ulceration.
Foals should also be observed for abnormalities of
the musculoskeletal system such as lameness and angu­
lar or flexural deformities; these are problems that the
owner may or may not be aware of. Lameness especially
warrants closer investigation as septic arthritis requires
immediate treatment and m ay decrease the prognosis
450
Figure 22.1 Foal with a ruptured bladder straining to
urinate frequently, the posture is characterized by spread
hind legs, a sunken back (concave shape), and elevated tail
significantly, the owner must be made aware of the
problem and appraised as to the potential for treatment
at this time or in the near future.
Foals that are straining can be observed in the
stall, to ascertain if they are straining to defecate or
urinate. Foals that are straining to defecate arch their
backs (convex shape) and elevate their tails, while
foals straining to urinate will usually spread their legs,
sink their backs (concave shape) and elevate their
tails (Figure 22. 1 ) . This distinction is important and
can help guide further diagnostics. Methods to pre­
vent excessive straining should be used such as
epidural anesthesia or lidocaine enemas. At the
author' s hospital foals have been seen to develop sec­
ondary uroperitoneum, because of excessive straining
to urinate or defecate.
Physical examination
After the distant examination is complete the foal
should be restrained for a thorough physical examina­
tion. During the physical examination it is again very
important to evaluate all body systems, not just the
gastrointestinal system. The age of the foal will dictate
normal parameters for the heart rate and respiratory
rate. A neonate will have an elevated heart rate and
respiratory rate compared to an older foal. Neonates
less than 1 week of age will have heart rates in the
range of 70-100 bpm and respiratory rates in the
range of 20-40 breaths per min, whereas older foals
will have heart rates in the range of 30-60 bpm and
respiratory rates in the range of 1 2-20 breaths per
min (Table 22. 1 ).

TeWl U.1 "rmal\fIl." ·tf hSrt rate�telplratotYiF.te. capilfary rE\flfl time,and rHtlI:tempe.'''''' 'fI�. .
Age Heart rate (bpm)
newborn 40-80 (at birth)
130-150 (during attempts
to stand)
70- 100 (first day)
7 days 70-100
3 months 30-60
Cardiovascular system
The cardiovascular system should be evaluated care­
fully. Mucous membranes should be moist and pink,
with a capillary refill time of 1-2 seconds. Tachycardia
can represent pain, hypovolemia, endotoxemia, and/ or
septicemia. However, bradycardia may represent hypo­
glycemia which may warrant immediate treatment with
intravenous dextrose. Bradycardia can also be present
with severe hyperkalemia as can be seen with uroperi­
toneum. Murmurs are only common during the neo­
natal period, usually caused by the incomplete closing
of the ductus arteriosus. This often results in a loud,
grade I-IV systolic left-sided murmur at the third inter­
costal space.
Respiratory system
The respiratory system should also be evaluated care­
fully. Breath sounds are easily auscultated in the new­
born, unlike the adult. Foals should be evaluated as to
the pattern of breathing and for any lack of breath
sounds indicating severe respiratory disease, greatly
increasing complications while under anesthesia.
Neonates should also be evaluated for the possibility of
fractured ribs - displaced rib fractures can lead to
laceration of the lung tissue and pneumothorax.
Gastrointestinal system
The gastrointestinal system should, of course, be evalu­
ated carefully for evidence of the cause of colic.
Abdominal distension can be detected on visual exami­
nation. Abdominal distension can be caused by fluid
inside or outside the gastrointestinal tract as well as gas
distension of the small or large intestine (see
Differential diagnosis and evaluation of the foal with
abdominal distension) . Unlike the adult, gas or fluid
distension of the small intestine can cause visible
CLINICAL EVALUATION OF THE FOAL 22
Capillary
Respiratory rate Temperature refill time
(breaths per min) (OC) (sec)
60-80 (first hour) 37.2-38.9 <2
20-40 (first day)
20-40 38.0-39.0 <2
12-20 37.5-38.5 <2
abdominal distension in the foal, whereas colonic
distension is more likely to cause visible abdominal
distension in the adult horse (see Chapter 1 7 ) .
Excessive fluid within the abdomen can be caused by
• ascites
• peritonitis
• uroperitoneum
• hemoperitoneum.
Fluid and/ or gas distension of the intestinal tract can be
caused by either enteritis or bowel obstruction (stran­
gulating or non-strangulating) and can not be defini­
tively diagnosed without radiographs or an ultrasound
examination of the abdomen. Abdominal distension can
be measured by shaving some hair on the dorsal aspect
of the foal's back as a marker and using white tape to
measure the circumference of the abdomen. This can be
effective at sequential examinations to determine if the
foal's abdomen is increasing or decreasing in size.
Rectal examination
A digital rectal examination can be performed, espe­
cially in the neonate to check for the presence of
retained meconium. The m econium is hard and
pelleted and usually felt at the brim of the pelvis. A
digital rectal examination should also be performed in
neonates without a history of meconium passage to
check for any fecal straining. The lack of fecal straining
and only the presence of mucus are indicative of a con­
genital disorder such as atresia coli or ileocolonic agan­
glionosis. If a digital examination is to be performed
the rectal temperature should be taken first. If the foal
is febrile and' colicky' , enteritis should be suspected.
Auscultation and palpation
Auscultation of the abdomen can be performed to
determine if there is gastrointestinal motility.
451
22 GASTROINTESTINAL DISEASE IN THE FOAL
Simultaneous percussion and auscultation and a char­
acteristic 'ping' can determine the presence of a gas­
distended viscus. Abdominal ballottement can be used
to detect fluid present within the abdominal cavity.
Abdominal palpation can be rewarding in some foals,
however it is not useful if the abdomen is tense or in
older foals. Palpation of the external umbilicus should
be performed in all young foals to evaluate for
drainage, heat, or enlargement. Umbilical hernias
should also be evaluated and determined if reducible.
Non-reducible hernias usually indicate entrapped
bowel. A transabdominal ultrasound examination is
needed to fully evaluate the umbilical remnants. Intact
male foals should also be palpated externally in the
scrotal area to determine if an inguinal ( scrotal) hernia
is present. If present, it must be determined if the her­
nia is reducible. Congenital inguinal hernias can be
manually reduced multiple times a day and after a few
weeks the vaginal ring will often decrease in size with
resolution of the hernia.
Examination of the eyes
An examination of the anterior chamber of the eye
should also be part of the physical examination of a
neonate. Uveitis characterized by fibrin within the ante­
rior chamber may indicate sepsis or blunt trauma to the
eye. The yellow fibrin in the anterior chamber may
make the normally brown iris appear green.
OTHER DIAGNOSTIC PROCEDURES
Nasogastric intubation
Another diagnostic procedure that can be performed
on foals of all ages is the passage of a nasogastric tube.
Obtaining gastric reflux in the neonate can be difficult,
even with a distended stomach. However, if gastric
reflux is obtained the presence of a functional or
mechanical obstruction of the stomach or small intes­
tine is indicated. For neonates, a stallion catheter can
often be used to check for reflux, in older foals a small
sized nasogastric tube can be used. Older foals may
need to be sedated to prevent injury to the foal, han­
dlers, or veterinarian.
Sedation during examination
Foals that are in severe pain can be hard to restrain, and
are dangerous and difficult to examine. Sedation of
these foals is warranted to prevent injury to handlers,
technicians, clients, and veterinarians. During the
examination, small doses of xylazine (0.5 mg/kg i.v.)
can be administered to allow both the physical
452
examination to proceed and the placement of ajugular
catheter to administer further medications and intra­
venous fluids. Xylazine, an alpha agonist, is a good
choice for short-acting sedation, also providing analge­
sia. The effects of xylazine usually last from 1 0-20 min­
utes with an intravenous dosage. This drug dosage can
also be administered with butorphanol, a mixed opioid
agonist/antagonist, to provide additional analgesia and
prolong the sedative effects. Other alpha agonists such
as detomidine, are not used in the author's hospital for
sedation of foals because of the profound sedation they
impart, as well as the duration of action which may
delay the decision for surgery. An overdose of the alpha
agonists can be reversed with yohimbine.
Radiography ( see section on Diagnostic imaging)
Although, because of their size, a rectal examination
can not be performed in foals, abdominal radiographs
can be taken easily. Lateral views are the standard views
taken, with the foal standing or in lateral recumbency
after sedation . Dorsoventral views are usually not neces­
sary, and can be quite stressful for a foal with moderate
to severe abdominal distension. From these radi­
ographs the nature of the distension - small versus large
intestine - can be determined. Large loops of distended
small intestine with hairpin turns, for instance, repre­
sent an obstruction of the small intestine. Fluid outside
the gastrointestinal tract can also be identified.
Contrast radiography can be used to identify
obstruction of the gastrointestinal tract and/or disrup­
tion of the u rinary tract. Barium can be used to identify
obstruction of the distal or proximal gastrointestinal
tract. Barium can be administered through a nasogas­
tric tube at 5 ml/kg (30% w/v) to identify delayed gas­
tric emptying and/or duodenal stricture. It has also
been reported that barium administered via a Foley
catheter as an enema at a dosage of 20 ml/kg has been
used to identify obstructions of the small and large
colon. According to one report, meconium impactions
and atresia coli have been identified using this
technique.
Ultrasonography (see section on Diagnostic imaging)
Ultrasonography has also been used to identify lesions
of the gastrointestinal tract in foals and adults, and can
provide valuable information for the foal with colic
and/ or distended abdomen. A 5-MHz probe can be
used to evaluate the abdomen and determine the
quantity and character of peritoneal fluid.
Abdominocentesis can be performed after fluid is iden­
tified to decrease the risk of enterocentesis.
Ultrasonography can also be used to identify abscesses
or enlarged lymph nodes within the gastrointestinal
 CLINICAL EVALUATION OF THE FOAL 22

tract and abnormalities or abscesses of the umbilical for best viewing. The mucosal surface of the duodenum
remnants. Both small and large intestine can be imaged should be evaluated for erosions, ulceration, or stric­
to determine wall thickness and motility. The small tures.
intestine can be imaged also to determine lumenal size
(diameter) . In a recent report, adult horses with acute Abdominocentesis
abdominal pain were evaluated via transabdominal
Abdominocentesis, a mainstay for evaluation of colic in
ultrasound prior to abdominal surgery. Horses within
the adult, is often not performed in the foal due to fears
this study with abnormal small intestine and lack of
of puncture or laceration of the bowel wall (see Chapter
motility detected on ultrasound prior to surgery, were
2 ) . Abdominocentesis however, can yield significant
found to have 1 00 per cent sensitivity, specificity, and
information in determining the cause of the acute
posi tive and negative predictive values for having a
abdomen or to determine surgical versus medical
strangulating small intestinal lesion at surgery.
therapy. At the author's hospital abdominocentesis in
Although a similar study needs to be performed in foals,
the foal is not performed before a complete transab­
from this study, it is highly predictive that foals with
dominal ultrasound examination of the foal has been
abdominal pain and similar ultrasonographic findings
made. This examination can determine the quantity
(dilated, non-motile small bowel) would likely require
and location of peritoneal fluid in the abdomen. Foals
surgery.
with excessive abdominal fluid are good candidates for
abdominocentesis as they can be heavily sedated,
Endoscopy placed in lateral recumbency, and restrained well for
the procedure. To prevent inadvertent laceration of the
Endoscopy is used in foals with abdominal pain to assess
bowel in a foal, a teat cannula is used rather than hypo­
the esophagus, stomach, and proximal duodenum (see
dermic needles. A disadvantage of using a teat cannula
Chapters 2 and 23) . It can also be used to assess the rec­
for abdominocentesis is that an omental hernia may
tum and small colon if other procedures fail to provide
subsequently occur in a small percentage of foals.
a diagnosis. Most commonly endoscopy is used to assess
Although this is a rather benign complication it can be
the stomach for gastric ulceration. The stomach is often
alarming to the owner. A small local block can be per­
assessed to confirm a diagnosis of gastric ulceration and
formed with 2% mepivacaine on the ventral abdomen
to monitor response to treatment. Foals should be
to the right of midline, or where fluid is located,
sedated or even anesthetized if necessary, to facilitate a
although avoiding the spleen and the umbilical rem­
complete endoscopic examination. To assess the
nan ts. A small stab incision is made with a no. 1 5 blade
stomach, foals will often need to be withheld from food
to penetrate skin and the abdominal musculature. The
and water and/or milk for 2-6 hours (depending on
sterile teat cannula is then gently introduced into the
age and amount of intake) before �he examination to
abdomen and fluid is collected for evaluation.
allow the stomach to empty.
Furthermore, from this position foals with uroperi­
Gastroscopy in foals under 1 month of age can be
toneum can have a drain placed to help evacuate the
performed using a scope that is 1 meter in length and
excessive fluid. In older foals abdominocentesis can be
10 mm or smaller in diameter. Older foals (4-6 months
performed from a standing position with an 1 8-gauge
of age) will require an endoscope 2 meters in length to
needle or teat cannula. Abdominocentesis can be per­
evaluate the stomach and duodenum. The endoscope
formed safely in these foals if the foal is adequately
should be passed through the nostril and then into the
sedated and restrained.
esophagus. Passage is continued until the stomach is
entered. At this time, the stomach should be distended
with air to facilitate a complete examination. If the
stomach contains fluid and/or feed material, it may be CLINICOPATHOLOGIC DATA
possible to suction off the fluid, alternatively the proce­
dure can be postponed for several hours. Retention of Information obtained from clinicopathologic tests can
fluid or feed material within the stomach may indicate shed valuable information about the condition and
pyloric or duodenal stricture. The surfaces of the prognosis of the foal. In all foals presented for evalua­
stomach should be evaluated for areas of ulceration or tion of colic, a complete blood count, chemistry panel,
erosions. After complete evaluation of the stomach and venous blood gas analysis should be performed. An
(squamous portion, glandular portion, and margo abdominocentesis should be performed when applica­
plicatus and pyloric antrum) then the scope can be ble. Immunoglobulin levels should also be evaluated in
advanced through the pylorus into the duodenum. neonates.
Again, the duodenum will need to be distended with air The complete blood count can detect and/or

453
22 GASTROINTESTINAL DISEASE IN THE FOAL
confirm sepsis, hypoproteinemia, or anemia. The pres­
ence of band neutrophils (left shift) with or without
toxic changes on the hemogram can also help deter­
mine the severity of infection.
Electrolyte analysis is also very important not only in
the diagnosis of abdominal disorders in foals, but can
direct initial treatment as foals with colic can have sig­
nificant fluid loss or sequestration. Portable electrolyte
units such as the I-Stat, can make electrolyte and blood
gas analysis in the field feasible, quick, and very afford­
able, thus reducing the time between recognition of the
problem and its treatment. Electrolyte values for foals
can be different to those for adults, as foals often have
higher phosphorus and lower sodium values than
adults. Electrolyte values for certain diseases are very
characteristic, such as uroperitoneum and enteritis.
Foals with uroperitoneum usually have
• hyponatremia
• hypochloremia
• azotemia
• hyperkalemia.
Whereas foals with enteritis often have
• hyponatremia
• hypochloremia
• acidemia.
Glucose should also be evaluated in neonates because
foals that are unable to nurse can develop profound
hypoglycemia. Glucose is usually part of a routine
chemistry panel but can also be evaluated with a gluco­
meter or reagent strip in the field for quick analysis.
Venous or arterial blood gas should be a routine part
of the complete clinicopathologic data set on a foal with
abdominal pain. Severe abdominal distention can
lead to respiratory compromise in the young foal.
Furthermore, if neonates are allowed to remain in lat­
eral or dorsal recumbency, they may also have difficulty
maintaining normal oxygenation.
Evaluation of the peritoneal fluid in foals includes
total protein, total nucleated cell count, red blood cell
count, and a cytologic examination. The normal range
of total protein in abdominal fluid is the same in foals
and adults, less than 2.5 g/dl. The total nucleated cell
count however, has been reported to be lower in foals
than adults and as such nucleated cell counts greater
than 1 .5 x 1 09/1 « 1 500 cellS/ill) are considered abnor­
mal. Cytologic examination of the fluid is also impor­
tant in the foal, as in the adult, to screen for bacteria,
plant material, or degenerative changes in the cells.
Foals with suspected uroperitoneum should have a sam­
ple of abdominal fluid evaluated for creatinine levels.
This level should be compared to the creatinine level in
serum, and if the ratio of peritoneal creatinine to serum
454
creatinine is greater than or equal to 2:1 , the diagnosis
of uroperitoneum can be confirmed.
Thorough evaluation of the foal with abdominal
pain including a complete physical examination, and
using additional modalities such as radiography, ultra­
sound, endoscopy, and clinicopathologic data, enables
the veterinarian to compile a list of differential diag­
noses, initiate treatment, and decide between medical
and surgical therapy in the foal. Although these cases
can be challenging, the outcome can be quite success­
ful.
Diagnostic imaging
procedures in the foal
JM Reimer
Ultrasonography of the gastrointestinal tract of the foal
is particularly rewarding because of the h igh incidence
of small intestinal disorders and the reduced digestive
development of the colon in the foal. In contrast to the
value of ultrasonography in identifying small intestinal
problems, the content of the colon often contains a
large amount of gaseous material which impedes ultra­
sonographic evaluation. Plain radiography may be use­
ful in the evaluation of disorders in the foal in which a
large amount of gas is present within the small intestine
or colon. Diaphragmatic hernias and pneumoperi­
toneum can also be diagnosed with radiography.
Contrast radiography is primarily useful in the diagno­
sis of meconium impactions, colonic atresia, and duo­
denal stricture in the foal.
ULTRASONOGRAPHY
The a,bdomen should be clipped as for exploratory
celiotomy. In lieu of clipping, liberal amounts of alco­
hol may be applied to the region to be examined in
some cases. If possible, the examination should be per­
formed with the foal in a standing position because
fluid-filled, edematous, or intussuscepted segments of
intestine, or any excessive peritoneal effusion, will tend
to gravitate to the dependent portion of the abdomen.
Such abnormalities may be difficult to visualize with the
foal in lateral recumbency. Otherwise an attempt
should be made to place the transducer as far beneath
the foal as possible, or to elevate the foal' s abdomen in
order that the transducer may be positioned ventrally.
Ultrasonography performed with the foal in dorsal
recumbency will rarely be rewarding as gas-filled seg­
ments of intestine will often obscure visualization of
 CLINICAL EVALUATION OF THE FOAL 22

underlying structures. Transducer frequencies in the which there is gastric distension due to increase in gas­
range of 7.5-5.0 MHz are recommended for evaluation tric fluid content, the lumen of the stomach and the
of the gastrointestinal tract of the foal. D epth display borders of the stomach may be visible (Figure 22.4) . A
depends in part on limitations of the transducer fre­ gas-fluid interface may also be noted in some cases.
quency used; generally using a depth display of 10 cm
initially, and altering it during the examination is Small intestine
appropriate. If there is a large amount of fluid ingesta
The small intestine normally has few contents within its
or peritoneal effusion present, then a greater depth dis­
lumen (Figure 22.5 ) , and grossly visible motility may be
play will enable visualization of deeper structures and a
difficult to discern. In disease states, the small intestine
lower frequency transducer may be necessary. A shorter
can be evaluated for wall thickness, lumen content,
depth display and possibly a higher frequency trans­
degree of distension, and motility. Amotile loops of
ducer will provide optimal diagnostic images if detailed
intestine that appear taut are typical of complete
imaging of a structure adjacent to the body wall is
mechanical obstruction such as small intestinal volvulus
desired. The presence of gas at any depth obviates an
(Figure 22.6), while a less taut appearance may be seen
increase in depth display as the ultrasound beam will
with incomplete mechanical obstruction, or functional
not penetrate beyond that point.
ileus as seen in some cases of enteritis (Figure 22.7 ) . In
Ultrasonography enables visualization of portions of
the stomach, duodenum, jejunum, and some segments
of the large intestine and small colon (if filled with fluid
contents or meconium).

The stomach

The stomach can be visualized from the left cranial

abdomen in the young foal. Occasionally the stomach
will be in contact with the ventral body wall, or at least
be visible immediately dorsal to the ventral aspect of the
liver when viewed from the ventral abdomen (Figure
22.2 ) . Mild curds surrounded by anechoic fluid, uni­
form echogenic fluid, or gas-bubble-Iaden fluid is nor­
mally seen in suckling foals within the stomach lumen
(Figure 22.3 ) . Otherwise only the stomach wall will be
seen as the high gas content of the ingesta will result in
a bright linear echo at the lumen, and the character of Figure 22.3 Normal stomach in a neonatal foal as viewed
the gastric contents will not be appreciable. In cases in from the left cranial abdomen. Notice the echogenic
material (presumed to be mild curds) surrounded by fluid

Figure 22.2 Normal stomach in a neonatal foal as viewed Figure 22.4 Markedly fluid-filled stomach in a neonatal
from the left cranioventral abdomen. Cranial is to the left. foal with anterior enteritis. Cranial is to the right. Notice
In this case the stomach is visible immediately dorsal to the the splenic vein (arrows) which can be used as a landmark
spleen

455
22 GASTROINTESTINAL DISEASE IN THE FOAL
Figure 22.5 Normal small intestine dorsal to the spleen, as
visualized from the ventral abdomen in a neonatal foal
Figure 22.7 Distended fluid-filled loop of small intestine
(amotile in real time) in a foal with ileus due to enteritis
Figure 22.9 Gas-bubble-Iaden fluid in the colon (long axis
view) of a young foal with colitis
456
Figure 22.6 Distended fluid-filled small intestine (short axis
view) with sedimentation of contents in one segment
(arrows) in a foal with complete mechanical obstruction
and ileus found to be due to small intestinal volvulus. It
should be noted that differentiation between mechanical
ileus and severe functional ileus may be difficult
Figure 22.8 Thickened or edematous small intestinal wall
(short axis view) with increased lumenal fluid content,
amotile in real time, in a neonatal foal with abdominal
pain and diarrhea. The foal died at 48 hours of age
because of clostridial enteritis
Figure 22.10 Small intestinal intussusception, short axis view
 CLINICAL EVALUATION OF THE FOAL 22

cases in which strangulation has resulted in devitaliza­

tion of the affected segment, differentiation of me chan­
ical ileus from enteritis with functional ileus may be
difficult. Devitalized segments of strangulated small
intestine may appear less taut because of loss of intesti­
nal tone, and thicker as edema of the wall develops.
Typically small intestine enteritis is manifest as hyper­
motile fluid-filled segments of small intestine with nor­
mal wall thickness. Infrequently, the wall may be
thickened or edematous (Figure 22.8 ) . In cases of
necrotizing enteritis gas may be seen within the wall of
the intestine (it should be noted that gas may also be
seen within the wall of devitalized strangulated small
intestine) or the wall may appear very thin. Increased
fluid content in the large intestine (Figure 22.9) may be Figure 22. 1 1 Meconium (arrows) in a foal with a
observed in some cases of enteritis, and its presence meconium impaction. Because meconium may be seen in
may be of help in the differentiation of functional from the intestine normally, the diagnosis of meconium
impaction should not be based on the results of ultra­
mechanical small intestinal ileus. The diagnosis may be
sonography alone
unclear in some instances and repeat ultrasound exam­
inations may be of benefit.
Small intestinal intussusceptions have a typical
'bull's eye' appearance when viewed in short axis
(Figure 22. 1 0 ) . Variable amounts of small intestinal dis­
tension proximal to the lesion may accompany intussus­
ception. It is particularly important to position the foal
standing if possible in order that the most dependent
portion of the abdomen can be examined with ultra­
sound. Affected loops of fluid-filled or edematous intes­
tine, or intussuscepted intestine; will tend to gravitate to
the most dependent area of the abdomen.

Colon

The colon often contains gaseous ingesta and its lumen

is generally not easily evaluated in the equine. In foals
with colitis, the contents of the colon may appear as
bubble-laden fluid (Figure 22.9) . Meconium appears as
hypoechoic structures within the large and/or small
colon (Figure 22. 11 ) . Because meconium can be visual­
ized in the normal equine neonate a diagnosis of meco­
nium impaction by ultrasound alone can be erroneous.
Peritoneum
Peritoneal effusions can be identified in foals with peri­
tonitis, uroperitoneum, hemoperitoneum, and transu­
dates. Effusions due to accumulation of transudate may
be identified in foals with mechanical gastrointestinal
obstructions. The fluid may appear anechoic in cases of
uroperitoneum, transudative effusions, and ruptured
viscus. In cases of ruptured viscus, the effusion may
range in appearance from anechoic to echogenic, and
may or may not contain a large amount of gas bubbles
or other echoes within the fluid (Figure 22.1 2 ) . Gas
echoes within the fluid are not always identified in cases
Figure 22.12 Marked peritoneal effusion with particulate
matter in a foal with a ruptured viscus. The spleen is
indicated by arrows
of ruptured viscus, however a gas-fluid or gas-spleen
interface may be seen from the left paralumbar fossa
(with the foal in a standing position) in cases with
significant pneumoperitoneum. Abdominocentesis
should be performed to confirm the type of fluid
present as the ultrasound appearance of effusions is not
specific. Visual inspection of the fluid, as well as exami­
nation of the fluid microscopically (particularly if the
cell count is normal) is very important to rule out a rup­
tured viscus.
Ultrasonography has obviated radiography for most
gastrointestinal disorders in the foal because of the

457
22 GASTROINTESTINAL DISEASE IN THE FOAL

Figure 22. 1 3 Distended barium-filled stomach, 30 minutes

after administration of barium sulfate via nasogastric
tube, in an unthrifty weanling foal with bruxism,
inappetance, and gastric reflux. Notice the absence of
barium in the small intestine. Duodenal stricture was
confirmed at surgery
Figure 22. 1 4 Lateral radiographic view following a barium
sulfate enema of a 30-hour-old foal with colic due to
meconium impaction. Notice the silhouetting of
meconium balls in the rectum and terminal small colon,
and the marked gas distension of the colon

portability of the ultrasound units and because of its

ability to both visualize intestinal motility in real time
and detect peritoneal effusions. It is often not possible
to distinguish mechanical from functional obstructions
with radiography, and ultrasonography may provide
more diagnostic information in such cases.
Diaphragmatic hernias may be identified radiographi­
cally, as with ultrasonography. Radiography, in combi­
nation with contrast studies, is most useful for the
diagnosis of atresia coli, meconium impactions, and
evaluation of gastrointestinal transit time. Standing
lateral radiographs are exposed at 1 0- 1 5 rnA and
80-120 kVp, with an 8:1 grid, film focal distance of
1 meter, and rare earth film screen combination. Gas
Figure 22. 1 5 Lateral radiographic view of the abdomen
caps are normally seen over the stomach, small intes­
following a barium sulfate enema of an 8-hour-old foal
tine, cecum, and colon. For contrast studies, barium sul­
with abdominal distension and colic. Notice the barium
fate is administered at 5-1 0 ml/kg as a 30 per cent w/v through the small colon, it has entered the large colon and
solution by nasogastric tube. The stomach should begin ended in a blind pouch. Exploratory celiotomy revealed a
to empty by 15 to 30 minutes and be nearly empty by 2 wall or diaphragm closure between the left and right ven­
hours, at which time contrast material may be seen in tral colons at the level of the sternal flexure, with intact
the cecum and colon. Duodenal stricture will result in mesentery. An anastomosis was performed and the foal
gastric distension and retention of barium (Figure recovered uneventfully. In the vast majority of cases of
22.13 ) . Retrograde contrast radiography is highly sensi­ atresia coli, a large segment of the large, transverse, or small
colon is absent, and surgical correction is rarely feasible
tive and specific for evaluating obstructions of the small
colon or transverse colon, such as those due to meco­
nium impaction. Approximately 500-1000 ml of barium immediately. Meconium impaction will appear as filling
sulfate solution (30% w/v) for a 50 kg foal is adminis­ defects within the small colon or rectum, with silhouet­
tered via enema into the rectum by gravity flow using a ting of the fecal balls by the barium (Figure 22.14) . If
soft flexible catheter. The author has found that a Foley the obstruction is just proximal to the pelvic inlet, a
catheter has been unnecessary for such studies. widening of the small colon at this location because of
Sedation of the foal may be required in some cases. meconium may be observed. Atresia coli may also be
Administration of barium should be discontinued when diagnosed by retrograde contrast radiography in most
the barium flows back around the catheter or the cases. The contrast material will stop abruptly in a blind
foal becomes uncomfortable. Radiographs are taken pouch (Figure 22. 1 5 ) . Tapering of the contrast material

458

Figure 22.16 Lateral radiographic view following barium
enema of the terminal small colon and rectum of a 1-day­
old foal with abdominal pain and distension. An inadequate
amount of barium sulfate has been administered to reach
the small colon, however notice the empty corrugated
appearance of the small colon. Because of intractable
abdominal pain, the foal was taken to surgery rather than
continue with the diagnostic procedure. Atresia coli was dis­
covered at exploratory surgery and the foal was euthanized
within the small colon indicates that an inadequate
amount of contrast material has been administered to
reach the transverse colon (Figure 22.1 6) and more
barium may be required. In general, standing radi­
ographic views have been sufficient in the author's
experience, however ventrodorsal views may be neces­
sary in some cases. Occasionally the atretic segment is
too proximal to be diagnosed with a retrograde contrast
study. Incidentally, a collapsed corrugated appearance
to the small colon has been observed by the author in
some cases of atresia coli ( Figure 22. 1 6) .
Differential diagnosis and
evaluation of the foal with
abdominal distention
CS Cable
INTRODUCTION
Abdominal distension can occur in foals of any age and
is most often accompanied by signs of abdominal pain.
Abdominal distension can occur in the foal however,
without signs of colic. Abdominal distention occurs
most commonly in adult horses with large colon disten­
sion (see Chapter 1 7) . However, in foals, small and
CLIN ICAL EVALUATION OF THE FOAL 22
large intestinal distention, as well as excessive abdomi­
nal fluid accumulation, will lead to abdominal disten­
tion. Abdominal distention in the foal is most
commonly caused by gastrointestinal disorders, usually
some type of intestinal obstruction (functional or
mechanical, congenital or acquired) . However, other
disorders such as rupture or leakage of the urinary tract
can lead to uroperitoneum and subsequent abdominal
distention. This section considers the differential diag­
nosis of abdominal distention in the foal and the evalu­
ation of foals with this condition.
History
Evaluation of the foal with abdominal distention begins
with a thorough history, including peripartum events.
Neonates should be evaluated as to their immunoglob­
ulin status and treated if partial or complete failure of
passive transfer is suspected.
PHYSICAL EXAMINATION
An initial step in the physical examination is to take
the rectal temperature as a fever may indicate infectious
causes of the distention. Foals with abdominal
distension often have elevated heart rates. When large
quantities of peritoneal effusion are present, the foal
often develops hypovolemic shock. When gram-nega­
tive bacterial infection is the culprit, endotoxemia may
also be a potential source of the tachycardia. Therefore,
thorough evaluation is necessary to treat the foal appro­
priately. Foals with abdominal distention may also have
elevated respiratory rates as excessive fluid can press
upon the diaphragm causing difficulty in breathing,
especially when the foal is recumbent. Furthermore,
the chest should be auscultated carefully to determine
if pleural fluid is present (possibly extending from the
abdomen) , also leading to difficulty in breathing.
Examination of the distended abdomen should include
external palpation, radiography, and/or an ultrasound
examination to determine the cause of the distention.
RADIOGRAPHY AND
ULTRASONOGRAPHY
To determine the exact location of the gastrointestinal
obstruction or site of urine leakage, contrast studies will
need to be performed. For the location of gastrointesti­
nal obstructions in the rectum and small colon, barium
enemas can be performed. The authors prefer to infuse
barium through a Foley catheter via gravity flow. The
Foley catheter after it is inflated, keeps the barium
459
22 GASTROINTESTINAL DISEASE IN THE FOAL
within the rectum and small colon. For identifYing the
site of leakage in cases of uroperitoneum. contrast cys­
tography or excretory cystography can be performed.
Retrograde injection of dye into the bladder followed
by simple abdominocentesis will allow the clinician to
determine whether or not uroperitoneum is present.
but the site of leakage will remain unknown. Further­
more. collection of abdominal fluid for cytology. creati­
nine measurement and culture and sensitivity should be
performed prior to retrograde injection of dye.
ABDOMINOCENTESIS
Abdominocentesis is best performed in cases of abdom­
inal distension after radiographs and/or ultrasound
examination has been performed. The risk of bowel
perforation is low if there is a large amount of peri­
toneal fluid within the abdomen. However. if large gas
distended or fluid distended loops of bowel are present
on radiography or ultrasound examination. then
abdominocentesis is often not performed to avoid the
risk of laceration of the bowel wall. To decrease the
risk of inadvertent bowel wall perforation when
abdominocentesis is performed. the foal should be well
restrained with adequate levels of sedation and sub­
cutaneous local anesthetic infiltration. Furthermore.
abdominocentesis with the use of a teat cannula is often
preferred over an 1 8-gauge needle to prevent bowel
laceration.
Cytologic evaluation of the abdominal fluid will help
narrow the list of differential diagnoses for foals with
abdominal distension. High nucleated cell counts with
bacteria present can represent bacterial peritonitis due
to sepsis. ruptured abscess. or ruptured viscera. As
mentioned in Evaluation of the foal with colic.
Clinicopathologic data the normal nucleated cell count
of abdominal fluid in foals is lower than that in adults.
NASOGASTRIC INTUBATION
Because small intestinal distension can lead to abdomi­
nal distension in the foal. then all foals that present with
abdominal distension should be evaluated for gastric
reflux. via a small bore nasogastric tube or stallion
catheter. Lack of reflux does not mean there is no accu­
mulation of fluid within the stomach. however obtain­
ing reflux indicates some form of bowel obstruction
(functional or mechanical) . Evaluation of the pH of the
sample can help determine if the reflux is from the
stomach or the small intestine. Intestinal fluid from the
small intestine will have a higher pH (6-8) than that
refluxed from the stomach which is more acidic.
460
EXPLORATORY SURGERY
There are many differential diagnoses for foals with
abdominal distension. and often the exact reason can­
not be elucidated until an exploratory celiotomy is per­
formed. However. careful and thorough diagnostics can
help guide the veterinarian toward the true nature of
the problem and help decide what treatment is
warranted. The following sections describe differential
diagnosis for foals with abdominal distension.
NEONATES
Neonatal foals are those within the first 2 weeks of age.
In these foals congenital as well as acquired disorders of
the gastrointestinal and urinary tract must be consid­
ered as differential diagnoses for foals with abdominal
distension. these include
• meconium retention
• intestinal atresia - atresia coli. atresia recti. atresia
ani
• ileocolonic aganglionosis
• uroperitoneum
• fecaliths
• peritonitis
• enteritis/colitis.
Meconium retention (see Chapter 25)
Meconium retention is one of the most common causes
of abdominal pain and abdominal distension in the
neonatal foal. Meconium is comprised of swallowed
amniotic fluid and intestinal secretions that accumulate
within the gastrointestinal tract in foals during gesta­
tion. Meconium is usually a dark color and pelle ted in
shape. These meconium pellets can be quite firm and
dry and often lead to difficulty in passage through the
newborn foal's narrow pelvis and rectum. Colts are
thought to be more commonly affected than fillies.
because of their relatively smaller pelvic size. Meconium
may be retained within the rectum. small colon. and even
within the large colon. Foals should begin to pass their
meconium within a few hours of birth. Foals may pass
small amounts of meconium then begin to show signs of
discomfort. Typical signs of meconium retention include
straining to defecate. colic, and gradual abdominal
distension as fluid and ingesta accumulate within the
gastrointestinal tract proximal to the obstruction.
Evaluation of these foals includes a thorough physi­
cal examination including evaluating the character of
straining if present. Foals that are straining to defecate
will have their backs arched with their tails in the air.
Digital palpation of their rectum will often reveal

retained m econium. Plain radiographs can reveal the
retained m econium within the rectum and/or small
colon with gas/fluid-distended colon proximal to the
obstruction. Contrast radiography with barium enemas
( administered through a Foley catheter) can also be
performed to help determine the location and nature
of the obstruction.
Intestinal atresia (see Chapter 1 6)
Intestinal atresia in the horse is a rare occurrence. It has
been reported to occur in the colon ( atresia coli) , and
in the rectum or anus ( atresia recti or ani) of the horse.
Atresia coli is approximately twice as common as other
types of atresia in the horse.
The most popular theory regarding the pathogene­
sis of intestinal atresia is that of a vascular accident. The
vascular accident is theorized to arrest growth and
result in atrophy of a bowel segment which becomes the
atretic segment. Louw's theory has been tested and
shown that every type of atresia can be duplicated by
selective ligation of mesenteric vessels.
Foals with intestinal atresia are born 'normal'.
However, they usually present within the first 24-48
hours of life for signs of colic, failure to pass their
meconium, and abdominal distension. Administration
of an enema will only produce clear water and mucous
- no fecal coloration. Foals with abdominal distension
and/or colic with no history of meconium passage
should be strongly suspected of intestinal atresia.
Evaluation of these foals should include a thorough
history, physical examination, and immunoglobulin
testing. Results of a complete blood count and chem­
istry panel are non-specific for this condition. Plain
radiographs of the abdomen and contrast studies may
help determine the site of obstruction.
Ileocolonic aganglionosis (lethal white
syndrome) (see Chapter 25)
This gastrointestinal disorder has been reported to
occur in white foals out of Overo-Overo Paint crosses.
Both male and female foals can be atfected. Recently it
was reported that a recessive gene is responsible for this
disease. The affected foals suffer from a lack of myen­
teric ganglia within the ileum, cecum, and/or the
entire large colon. The lack of myenteric ganglia results
in lack of propulsive motility within the gastrointestinal
tract.
These foals, although normal at birth, will begin to
show signs of colic within 1 2-24 hours of birth, they will
not pass any meconium, and digital palpation or admin­
istration of enemas will not produce any fecal material.
There is no treatment for these foals at the time of writ­
ing and euthanasia is recommended. However, horses
CLIN ICAL EVALUATION OF THE FOAL 22
can now be tested prior to breeding to determine if they
carry the gene responsible for the disease, using a DNA
test on the animal's blood or hair. The veterinary genet­
ics laboratory at the University of California, Davis can
perform the test.
Uroperitoneum
Uroperitoneum is a common cause of abdominal dis­
tension in foals and is the result of urine l eaking from
the urinary tract into the abdomen. Possible sites of
urine leakage include the urachus, ureter, urethra, or
most commonly, the bladder. Colts and fillies can be
affected, however colts are more commonly affected.
The pathogenesis of uroperitoneum includes increased
abdominal pressure during delivery, external trauma,
infection within the urachus, or necrotic cystitis. Tears
or defects within the bladder occur most commonly on
the dorsal aspect of the bladder.
Foals that develop uroperitoneum may not show
clinical signs for 2-3 days following the formation of the
defect within the urinary tract. Clinical signs include
progressive abdominal distension, tachycardia, tachyp­
nea, depression, and decreased interest in nursing.
Although m any foals will have stranguria or oliguria,
foals with defects within the urinary tract have been
known to urinate normally.
The evaluation of foals with suspected uroperi­
toneum involves a thorough physical examination. The
external umbilicus, prepuce, and vulva of foals should
be examined closely. Urine leakage into the subcuta­
neous tissues or retroperitoneally from tears of the ura­
chus, ureters, or urethras can lead to subcutaneous
swelling and edema. Complete blood counts m ay only
reveal hypovolemia, unless concurrent sepsis or infec­
tion is present. Electrolyte abnormalities resulting from
uroperitoneum classically include hyponatremia,
hypochloremia, hyperkalemia, and azotemia. An ultra­
sound examination of the abdomen should reveal
excessive amounts of peritoneal fluid (Figure 22. 1 7) .
Imaging a fluid-distended bladder should not lead to
discounting uroperitoneum as the diagnosis, as the
urine accumulation can, of course, originate from a dif­
ferent site. The diagnosis can be confirmed through the
collection of abdominal fluid. Abdominocentesis
should yield voluminous clear, pale yellow fluid. The
fluid should be evaluated via cytology and comparison
of the creatinine values from serum versus abdominal
fluid. The diagnosis can be confirmed when the creati­
nine concentration of the abdominal fluid is twice that
of the serum concentration.
Treatment of foals with uroperitoneum almost
always requires surgical repair of the defect. How­
ever, stabilization of the electrolyte and acid-base
461
22 GASTROINTESTINAL DISEASE IN THE FOAL
Figure 22.17 Abdominal ultrasonogram of a foal with a rup­
tured bladder. There is a large excess of anechoic peritoneal
fluid in which the collapsed bladder is seen 'floating'
abnormalities must be performed prior to surgery to
prevent anesthetic complications or even death.
Medical stabilization should include drainage of the
excessive abdominal fluid, either through a teat can­
nula or small chest trocar (for more continuous
drainage over several hours ) . Removal of the urine will
not only reduce pressure on the diaphragm allowing
the foal to breathe more easily, but will decrease both
serum creatinine and more importantly potassium con­
centrations.
Intravenous fluids should be administered to correct
hypovolemia and electrolyte abnormalities. Normal
saline can be administered intravenously along with
dextrose to combat hypoglycemia and promote move­
ment of potassium intracellularly. Severe or non­
responsive hyperkalemia can also be treated with
intravenous calcium (4 mg/kg slowly LV. over 1 0 min­
utes) or subcutaneous insulin (0. 1 IV/kg) regular
insulin LV. Furthermore, for foals with severe or non­
responsive hyperkalemia, attempts at complete
drainage of abdominal fluid should be made along with
catheterization of the bladder to prevent further accu­
mulation of urine within the abdomen. At the author's
hospital, foals with uroperitoneum are not anesthetized
until the serum potassium is below 5.5 mEq/dl. We
believe that at this level, the risk of cardiac arrhythmias
is much less under general anesthesia.
Fecaliths (see Chapter 16)
Fecaliths occur more commonly in pony or miniature
horse foals than in the larger breeds. These concretions
of fecal material and other ingested material (such as
shavings) can occur in neonates, but also cause obstruc-
462
tions in older foals. Fecaliths cause abdominal disten­
sion and mild to moderate colic, similar to that seen
with meconium impactions, as gas and ingesta accumu­
late proximal to the obstruction. The obstruction is
commonly within the small colon. Although the
obstruction is usually quite distal within the intestinal
tract, enemas are usually not effective and surgical
removal of the object is often necessary.
Peritonitis
Peritonitis can occur in any age foal and often results in
abdominal distension and low-grade colic with profound
depression. Peritonitis in foals can have many different
etiologies, including bacterial, chemical, or traumatic.
Neonates can develop bacterial peritonitis from
• systemic bacterial infection (sepsis)
• severe bacterial enteritis
• leakage of bacteria from a gastroduodenal ulcer
that has perforated
• leakage of bacteria from an umbilical remnant
abscess
• a mesenteric abscess
• damage of the gastrointestinal tract from parasite
migration.
Chemical peritonitis can occur from uroperitoneum or
hemoperitoneum. Trauma to the abdomen of foals can
result in hemoperitoneum from several different sources,
including the spleen, liver, or umbilical remnants.
OLDER FOALS
The more common causes of abdominal distention in
older foals are
• small intestinal obstructions - intussusceptions,
volvulus
• fecaliths
• peritonitis
• enteritis/ colitis.
Small intestinal obstructions such as intussusception
can lead to abdominal distention; these typically occur
in foals that are 3-5 weeks of age, however, older foals
and horses can be affected as well. Intussusceptions can
occur in two forms, acute and subacute. The acute form
is indicated by a sudden onset of severe unrelenting
pain. The subacute form includes chronic colic,
anorexia, and an unthrifty appearance.
Small intestinal volvulus can also result in abdominal
distension, but again the acute nature of the pain often
precedes the development of distention. Small intesti­
nal volvulus commonly occurs in foals that are 2-4
months of age.
 CLI NICAL EVALUATION OF THE FOAL 22

Medical therapy in the foal H ypovolemic shock is suspected when the following are
observed
with abdominal pain • decreased distensibility of the j ugular vein
• prolonged capillary refill time
G Perkins
• cold extremities
• increased heart rate
• decreased pulse pressure
INTRODUCTION
• decreased skin turgor.

This section provides a general guide to the medical Increases in the packed cell volume and total protein
management of a foal with colic. The goals of medical are indicators of dehydration but are not specific.
therapy are to Azotemia, elevated blood urea nitrogen and creatinine,
can occur secondarily to dehydration but renal failure
• correct the primary cause of colic
should be ruled out by urinalysis and response to fluid
• correct electrolyte and metabolic imbalances
therapy. Interestingly, even without clinically detectable
• provide pain relief
dehydration, fluid therapy can be very beneficial in the
• provide continued nutritional support
management of colic in foals and adult horses.
• provide decompression of the bowel
Calculations for fluid volume are
• provide intestinal rest if distension persists.
volume deficit = (% dehydration) x (body weight (kg»
Treatment for gastric ulceration is covered elsewhere
(see Chapter 23) . maintenance fluids = (60 - 1 20 ml x
Foals are more likely to show signs o f colic with (body weight (kg» per day plus
en teritis than adults, therefore ' colicky' foals are often ongoing losses = (estimated volume) =

treated medically. If aggressive medical management

does not relieve the pain or distension, or if ancillary (liters) to be given over 1 day
tests such as ultrasound and radiography suggest The electrolyte abnormalities most commonly
obstruction , surgical exploration should be considered encountered with gastrointestinal disease in the foal
(see Evaluation of the foal with colic) . include

• hyponatremia
• hypochloremia
• hypokalemia
FLUID THERAPY
• hypoglycemia
• metabolic acidosis.
Supportive care of the equine neonate begins with fluid
therapy to restore and maintain fluid homeostasis. The Mild colic with a hypermotile intestine and no obstruc­
total body water of a foal accounts for 70-75% of its tion can occasionally be managed with small amounts of
body weight. Gastrointestinal disease can result in fluid given via a nasogastric tube. The total volume to
severe fluid shifts because of loss of sodium, protein, be placed directly into the stomach should be small
and fluid into the gastrointestinal lumen or peri­ (8- 1 2 ml/kg ) . In most instances intravenous adminis­
t(meum. Endotoxemia and the resultant activation of tration of a balanced polyionic electrolyte solution such
the inflammatory cascade results in pooling within the as plasmalyte or lactated Ringer' s solution is preferred.
gastrointestinal capillary beds and increased permeabil­ Bicarbonate is required for the treatment of severe
ity to macromolecules, exacerbating the fluid shifts. metabolic acidosis (HC03 < 1 6 mEq/dl) with a normal
The resultant hypovolemia, if progressive, can lead to anion gap. The following calculation should be used to
decreased perfusion of the tissues, anaerobic metabo­ determine the bicarbonate deficit
lism, and metabolic acidosis.
(base deficit) x (0.4) x (body weight (kg» = HC03
Indicators of dehydration that can be used to calcu­
deficit (mEq)
late the percentage dehydration include
or
• decreased skin turgor
(normal HC03 - measured HC03) x (0.4) x
• dry mucous membranes
(body weight (kg» HC03 deficit (mEq)
=

• decreased urinary output

• sunken eyes One half of the deficit should be replaced over
• muscle weakness. 1-4 hours and the remainder over the following

463
22 GASTROI NTESTINAL DISEASE IN THE FOAL
1 2-24 hours. Isotonic bicarbonate is nearly 1 .25% and
intravenous bicarbonate solution comes commercially
prepared as 8.4% ( 1 mEq/ml) and 5% (0.6 mEq/ml)
solutions. Successful management of metabolic acidosis
in the foal with diarrhea can sometimes be achieved by
administering oral bicarbonate. This should be
attempted only when the foal is well hydrated and the
anion gap is normal. The base deficit can be calculated
by converting I gram bicarbonate into 1 2 mEq and dos­
ing orally.
Hypokalemia occurs as a result of decreased intake
and loss through the gastrointestinal tract and urine.
Potassium may be added to the intravenous fluids at
approximately 20-40 mEq/liter. The potassium supple­
mentation should not exceed 3-5 mEq kg/d and 0.5 mEq
kg/h. Hyperkalemia in the foal with gastrointestinal dis­
ease is usually secondary to metabolic acidosis and
translocation of the potassium to the extracellular space.
In a rare case it may be a result of acute renal failure.
Treating the metabolic acidosis with bicarbonate-rich
fluids generally corrects the hyperkalemia. Dextrose
solutions (2.5-5.0%) promote the movement of potas­
sium back into the cells. Insulin (O. l IU /kg regular
insulin i.v.) can also be used but is generally not recom­
mended. If severe cardiac arrhythmias or atrial standstill
are detected, calcium gluconate can be administered at
4 mg/kg i.v. slowly over 10 minutes to protect the heart.
NUTRITION
En teral nutrition III foals with abdominal distension
and colic can be contraindicated. A muzzle can be
placed on a foal that is reasonably bright and active to
prevent nursing until the colic subsides. Foals with colic
that are being fed with a nasogastric tube should be fed
only very small amounts of milk. If the foal tolerates the
small quantities, the amount can be increased slowly
over a few days to maintenance levels of 1 5-20% body
weight per day. Parenteral nutrition should be consid­
ered in foals that may be unable to receive enteral nutri­
tion for more than 24-36 hours. Since neonates have
minimal reserves of glycogen and fat, food deprivation
for 1 day may have profound effects. Parenteral nutri­
tion is also indicated in prematurity, septicemia, and
diarrhea where the gastrointestinal tract is unable to
transport and digest milk. The decision to do partial or
total parenteral nutrition is based on the gastrointesti­
nal tract fun ction. It is important to continue stimulat­
ing the enterocytes by feeding small amounts of milk
(50 ml q. 1-2 hr) if possible. Any electrolyte abnormali­
ties should be corrected with fluids prior to initiating
TPN. A foal should receive approximately 1 00-150 kcal
kg-I day-I. Parenteral nutrition derives its energy from
464
Foal's weight (50 kg)
Level of nutritional support 1 00 kcal/kg/d
Total daily calories 100 kcal x 50 kg
= 5000 kcal
Non-nitrogen calorie distribution
40% dextrose = 2000 kcal dextrose
60% lipid = 3000 kcal lipid
fr21iln
A. Ratio of 300 non-nitrogen cal/g of nitrogen
5000 total daily kcal / 300 (ratio) = 1 6. 5 9
nitrogen
B. 16.5 9 nitrogenl16% nitrogen in protein = 1 00 9
protein
C. Example to determine volume of an amino 8.4%
acid solution:
100g nitrogen/0.084 a m i no acid solution =
1 1 76.5 ml
three sources; amino acid solutions, dextrose, and
lipids. The non-protein nitrogen sources; dextrose and
lipids should be distributed at 40% and 60% , respec­
tively. The ratio of non-nitrogen calories to grams of
nitrogen has been extrapolated from humans to be
approximately 1 50-300. Protein contains 16% nitrogen,
therefore an amino acid solution can be approximated
by dividing the protein by 6.25. The kcal derived from
protein is 4 kcal/g, glucose i s approximately 4 kcal/g,
and fat is 9 kcal/g. This value should lie within the ratio
of non-nitrogen calories to grams of nitrogen.
Strict attention to aseptic techniques should be paid
when managing the TPN solutions since they can sup­
port the growth of bacteria and fungi. The amino acids
should be mixed with the dextrose before adding the
lipids. A freshly made bag can be kept refrigerated for
24 hours prior to use. The solution should be delivered
through a TPN dedicated intravenous line and very
careful handling of the catheter ports and intravenous
lines should be undertaken with daily replacement of
the lines. When beginning the TPN, start at approxi­
mately one-third of the desired rate. Monitor the blood
frequently for lipemia, and the urine and blood for
hyperglycemia (blood glucose > 1 80 mg/dl ) . Increase
the flow rate slowly if normoglycemia is maintained.
ANALGESICS
Controlling pain in a colicky foal that is rolling is
important in reducing self inflicted trauma, as well as

decreasing inflammation that is causing ileus. Non­
steroidal anti-inflammatory drugs (NSAIDs) can be of
benefit but should be used judiciously because of the
ulcerogenic effects on the glandular portion of the
stomach and renal papillary necrosis. Drugs with a low
cyclooxygenase-l :cyclooxygenase-2 ratio are thought to
be safest. Unfortunately, pharmacokinetics and toxicity
trials of NSAIDs in the foal are not well documented.
Flunixin meglumine (0.5- 1 .0 mg/kg i.v.) has been
reported to be the most effective drug for gastrointesti­
nal pain. Ketoprofen has been documented as the least
ulcerogenic NSAID compared with phenylbutazone
and flunixin meglumine in the horse, but anecdotal
reports indicate that its pain relief in colic is not as pro­
nounced as flunixin meglumine. Butorphanol, an opi­
oid analgesic, (0.01-0.04 mg/kg i.m. or i.v. ) can be used
in addition to, or to limit the amount of, NSAIDs given
when gastroduodenal ulceration is a concern. Xylazine
(0. 1-0.5 mg/kg i.v.) provides sedation and analgesia,
but can cause profound decreases in gastrointestinal
motility. If repeated doses of analgesics are required
surgical exploration should be considered.
DECOMPRESSION
A nasogastric tube can be passed to relieve gastric dis­
tension. Unfortunately, the diameter of a foal's nasal
passages limits the size of the nasogastric tube to either
a stallion catheter or a 1 em diameter nasogastric tube.
A stylet can be used for ease of swallowing and passage
of the tube from the nasopharynx into the esophagus.
The stomach can be lavaged gently with small amounts
of water (60 ml at a time) . Frequently, even if reflux is
present in the stomach, it is difficult to manually extract
the fluid. The tube should be left in place and capped
to prevent air aspiration.
Percutaneous bowel trocarization is indicated if
severe abdominal distension coupled with respiratory
compromise persists. The owner should be warned of
the inherent risks of peritonitis and that the foal may
require surgical exploration if the condition persists.
The foal should be sedated and/or placed in lateral
recumbency. The abdomen should be percussed for a
prominent gas ping. The area where the ping is heard
best should be clipped and prepared aseptically. A small
lidocaine bleb should be infused at the puncture site. A
1 6-1 8-gauge 1 .5-inch needle or 3.5-inch catheter over
stylet can be advanced through the skin and body wall
into the distended viscus and air should be drained. A
small volume of antibiotic (i.e. amikacin or gentamicin)
should be infused as the needle/catheter is withdrawn.
The foal should be maintained on systemic antibiotic
therapy for 3-5 days following trocarization.
CLIN ICAL EVALUATION OF T H E FOAL 22
PROKINETICS
Motility enhancing drugs are considered controversial
in the foal with colic. Surgical and/or obstructive dis­
eases should be ruled out before administering proki­
netic agents. The most common indication for
prokinetic agents in a foal is ileus secondary to sep­
ticemia, enteritis or neonatal maladjustment. The
dosages and side effects have been extrapolated for the
most part from human and small animal studies, and
little data exists in the literature on foals. Cisapride
(0.2-0.4 mg/kg p.o. q. 4-8 h) is a third generation ben­
zamide that acts as a serotonin agonist within the myen­
teric plexus. Cisapride has effects on the colon,
esophagus, stomach, and small intestine and, therefore,
can impact the entire gastrointestinal tract. Cisapride
has been well tolerated in adult horses. Metoclo­
pramide (0.25-0.50 mg/kg i.v. as a I-h infusion q. 4-8 h
or 0.6 mg/kg p.o. or per rectum q. 4-6 h ) , a dopamine
antagonist, has been well documented to increase gas­
tric emptying with coordinated increase in tone of the
lower esophageal sphincter and contraction of the
stomach. Caution and constant monitoring for neuro­
logic signs should be used when giving this medication
because of the permeability of the blood-brain barrier
and extra-pyramidal signs. Erythromycin, ( 1 .0-2.0 mg/
kg i.v. administered as a I-h infusion q. 6 h or p.o. q.
6 h) at sub-antibiotic levels stimulates motilin receptors.
Ranitidine ( 1-2 mg/kg p.o. or i.m. q. 8-12 h ) , an H2-
blocker, has also been shown to have effects on gas­
trointestinal motility and positive effects on gastric
emptying disorders. Ranitidine w.ould be a wise choice
since it is also useful in treating gastric ulceration. An
acetylcholine esterase inhibitor, neostigmine (0.02 mg/
kg s.c.) , is a potent prokinetic agent and can sometimes
cause severe cramping and colic in the horse. It has
been used successfully along with sedation in foals with
non-obstructing large colon gas distension.
Surgical decision for the foal
with colic
CS Cable
INTRODUCTION
Foals with colic are challenging cases to manage.
Often the most difficult aspect of their management is
determining when and if the foal requires surgery.
Delaying surgery may unnecessarily compromise the
foal's physical condition and increase the risks of
465
22 GASTROINTESTINAL DISEASE I N THE FOAL
general anesthesia. Furthermore, delaying surgery
when devitalized bowel is involved can change a
closed bowel operation into a resection and anastomo­
sis, thereby greatly reducing the overall prognosis. On
the other hand, placing a neonatal foal under general
anesthesia to perform an exploratory celiotomy can
greatly increase the risk of pneumonia and/or peri­
tonitis. Furthermore, there is still a great deal of con­
troversy regarding the risk of foals developing
postoperative intra-abdominal adhesions, despite
recent publications suggesting that foals are not at
greater risk than adult horses of these complications.
These conflicting factors make the surgical decision
for abdominal surgery in foals difficult.
The decision to perform surgery in a foal should be
made only after a complete and thorough physical
examination has been performed with careful atten­
tion being paid to the historical events preceding the
colic. In addition, laboratory values (along with radio­
graphs, ultrasound, and possibly an endoscopic exami­
nation) can be very helpful in making the surgical
decision.
HISTORY AND PHYSICAL
EXAMINATION
As mentioned in previous chapters, a complete history
can be very beneficial in providing clues to the origin of
the colic episode. The following can provide valuable
information
• peripartum events
• age of the foal at the onset of clinical signs
• farm history of disease
• previous illness or surgery
• feeding program
• anthelmintic history
For example, a poor-doing weanling with a history of
chronic intermittent colic is highly suggestive of a
chronic ileocecal intussusception.
The physical examination should be performed
keeping in mind the differences in the normal values of
heart rate and respiratory rate between neonates and
older foals (see Evaluation of the foal with colic) . Those
foals with an elevated temperature should be closely
evaluated for sepsis and/or enteritis as the cause of
colic. Enteritis in foals can be especially difficult to dis­
tinguish from surgical lesions, as the foal often becomes
quite painful from intestinal distension before diarrhea
is present. In the author' s experience, Clostridial
enteritis in particular causes moderate to severe pain in
the foal requiring frequent analgesia.
Foals with colic often have distended abdomens.
466
The severity of distension can be monitored by repeat­
edly measuring around the foal' s abdomen at specific
points with a tape to detect changes. Foals with severe
abdominal distension can have great difficulty breath­
ing properly. These foals will require decompression
(percutaneous or surgical) of the gas-distended bowel
even if the lesion is usually amenable to medical ther­
apy. Percutaneous methods of bowel decompression
carry risks in the neonatal foal, mostly from peritonitis
after the bowel puncture because of the thinness of the
intestinal wall.
Palpation of the foal externally can aid in identifying
large obstructions within the abdomen, but is often
impossible on a larger foal or one in severe pain. The
foal with colic should always be evaluated for hernias
(umbilical or inguinal/scrotal) and other congenital
defects. Reducible hernias are not a surgical emer­
gency, but entrapped (non-reducible) hernias require
immediate surgery. Ruptured indirect inguinal hernias,
(inguinal hernias that have broken through the vaginal
tunic) , although not strangulating in nature, often
require immediate surgery as they can dissect through
the subcutaneous tissues becoming very large and much
more difficult to manage.
A nasogastric tube (small size) should also be passed
in foals with colic, however, the presence of reflux does
not always indicate a mechanical obstruction.
Furthermore the lack of reflux does not rule out a small
intestinal surgical lesion. The presence of reflux alone
therefore is not conclusive for a surgical lesion. The pH
of the reflux can help identify its source - acidic reflux
originating in the stomach and basic reflux usually orig­
inating in the small intestine. Furthermore, a gram
stain of a reflux sample may help identify bacterial
enteritis, especially if an overwhelming population of
one type of bacteria is found.
Foals tend to be more sensitive to gastrointestinal
pain than adults, and this makes it difficult to decide to
perform surgery on a foal, on the basis of signs of pain.
However, the foal displaying persistent, severe pain that
is not responsive to analgesia is a candidate for an
�xploratory celiotomy. Even if ileus alone is the culprit,
decompression of the bowel can relieve the pain and
speed recovery.
LABORATORY EXAMINATION
As in the adult, a foal should be evaluated using a com­
plete blood count, chemistry panel, and abdominocen­
tesis if possible. The presence of leukopenia, left shift,
or evidence of toxic neutrophils suggests sepsis; infec­
tious causes of colic, such as enteritis, should then be
considered. Neonatal foals should be evaluated further

by gamma globulin levels (IgG) to assess passive transfer
of immunoglobulins and the likelihood of sepsis. Foals
that have less than 800 mg/dl (80 g/I) of IgG are
treated for failure of passive transfer in the author's
hospital.
Chemistry panels are performed to evaluate the
foal 's electrolyte status. Marked hyponatremia and
hypochloremia suggest enteritis. Hyperkalemia with
hyponatremia and hypochloremia suggests uroperi­
toneum.
Abdominocentesis can be very helpful in identifying
surgical lesions in foals. Care must be taken to avoid
inadvertent bowel puncture when acquiring the sam­
ple, so in the author's hospital an ultrasound examina­
tion of the abdomen is performed to locate the area
where fluid is most likely to be obtained. Foals with
moderate to marked abdominal distension from bowel
distension are usually not evaluated via abdominocen­
tesis because of the higher risk of bowel perforation.
The fluid is analyzed for white blood cell count, total
protein, and cytology. White blood cell counts greater
than 1 500-3000/111 ( 1 .5-3.0 x 1 09/1) are considered
abnormal in foals. If uroperitoneum is suspected, the
fluid should be evaluated for creatinine concentration
and its level compared with serum creatinine concen­
trations. If the ratio is greater than 2: 1 urinary tract
rupture/perforation is likely.
ADDITIONAL DIAGNOSTIC
PROCEDURES
The use of radiographs and/or ultrasound has greatly
enhanced the veterinarian's ability to determine the
location of the gastrointestinal obstruction in the foal
and decide if surgery is necessary. Although plain radi­
ography can help determine the nature of the foal's
abdominal distension if present (i.e. small versus large
bowel distension) , contrast radiography is often much
more specific in giving the location of the lesion.
Contrast radiographs taken after barium has been
administered can enhance the view of the gastroin­
testinal tract and locate specific sites of obstructions.
Barium can be administered to the foal through a
nasogastric tube, dose syringe, or through a Foley
catheter (barium enema) . Barium administered
through a dose syringe can help identify problems
with the oral cavity, soft palate, esophagus, or cardia.
Barium administered through a nasogastric tube
should be made into a solution (30% w/v) and dosed
at 5 ml/kg. This can help identify lesions of the car­
dia, stomach (e.g. gastric ulcers) , or duodenal stric­
tures. Barium administered via an enema can help
identify lesions of the rectum, small colon, and even
CLIN ICAL EVALUATION OF THE FOAL 22
the distal large colon at a dose of 1 8-20 ml/kg. Foals
are best sedated for this procedure
Evaluation of the foal's abdomen via ultrasound can
also greatly help in the decision for medical versus sur­
gical treatment. Although a rectal examination (a stan­
dard and often vital part of the examination of an adult
horse with colic) cannot be used in the foal, an ultra­
sound examination can help provide the information
needed to make the decision for surgery. Identification
of thickened and non-motile small intestine is highly
suggestive of a strangulating small intestinal lesion.
Other lesions that can be identified include intussus­
ceptions which appear as a 'bull's-eye' lesion (rings with
a circular echogenic core) , and copious amounts of
abdominal fluid suggesting either uroperitoneum or
peritonitis if the fluid is echogenic.
CONCLUSION
Differentiating surgical versus medical therapy in a foal
with colic can be a formidable task. Severe pain often
dictates our decision, but this degree of pain can some­
times be caused by relatively minor obstructions.
Initially medical therapy is often chosen for the less
obvious surgical patients. However, progressive abdom­
inal distension, persistent pain, and/or changing
abdominocentesis values all warrant an exploratory
celiotomy. I mproved surgical techniques and medica­
tion used to minimize adhesion formation (see
Chapters 10 and 1 1 ) appear to have kept the rate of
adhesion formation following exploratory celiotomy
low. In this author's opinion, it is better to perform a
careful, early exploratory celiotomy on a relatively sta­
ble foal than frantic, desperate surgery on a dying one.
BIBLIOGRAPHY
Evaluation of the foal with colic
Chaffin M K, Cohen N D ( 1 995) Assessing the history,
signalment, and examination findings in foals with colic.
Vet. Med. 8:765-9.
Chaffin M K, Cohen N D ( 1 995) Diagnostic tests and
procedures in foals with colic. Vet. Med. 8:770-6.
Cohen N D, Chaffin M K ( 1 995) Assessment and initial
management of colic in foals. Compo Cont. Educ. Pract. Vet.
1 7 ( 1 ) :93-102.
Cudd T A ( 1 990) Evaluation of acute abdominal pain. In
Equine Clinical Neonatology, A M Koterba, W H Drummond,
P C Kosch (eds. ) . Lea and Febiger, Philadelphia, pp.
367-78.
Cudd T A, Wilson ] H ( 1 990) Diagnostic techniques for
abdominal problems. In A M Koterba, W H Drummond,
P C Kosch (eds.) Equine Clinical Neonatology, Lea and
Febiger, Philadelphia, pp 379-412.
467
22 GASTROINTESTINAL DISEASE I N THE FOAL
Klohnen A, Vachon A M, Fisher A T ( 1996) Use of diagnostic
ultrasonography in horses with signs of acute abdominal
pain.] Am. Vet. Med. Assoc. 209 ( 9 ) : 1597-160 1 .
Koterba A M ( 1 990) Physical examination. I n A M Koterba,
W H Drummond, P C Kosch (eds.) Equine Clinical
Neonatology, Lea and Febiger, Philadelphia, pp 71-83.
Murray M] ( 1 997) Foal stomach and duodenum. In Equine
Endoscopy] L Traub-Dargatz, C M Brown (eds.) 2nd edn.
Mosby, Baltimore, pp 159-7 1 .
Orsini,] A ( 1 997) Abdominal surgery i n foals. Vet. Clin. North
Am. Equine Pract. 1 3 ( 2) :393-413.
Diagnostic imaging procedures in the foal
Fisher A T, Yarbrough T Y ( 1 995) Retrograde contrast
radiography of the distal portions of the intestinal tract in
foals. ] Am. Vet. Med. Assoc. , 207:734-7.
Reef V B ( 1 992) Pediatric abdominal ultrasonography. In
Equine Diagnostic Ultrasound, WB Saunders, Philadelphia,
pp. 364-403.
Reimer] M and Bernard W V ( 1 998) Abdominal sonography
of the foal. In Equine Diagnostic Ultrasonography, N W
Rantanen and AO McKinnon (eds): Williams and Wilkins,
Baltimore, 627-36.
Reimer] M ( 1998) The Gastrointestinal Tract: The Foal. Atlas 0/
Equine Ultrasonography. Mosby, St Louis, pp. 200-1 1 .
Differential diagnosis and evaluation of the
foal with abdominal distension
Benamou A E, Blikslager A T, Sellon D C ( 1 995) Intestinal
atresia in foals. Compo Cont. Educ. Pract. Vet.
1 7 ( 1 2 ) : 1 5 10-16.
Chaffin M K, Cohen N D ( 1995) Assessing the history,
signalment and examination findings in foals with colic.
Vet. Med. 8:765-776.
Cohen N D, Chaffin M K ( 1 994) Intestinal obstruction and
other causes of abdominal pain in foals. Compo Cont. Educ.
Pract. Vet. 1 6 (6) :780-90.
Cohen N D, Chaffin M K ( 1 995) Assessment and initial
management of colic in foals. Compo Cont. Educ. Pract. Vet.
17 ( 1 ) :93-9.
468
Fisher A T ]r, Yarbrough T B ( 1 995) Retrograde contrast
radiography of the distal portions of the intestinal tract in
foals.] Am. Vet. Med. Assoc. 207:734.
Medical therapy in the foal with abdominal
pain
Cohen N D, Chaffin M K ( 1 995) Assessment and initial
management of colic in foals. Compo Cont. Educ. Pract. Vet.
1 7 ( 1 ) :93-103.
MacAllister C G, Morgan S], Borne A T, Pollet R A ( 1 993)
Comparison of adverse effects of phenylbutazone, flunixin
meglumine and ketoprofen in horses. ] Am. Vet. Med.
Assoc. 202 ( 1 ) :71-7.
Spurlock S L, Ward M V ( 1 99 1 ) Parenteral nutrition in
equine patients: principles and theory. Compo Cont. Educ.
Pract. Vet., 1 3 (3) :461-8.
Vaala W E ( 1 998) Neonatology. In Manual o/Equine
Emergencies: Treatment and Procedures,] A Orsini, T] Divers
(eds ) . W B Saunders, Philadelphia, pp. 473-503.
Surgical decision for the foal with colic
Bernard W V ( 1 992) Differentiating enteritis and conditions
that require surgery in foals. Compo Cont. Educ. Pract. Vet.
14: 535-7.
Cable C S, Fubini S L, Erb H N et aL ( 1 996) Abdominal
surgery in foals: a review of 1 19 cases ( 1 977-1994) . Equine
Vet. ] 29(4) :257-6 1 .
Klohnen A , Vachon A M, Fisher A T ( 1 996) Use of diagnostic
ultrasonography in horses with signs of acute abdominal
pain. ] Am. Vet. Med. Assoc. 209(9) : 1 597-60 1 .
Orsini,] A ( 1 997) Abdominal surgery i n foals. Vet. Clin. N.
Am. Equine Pract. 1 3 (2) :393-4 13.
Ragle C A ( 1 999) The acute abdomen: diagnosis,
preoperative management and surgical approaches. In
Equine Surgery, ] A Auer. and] A Stick (eds) : 2nd edn WB
Saunders, Philadelphia, p 224-32.
Vatistas N ], Snyder] R, Wilson W D ( 1996) Surgical
treatment for colic in the foal (67 cases) : 1980-1992.
Equine Vet. ] 28 ( 2 ) : 1 39-45.
 23
Stomach diseases of the foal
MJ Murray
Gastroduodenal ulceration
INTRODUCTION
There are many similarities between gastric ulceration
in foals and adult horses, but there are also important
differences
• the clinical signs are frequently more severe in foals
• involvement of the duodenum is common in foals
but rare in adult horses
• there is greater potential for debilitating or fatal
sequelae to gastroduodenal ulceration in foals.
Peptic disorders affecting the esophagus, stomach,
and duodenum have been recognized as important
conditions in foals for many years. In a 1964 report of
post-mortem findings of severely ulcerated stomachs
from foals, the author suggested that lesions might have
resulted from Gasterophilus intestinalis larvae, foreign­
body trauma (stones), or corticosteroid administration.
In the 1970s and early 1980s the veterinary literature
saw clinical reports that described fatal consequences of
severe, perforating gastroduodenal ulcers in foals. For
several years thereafter the typical 'ulcer' cases were
considered to be either foals which died suddenly as a
result of gastroduodenal perforation or foals showing
bruxism, ptyalism, or dorsal recumbency. In subse­
quent years, the number of foals examined for gastro­
duodenal lesions greatly increased and an expanded
spectrum of gastroduodenal lesions and clinical syn­
dromes was described. Recently, more has been learned
about gastric development and physiology from endo­
scopic and clinical findings, and methods of treatment
and prevention of gastroduodenal ulcers in foals have
changed.
ETIOPATHOGENESIS
The anatomy and physiology of the stomach of foals is
inherently the same as that in adult horses (see Chapter
12), but there are developmental issues that are perti­
nent to gastroduodenal ulceration in foals. The gastric
stratified squamous and glandular epithelia undergo
substantial development during late gestation and the
neonatal period. During mid-gestation the gastric squa­
mous epithelium is eight to ten cells thick, with a single
layer of basal cells. Cells are polyhedral in shape and are
not stratified. In the last month of gestation the basal
layers of the squamous mucosa become more numer­
ous, epithelial cells become flattened and stratified,
and a superficial layer of keratinized cells develops.
Differentiation of the glandular mucosa can be appreci­
ated by mid-gestation, and there is some staining for
mucosubstances in superficial cells. By the last month of
gestation the glandular mucosa appears more differen­
tiated and surface epithelial cells stain strongly for
mucosubstances, but there is no mucus layer over the
epithelium.
Mter birth, the gastric squamous epithelium under­
goes vigorous epithelial hyperplasia, including
increased epithelial cell layers, thickening of the kera­
tinized layers, and pronounced epithelial projections
extending into the lamina propria. The squamous
mucosal hyperplasia probably results from increasing
exposure to an acidic environment, in conjunction with
responses to local and possibly milk-derived growth
factor effects. The glandular mucosa appears fully
469
23 GASTROINTESTINAL DISEASE IN THE FOAL
differentiated, and there is a substantial mucous layer
covering the mucosal surface.
Recent studies have demonstrated that foals are
capable of substantial gastric acidification by 2 days of
age. In one report, I-day-old foals tended to have a rela­
tively high gastric pH and had few pH recordings less
than 4.0, but by 2 days of age, highly acidic pH values
were recorded more frequently. By 1 week of age,
gastric pH recordings were frequently less than 2.0. In
another report a similar temporal association with age
was found, and nursing was associated with an abrupt
increase in gastric pH, and conversely, gastric pH
became highly acidic when foals remained recumbent
and did not nurse for more than 20 minutes.
Gastric ulceration is classically considered to result
from an imbalance of aggressive factors (hydrochloric
acid and pepsin) and protective factors (mucus/bicar­
bonate barrier, mucosal blood flow, etc.), and in the
young foal this balance can easily be shifted toward pep­
tic injury. The gastric squamous epithelial mucosa has
minimal resistance to peptic i�ury, whereas the gastric
glandular mucosa has an array of protective mecha­
nisms. Thus, lesions in the gastric squamous mucosa are
primarily due to excessive exposure to hydrochloric
acid and lesions in the gastric glandular mucosa are
primarily due to impaired mucosal defenses.
Gastric acid secretion is regulated by several endo­
crine and paracrine mediators, and the balance between
stimulation and inhibition of acid secretion may be more
easily perturbed in the young animal than in an adult.
Mucosal protection also may be more easily perturbed
in foals compared to adult horses. Lesions in the gastric
glandular mucosa have been observed with greater
prevalence in young foals compared to adult horses.
In normal foals, glandular mucosal lesions are typi­
cally erosions, and these usually heal spontaneously. In
foals with a clinical disorder, this can range from a
painful musculoskeletal problem to septicemia, there
is an increased prevalence and severity of gastric
glandular mucosal lesions, presumably resulting from
impaired gastric mucosal blood flow, which reduces
gastric mucosal resistance to peptic injury.
Young foals also have a high prevalence (up to 50%)
of squamous mucosal lesions, which are primarily ero­
sions (Plate 23. 1). The gastric mucosa in the young foal
(up to 30 days old) is relatively thin and is characterized
by desquamation of superficial epithelial layers. These
traits may render this mucosa more susceptible to
peptic injury. Fortunately, in most cases the squamous
mucosal erosions heal without consequence.
We have not observed gastric lesions on post­
mortem examinations of aborted fetuses or in term
foals that died as a result of dystocia. However, we have
observed gastric lesions in foals as young as 2 days old,
470
regardless of the length of gestation. It appears that the
neonatal foal stomach secretes hydrochloric acid soon
after birth, even if the foal is born prematurely.
The pathophysiology of duodenal ulcer disease in
foals is assumed to involve peptic injury to the duodenum;
this may result from insufficiencies in duodenal mucosal
defenses or pancreatic secretions that can neutralize
acidic gastric effluent. Conversely, in some foals duode­
nal disease appears to reflect more widely distributed
enteritis and may not result directly from peptic injury.
In humans, duodenal ulcer disease is considered to
be a peptic disorder, but recently Helicobacter pylori has
been considered to be the primary direct cause of duo­
denal ulceration. The bacteria only colonize gastric
glandular mucosa, so infection of the duodenum must
be preceded by metaplasia of areas of duodenal mucosa
to gastric mucosa, which probably results from peptic
injury. Helicobacter spp. have been identified in many
animal species. Several investigators have examined
equine gastric mucosa for Helicobacter spp. by light
microscopy, mucosal urease activity, and by using poly­
merase chain reaction, but to date no evidence of
Helicobacter infection in equids has been reported.
Whereas glandular and squamous mucosal lesions
typically heal spontaneously, the inherent susceptibility
of the foal gastric mucosa to peptic injury enhances
the possibility for severe and catastrophic ulceration to
occur. Any condition that shifts the balance from heal­
ing to further peptic injury will promote the type of
gastroduodenal ulcer disease that is classically associ­
ated with foals.
ULCER SYNDROMES
There are several manifestations and complications of
gastroduodenal ulcers in foals
• mild gastric erosions with no apparent clinical signs
('silent ulcers')
• stress-induced gastric lesions in foals with another
disorder
• sudden onset severe gastric ulceration
• duodenal ulcer and duodenitis
• gastric outlet obstruction
• gastric or duodenal perforation with peritonitis
• pyloric ulceration
• duodenal ulceration
• gastroesophageal reflux
• pyloric or duodenal stricture.
'Silent ulcers'
This term refers to the absence of clinical signs in a foal
with gastric lesions. It is unlikely that foals with duode-

nal lesions will be free of clinical signs. The large major­
ity of foals with 'silent ulcers' have mild erosive lesions
that heal spontaneously. A small subset of foals with
gastric lesions but no clinical signs will develop more
severe gastric lesions and may present with a sudden
onset of severe or catastrophic signs reflecting gastric
outlet obstruction or pseudo-obstruction, or perfora­
tion.
Stress-induced gastric lesions
Foals with any clinical disorder have a greater preva­
lence of lesions in the gastric glandular mucosa (Plate
23.2) than normal foals. Also, there may be greater risk
for ulceration of the gastric squamous mucosa if the
foal's appetite and milk or feed intake is diminished
because of illness. In a prospective study, the prevalence
for gastric glandular lesions in foals in a neonatal inten­
sive care unit that did not receive ulcer prophylaxis was
40 per cent. This included foals born prematurely,
demonstrating that sufficient gastric acid can be
secreted to cause peptic injury in a premature foal.
Gastric ulceration is highly prevalent in human
intensive care units, and the incidence approaches 100
per cent in patients with severe burns. Gastric ulcera­
tion secondary to physiologic stress probably results
from disturbances in mucosal blood flow. In several
animal models of stress, exposure to a physiologic stres­
sor has been shown to reduce mucosal blood flow and
cause gastric lesions. Recently, investigators have shown
that reducing gastric mucosal constitutive nitric oxide
synthesis causes mucosal lesions whereas enhancing
nitric oxide synthesis protects against stress-induced
gastric mucosal lesions.
Stress is commonly considered to be a factor in
gastric ulcer development in people, and the term is
typically used to refer to psychological stress. In fact,
this type of stress has not been associated with an
increased prevalence of gastric lesions in most human
studies. Situations that we might perceive as being
stressful, such as long-distance transportation, herd
pressures, etc., have not been documented to affect the
incidence or prevalence of gastric lesions in foals. In
individual animals, however, many clinicians believe
that these situations may be stressful and contribute to
ulcer development.
Sudden onset severe gastric ulcers
Occasionally, foals will present because of acute abdom­
inal discomfort or depression, and will have no history
of a current problem or other disorder found on exam­
ination. Gastroscopy will reveal substantial ulceration,
typically in the gastric antrum and at the pylorus (Plate
23.3), but also in the gastric squamous mucosa. It is
STOMACH DISEASES OF THE FOAL 23
usually not possible to determine a cause for the severe
ulceration, which can be worse than lesions found in
foals that have an underlying disorder. The appearance
of the glandular mucosal ulcers often implies some dis­
turbance to gastric mucosal blood flow, and treatment
that should improve mucosal blood flow (sucralfate,
misoprostol) has appeared to benefit these foals.
Duodenal ulceration and duodenitis
Duodenal ulceration occurs with much less frequency
than gastric ulceration and in one retrospective study
duodenal ulcers were found in 28 of 511 (5%) foals
necropsied at a veterinary teaching hospital. Duodenal
ulcer disease is found almost exclusively in foals, and
foals of any age can be affected. Predisposing causes of
duodenal ulceration in foals are not known. Duodenitis
often accompanies enteritis, regardless of the cause.
Lesions occur primarily in the proximal duodenum,
and range from diffuse inflammation to focal, bleeding
ulcers. Lesions are seldom confined to the duodenum.
Gastric ulceration, and often esophagitis, accompanies
duodenal ulceration, because of impaired gastric
emptying. In fact, presenting signs often appear to
relate more to complications of duodenal ulceration
rather than the duodenal disease itself.
Duodenal ulceration can be difficult to confirm ante
mortem. Most cases present with acute abdominal dis­
comfort or with depression. Foals that have the 'classic'
gastroduodenal ulcer signs of bruxism and ptyalism
often have duodenal ulcer disease. Fever is often pre­
sent, due to either a concurrent enteritis or peritonitis
secondary to ulcer perforation. Duodenoscopy is the
most specific means of diagnosis (Plate 23.4).
Alternatively, if one can only examine the esophagus
and stomach, the presence of esophageal erosion or
ulceration and severe gastric ulceration is consistent
with duodenal ulceration and impaired gastric empty­
ing.
The prognosis for duodenal ulceration is worse than
for simple gastric ulceration, because of associated com­
plications (see below). Duodenal ulceration does not
seem to recur, as gastric ulceration often does, and
there can be complete resolution if there are no com­
plications.
Gastric outlet obstruction or pseudo­
obstruction
Gastric emptying results from coordinated myoelectric
activity that originates in the gastric antrum and is
propagated toward the pylorus and into the proximal
duodenum. Inflammation, erosion, and ulceration
affecting the pylorus or duodenum can impair gastric
emptying and cause pseudo-obstruction. Fibrosis may
471
23 GASTROINTESTINAL DISEASE IN THE FOAL
result from severe ulceration and can cause stricture of
the pylorus or duodenum.
There are several potential sequelae to impaired gas­
tric emptying. Retention of acidic gastric contents can
cause severe gastric ulceration. Reflux of acidic gastric
contents into the esophagus often occurs with impaired
gastric emptying, leading to esophagitis, esophageal
ulceration, and megaesophagus. Gastric pseudo­
obstruction implies a reversible condition, and if an
affected foal is treated aggressively, normal gastric
emptying can usually be restored. If ulceration has
progressed to fibrosis and stricture (Plate 23.5), the
long-term prognosis is less favorable.
Signs associated with impaired gastric emptying
include
• poor appetite
• abdominal discomfort
• belching
• poor body condition
• spontaneous nasal reflux of gastric contents
• ptyalism (secondary to esophagitis).
If impaired gastric emptying is suspected, endoscopy is
crucial to determine the nature and location of the
obstruction (stricture or pseudo-obstruction), and
whether medical or surgical treatment is indicated. In
lieu of endoscopy, barium contrast radiography may be
useful to document delayed gastric emptying. Scinti­
graphy has also been used.
Treatment of gastric pseudo-obstruction with a pro­
kinetic drug is usually effective. The author prefers
bethanecol, 0.02 mg/kg s.c., q. 6-8 h initially, then
0.35 mg/kg p.o., q. 8 h. If impaired emptying is due to
a partial stricture of the pylorus, medical management,
which includes bethanecol and treatment for ulcer
healing, can be effective, but must be maintained con­
tinuously. With severe stricture of the pylorus or duode­
num, surgical bypass (see below) will be required.
Perforation of the stomach or duodenum
Perforation is a dramatic, although infrequent, sequel
to gastroduodenal ulceration. In many cases, perfora­
tion is not preceded by typical gastric ulcer signs and
foals are found acutely depressed, in pain, or dead.
Most foals presented with perforation have widespread
peritonitis, which can have a tremendous fibrinous
component. In such cases it is possible for peritoneal
fluid cell count and protein to be normal because of
sequestration of cells and protein in fibrin clots within
the omentum. Careful inspection of a Wright's or gram­
stained slide for bacteria may confirm a perforated vis­
cus. Occasionally, a perforation in the stomach or in the
duodenal ampulla will be sealed by the greater omen-
472
tum. In these cases there will be evidence of peritonitis
(fever, shock, peripheral blood leukocytosis or leuko­
penia, hyperfibrinogenemia, increased peritoneal white
blood cell count, and protein concentration) but the
foal's condition will stabilize with intensive treatment.
Clinical signs vary depending on the location and sever­
ity of gastroduodenal lesions. Foals with gastric squa­
mous or glandular mucosal erosions often will have no
apparent clinical signs. Conversely, it is probable that
clinical signs will be expressed in a large majority of
foals with duodenal lesions.
The clinical signs most often associated with gastro­
duodenal lesions include
• abdominal discomfort
• poor nursing
• bruxism
• dorsal recumbency
• depression
• ptyalism
• diarrhea without fever or abnormalities in the
leukogram
• chronic poor condition.
Whereas these clinical signs are considered to be evi­
dence of gastroduodenal ulcers, they are not specific
for this condition. Poor nursing, diarrhea, and abdomi­
nal discomfort are associated with a number of gastro­
intestinal disorders in foals. Bruxism is a non-specific
sign of abdominal pain. Ptyalism is a sign of esophagitis,
and while most cases of esophagitis in foals are
secondary to gastroesophageal reflux, other causes
(foreign body, candidiasis) should be considered. Fever
often accompanies gastroduodenal ulcer conditions,
particularly if there is duodenitis or perforation of a
gastric or duodenal ulcer.
Importantly, if a foal is showing signs characteristic
for gastroduodenal ulcer disease, then the veterinarian
should presume that the foal has severe gastroduodenal
disease. One should perform or refer the animal for
further evaluation and treat very aggressively to reduce
the likelihood of catastrophic consequences.
DIAGNOSIS
Although the clinical signs described for gastroduode­
nal ulceration in foals may be non-specific they should
alert the veterinarian to the strong possibility that
gastroduodenal ulceration is a problem in the foal. If
gastroduodenal ulceration is suspected, an endoscopic

examination should be performed. It is vital to deter­
mine the extent and severity of ulceration so that appro­
priate treatment and management of the foal can
commence in order to avoid or minimize catastrophic
consequences. In cases with severe ulceration with
hleeding, aspiration of gastric contents will recover
brown-black fluid or material similar in appearance to
coffee grounds.
Because gastroduodenal ulceration may be sec­
ondary to other disorders or can cause significant com­
plications, a thorough evaluation of the foal is required.
A minimum database (CBC, serum chemistry profile,
urine analysis) should be collected. Other useful diag­
nostic procedures may include abdominal radiography,
abdominal ultrasonography, and peritoneal fluid analy­
sis. In neonatal foals with hleeding gastroduodenal
ulcers, fecal occult blood tests may be positive. In older
foals, the test is usually negative because of colonic
bacterial digestion of hemoglobin.
Radiography can be used to detect intestinal atony
or, using a barium contrast agent, to detect delaye�
gastric emptying. With severe duodenal or pyloric ulcer­
ation, survey radiographs of the cranial abdomen may
reveal accumulation of fluid within the stomach.
Contrast radiography has not been reported to be a reli­
able method for detecting gastric lesions in foals, with
the possible exception of very severe lesions. In many
foals with ulceration at the pylorus or in the duodenum
complete emptying of barium contrast is usually
delayed (> 2 hours), and an irregular mucosal border
may be noted in the descending duodenum. If stricture
has occurred, this may be noted. If the descending duo­
denum is to be imaged, the volume of contrast material
(20-40% aqueous suspensions of barium sulfate)
placed into the stomach should not exceed 0.5-1 liter
in a foal, and 1-2 liters in a weanling/yearling, or the
proximal descending duodenum will be obscured by
contrast within the stomach.
Abdominal ultrasonography and paracentesis can be
useful when gastric .or duodenal perforation is sus­
pected. Ultrasonography may reveal gastric or small
bowel distension with fluid, free fluid in the peritoneal
cavity, or fluid with gas (anaerobic growth) in the peri­
toneal cavity. Paracentesis may reveal an inflammatory
reaction with gastric or duodenal perforation, but in
some cases peritoneal fluid analysis can be misleading
because inflammatory cells may be sequestered in
fibrinous exudate.
In lieu of an endoscopic examination, the veterinar­
ian will need to rely on clinical signs and treatment
response, as well as the results of a thorough evaluation.
STOMACH DISEASES OF THE FOAL 23
Treatment must include aggressive suppression of
gastric acidity and may include mucosal protectants
and drugs that enhance gastric emptying. With simple
gastric ulcer disease, clinical signs should subside within
1-2 days. For example, if a foal's appetite is poor
because of ulcers, treatment with effective acid suppres­
sion will result in improved appetite within 24-48
hours. If abdominal discomfort is caused by ulcers, this
should resolve within 24 hours of the start of treatment.
With gastric emptying disorders or duodenal ulcera­
tion, response to treatment may be less satisfactory.
Conversely, clinical improvement may be noted in the
absence of improvement in lesions, because suppres­
sion of gastric acidity may be sufficient to alleviate pain,
but insufficient to facilitate healing. In such cases, there
can be a false belief in treatment success, only to have
catastrophic complications develop later.
TREATMENT (Tables 23.1. 23.2)
The treatment objectives for gastroduoden;!! ulcers in
foals are similar to those in adult horses (see Chapter
12), the main aim being the suppression of gastric acid­
ity, but there should be a heightened sense of urgency if
the foal is exhibiting clinical signs characteristic of
gastroduodenal ulceration. Because glandular mucosal
lesions form in a relatively large percentage of foals,
treatment with a mucosal protectant is often indicated.
Also, treatment with a drug that stimulates gastric
emptying is indicated whenever ptyalism is noted.
If the foal has abdominal discomfort or if gastric
obstruction or pseudo-obstruction are suspected, the
foal should be given an H2 antagonist intravenously or
intramuscularly. Use of a prokinetic drug should be
restricted until diagnostic evaluation is completed,
although in the author's experience administration of
bethanecol to foals with known pyloric or duodenal
strictures did not induce discomfort or worsen their
condition.
Oral treatment can be given when the foal is permit­
ted to nurse or ingest feed. Use of an H2 antagonist or
omeprazole (proton pump inhibitor) is indicated,
rather than an acid neutralizing product. Sucralfate,
and in selected cases misoprostol, can be added to the
treatment when oral intake is permissible. As with adult
horses, misoprostol can cause abdominal discomfort
and diarrhea in foals, and if given it should be adminis­
tered at the lower end of the dosage range (1.5 j1g/kg
p.o., b.i.d.) to test for tolerance, then gradually
increased.
473
23 GASTROINTESTINAL DISEASE IN THE FOAL

T,b" U.1 Typical tre.tmlmw':us�ln ttl.mlldlcal Tlble�34 �nttnued

man.rUnt of g��� ulctl'atlon.lnfOJls
Scenario 3: Foal is not nursing well, it has frequent mild
Drug (size) Recommended abdominal discomfort, and is lethargic. Physical
dosage examination and results of minimum database are within
normal limits. Endoscopy reveals extensive erosion and
Antacid ulceration of the gastric squamous mucosa, ulceration in
the glandular mucosa of the antrum, and hyperemia of the
MaaloxTC 240 ml (8 oz.), q. 4 h
mucosa at the pylorus.
Mylanta double strength 240 ml (8 oz.), q. 2 h

Treatment recommendation Treatment

H2antagonist
Cimetidine (800 mg tablets)
(150 mg/ml)
Ranitidine (300 mg tablets)
(25 mg/ml)
Proton pump inhibitor
Omeprazole (20 mg capsules
of enteric coated granules)
Omeprazole (paste
formulation)
Mucosal protectant
Sucralfate (1 9 tablets)
Misoprostol (200 IJg tablets)
Motility modifier
Bethanecol (5.15 mg/ml)
Bethanecol (50 mg tablets)
TJIjIt al�a. GllideliMs fOI'ti1emedlcal
"""___t of IastrOduOi:!tn.' !.Iletl'S in fOJls, fQ!.Ir
.
duration
25 mg/kg p.o., q. 8 h
7 mg/kg Lv., q. 6-8 h
Initial treatment
7 mg/kg p.o., q. 8 h
• cimetidine, 7 mg/kg Lv., q. 6 h, or 2-4 days, until
1.5 mg/kg Lv., q. 8 h
• ranitidine, 1.5 mg/kg Lv., q. 8 h, and foal nurses or
bethanecol, 0.02 mg/kg s.c., q. 8 h ingests feed
1 mg/kg p.o., s.Ld.
Subsequent treatment
• omeprazole paste, 4 mg/kg s.i.d. or • 3 weeks
4 mg/kg, p.o., s.Ld. • ranitidine, 7 mglkg p.o., q. 8 h, and
sucralfate, 10-20 mg/kg p.o., q. 8 h, and • 3 weeks
bethanecol, 0.35 mglkg p.o., q. 8 h • 10-21 days
Repeat endoscopy
10-20 mglkg p.o., q. 8 h after treatment
1.51J9/kg p.o., q. 8-12 h
up to 2.5 IJg/kg p.o., Scenario 4: Foal is presented because of depression and mild
q. 8 h abdominal discomfort. Physical examination reveals signs of
cardiovascular shock and fever. CBC reveals leukopenia and
mild anemia. Peritoneal centesis yields a small volume of
0.02 mg/kg s.c., q. 6-8 h fluid with the appearance of increased neutrophils and a
few intracellular bacteria. Gastroscopy reveals severe
0.35 mg/kg p.o., q. 8 h
ulceration of the gastric squamous mucosa and ulceration
of the glandular mucosa of the antrum and pylorus.
Because of poor gastric contractility the endoscope cannot
be advanced into the duodenum.

Treatment recommendation Treatment

dlfft_dl�c1Isca�· . . . .
duration

Scenario 1: Foal has mild signs of diminished nursing, Initial treatment

occasional mild abdominal discomfort, mild lethargy. • cimetidine, 7 mg/kg Lv., q. 6 h. or 4-7 days, until
Physical examination and results of minimum database are • ranltidine, 1.5 mg/kg Lv., q. 8 h, and foal nurses or
within normal limits. Endoscopy not done. bethanecol, 0.02 mg/kg s.c., q. 8 h ingests feed

Treatment recommendation Treatment Subsequent treatment

duration • omeprazole paste, 4 mg/kg s.Ld. or 3-12 weeks
• ranltldlne, 7 mg/kg p.o., q. 8 h, and
• omeprazole paste, 4 mg/kg, s.Ld., or • 2-3 weeks sucralfate, 10-20 mg/kg p.o., q. 8 h, and 3-4 weeks
• ranitidine, 7 mg/kg p.o., q. 8 h, or • 2-3 weeks bethaneco.l, 0.35 mg/kg p.o., q. 8 h 3-12 weeks
• cimetidine, 25 mglkg p.o., q. 6 h • 2-3 weeks Repeat endoscopy
after 4-7 days,
Scenario 2: Foal is not nursing well, it has frequent mild then every
abdominal discomfort, and is lethargic. Physical 7-14 days
examination and results of minimum database are within
normal limits. Endoscopy not done. Associated treatment
• broad spectrum antimicrobial treatment • 2-4 weeks
Treatment recommendation Treatment • anti-Inflammatory therapy • as needed
duration • intravenous fluid support • as needed
• intravenous nutritional support • while foal is nil
• omeprazole paste, 4 mg/kg s.i.d., or • 3-4 weeks per os
• ranitidine, 7 mg/kg p.o., q. 8 h, and
sucralfate, 10-20 mg/kg p.o., q. 8 h • 3-4 weeks

474
 STOMACH DISEASES OF THE FOAL 23

The duration of treatment depends on the severity feed intake, and thus contribute to ulcer formation in
of the gastroduodenal lesions as determined by individual animals.
endoscopy. Some lesions can heal remarkably quickly
(within 10 days); this is probably an age-related phe­
nomenon. In other cases treatment will be required for
several weeks. If treating empirically, the duration of Gastric endoparasitism
treatment should be based on the severity of presenting
signs and evidence for complications rather than the MJ Murray
clinical response to treatment, which can occur within a
few days and thus be misleading as to the progress of Endoparasitism of the stomach of foals is relatively
healing. A minimum duration of 2 weeks' treatment is uncommon because modern anthelmintics and para­
necessary, but 3 weeks is more prudent. If clinical signs site control programs are highly effective against para­
are severe, a treatment duration of 4--6 weeks is reason­ sitic species that may infect the stomach. Gasterophilus
able to ensure complete healing. spp. ( G. intestinalis, G. nasalis, and G. haemorrhoidalis) are
Surgery has been performed to bypass a strictured the most common gastric endoparasites, but occasion­
pylorus or duodenum with mixed results. The bypass ally infection with spirurid nematodes (Draschia mega­
procedure itself is relatively straightforward for experi­ stoma, Habronema muscae, H. majus) and the minute
enced surgeons, but several weeks are usually required worm (Trichostrongylus axei) occur.
for coordinated motility patterns to be established with
the stomach and the anastomosis site. In the interven­
ing period, treatment to suppress gastric acidity and GASTEROPHILUS SPP.
enhance motility should be maintained. Many foals that
require gastroduodenal bypass surgery are severely ill at Etiopathogenesis
the time of surgery and the surgery is attempted as a
The most common infestation of the stomach is with
salvage procedure. In most cases this either fails or the
larvae of the common bot fly Gasterophilus intestinalis.
foal fails to thrive. However, some foals have gone on to
Infestation is seasonal, primarily in the fall and winter
thrive and perform well. For the procedure to be suc­
months, and the larvae are readily killed by the iver­
cessful, the owner must accept a substantial long-term
mectin anthelmintics. Occasionally a foal may present
commitment, both financially and in the care of the
with a severe infestation of G. intestinalis or G. nasalis
foal.
larvae and have clinical signs referable to the gastro­
intestinal tract. The eggs (nits) of the common bot fly
are laid on the horse's legs from where they are
PREVENTION
ingested. The larvae of G. intestinalis develop within the
stomach and attach to the squamous or glandular
Prevention of gastric ulceration in foals at high risk of
mucosa, usually adjacent to the margo plicatus or in the
developing ulcers is best accomplished using acid sup­
dorsal fundus. The larvae will move within the stomach
pressive treatment. Foals of all ages admitted to our hos­
periodically. Usually the larvae are solitary, but occa­
pital are routinely treated with an acid suppressive drug,
sionally they will congregate into large clusters. The
and of these foals examined at post mortem, virtually
larvae of G. nasalis tend to develop and accumulate
none had gastric ulcers. This contrasts sharply with the
within the proximal duodenum.
stomachs of foals not treated prophylactically. The prac­
The larvae make a small defect in the mucosa, but
tice of ulcer prevention has become commonplace in
even with a large number of larvae there usually is only
equine neonatal ICUs in the United States. There has
minimal damage to the mucosa. There are reports,
not been a study to determine the optimal prophylactic
though, of gastric rupture associated with Gastero­
dose of acid suppressive drug for foals, and in our hospi­
philus larvae infestation.
tal we typically use either cimetidine at 7 mg/kg Lv., q.
6-8 h, or ranitidine 7 mg/kg p.o., q. 8 h. Use of a mucosal
Clinical signs
protectant such as sucralfate is reasonable, but should be
given in conjunction with an acid suppressive drug. Usually there are no associated clinical signs. Clinical
Other situations that may warrant ulcer prophylaxis signs do occur however when there is a large number of
in f()als include transportation, weaning, showing, or Gasterophilus larvae within the stomach or duodenum,
housing the foal in overcrowded conditions. None of particularly if they are in a large cluster. The signs of
these situations has been shown to increase the risk for Gasterophilus infestation can mimic those of gastro­
gastric ulceration, but they may affect the foal's milk or duodenal ulceration or there may be vague signs of

475
23 GASTROINTESTINAL DISEASE IN THE FOAL
abdominal discomfort. If lmvae are congegrated at the
cardia the foal may have signs of bruxism and ptyalism.
If many larvae are attached to the mucosa of the proxi­
mal duodenum there may be signs of gastric pseudo­
obstruction.
Diagnosis
Endoscopy is required for a definitive diagnosis.
Gastroscopy is performed because the foal presents with
either signs of abdominal discomfort or signs more sug­
gestive of gastroduodenal ulceration. Some foals will
have concurrent gastric ulceration, but because most
foals with Gasterophilus larvae do not have gastric
ulcers the association between the ulceration and the
Gasterophilus infestation is unclear.
Treatment
Larvae of Gasterophilusspp. are highly susceptible to treat­
ment with ivermectin, 200 llg/kg. There can be complete
elimination of the larvae within 24-48 hours of treat­
ment. The benzimadazole and pyrimidine anthelmintics
are ineffective in eliminating Gasterophilus larvae.
SPIRURID NEMATODES
The spirurid nematodes that can infect the equine
stomach are Draschia megastoma, Habronema muscae, and
H. majus. Once relatively common, gastric infection
with these parasites is now rarely encountered. Clinical
problems resulting from spirurid infection are uncom­
mon, but those that do occur result from infection with
D. megastoma which produces large, tumor-like lesions
in the gastric glandular mucosa. These lesions contain a
large number of larvae, and clinical problems result
only if the lesion obstructs the pylorus or if stomach
perforation occurs.
MINUTE STOMACH WORM
Typically, infection with Trichostrongylus axei is light and
causes no clinical problem. The larvae invade the gastric
glandular mucosa and may cause hypertrophic thicken­
ing and inflammation ifthe infestation is acute and heavy.
Infection with this parasite can cause sudden weight loss
in horses. The larvae are effectively eliminated by the
benzimadazole anthelmintics and ivermectin.
476
Gastric abscess
MJ Murray
Abscessation in the wall of the stomach is an infrequent
finding. Abscesses can form secondary to severe gastric
ulceration, Rhodococcus equi bacteremia, foreign body
penetration, or septic peritonitis. Signs of gastric absces­
sation are variable and similar to abscessation in other
organs
• fever
• neutrophilia
• hyperfibrinogenemia
• anemia
• weight loss
• and possibly colic.
Diagnosis may be made endoscopically, radiographi­
cally, or ultrasonographically. Treatment should
include drainage, but since this is usually not possible,
outcomes are usually poor. There is often extensive
involvement of abdominal viscera.
BIBLIOGRAPHY
Gastroduodenal ulceration
Furr M 0, Murray M] and Ferguson D C (1992) The effects
of stress on gastric ulceration, T" T4, rT" and cortisol in
neonatal foals. Equine Vet.J 24:37-40.
Murray M, Hart], Parker G A (1987) Equine gastric ulcer
syndrome: Prevalence of gastric lesions in asymptomatic
foals. Proc. Am. Assoc. Equine Pract. 33:769.
Murray M] (1989) Gastroendoscopic appearance of gastric
lesions in foals: 94 cases (1987-1988}.J Am. Vet. Med.
Assoc. 195:1135-42.
Murray M], Mahaffey E A (1993) Age-related characteristics
of the equine gastric squamous epithdial mucosa. Equine
Vet.J 25:514-17.
Sanchez L C, Merritt A M, Lester G D (1998) Effect of
ranitidine on intragastric pH in clinically normal neonatal
foals.J Am. Vet. MedAssoc. 212:1407-12.
Wilson] H (1986) Gastric and duodenal ulcers in foals: A
retrospective study.Proc. Second Equine Colic Res. Symp.
pp.126-8.
Gastric endoparasitism
Drudge] H, Lyons E T (1986) Internal parasites of horses.
Hoechst-Rousse1 Vet. Company [place].
 24
Small intestinal diseases associated
with colic in the foal

J Orsini

INTRODUCTION CONGENITAL DEFECTS ASSOCIATED

WITH COLIC
There are a number of congenital defects and anom­
alies that may cause colic and/or small intestinal Scrotal and inguinal hernia
obstruction or strangulation in foals. These include
Scrotal hernia may be noticed within a few days of birth
scrotal or inguinal hernia, umbilical hernia, and the
as a soft, fluctuant swelling in the inguinal region and
congenital anomalies called Meckel's diverticulum
scrotum. The hernia can be reduced easily when the
and mesodiverticular band. Diaphragmatic hernia can
foal is rolled onto its back. Scrotal hernias in adult
occur in foals but it is usually the result of trauma
horses are not easily reduced and the difference
and is a very rare congenital defect. Other very rare
between adults and foals is probably because of the rel­
congenital defects that may cause colic in foals
atively shorter, wider, and more direct configuration of
include segmental lymphatic aplasia with chyloab­
the foal's inguinal canal. Scrotal hernias in foals often
domen (chyloperitoneum) , and jejunal diverticulum.
resolve spontaneously, and strangulation of small intes­
Congenital mesenteric defects, especially in the
tine is rare. The size of the external inguinal ring does
mesentery of the small intestine, may lead to incar­
not seem to play a role in the problem, usually the
ceration of a loop of small intestine ending in stran­
external rings are 5 cm in length on both sides. Scrotal
gulation or volvulus. A persistent mesodiverticular
hernias usually occur on one side only, but bilateral her­
band may predispose the adjacent mesentery to
nias may occur (Figure 24.1) .
rupture.
A figure-of-eight bandage may be applied over the
The major challenge, in fact, is diagnostic. Rectal
scrotum and prepuce to encourage resolution of the
palpation yields helpful, sometimes definitive, diagnos­
hernia. The bandage should be made of adhesive elastic
tic information in the adult horse but is not generally
material and care must be taken not to cover the anus
feasible in the foal because of its small size. It therefore
or end of the prepuce with the bandage. Surgical cor­
can be difficult to distinguish medical from surgical
rection is recommended for an uncomplicated hernia if
cases of colic. Frequently a 'watch and wait' or 'medical
it does not resolve spontaneously by 3-6 months, or if
treatment first' approach can carry as much risk as
the owner is concerned because of an apparent increase
exploratory surgery.
in the size of the hernia. Correction with castration is
Other acquired small intestinal diseases in foals
recommended. Surgical correction may be done by
causing colic and which may require surgical correction
include • an inguinal approach with castration
• laparoscopic repair with castration
• volvulus • an inguinal approach without castration
• impaction by ascarids or meconium • a midline celiotomy with closure of the vaginal ring.
• intussusception
• abdominal abscess. The last two methods may cause atrophy of the

477
24 GASTROINTESTINAL DISEASE IN THE FOAL
Figure 24.1 Sonogram obtained from a 1-week-old
Standardbred colt with a bilateral inguinal hernia. Notice
the excess fluid contained within the scrotum, the normal
testicle (three arrowheads), and the adjacent jejunum
with normal peristalsis (five arrowheads). From Reef V B
(ed.) (199B) Equine Ultrasonography, W B Saunders,
Philadelphia, with permission
testicle, and the last method may cause intra-abdominal
adhesions. The intestines need not be exposed or eval­
uated if strangulation has not occurred and there is no
clinical evidence of intestinal abnormality.
Although most inguinal hernias are indirect in
horses (Le. the intestine passes through the vaginal ring
into the vaginal tunic) , foals can present 4-48 hours
after birth with a direct inguinal hernia. This occurs
when there is rupture of the common vaginal tunic and
jejunum and occasionally a testicle escapes through this
rupture into the subcutaneous space of the scrotum
and prepuce. Direct or ruptured inguinal hernia in
foals causes intermittent colic, severe scrotal and
preputial swelling and edema, with skin excoriation and
splitting caused by abrasion against the inside of the
thigh. These hernias are usually not reducible and
surgery is required. The torn edges of the common
vaginal tunic should be repaired as much as possible to
the level of the vaginal ring. The superficial or external
inguinal ring should also be sutured, preferably with a
continuous pattern to obtain a more complete seal.
Usually the intestine is viable, but progressive necrosis
has been reported.
Umbilical hernia
Umbilical hernia occurs in 0.5-2 per cent of young
horses. It is considered the second most common con­
genital defect in horses (the most common being cryp­
torchidism, accounting for 1 per cent of hospitalizations
478
of young horses in one study) . Females are at greater
risk for the defect, with an odds ratio of about 2: 1.
Digital palpation and ultrasonography (Figure 24.2)
are used to determine the size and shape of the hernial
ring, contents of the hernial sac, its reducibility, and the
nature of the tissue surrounding the ring. A thickened
fibrotic ring holds sutures more reliably if the hernia is
repaired surgically. Hernial contents may include
omentum,jejunum, ileum, cecum, and ventral colon, as
well as an antimesenteric portion of small intestinal wall
called a Richter's or parietal hernia.
Smaller hernias may resolve spontaneously and
incarceration of intestine in the hernial ring is rare. In
one report, 13 of 147 horses with umbilical hernias
admitted to a university hospital had developed compli­
cations, including intestinal strangulation, abscessation,
and enterocutaneous fistula. Surgical repair is usually
undertaken for cosmetic reasons. Frequent monitoring
of hernias and early repair of large hernias (> 10 cm) is
recommended, because strangulation may develop at
any time. Strangulation should be suspected in a non­
reducible umbilical hernia that increases in size and
warmth, and is painful, firm, or edematous. Severity of
pain is not a reliable indicator of strangulation or other
complications. When a loop of small intestine is
involved, it usually dissects back to the inguinal region
where most of the swelling occurs.
Surgical reduction is necessary for umbilical hernias
that contain incarcerated intestine. With the foal in a
dorsal recumbent position, a 10-15 cm incision is made
cranial to the hernia ring to avoid accidental puncture
of incarcerated bowel. Once the abdomen has been
opened and the involved intestine identified, the inci­
sion is extended to and around the hernial ring. The
incarcerated bowel and its attachments to the hernial
ring may be resected. If an enterocutaneous fistula is
involved, special care should be taken to clean the fis­
tula and isolate it from the surgical field by packing it
and suturing skin over it.
Meckel's diverticulum and mesodiverticular
band
Meckel's diverticulum and the mesodiverticular bands
are congenital anomalies that arise from remnants of
the vitelline duct and arteries. In the embryo, the
vitelline duct connects the lumen of the gut to the yolk
sac. The vitelline arteries run on either side of the
mesentery from the aorta to the yolk sac. As the yolk sac
regresses and involutes at 5-10 weeks of gestation, the
right vitelline artery becomes the cranial mesenteric
artery, the left vitelline artery regresses, and the vitelline
duct also involutes. Anomalies result if the vitelline duct
persists as a tubular projection from the distal jejunum
 SMALLINTESTINAL DISEASES ASSOCIATED WITH COLIC IN THE FOAL 24

Figure 24.2 Sonograms of the umbilicas and ventral abdomen obtained from a 9-month-old Quarter horse colt with an
umbilical hernia. The right side of these sonograms is cranial, and the top is ventral, a) sonogram of the umbilical swelling
demonstrating the large umbilical abscess (arrows) associated with the umbilical hernia, b) sonogram of the thickened
ileum trapped within the hernia. From Reef V B (ed.) (1998) Equine Ultrasonography, W B Saunders, Philadelphia, with
permission

or ileum or if the left or right vitelline arteries persist as present, they are often if not always implicated in mor­
bands of tissue (Figure 24.3) . Any of these anomalies bidity and mortality.
may cause incarceration, strangulation, or volvulus of
the small intestine, and the diverticulum may become Mesenteric defects
infected and necrotic. Most of the reported cases have
Congenital mesenteric defects, especially in the mesen­
been in adult horses, although there are reports of a 3-
tery of the small intestine, may lead to incarceration of
month-old foal and a 6-month-old foal that were
a loop of small intestine, and may end in strangulation
affected. It was initially thought that these anomalies
or volvulus. These defects are rare. A persistent mesodi­
were quite common in horses, but recent studies sug­
verticular band may predispose the acljacent mesentery
gest that they are quite rare. However when they are
to rupture.

Chyloabdomen

Chyloabdomen is a rare condition that may cause colic

Figure 24.3 A large Meckel's diverticulum with a diameter
equal to that of the small intestine
in foals 12-36 hours after birth. Affected foals seem
healthy initially and then develop signs of colic but usu­
ally without reflux or abdominal distension.
Abdominocentesis yields a copious flow of milky,
opaque fluid with a triglyceride concentration 100
times the reference value. The cell count may be nor­
mal and the nature of the fluid precludes protein deter­
minations with a refractometer.
Surgical findings include an abdomen full of white,
opaque fluid and a variable length of jejunum that is
thick-walled, turgid, and discolored white to yellow.
Associated mesenteric lymphatics are white and
markedly distended. Subserosal lymphatic vessels are
distended with lymph, and some rupture to form coa­
lescing yellow-white plaques. The condition seems to be
caused by congenital absence of a communication
between afferent and efferent lymph vessels from the
involved lymph nodes, with subsequent mesenteric lym­
phangitis and lymphangiectasis. Intestine proximal to

479
24 GASTROINTESTINAL DISEASE IN THE FOAL
Figure 24.4 Sonogram of the left side of the thorax
obtained in the tenth intercostal space from a 1-month­
old Standardbred filly with a diaphragmatic hernia. The
fluid-distended small intestine (SI) is immediately adjacent
to the ventral lung with no diaphragm separating them
the affected segment is usually distended, and this, pos­
sibly associated with the irritation of chyle in the
abdomen, could explain the signs of colic.
Resection of the affected intestine can produce a sat­
isfactory outcome. Conservative treatment with anal­
gesics, antibiotics, and intravenous fluids led to a full
recovery in one foal with chyloabdomen.
Diaphragmatic hernia
Diaphragmatic hernias can occur in foals, either as a
rare congenital defect in which there is incomplete
fusion of the pleuroperitoneal folds in the dorsal tendi­
nous portion of the diaphragm, or more commonly as a
result of trauma. They can be treated successfully by
direct closure or by insertion of a mesh implant.
Presenting signs are usually non-specific, but ultra­
sound (Figure 24.4) and radiographic examinations
may reveal loops of bowel in the thoracic cavity. Most
cases are diagnosed at surgery without a preoperative
diagnosis.
ACQUIRED SMALL INTESTINAL
DISEASES ASSOCIATED WITH COLIC
Gastroduodenal ulcers and obstructions (see
Chapter 23)
Gastric ulcers are common in foals of all ages, particu­
larly those treated with non-steroidal anti-inflammatory
drugs or subjected to various forms of stress. Diarrhea is
the most common clinical sign of gastroduodenal
480
ulcers, but teeth grinding, salivation, and signs of colic
are also suggestive of ulcers. Gastric reflux and fever
may also be observed. Ulcers may not always be mani­
fested by signs of acute colic. Laboratory studies may
show high total white blood cell counts or elevated
plasma fibrinogen levels. The medication history is
helpful in evaluating the possibility of ulcers. In foals, a
regimen of phenylbutazone at 10 mg kg-I d-I may pro­
duce severe gastrointestinal ulcers and diarrhea as early
as day 3 of treatment. Flunixin meglumine is also poten­
tially ulcerogenic, but low doses (0.5-1.1 mg kg-I d-I)
have been used safely in neonates. Ulceration may be
suspected in a foal with colic if there is a history of non­
steroidal anti-inflammatory drug treatment or of signif­
icant stress such as surgery, transportation, or other
illness; however these factors can be difficult to docu­
ment. There can sometimes be an outbreak of duo­
denal ulcers in a herd.
Ulcers with outflow obstruction can be difficult to
confirm by contrast radiography. Diagnostic signs on
plain radiographic films include aspiration pneumonia,
dilated fluid-filled esophagus, and gastric distension;
gas may be present in the hepatic duct. Endoscopy is
more sensitive and specific than radiography in diag­
nosing esophageal and gastric lesions, and it also allows
biopsy. Endoscopic studies have shown erosions and
ulcers in a substantial proportion of foals that do not
have signs of colic.
Ulcers can be managed medically, although duode­
nal and gastric ulcers can perforate. Severity of pain is
not always a reliable guide. Perforation has occurred in
moribund foals showing no or only mild signs of gas­
trointestinal disease and in which ulcers were not sus­
pected. Surgery is indicated if barium contrast
radiographs suggest gastroduodenal obstruction, illus­
trated by reflux of fluid from the stomach to esophagus,
an enlarged gastric silhouette, and delayed gastric emp­
tying (> 2 hours) . Surgery is undertaken to prevent
complications - primarily ulcer perforation and gastric
outflow obstruction - as well as to relieve colic and pro­
mote mucosal healing. Surgery has been used success­
fully to repair a perforated gastric ulcer in a foal.
Foals younger than 4 months of age are at a greater
risk of developing gastroduodenal obstruction sec­
ondary to ulcers. Potential sites of obstruction are the
cardia, gastric antrum, pylorus, and duodenum. Many
affected foals have been depressed, weak, and anorectic
in the days or weeks preceding examination, and radi­
ographic views show gastric and esophageal distension.
Volvulus of the small intestine
Volvulus of the small intestine is the most common indi­
cation for intestinal surgery in the foal. It most often
 SMALLINTESTINAL DISEASES ASSOCIATED WITH COLIC IN THE FOAL
Figure 24.5 Sonogram of the abdomen obtained from a
3-week-old Thoroughbred colt with a small intestinal
volvulus. Turgid distended loops of jejunum are filled
with anechoic fluid with only a small amount of ingesta
distended (white arrow). From Reef V B (ed.) (1998)
Equine Ultrasonography, W B Saunders, Philadelphia,
with permission
involves the distal jejunum and ileum. Any length of
small intestine ranging from a few centimeters to sev­
eral meters may be twisted or knotted. Volvulus is seen
most often in foals younger than 3 months and may be
a result of changing feeding habits as the foal adapts to
digesting bulkier adult food. Other reported risk factors
include peritonitis, previous abdominal surgery, and
parasite burden.
Pain may seem to fluctuate but quickly becomes
severe, and affected foals often lie on their sides or
assume a position of dorsal recumbency. As the foal's
condition deteriorates, the small intestine begins to dis­
tend with gas; at this point, the abdomen becomes dis­
tended and peristalsis is not evident on abdominal
auscultation. Rapid and labored respiration, high fever,
a weak and rapid pulse, and injected mucous mem­
branes indicate a deteriorating condition, and differen­
tiate volvulus (sometimes too late for successful
intervention) from ileus. Ultrasonography has proven
to be a useful ancillary diagnostic modality (Figure
24.5) .
At surgery, the twisted loop is often located close to
the ileocecal valve and is generally recognized easily by
its purple congested appearance. In some cases the twist
is very loose and easily freed, whereas in others it is dif­
ficult to reduce. After correcting the volvulus, resection
and anastomosis can be p t;:rformed.
24
Small intestinal impaction
Ascarid impaction (see Chapter 13)
Intestinal stages of Parascaris equorum may cause intesti­
nal obstruction, intussusception, abscessation, and even
rupture in older foals (2-4 months) , but this is more
common in weanlings (median age 5 months; range
4-24 months) . Affected foals usually appear parasitized
and unthrifty, and impaction usually follows
anthelmintic treatment by 1-5 days. A history of recent
anthelmintic administration should always raise the
question of a possible ascarid impaction in a foal with
acute colic. Impactions may occur without anthelmintic
treatment however. Because foals develop a natural
immunity to this parasite, infection rates decline after 6
months of age. Ultrasonography has been used to con­
firm an ascarid impaction in those cases where the
cause for the acute abdominal crisis is unclear (Figure
24.6) .
Surgical removal of impacted ascarids is indicated in
foals with clinical signs of obstruction. Impactions may
occur at more than one site, but distal jejunum and
ileum are the most common sites, followed by the
cecum and other parts of the jejunum, and the pelvic
flexure. Enterotomy is required to relieve the
impaction and resection may be indicated if the bowel
Figure 24.6 Sonogram of the abdomen obtained from a 5-
month-old Paint colt with an ascarid impaction. The thick
echogenic ascarid worm (arrow) is surrounded by fluid in
the small intestine. From Reef V B (ed.) (1998) Equine
Ultrasonography, W B Saunders, Philadelphia, with
permission
481
24 GASTROINTESTINAL DISEASE IN THE FOAL

is devitalized. Damage to the intestinal wall at the site of

the impaction often causes peritonitis and adhesions,
and the mortality rate may be as high as 92 per cent.
To prevent ascarid impaction, heavily parasitized
f()als should be wormed with a slow-acting drug such as
a benzimidazole (e.g. thiabendazole - the least effective
and therefore the safest, and fenbendazole) .
Ivermectin, also slow acting but highly effective against
this parasite, can be given 3 weeks later. The goal of
treatment is to reduce the numbers gradually, rather
than kill all the ascarids simultaneously leaving a mass
of dead worms in the lumen of the bowel.

Meconium impaction (see Chapter 25)

Retention of meconium is a frequent cause of intestinal Figure 24.7 Sonogram of the ventral abdomen obtained
obstruction in neonates, most commonly involving the from a 3-day-old Thoroughbred colt with an intussuscep­
rectum and small colon. Most cases respond to medical tion. Notice the characteristic target or 'bull's-eye' sign of
the intussusception. The 'bull's-eye' sign is created by the
treatment with enemas, intravenous fluids, and laxa­
edematous outer intussuscipiens (solid arrow), a fluid layer
tives. Meconium impaction may be difficult to differen­
between the outer intussuscipiens and the inner intussus­
tiate from ruptured bladder and from atresia ani, a ceptium, and the more echogenic inner intussusceptum
relatively rare congenital defect. Foals with ruptured (open arrow). From Reef V B (ed.) (1998) Equine
bladder are usually older (usually at least 3-4 days of Ultrasonography, W B Saunders, Philadelphia, with
age) . If medical treatment does not result in the passage permission
of meconium, or if colic signs persist, surgery may be
indicated.
In a recent study, 8 of 24 foals with meconium
impaction required surgery, and 2 of these 8 required
an enterotomy. Of these 8 foals, there were 7 with fol­
low-up information after surgery; 2 were euthanized
because of serosal adhesions after enterotomies to evac­
uate the impaction, and 4 matured and raced without
complications.

Intussusception

Small intestinal intussusception has been regarded as

being a common condition in foals, but recent clinical
experience and the results of two retrospective studies
which did not identify a single case in a series of 87 foals
with colic, suggest that it is very rare. The small intestine
can invaginate into the cecum or into itself, conditions
that may begin as simple obstructions and progress to
strangulation as the tissue becomes edematous and the
vascular supply is compromised (Figures 24.7 and 24.8) .
The cause of intussusceptions is not known, but they
have been associated with bacterial and protozoal
(Eimeria leukarti) infection in one case, and treatment
with an organophosphate anthelmintic in another.
Intussusception can present as acute colic that is dif­
ficult to distinguish from volvulus. In other cases signs
may be subacute or chronic. The subacute form may fol­
Iow a bout of diarrhea in young foals, they may also grind
their teeth and show moderate signs of colic. Those with
the chronic form become anorectic and unthrifty and
Figure 24.8 Sonogram of the ventral abdomen obtained
from a 5-day-old Thoroughbred colt with an intussuscep­
tion. Notice the fibrin between the thick outer intussuscip­
iens (outer arrows) and the inner intussusceptum (inner
arrow). From Reef V B (ed.) (1998) Equine
Ultrasonography, W B Saunders, Philadelphia, with
permission
they are often only diagnosed at necropsy, underscoring
the importance of exploratory celiotomy in diagnosing
unexplained and persistent colic. Gentle traction and
manipulation can relieve an intussusception, although a
jejunocecostomy is sometimes necessary.

482
 SMALLINTESTINAL DISEASES ASSOCIATED WITH COLIC IN THE FOAL
Necrotizing enterocolitis
This is a rare but highly fatal disease of newborn foals,
particularly those stressed at birth by dystocia, placental
disease, and other causes of immaturity. The cause is
probably multifactorial, although intestinal ischemia or
hypoxia is a predisposing factor for this disease in
human infants. In foals, the intestinal mucosa is usually
intact but gas-forming bacteria seem to colonize the
bowel wall and cause gas accumulation. Bowel perfora­
tion can follow. Gross appearance of the affected bowel
includes submucosal emphysema, hemorrhage, edema,
and inflammation in the intestinal wall.
Radiographs are often diagnostic. Segments of intes­
tine viewed in cross section have a double-ring appear­
ance caused by a radiolucent layer of gas separating
layers of the bowel wall. Many linear strips or 'bubbles'
of gas can be seen in the intestinal wall (pneumatosis
intestinalis, Figure 24.5) and gas distension of the
affected segment should be evident. Gas in the peri­
toneal cavity is evidence of rupture.
Surgery to resect affected intestine; nutritional, fluid,
and electrolyte support; and antibiotics are required.
The prognosis is poor especially if surgery is delayed, the
lesions are too extensive for intestinal resection, or the
foal is too debilitated for other reasons.
Abscess
Mesenteric and intestinal abscesses can cause intestinal
obstruction and colic in foals. Foals with abscesses in
the umbilical remnants are usually younger than
Figure 24.9 Sonogram obtained from a 2-month-old
Thoroughbred filly with an abdominal abscess. The
abscess (arrows), which is lying against the floor of the
ventral abdomen, has a multi loculated appearance. From
Reef V B (ed.) (1998) Equine Ultrasonography, W B
Saunders, Philadelphia, with permission
24
6 weeks of age. Foals with mesenteric abscesses
(Streptococcus spp. and Rhodococcus equi) are usually 2-6
months old, and may have no pulmonary involvement.
Clinical signs of abscesses in foals include recurrent,
mild colic in some but not all cases, fever unresponsive
to antibiotics, neutrophilic leukocytosis, and hyperfib­
rinogenemia. Mesenteric abscesses are heavy and tend
to migrate to the ventral abdomen where they can be
detected by ultrasound examination (Figure 24.9) .
Surgical treatment by bypass or marsupialization is pos­
sible in some cases.
POSTOPERATIVE MANAGEMENT AND
COMPLICATIONS
Close postoperative monitoring is needed to avoid
potentially fatal complications of abdominal surgery in
foals. The main concerns in the immediate postopera­
tive period are ileus and hypovolemic or endotoxic
shock. Sepsis accounts for significant morbidity and
mortality in foals following abdominal surgery, and
antibiotic therapy must be tailored to the different
metabolism of very young foals, with adequate coverage
for gram-negative bacteria in any septicemic foal.
Peritonitis may occur following leakage of bacteria from
the bowel into the peritoneal cavity. Foals seem to be
especially prone to intestinal adhesions after abdominal
surgery, and may require a second procedure when
signs of colic and obstruction recur. Small intestinal
lesions are associated with a higher incidence of abdom­
inal adhesions than colonic lesions. Experimentally,
adhesions have been shown to result from ischemia or
distension of the small intestine.
OUTCOME AND PROGNOSIS
In certain respects foals are good candidates for
surgery. Their size mitigates some of the problems of
abdominal surgery in adult horses, and survival rates of
foals do not seem to be significantly worse than survival
rates of adults. This is not true for very young foals, how­
ever. Foals younger than 1 week of age had the worst
odds of survival, and the odds improved for the 1-
month-old group, and improved even further for the
1-3-month-old foals. In a recent report of 67 foals with
surgical colic, only 10 per cent of foals under 14 days of
age survived to maturity compared to 46 per cent of
foals between 15-150 days of age. Short-term survival
for foals of this age with colic surgery has been reported
as 63-65 per cent, and long-term survival is about 40 per
cent, similar to the reported long-term survival of older
horses undergoing colic surgery (45 per cent) . As
483
24 GASTROINTESTINAL DISEASE IN THE FOAL
expected, colic surgery survival rates vary widely accord­
ing to the diagnosis, the compromised condition of
many surgical colic patients is also a significant con­
founding factor in survival. One of the major challenges
in foals is diagnostic. Because rectal examination is not
possible, it may be even more difficult to distinguish
medical from surgical cases of colic. Frequently a 'watch
and wait' or 'medical treatment first' approach can
carry as much risk as exploratory surgery.
BIBLIOGRAPHY
Crowe M W, Swerczek T W (1985) Equine congenital defects.
Am.]. Vet. Res. 46(2): 353-8.
Edwards G B, Scholes S R, Edwards S E R, et al. (1994) Colic in
four neonatal foals associated with chyloperitoneum and
congenital segmental lymphatic aplasia. In: Proceedings of
the Fifth Equine Colic Research Symposium, Athens, GA, p. 35.
Freeman D E, Koch D B, Boles C L (1979) Mesodiverticular
hands as a cause of small intestinal strangulation and
volvulus in the horse.]. Am. Vet. Med. Assoc.
175(10):1089-94.
Freeman D E, OrsiniJ A, Harrison I W, et al. (1988)
Complications of urn hilical hernias in horses: 13 cases
(1972-1986).]. Am. Vet. Med. Assoc. 192:804-7.
Freeman D E, Spencer P A (1991) Evaluation of age, breed,
and gender as risk factors for umbilical hernia in horses of
a hospital population. Am.]. Vet. Res. 52:637-9.
484
Hooper R N (1989) Small intestinal strangulation caused by
Meckel's diverticulum in a horse.]. Am. Vet. Med. Assoc.
194(7):943-4.
Klohnen A, Wilson D G (1996) Laparoscopic repair of scrotal
hernias in two foals. Vet. Surg. 25:414-16.
Lundin C S, Sullins K E, White N A, et al. (1989) The
pathogenesis of peritoneal adhesions in the foal
(abstract). Vet. Surg. 18:65.
Markel M D, PascoeJ R, Sams A E (1987) Strangulated
umbilical hernias in horses: 13 cases (1974-1985).]. Am.
Vet. Med. Assoc. 190:692-4.
OrsiniJ A (1997) Abdominal surgery in foals. Vet. Clin. N. Am.
Equine Pract. 13(2) :393-413.
Priester W A, Glass M D, Waggoner, N S (1970) Congenital
defects in domesticated animals: general considerations.
Am.] Vet. Res. 31:1871-9.
RobertsonJ T (1982) Obstructive diseases - congenital
diseases. In: Equine Medicine and Surgery 3rd edn, RA
Mansmann, E S McAllister, P W Pratt (eds). American
Veterinary Publications, Santa Barbara, CA, 1982, pp.
559-71.
Sprinkle F P, Swerczek T W, Crowe M W (1984) Meckel's
diverticulum in the horse. Equine Vet. Sci. 4(4):175-6.
Spurlock G H, RobertsonJ T (1988) Congenital inguinal
hernias associated with a rent in the common vaginal
tunic in five foals.]. Am. Vet. Med. Assoc. 193:1087-8.
van der Velden M A (1988) Ruptured inguinal hernia in new­
born colt-foals: A review of 14 cases. Equine Vet.].
20:178-81.
YovichJ V, Horney F D (1983) Congenital jejunal
diverticulum in a foal.]. Am. Vet. Med. Assoc. 183:1092.
 25
Large and small colon diseases
associated with colic in the foal

that of high impactions. High impaction is a more prox­

Retained meconium imal obstruction of the gastrointestinal tract, in the
author's experience this generally occurs in the trans­
WV Bernard verse or right dorsal colon.

INTRODUCTION Clinical signs

Clinical signs of meconium retention may include any
Meconium is a product of glandular secretions, swal­
combination of the following
lowed amnionic fluid, epithelial cells, mucus, and bile.
Throughout gestation this material is moved along the • repetitive unproductive tenesmus
fetal gastrointestinal tract by peristalsis and is stored in • tail flagging/swishing
the colon and rectum. Meconium varies in color from a • stretching
glossy black to a dark brown. The consistency and form • posturing as if to defecate (kyphotic posture -
of this first stool can be hard, grape-size pellets or a humped back)
sticky, tarry toothpaste-like material. The change to a • abdominal pain
less tenacious material generally indicates that the • abdominal distension
meconium has been passed. • lack of interest in suckling.
The initial passage of meconium usually begins in
the first few hours after birth. Meconium passage is gen­
erally complete within 24 hours, however it can take up
to 48 hours. The time spent evacuating meconium is
not the critical factor when considering meconium
retention. The degree of pain, discomfort, and strain­
ing, and alterations in the routine foal behavior are the
critical factors to be considered when evaluating the
possibility of meconium retention. It is not atypical for
newborn foals, standing or in lateral recumbency, to
strain considerably when passing meconium. These
attempts should be productive. Male foals (possibly as a
result of narrowed pelvic inlet) and foals resulting from
prolonged gestation appear to be predisposed to meco­
nium retention. Meconium retention has been classi­
fied as either high or low impaction. A low impaction is
an obstruction of the small colon/rectum at the pelvic Figure 25.1 Meconium retention in a 24-hour-old foal.
inlet. The incidence of low impactions far outnumbers Dorsal recumbency

485
25 GASTROINTESTINAL DISEASE IN THE FOAL
Frequent efforts at defecation may be confused with
attempts to urinate. Advanced signs of abdominal pain
include dorsal recumbency (Figure 25.1), rolling from
side to side, or violent collapse. Meconium retention is
the most common cause of abdominal pain in the new­
born foal (see Chapter 22). It should be noted that the
clinical signs seen with meconium retention are non­
specific, and other differentials of abdominal pain
should be considered.
DIAGNOSIS
Diagnosis of the condition is based upon clinical signs,
physical examination findings, and other diagnostic
testing. Digital examination can identifY fecal material
at the pelvic inlet, however, absence of a positive digital
finding should not rule out meconium retention. If
retention is suspected, response to a mild enema can be
diagnostic. If clinical signs of abdominal pain persist,
then abdominal radiology and ultrasonography should
be pursued. Passage of a nasogastric tube may identifY
gastric reflux, and peritoneal fluid analysis may be use­
ful in ruling out other causes of abdominal pain.
Abdominal ultrasound can be used to identifY the pres­
ence of meconium in the gastrointestinal tract (this is
not necessarily indicative of impaction) and to rule out
other disease processes. Radiographs of the abdomen
can identifY meconium and/or gas distension of the
small or large intestine. Contrast radiography (barium
enema), can be very useful if other diagnostics are not
definitive. A barium enema is performed using a soft
rubber catheter, and gravity flow of 500-1000 ml of liq­
uid barium contrast material.
Differential diagnoses for foals showing clinical signs
of meconium retention include
• bladder rupture
• rectal irritation
• congenital atresias
• ileocolonic aganglionosis.
TREATMENT
Treatment of meconium retention varies with severity
and duration. Simple, cautious manual removal of fecal
. material can occasionally be all that is necessary. Mild
enemas usually provide adequate softening and lubrica­
tion for passage of retained material. Enema solutions
vary in quantity and contents. Commercial products are
available and can be effective. A safe, non-irritating
enema solution consists of 500-1000 ml of warm water
with 5-10 ml of soft, non-irritating soap. Repetitive
486
enemas can be irritating to the sensitive rectal mucosa,
it is preferable to use fewer large volume enemas rather
than frequent small volume procedures. Foals that
develop rectal irritation from enemas can demonstrate
the same clinical signs as meconium impaction, this may
lead to further enema administration and further irrita­
tion. Eventually the foal may develop toxemia unless the
irritating enemas are discontinued. So�t flexible
catheters are much preferred over the rigid counterparts.
Gravity flow, retention enemas containing 4% acetylcys­
teine have been recommended and can be effective.
The use of laxatives or cathartics given via nasogas­
tric tube may be beneficial particularly if the impaction
is suspected to be proximal. Mineral oil (200-400 ml),
castor oil (30 ml) and milk of magnesia (120 ml) have
been recommended. The effectiveness of these prod­
ucts is more likely via stimulation of gastrointestinal
motility rather than a direct effect on the meconium.
Cathartics should be used cautiously as they can be very
irritating to the mucosal lining of the gastrointestinal
tract. It is unlikely that fluid therapy is useful in soften­
ing meconium impactions. A straining foal with a pelvic
obstruction and full bladder (as a result of fluid ther­
apy) may be more prone to bladder rupture.
Pain control is an important aspect of therapy. A col­
icky foal can not effectively pass meconium. Analgesics
are beneficial when used judiciously. Passage of a naso­
gastric tube to assess the presence of gastric distension
should be a routine procedure in the diagnostics and
therapy of a colicky foal. If abdominal distension
becomes excessive despite therapy, then cecal trocariza­
tion and/or surgical exploration may become neces­
sary. It is rare that abdominal surgery is required to
resolve low impactions. Surgery may be necessary if
there is unrelenting, non-responsive pain and/or
severe gas distension. In these circumstances an alter­
native cause of abdominal pain or a proximal meco­
nium obstruction (right ventral or transverse colon) is
generally identified.
Atresia coli
EM Santschi
INTRODUCTION
Atresia coli is an uncommon, apparently sporadic con­
dition of neonatal foals. Foals affected with atresia coli
initially nurse well, but can not pass meconium. The
ingestion of food causes fluid and gas to accumulate,
and the intestine becomes distended causing colic.
 LARGE AND SMALL COLON DISEASES ASSOCIATED WITH COLIC IN THE FOAL 25

EPIDEMIOLOGY

Age
Atresia coli is a congenital condition, therefore clinical
signs of colic and bloating are seen only in foals within
48 hours of birth.

Gender
There is no gender predisposition.

Genetics
Atresia coli has been reported in American Paint
horses, Arabians, Appaloosas, Morgans, Quarter horses,
Standardbreds, and Thoroughbreds. No genetic predis­
position has been noted. Figure 25.2 Surgical photo of a foal with atresia coli. The
blind end of the right ventral colon is closest to the cam­
era. The pelvic flexure and all large colon aboral were not
present in this foal.
ETIOLOGY

The cause of atresia coli is unknown. The condition is

thought to be caused by a congenital loss of blood sup­
ply to a portion of the colon leading to ischemic local
necrosis of the gut. Because of the rare occurrence of
atresia coli, such vascular accidents are presumed to be
random events.
and central nervous system have been reported in foals
affected with atresia coli, and may be discovered on
post-mortem examination.

CLINICAL SIGNS
Foals affected with atresia coli will usually show signs of
abdominal pain and progressive abdominal distension
within 24 hours of birth. No meconium is passed and
none can be detected by palpation or enemas.
Occasionally, a blind-ended rectum can be palpated
digitally. Abdominal radiographs and ultrasound
demonstrate gas and fluid-filled intestinal segments.
CLINICAL PATHOLOGY
There are no pathognomonic pre-mortem tests for atre­
sia coli. As the foal becomes moribund, alterations in
blood clinical chemistry and hematological parameters
can be seen due to dehydration and endotoxemia.
PATHOLOGY
DIAGNOSIS
The major differential diagnoses of atresia coli are
Overo lethal white syndrome and meconium
impaction. Overo lethal white syndrome can be elimi­
nated in the majority of foals by examination of pedi­
gree and physical appearance of the foal. One useful
clinical sign that will discriminate between atresia coli
and an impaction is that most foals with meconium
impaction will produce some feces or fecal staining.
Abdominal radiographs using barium enemas can also
be used to discriminate between a foal with atresia coli
and one with a meconium impaction.
Proctoscopy may be helpful in some foals with
atresia coli. Confirmation of colonic atresia can only
be made at exploratory laparotomy. However, a pre­
sumptive diagnosis of colonic atresia can be made in
non-Overo lineage horses by the appearance of colic
signs within 24 hours of birth and the lack of fecal
staining.

Gross pathology
Segments of the colon are not present. Most foals with
atresia coli are type 1, a blind-end atresia - the oral dis­
connected segment is dilated with meconium, fluid,
and gas, and the rectal segment is usually atretic (Figure
25.2). Other congenital abnormalities of the cardiac
TREATMENT
Treatment of atresia coli requires either surgical anas­
tomosis of the discontinuous segments or a colostomy
of the blind end of the oral segment. Several attempts
have been made at surgical correction, but to the

487
25 GASTROINTESTINAL DISEASE IN THE FOAL
author's knowledge, none of the treated foals have
survived to adulthood. One foal was followed for 18
months after surgery and reported as healthy but was
then lost to follow up, and another foal survived 16
months after the surgery, but succumbed to colic
caused by intestinal adhesions (Ducharme, personal
communication, 1999). Ileus, adhesions, and peritoni­
tis are the most common reasons for failure. Because of
the guarded prognosis and the high cost of treatment,
most foals with atresia coli are euthanized after
exploratory surgery. An additional concern is the
reported concurrent occurrence of other congenital
abnormalities. Foals should receive a thorough physical
examination before surgery to try and detect other con­
ditions. If correction is attempted, owners should be
advised that other conditions could become apparent at
a later date.
Surgical correction is not possible in all foals
affected with atresia coli because of an inability to phys­
ically reappose the blind-ended segments. Permanent
colostomy is unlikely to be successful. If anastomosis is
attempted, it should focus on removing as much ingesta
as possible from the proximal segment, removing any
compromised bowel in the proximal blind-ended sec­
tion, and suturing the sections together. Because of the
disparate sizes of the lumens of the segments, hand
suturing is recommended using 3-0 monofilament
absorbable suture material, and an end-to-side anasto­
mosis is usually performed to maximize the lumen size
of the distal segment. Two suture lines are recom­
mended, the first appositional and the second invert­
ing. Feeding after surgery should begin slowly as
initiation of motility in the previously distended seg­
ments may be delayed.
Ileocolonic aganglionosis
EM Santschi
INTRODUCTION
Ileocolonic aganglionosis is a congenital absence of
myenteric ganglia in the terminal portion of the ileum,
'cecum, large colon, and small colon. The disease was
first reported in the US in 1977 and primarily occurs in
all-white offspring born to parents of theOvero spotting
pattern. The condition is always fatal. Fmils affected
with ileocolonic aganglionosis are referred to as 'Lethal
whites', so the condition is referred to as Overo lethal
white syndrome (OLWS).
488
EPIDEMIOLOGY
Age
Overo lethal white syndrome is a congenital agan­
glionosis, therefore clinical signs are seen only in foals
within 48 hours of birth.
Gender
There is no gender predisposition.
Genetics
Overo lethal white syndrome is seen in foals born to
parents ofOvero lineage. The parents are not always of
Overo coloration, but often are because the gene
responsible for OLWS also causes a prominent Overo
color pattern.
ETIOLOGY
The cause ofOLWS is the inheritance of two alleles of a
specific mutation in the gene that codes for endothelin
receptor B. Allele-specific testing reveals that the muta­
tion is most common in American Paint horses, but is
also found in Quarter horses, American Miniature
horses, Pintos, Thoroughbreds, Saddlebreds, and
Standardbreds. The lethal mutation in the endothelin
receptor B gene results in a single amino acid substitu­
tion in the first transmembrane domain of the seven
transmembrane domain g-protein coupled receptor.
This alteration in the protein composition is thought to
be sufficient to substantially alter the function of the
endothelin B receptor. The mechanism by which the
receptor causes aganglionosis is not known. However,
multiple investigations in multiple species indicate the
importance of the endothelin signaling pathway in the
normal development of the neural crest cells that
become epidermal melanocytes and enteric neurons.
CLINICAL SIGNS
Foals born affected with OLWS are born white or
almost entirely white (Plate 25. 1). Small areas of pig­
ment can occur on the body, especially the forelock and
tail. They have pigmented retinas but their irises are
white, giving an appearance of 'glass eyes'. OLWS foals
are apparently normal at birth, and will stand and nurse
well. However, they eventually show signs of colic from
intestinal distension caused by a functional obstruction.
The appearance of signs of colic are variable, but most
often occur within 24 hours of birth. Lethal white foals
most commonly do not pass feces, but occasionally
some fecal staining can be obtained after enemas.
 LARGE AND SMALL COLON DISEASES ASSOCIATED WITH COLIC IN THE FOAL
Abdominal ultrasound and radiographs will demon­
strate variable amounts of intestinal distension, and
foals will generally bloat and die within 48 hours of
birth.
CLINICAL PATHOLOGY
There are no pathognomonic pre-mortem tests for
OLWS. As the foal becomes moribund, alterations in
blood clinical chemistry and hematological parameters
can be seen, presumably because of dehydration and
endotoxemia.
PATHOLOGY
Gross pathology
Milk is found in the stomach and duodenum.
Meconium is found in the ileum, cecum, and colon but
is not impacted and is typically not found in the small
colon, which contains only mucus. Gas and fluid disten­
sion of the intestine varies, but always involves the small
intestine over much of its length. The small colon is
atretic and appears tortuous and tightly contracted
(Figure 25.3).
HISTOPATHOLOGY
Myenteric ganglia are absent in the ileum, cecum, and
colon of affected foals.
Figure 25.3 Gross necropsy photo of the small colon of a
foal affected with Overo lethal white syndrome. The small
colon is atretic and contracted, and contains no meco­
nium.
25
DIAGNOSIS
Confirmation of OLWS can be made by demonstrating
the lack of myenteric ganglia in the small colon of foals
at necropsy and by demonstration of homozygosity for
the OLWS mutation in the gene encoding endothelin
receptor B. The major differential diagnoses of OLWS
are atresia coli and meconium impaction. Meconium
impaction can be diagnosed by digital examination,
abdominal radiographs with contrast material, and by
ultrasound. Atresia coli can sometimes be diagnosed by
abdominal radiographs with contrast material, but is
definitely found by exploratory laparotomy. A presump­
tive diagnosis ofOLWS can be made in all-white foals of
Overo parentage that bloat and colic within 48 hours of
birth, and that do not pass feces.
TREATMENT
Attempts to treat OLWS either medically or surgically
are doomed to fail because of the extensive nature of
the lesion. The intractable nature of the condition
means that foals should be euthanized once a presump­
tive diagnosis is made.
PREVENTION
Allele-specific testing is available to test breeding stock
for the presence of the genetic mutation that causes
OLWS. By testing breeding stock and not breeding
heterozygotes the occurrence of OLWS can be elimi­
nated.
BIBLIOGRAPHY
Retained meconium
Shires G M (1991) Diseases of the small colon. In: Equine
Medicine and Surgery, P T Colahan, I G Mayhew, A M
Merritt,] N Moore (eds). American Veterinary
Publications, Goleta, CA, pp. 659-60.
Atresia coli
Estes R, Lyall W (1979) Congenital atresia of the colon: a
review and report of four cases in the horse.] Equine Med.
Surg. 3:495-8.
Fischer A T, Yarborough T Y (1995) Retrograde contrast
radiography of the distal portions of the intestinal tract of
foals.] Am. Vet. Med. Assoc. 207:734-7.
Nappert G, Laverty S, Drolet R, Naylor] (1992) Atresia coli in
7 foals (1964-1990). Equine Vet.] supp!. 13:57-60.
Young R L, Linford R L, Olander H] (1992) Atresia coli in
the foal: a review of six cases. Equine Vet.] 24:60-2.
489
25 GASTROINTESTINAL DISEASE IN THE FOAL

Ileocolonic aganglionosis progeny of overo spotted horses. J. Am. Vet. Med. Assoc.
180:289-92.
Gariepy C E, Cass D T, Yanagisawa M (1996) Null mutation of Santschi E M, Purdy A K, Valberg SJ, Vrotsos P D, Kaese H,
endothelin receptor B gene in spotting lethal rats causes MickeisonJ R (1998) Endothelin receptor B mutation
aganglionic megacolon and white coat color. Proc. Nat. associated with lethal white syndrome in horses. Mamm.
Acad. Sci. 93:867-72. Gen. 9:306-9.
Hultgren B D (1982) Ileocolonic aganglionosis in white

490
 27
Diarrhea in the foal
Foal heat diarrhea
.,,------
J Freestone
INTRODUCTION
Foal heat diarrhea is experienced by 75-80 per cent of
normal foals. Foal heat diarrhea, as the term implies,
occurs in foals from 6-1 4 days of age and coincides with
the first estrus cycle in the post-partum mare. This
appears to be coincidental as foals separated from their
dams and fed a controlled diet will still develop diar­
rhea at the same age. The cause of foal heat diarrhea
has been widely debated with strongyloidosis and
changes in milk composition largely eliminated as pos­
sible causes. From the work of Masri et at. ( 1 986) it
appears that the diarrhea results from a physiological
change within the gastrointestinal tract as the foal
develops a normal bacterial flora.
CLINICAL SIGNS
Foal heat diarrhea is most commonly a mild diarrhea
that is malodorous and self limiting over a 7-day period.
In a small number of foals the diarrhea may be profuse
and may be prolonged, or it may initially resolve and
then reoccur for an additional 2-3 days. The odor of
diarrhea caused by rotavirus can often be distinguished
from that of foal heat diarrhea. Foals show no adverse
clinical signs with foal heat diarrhea, and remain bright,
alert and responsive, afebrile, and they continue to
suckle. The diarrhea 'scalds' the perineal area resulting
in hair loss.
DIAGNOSIS
The diagnosis of foal heat diarrhea relies on the clinical
signs presented by the foal. Routine hematology and
biochemistry is normal. Foal heat diarrhea needs to be
differentiated from other infectious causes of diarrhea
including nutritional causes, viral diseases, and salmo­
nellosis. On a large Thoroughbred stud the most likely
differential diagnosis is rotavirus diarrhea. A good rule
of thumb is to monitor the foal's nursing behavior and
the size of the mare's mammary glands - foals with foal
heat diarrhea will rarely go 'off suck' in contrast to foals
with infectious causes of diarrhea.
TREATMENT
There is no treatment necessary for foal heat diarrhea
as the condition is self limiting. The foal's perineal area
can be cleaned and protected from scalding with the
application of petroleum jelly or zinc oxide. If the foal
deteriorates or the diarrhea is prolonged another cause
for the diarrhea should be considered and the use of
anti-ulcer medications, intestinal protectants, antibi­
otics, and fluid therapy considered.
Viral diarrhea in foals
TD Byars
INTRODUCTION
Foals are most susceptible to viral diarrheas during the
neonatal, perinatal, and suckling periods by virtue of
493
27 GASTROINTESTINAL DISEASE IN THE FOAL
being immunologically naive. The causative or associ­
ated viruses include
• equine herpesvirus Type-l (EHV-l)
• adenovirus
• coronavirus
• equine viral arteritis (EVA)
• rotavirus
• parvovirus
• viral infections that have not been completely
identified but noted on fecal electron microscopy.
Most viral diarrheas are considered to be highly
infectious and are rarely diagnosed at the time the
symptoms are present. The exception is rotavirus, the
most commonly recognized viral gastroenteritis in foals
that is readily diagnosed by ELISA testing. Viral diar­
rheas should be suspected whenever an outbreak of foal
diarrhea is present and routine microbiology is non­
diagnostic. Viral diarrhea can be diagnosed by
• ELISA (rotavirus A)
• electron microscopy of tissues and feces
• polymerase chain reaction testing and
immunoperoxidase (EHV-l)
• virus isolation from fecal or tissue samples obtained
at post-mortem examination.
Unlike food animals where sacrifice to confirm a
diagnosis may be elected, foals represent a population
of companion animals where viral infections may be sus­
pected but not confirmed, since the time involved in
treatment can compromise ante-mortem diagnosis and
post-mortem viral isolation. Koch's postulates are rarely
documented in identifYing viral causes of enteritis in
the equine species.
CLINICAL SIGNS
Often viral diarrheas can not be differentiated from
bacterial diarrheas since incubation periods may be
similar and the clinical presentation can vary from
acute to moderate severity, dependent upon the degree
of insult and age of the foal. Clinical signs can vary from
slight - a febrile foal that is not nursing, to profound -
profuse watery to lightly hemorrhagic diarrhea accom­
panied by colic. The diarrhea can be fetid, and vary in
color and consistency. In some cases atypical enteritis
may be present in that the clinical assessment and blood
values are consistent with enteritis but diarrhea is not
present at the time of examination. Colic caused by
enteritis may be difficult to differentiate from a surgical
colic if blood values are reasonably normal and fever is
not present (see Chapter 22) . Abdominal pain associ­
ated with the early stages of viral enteritis can be severe,
494
with tympany and occasionally gastric reflux. Further
clinical diagnostic procedures are indicated in these
cases with ultrasound examination being the diagnostic
method most useful to rule out intussusception, volvu­
lus, torsion, or peritonitis. A percentage of enteritic
foals are unresponsive to analgesics and cannot be dif­
ferentiated from surgical cases until tympany has been
relieved by the use of prokinetics or, more rarely, per­
cutaneous trocarization. Trocarization is usually con­
traindicated wherever surgical options are available
since foals should be considered more susceptible to
secondary peritonitis than adults.
TREATMENT
Treatments for viral diarrheas are generally empirical
and symptomatic
• fluid and electrolyte therapy
• plasma
• antibiotics
• anti-ulcer therapy
• anti-diarrheal medications
• analgesics
• antipyretics
Precautionary antibiotics and anti-ulcer medications
(see Chapter 23) should be prescribed. Fluid therapy,
oral or parenteral, for maintenance of normal hydra­
tion is the main objective of treatment. Fluid therapy is
necessary to correct dehydration, shock, and electrolyte
imbalances. In some cases colloids (plasma, albumin, or
hetastarch) may assist in the intravascular retention of
crystalloid (fluid) therapy. Other treatments include
the use of antidiarrheal medications, analgesics, and
antipyretics. The fluids and colloids selected are based
on laboratory findings, electrolyte and acid-base imbal­
ances, and clinical signs. Oral supplementation should
include access to fresh and electrolyte water, and a salt
block. Potassium deficits can be corrected in intra­
venous fluids at a rate of 0.5 mEq kg-1 h-1 or orally as
potassium chloride in the form of 'lite' salt mixed with
yogurt. Patients with reflux, ileus, or extreme cachexia
may benefit from the initiation of total parenteral nutri­
tion (with or without lipids) . Antidiarrheal medications
are rarely effective in altering the course of the diarrhea
but medications such as bismuth subsalicylate and
kaolin may help reduce bowel inflammation and pro­
vide for secondary toxin absorption and resorption
when combined with activated charcoal. Oral plasma
from adult donors has been used in cases of viral diar­
rhea in foals with questionable efficacy. Analgesic use in
viral diarrheas should emphasize the discriminating use
of ulcerogenic non-steroidal anti-inflammatory drugs

(NSAlDs). Dipyrone is not currently available commer­
cially but has provided excellent analgesia in mild colic,
along with its anti-pyretic activity, in foals with diarrhea
of various causes. Intravenous and intramuscular butor­
phanol (in small animal dilutions) is useful in the con­
trol of colic without cardiovascular or ulcerogenic side
effects. Xylazine may also be used to control colic but
temporarily affects cardiovascular function and potenti­
ates ileus.
ROTAVIRUS AND SIMILAR VIRAL
INFECTIONS
Rotavirus diarrhea is considered to be species specific
but may involve variant strains in foals. Exposure is from
carrier adults, infected foals, and mechanical transmis­
sion by humans and fomites. The incubation period is
1-2 days and it is highly infectious to suckling foals of
any age. The pathogenesis of infection primarily
involves the intestinal epithelial cells. Villi become
shortened or denuded, crypts become hyperplastic, and
the ensuing diarrhea is combined secretory and malab­
sorptive enteritis. Additionally carbohydrate enzymes
and lactose become deficient. The diarrhea, if present,
is usually watery and distinctly fetid. Diagnosis is by
ELISA testing or electron microscopy of feces for viral
particle identification. Treatment is non-specific and
the virus can be shed for approximately 5-7 days after
the diarrhea has resolved. Medications containing lac­
tase have been used to improve digestion of milk lac­
tose, but the efficacy of this treatment remains
unproven. A commercial modified live virus vaccine is
currently available for use in mares prior to foaling to
accentuate colostral antibodies. Foals from vaccinated
mares can still become infected with rotavirus although
the clinical signs may be attenuated.
In Ireland and central Kentucky a unique cyclic epi­
zootic of a suspected form of rotavirus diarrhea was
noted in 1987 and 1995, nicknamed the 'pink-rosewater
diarrhea' or '36-hour scours'. The disease was highly
infectious with virtually every foal at respective farms
heing clinically affected within 36 hours of birth. The
clinical signs include a pinkish watery diarrhea, rela­
tively non-fetid, usually complicated by dehydration
and colic associated with abdominal tympany. Colics
were often severe and unresponsive to analgesics.
Neostigmine used to relieve tympany was most effective
in the resolution of colic. Often treatments were empir­
ical or symptomatic. Routine sanitation procedures,
including pressure washings and disinfection, were inef­
fective. Washings and disinfection of the mares' udders
were also ineffective. Foaling in paddocks or pens out­
side the barn environment resulted in a dramatic cessa-
DIARRHEA IN THE FOAL 27
tion of new clinical cases. Viral particles were noted on
fecal electron microscopy without a definitive identifi­
cation of the causative viral etiology.
PROGNOSIS
The prognosis for foals with viral diarrhea is usually
favorable with fluid therapy and supportive care.
Secondary complications with bacterial infections or
the gastric ulcer syndrome can reduce the number of
favorable outcomes. Foals having survived viral diarrhea
are usually immune to subsequent infections, although
rotavirus is known to recur occasionally, albeit with
reduced clinical severity.
Salmonellosis in the foal
J L Whiting and TD Byars
Salmonella spp. are the most commonly diagnosed
causative agents of bacterial enterocolitis in the adult
equine, and has been reported as the most common
cause of bacterial diarrhea in the foal. In foals less than
14 days of age, Salmonella infections can lead to bac­
teremia, septicemia, septic shock, and death, with diar­
rhea occurring secondarily. Other bacteria, including
Actinobacillus equuli, Escherichia coli, Streptococcus spp. and
Klebsiella spp. may also cause diarrhea secondarily to
septicemia.
Young and immunocompromised animals are more
susceptible to Salmonella infections, in that exposure to
a lower dose of the organism can result in infection. This
increased susceptibility of the young may in part be
because of a less sophisticated or less well established
microflora within the gastrointestinal tract. Experimental
data have shown the significance of normal gastroin­
testinal flora in restricting the ability of the Salmonella
organism to establish and proliferate within the intestine.
The most common source of exposure and infection
in the foal is another horse. Often the mare herself is an
asymptomatic carrier, shedding the organism during
the stress of parturition and exposing the foal to the
pathogen in utero or in the post-foaling environment.
PATHOGENESIS
Salmonella spp. are gram-negative, facultative, anaerobic
bacteria, which usually gain access to the gastrointesti-
495
27 GASTROINTESTINAL DISEASE IN THE FOAL
nal tract via the fecal-oral route. The bacteria must
combat a number of non-specific host defense mecha­
nisms - gastric acidity, normal intestinal flora, peristal­
sis, intestinal mucus, lactoferrin and lysozyme
secretions within the gastrointestinal tract - in order to
establish infection. Salmonella organisms have many
virulent properties enabling them to establish infection
within the host. Among these are flagellar and chemo­
tactically directed motility, capsular and surface anti­
gens, macrophage-induced proteins, endotoxin,
enterotoxin, cytotoxin, plasmids, and iron-chelating
enzymes. Once Salmonella organisms come in close
proximity to, or possibly in contact with, the brush bor­
der of enterocytes, the microvilli and tight junctions
undergo degeneration. Flagellar motility may enable
the organism to approach enterocytes close enough for
adhesion to occur. Surface 0 antigens and fimbriae
may then facilitate adherence of the bacteria to the host
receptor cells.
The bacteria migrate through the enterocyte and
access the lamina propria where their presence stimu­
lates an inflammatory response. The macro phages and
neutrophils recruited will phagocytize the bacteria, and
it is within these phagocytic cells that Salmonella organ­
isms survive and multiply, while remaining protected
from antibiotics, antibodies, and complement. Flagella
are thought to protect the organism from intracellular
killing, while macrophage-induced proteins produced
by Salmonella spp. have been shown to block fusion of
the phagosome and lysosome, allowing intracellular
survival and multiplication.
Both phagocytized and free Salmonella organisms
travel via the lymphatics to regional lymph nodes where
they persist in stimulating an inflammatory response.
From here the bacteria continue via efferent lymphatics
to drain into the blood circulation. Once in the circula­
tion, the bacteria are generally cleared via the reticu­
loendothelial system, primarily through the liver and
the spleen. Septicemia and its sequelae (more common
in the neonate than the adult) can occur if the infection
is not contained by the mononuclear phagocytic system.
Immunity against Salmonella spp. requires both cell­
mediated and humoral immunity as the bacteria are
intracellular pathogens. The neonate's predisposition
toward bacteremia and septicemia may be because of
factors such as delayed gut closure at birth, immature
cellular immune response, and decreased complement
activity.
Inflammation within the bowel wall results in villus
blunting and degeneration and abnormal extrusion of
enterocytes. Cytotoxins may in part be responsible for
cellular destruction by inhibiting protein synthesis. The
diarrhea in the disease process of Salmonella infections
is a result of malabsorption because of this destruction
496
of epithelial cells. Additionally, enterotoxins may
induce secretion of fluid from intact intestinal epithe­
lial cells.
Lipopolysaccharide (LPS), or endotoxin, is a com­
ponent of the outer membrane of gram-negative bacte­
ria, and contributes greatly to the pathogenesis of
salmonellosis. Endotoxin activates a variety of host cells
(platelets, macrophages, endothelial cells, leukocytes)
and host tissues to release inflammatory mediators such
as arachidonic acid metabolites, prostaglandins,
leukotrienes, tumor necrosis factor, interleukins, gran­
ulocyte and macrophage stimulating factor, and reac­
tive oxygen radicals. LPS can also stimulate both the
intrinsic and extrinsic clotting cascades and activate
complement by the classical and alternative pathways.
Endotoxemia leads to alterations in hemodynamics,
homeostasis, metabolism, and endothelial integrity,
resulting in tissue injury, vascular collapse, and multi­
ple-organ system failure (see Chapter 1 1 ) .
CLINICAL SIGNS
Clinical signs of salmonellosis are variable and can
range from mild enteritis to fulminating septicemia
(Table 27. 1 ) .
Manifestations are attributed to enterocolitis, sep­
ticemia, and endotoxemia. Early in the course of the
disease, fever, decreased nursing, and depression are
commonly found. Neonates can present with hypother­
mia. Foals frequently show signs of moderate to marked
abdominal pain and can have associated abdominal dis­
tension. Other differential diagnoses must be consid­
ered in the neonate as colic symptoms may accompany
mechanical gastrointestinal obstruction, for example
meconium impaction, intussusception, volvulus, and
colon torsion (see Chapter 22 ) . Ileus often occurs, con­
tributing not only to colic and distension, but also to
decreased or absent normal progressive motility
Pyrexia
Depression
Decreased nursing
Abdominal pain
Abdominal distension
Ileus
Dehydration
Congested mucous membranes
Prolonged capillary refill time
Diarrhea

sounds. Fluid and gas sounds are frequently appreci­
ated when auscultating the abdomen. Dehydration, as
evidenced by decreased skin elasticity, dry mucous
membranes, and sunken eyes, can become severe with
ongoing fluid losses that may lead to poor tissue perfu­
sion. Endotoxemia contributes to decreased perfusion
by stimulation of various inflammatory mediators
(thromboxanes, prostaglandins, leukotrienes, and cate­
cholamines) which can cause both vasoconstriction and
hypotension. Clinically, vasoconstriction is seen early in
the course of endotoxemia and is represented by pale
mucous membranes, whereas decreased vascular tone
appears as muddy, dark-red, congested mucous mem­
branes with a toxic line along the gingiva. Additional
findings associated with poor perfusion include tachy­
cardia, elevated pulse rate and intensity, prolonged cap­
illary refill time, cold extremities, and depressed
mentation.
Clinical signs of bacteremia may manifest as infec­
tions evident in other organ systems such as
• pneumonia
• septic arthritis
• uveitis
• osteomyelitis
• skin abscesses
• meningitis
• nephritis.
Severe septicemia can lead to septic shock, multiple
organ system failure, and circulatory collapse.
Diarrhea may not be present initially and neonates
may die rapidly from severe septic shock before diar­
rhea develops. Diarrhea associated with acute
Salmonella enterocolitis is most often profuse and liq­
uid with little solid material present. Flecks of blood
may rarely be present. Foals will defecate in increased
frequency and volume. Colic and straining during defe­
cation are common features associated with the high
volume of diarrhea produced, while rectal prolapse can
occur.
CLINICAL PATHOLOGY
Although not diagnostic for the disease, the most con­
sistent hematological abnormalities found with severe
Salmonella diarrhea infections are
• leukopenia
• neutropenia with a degenerative left shift
• toxic changes (cytoplasmic vacuolation and toxic
granules) seen in granulocytes.
An inversion of the neutrophil:lymphocyte ratio can
indicate sepsis. A rebound neutrophilic leukocytosis
DIARRHEA IN THE FOAL 27
may occur later in the course of disease, sometimes
indicating recovery. Thrombocytopenia can be found
in some cases. Fibrinogen can be variable, with low
« 1 00 mg/dl) values being attributed to coagulopathy
and elevated (> 1 000 mg/dl) values being attributed to
inflammation. Hematocrit is generally markedly
increased because of hemoconcentration and splenic
contraction. Total plasma protein is initially quite ele­
vated because of hemoconcentration, but will decrease,
along with serum albumin levels, with ongoing enteric
losses secondary to mucosal damage or generalized
endothelial damage. Many neonates will have
decreased serum immunoglobulin G (IgG) levels
because of protein catabolism commonly associated
with septicemia. Foals that experience a failure of pas­
sive transfer (FPT) are predisposed to septicemia, and it
can be hard to differentiate if the low IgG led to sep­
ticemia or if it was a result of septicemia.
Electrolyte and acid-base imbalances can be pro­
found with Salmonella enterocolitis and commonly
include
• hyponatremia
• hypokalemia
• hypochloremia
• hypocalcemia
• metabolic acidosis.
Hypoglycemia in foals may be marked as a conse­
quence of decreased glycogen stores in the liver and
bacterial depletion due to sepsis. Azotemia is usually
prerenal in origin, but can be caused by acute renal fail­
ure or bacterial nephritis in profoundly dehydrated,
endotoxemic, or septicemic animals. Hepatic enzymes
may be mild to moderately increased as a consequence
of absorption of bacterial toxins (endotoxins) .
Endotoxin-mediated lactic acidosis can result from
poor perfusion. Mediators of inflammation stimulated
by endotoxemia can lead to a hypercoagulable state fol­
lowed rarely by disseminated intravascular coagulation
(DIC), as evidenced by prolonged prothrombin time,
partial thromboplastin time, depletion of antithrombin
III and increased fibrin degradation products.
DIAGNOSIS
Diagnosis of Salmonella spp. as the causative agent of
diarrhea is demonstrated by a positive fecal culture,
while a positive blood culture is needed to diagnosis
Salmonella septicemia. Isolation of the organism from
fecal material is variable as Salmonella spp. may be inter­
mittently shed in the feces. With acute enteritis, the
feces can have little solid material and the chance of
culturing the bacteria is diminished (although better
497
27 GASTROINTESTINAL DISEASE IN THE FOAL
than in adult horses) . A minimum of three to five con­
secutive 1 gram fecal cultures taken 24 hours apart are
recommended to increase the chance of isolating the
organism. Fecal cultures from the mare should also be
submitted to assist in determining the source of infec­
tion.
TREATMENT
Therapy for salmonellosis is aimed at maintaining
hydration and electrolyte balance in the face of ongo­
ing losses, reducing the effects of endotoxemia, pre­
venting or treating bacteremia, and gastroprotectant
therapy (Table 27.2 ) .
Aggressive intravenous fluid therapy may be
required as dehydration can rapidly become severe in
the foal with enterocolitis, and effects of decreased
intravascular volume can be profound. Electrolyte and
acid-base abnormalities can be marked and serum
parameters should be monitored frequently to main­
tain balance. Isotonic fluids are routinely used to
restore and maintain hydration status, with additional
electrolytes, for example potassium and bicarbonate,
added as indicated by deficits found in serum chemistry
analysis. Potassium chloride should not be adminis­
tered at a rate greater than 0.5 mEq kg-I h-I in the foal.
In the severely affected foal with poor perfusion, signs
of septic shock or reduced plasma oncotic pressure
(hypoproteinemic: <4.0 mg/dl or 40 gil; hypoalbu­
minemic: < 1 .8 mg/dl or 18 gil; and hemoconcen­
trated with ventral or distal limb edema) , colloids such
as hydroxyethyl starch, at a dose of 10 ml/kg, can be
Intravenous fluid therapy
Isotonic fluids
Bicarbonate
Potassium chloride
Colloids
Plasma
Hyperimmune plasma
Dextrose
Partial or total parenteral nutrition
Antibiotics
Polymyxin B
Flunixin meglumine
Pentoxifylline
Bismuth subsalicylate
Activated charcoal
Live yogurt
Anti-ulcer therapies
498
beneficial. Intravascular volume can be expanded, and
vascular perfusion and oncotic pressure improved with
a decrease in interstitial fluid accumulation. Colloids
are generally followed by continued crystalloid fluid
therapy. When used in conjunction with colloids, a
decreased amount of crystalloid fluids are required.
Plasma is recommended in the hypoproteinemic foal
with hypoalbuminemia and/or low IgG levels. In addi­
tion, plasma contains coagulation factors and
antithrombin III, which could benefit the endotoxemic
patient. Hyperimmune plasma containing
immunoglobulin-recognizing LPS core antigen has
been recommended in horses with Salmonella infec­
tions at a dose of 0.4 ml/kg. Fluids containing dextrose
(5% solution) or oral supplementation via a nasogastric
tube may be required in the foal that has stopped nurs­
ing. Alternatively, the catabolic patient may benefit
from oral supplementation with high-nitrogen oral
solutions (osmolite) , partial parental nutrition (PPN)
or total parental nutrition (TPN) .
Although antibiotic therapy will not alter the course
of the diarrhea or reduce the incidence of shedding of
the Salmonella organism, it is recommended that foals
with Salmonella infections be treated with antibiotics in
the hope of preventing bacteremia and to treat any sites
of secondary infection. Appropriate antibiotic therapy
should be established based on sensitivity results of fecal
or blood cultures. Ideally lipid-soluble antibiotics such
as trimethoprim-sulfonamides and chloramphenicol,
should be used as the Salmonella organism survives
intracellularly. Often the Salmonella spp. isolated, espe­
cially in nosocomial infections, will be resistant to the
aforementioned antibiotics, and other broad-spectrum
choices such as third generation cephalosporins or
penicillin and aminoglycoside combinations are found
to be more effective. Antibiotics may contribute to the
release of endotoxins in cases of rapid bacterial death.
For this reason patients can be treated with medications
that decrease the effects of circulating endotoxin prior
to initiation of antimicrobial therapy. Polymyxin B, at a
low dose of 6000 IU/kg, binds and removes endotoxin
from circulation. Cyclooxygenase inhibitors such as flu­
nixin meglumine (0.25 mg/kg Lv. t.Ld.) will both ame­
liorate the effects of endotoxemia by decreasing
synthesis of prostaglandins and thromboxanes, and
decrease the secretory component of diarrhea by block­
ing prostaglandin-mediated hypersecretion of entero­
cytes. Non-steroidal anti-inflammatory drugs should be
used cautiously in foals because of the greater risk of
gastroduodenal ulcers. Pentoxifylline (7.5 mg/kg p.o.
bj.d.) has been shown to reduce endotoxin-induced
synthesis of tumor necrosis factor, a contributor to
endotoxemia associated with sepsis. In addition, pen­
toxifylline increases red blood cell deformability,

decreases blood viscosity, decreases platelet aggrega­
tion, and decreases thrombus formation, thereby com­
bating conditions contributing to impairment of
regional blood flow.
Bismuth subsalicylate is commonly used as an intesti­
nal protectant. The bismuth is thought to have anti­
endotoxic and weak antibacterial properties while the
salicylate has anti prostaglandin activity which may
decrease enterocyte hypersecretion. Activated charcoal
and/or mineral oil can be used to decrease absorption
of endotoxin. Yogurt or other lactobacillus-containing
products can be used to help reintroduce beneficial
flora to the gastrointestinal tract.
Anti-ulcer medication is routinely recommended
and administered prophylactically and therapeutically
to ill foals because of their predisposition to gastric
ulcer syndrome. Omeprazole (a gastric acid (proton)
pump inhibitor), or famotidine, ranitidine, cimetidine
(H2 antagonists) , and sucralfate (a cytoprotective
agent) are commonly used medications. It is interesting
10 recall that one important host barrier to Salmonella
infections is the ability of acidic pH in the stomach to
prevent live bacteria from gaining access to the intes­
tine. Changing gastric pH with anti-ulcer medication
may in fact enhance infection.
PREVENTION AND CONTROL
The Salmonella organism is relatively prevalent within
the environment and can be shed in the feces of clini­
cally normal horses. The most common route of infec­
tion is fecal-oral. The mare is often found to be
shedding the organism and the foal has probably con­
tracted it from her. Neonates are at greater risk during
the first 24 hours of life as the organism may gain access
via the gastrointestinal tract prior to gut closure.
Overcrowding, improper sanitation, and inadequate
umbilical care all put the neonate at risk for Salmonella
bacteremia and consequent septicemia.
Adequate colostral antibody absorption is important
to develop the foal's immune defense system. A serum
IgG concentration of more than 800 mg/dl at 24 hours
of age is recognized as optimal passive conference of
immunity in the neonatal foal. This immunity is espe­
cially important in the neonate at risk for sepsis. Plasma
transfusions with hyperimmune plasma from donors
vaccinated against mutant strains of]-5 Escherichia coli or
Salmonella typhimurium have been reported to provide
IgG protection against gram-negative core antigens, but
clinical response to this therapy is variable. In addition,
plasma provides opsonins which improve the foal's
immune function. Sick neonates can experience
increased immunoglobulin consumption, possibly
DIARRHEA IN THE FOAL 27
because of sequestering of IgG within the intravascular
space or at sites of inflammation, and can benefit from
plasma transfusions even if initial colostral absorption is
adequate. Autogenous vaccines have been used to stim­
ulate immunity against Salmonella spp., but approved
and proper preparation is difficult.
Animals identified as infected with Salmonella spp.
should be kept isolated from the general population
until they culture negative. Both mares and foals should
be cultured. Infected animals can continue to shed
organisms in their feces intermittently for several days
to weeks. Daily fecal cultures should be taken beginning
at 4 weeks after the cessation of clinical signs, and three
to five negative cultures are needed before putting the
animal in contact with other foals can be considered.
Clostridial enterocolitis in
foals
TJ Divers
Clostridial diarrhea has been diagnosed in foals at an
increasing rate over the past 5 years. It is unclear if this
is a result of increased prevalence of the disease or
increased use of more sensitive diagnostic tests for
intestinal clostridial toxins.
ETIOPATHOGENESIS
Clostridium perfringens type C is a well-proven cause of
colic and diarrhea (often hemorrhagic) in young foals.
The disease almost always occurs in foals less than 5 days
of age ,that have received sufficient colostrum.
Pancreatic trypsin is inhibited by a trypsin inhibitor in
colostrum, which undoubtedly plays a role in the poten­
tial for C. perfringens colonization and increased toxin
concentration in the foal's small intestine during the
first week of life. C. perfringens type C produces a beta
toxin which causes severe intestinal necrosis and hem­
orrhagic diarrhea. As the intestinal wall becomes dam­
aged the organism can be found in the blood of many
affected cases. In later stages of the disease the organ­
ism can be found in the peritoneal fluid. C. perfringens
type C diarrhea can be either a farm problem or it can
present as an isolated case. Foals, such as orphan foals,
that may be given both colostrum and milk in unusually
large amounts via a nasogastric tube may be at
increased risk. Although unconfirmed, exposure to the
organism may be via the mare rather than environmen­
tal contamination.
499
27 GASTROINTESTINAL DISEASE IN THE FOAL
Clostridium peifringens type A has been incriminated
as a cause of diarrhea in foals of all ages. Proof of the
relationship between C. perfringens type A in the foal's
stool, and diarrhea in foals has been difficult. As in
adult horses, C. peifringens type A organisms are more
common in foals with diarrhea than in healthy foals,
but no toxin marker has been found in the foal that dis­
tinguishes a pathogenic strain of C. perfringens type A
from non-pathogenic strains. C. perfringens type A
enterotoxin and/or its enterotoxin gene can be found
in both normal and diseased foals. C. perfringens type A
may cause diarrhea in foals, but more research is
needed to prove cause and effect. A similar situation
exists with C. dijjicile and its relationship to foal diar­
rhea. C. dijjicile has been reported, and has frequently
been incriminated as causing outbreaks of diarrhea in
young foals (generally < 3 weeks of age) . In these out­
breaks there has been no history of prior antibiotic
treatment to predispose the animals to the proposed C.
dijjicile diarrhea. Proving cause and effect has been dif­
ficult since normal foals may have both C. dijjicile and its
toxin in their stool. This situation is also well-known in
children. It may be that C. dijjicile is a primary pathogen
in some cases of foal diarrhea, or it may be present in
the stool in greater numbers because of the diarrhea, or
it may be acting with another pathogen to cause diar­
rhea. Other pathogens that may be present simultane­
ously include Cryptosporidium spp., Bacteroides fragilis,
rotavirus type A, or a virus similar to rotavirus but
smaller than type A.
CLINICAL SIGNS
Colic often precedes the diarrhea by a few hours and
can be severe. Mild to moderate abdominal distension
generally precede the diarrhea. There may be some
reflux after passage of a soft nasogastric tube, but more
commonly reflux is absent or minimal. Fever is often
present. Clostridium perfringens type C generally causes a
hemorrhagic enteritis with blood-stained diarrhea
(Plate 27. 1 ) . Diarrhea associated with C. dijjicile or C.
perfringens type A is more commonly brown and fetid.
DIAGNOSIS
The diagnosis of clostridial enteritis, or any enteritis in
foals, should be based on signalment and historical
information, for example age of the foal, clinical find­
ings, fever, leukopenia, low serum sodium and chloride,
liquid gut sounds on auscultation, in addition to fecal
cultures and toxin assays. Radiographic examination,
performed using 85 kVp and 20 rnA with rare earth
500
screen cassettes, is useful in distinguishing ententls
from surgical conditions, for example intussusception,
in the colicky foal. Small intestinal obstructive lesions
have a few distinct inverted U-shaped loops of bowel and
there is less intestinal gas distension than with enteritis.
Ultrasound examination of the abdomen using a 5-mHz
probe is most helpful in differentiating between surgical
disorders and enteritis as causes of abdominal pain. The
small intestine of foals with enteritis is generally more
hypoechoic than normal (Figure 27. 1 ) and the motility
may be increased. With strangulating diseases of the
small intestine, motility of the distended intestine is usu­
ally absent. The ultrasound examination should be per­
formed with the foal standing if possible.
Fecal cultures should be submitted for Clostridium
spp. culture (anaerobic media) and toxin assay (c. diffi­
cile toxin A and B, and C. peifringens alpha and entero­
toxin) . For toxin assays, the sample should ideally be
delivered immediately to the laboratory or the feces
frozen and sent by overnight mail. An estimate of the
number of C. peifringens organisms in the feces may be
helpful in determining significance, but quantitative
cultures require that a fresh sample (ideally taken from
the rectum) be kept under anaerobic conditions and
delivered immediately to the laboratory. Large num­
bers of C. perfringens (> 1 03 colony-forming units/ml of
feces) would be supportive of the diagnosis. A gram
stain of the feces is helpful in the diagnosis if there are
Figure 27.1 Ultrasonogram of the abdomen of a foal
affected by dostridiosis showing multiple distended loops
of small intestine with grossly thickened intestinal walls. In
real time hypermotile movement of intestinal contents is
evident, helping to differentiate enteritis from mechanical
obstructions of the small intestine

a large number of gram-positive rods. Spores are more
commonly seen with C. difficile and the organism can
often be more curved in appearance and have a darker
gram-positive stain than C. perfringens. Genotyping
would be needed to determine C. perfringens type (A-E) .
Blood cultures should be performed on young foals
« I week of age) with diarrhea as C. perfringens type C
can often be found in the blood or peritoneal fluid in
the later stages of the disease.
TREATMENT
Treatments that can be helpful for clostridial diar­
rhea are shown in Table 27.3.
Signs of abdominal pain should be controlled to
minimize injury to the foal. Dipyrone (22-33 mg/kg
i.v.) or butorphanol (4-6 mg/kg i.m.) can be used ini­
tially. Low doses of flunixin meglumine can be used
sparingly. Foals with colic, ileus, and severe or progres­
sive 'gaseous' abdominal distension that have been
unresponsive to appropriate medical treatment and are
believed not to have an obstructive disorder, can be
given neostigmine (0.2-0.4 mg/foal s.c.) after sedation
with xylazine in an attempt to evacuate the gas.
Lactated Ringer's solution should be given to reduce
fluid deficits. Potassium chloride (20 mEq/l) should be
added if the foal is hypokalemic, or if sodium bicarbon­
ate and dextrose have been administered, and if the
foal has been seen to urinate. Additional potassium is
generally needed in foals having diarrhea for more than
2 days or in foals receiving large volumes of intravenous
fluids. If the foal appears weak add 10 g dextrose/I
unless the blood glucose concentration is normal. If the
Analgesics - dipyrone
- butorphanol
- flunixin meglumine
Neostigmine
Lactated Ringer's solution
Potassium chloride
Dextrose
Sodium bicarbonate
Plasma
Dobutamine
Antibiotics - penicillin
- amikacin
- metronidazole
H2-blockers - ranitidine
- famotidine
Pepto bismol/yogurt
DIARRHEA IN THE FOAL 27
blood glucose is normal add 5 gil. Bicarbonate should
only be used if the acidosis is severe and/or persistent.
Two liters of plasma should be given intravenously
(preferably the plasma should have antibodies against
endotoxin, although the LPS antibodies may not be as
important as some naturally occurring factors in
plasma, e.g. anti-thrombin III). Clostridium perfringens
type C and D antiserum can be given orally to affected
foals. If the foal is in hypotensive shock and the plasma
and polyionic fluids do not improve the condition (as
determined by monitoring the blood pressure or by
clinical impressions, e.g. poor capillary refill, severe and
persistent tachycardia, and cold extremities) , dobuta­
mine (5-10 I-lg kg-J min-I) should be administered via a
slow intravenous drip.
Antimicrobial therapy should include intravenous
penicillin, 44 000 IV/kg i.v. q. 6 h, and amikacin,
18 mg/kg q. 24 h, (carefully monitor urine production,
serum creatmme, and amikacin trough levels) .
Metronidazole, 1 0 mg/kg p.o. q. 1 2 h, may also be
administered. Broad spectrum antibiotics are indicated
as bacterial translocation to other organs can occur.
Ranitidine 1 . 5-2.2 mg/kg i.v. q. 8 h or famotidine
0.7-1.4 mg/kg i.v. once daily should be used in the
hope of preventing gastric ulcers. Once the colic sub­
sides, these or other H2-blockers or proton pump block­
ers can be given per os.
Pepto bismol (56-1 1 2 g ( 2-4 oz) p.o. q. 4-6 h) with
28-56 g ( 1-20z) yogurt may be of some benefit in
reducing toxin absorption and re-establishing normal
intestinal flora. The foal can be allowed to nurse but
should not be force-fed milk.
PROGNOSIS
The prognosis with Clostridium perfringens type C is vari­
able, intestinal necrosis rapidly occurs in a few cases
with large numbers of the organism being identified in
both blood and peritoneal fluid. Less severely affected
cases respond dramatically to treatment and may
appear normal within 2-3 days. C. difficile and C. perfrin­
gens type A-associated disease seems to produce a more
protracted diarrhea. The prognosis for either infection
is generally good if the foal is nursing at recognition of
the disease, or if nursing is strong after 24 hours of
treatment. Gastric ulceration, electrolyte imbalances,
and cachexia may be significant problems in a few foals.
CONTROL
Clostridium perfringens type C diarrhea is often an iso­
lated event on a farm requiring few control measures.
501
27 GASTROINTESTINAL DISEASE IN THE FOAL
Cleaning the mare's udder prior to the foal nursing
may be the most appropriate control measure and
should be routinely recommended. C. perfringens type C
toxoids are available but would not routinely be recom­
mended for the pregnant mare unless the farm has a
proven problem with C. perfringens type C. A more sig­
nificant problem exists with farm outbreaks of foal diar­
rhea presumed to be associated with either C. difficile or
C. perfringens type A. It may help to ensure cleanliness of
the mare at parturition, disinfect the foaling area, and
avoid using a common foaling stall. Prophylactic use of
metronidazole, 10 mg/kg q. 1 2 or 24 h, from day 1 (do
not administer prior to colostrum) to day 5 appears to
be helpful in stopping outbreaks on some farms.
Lactobacillus acidophilus probiotics may be administered
for either prophylaxis or treatment but their efficacy is
not proven. Hospitalized foals, either with or without
diarrhea may be shedding C. difficile in the greatest
numbers. Their stalls should be disinfected with an
appropriate disinfectant (hypochlorite, glutaraldehyde,
or phenolics) , and all personnel entering and leaving
the stall should wash hands and wear protective cloth­
ing and boots.
Rhodococcus equi as an
agent of intestinal disease
KA Sprayberry
INTRODUCTION
Rhodococcus equi is a gram-positive, facultative intracellu­
lar aerobe, it is known primarily as a pathogen of the
respiratory tract of the juvenile horse. The organism is a
saprophytic inhabitant of the soil, favoring soils in warm
climates where the manure of herbivores is present.
Such soils promote survival and amplification of R. equi
populations because molecules produced by fermenta­
tive digestion in the equine hindgut are growth factors
for the organism. The typical manifestation of disease
caused by this bacterium is an abscessing, pyogenic,
granulomatous bronchopneumonia in foals aged 1-6
months, but many extrapulmonary manifestations of
infection, including colitis and abdominallymphadeni­
tis, have been described.
Originally classed taxonomically in the genus
Corynebacterium, the organism was reclassified as
Rhodococcus spp. on the basis of genetics, chemistry, and
ecology. Members of this genus are soil inhabitants,
having in common the production of red pigment, but
only R. equi has been reported as a pathogen in animals
502
or humans. The organism IS m the same taxonomic
order (Actinomycetales) as mycobacteria. Myco­
bacteria, like R. equi, are primarily pathogens of the res­
piratory and intestinal tracts, causing pulmonary and
intestinal tuberculosis in humans (M. avium, M. bovis,
and M. tuberculosis) andJohne's disease, a chronic, gran­
ulomatous inflammation of the intestinal tract of ungu­
lates (M. paratuberculosis). The tuberculous, pyogenic
granulomas of mycobacteria infections are histologi­
cally similar to rhodococcal abscesses in their composi­
tion of infected macrophages and multinucleate giant
cells with neutrophilic infiltration.
EPIDEMIOLOGY AND PATHOGENESIS
Because the bacterium resides endemically in types of
soils which support populations of horses, it is an agent
to which most, if not all, horses are exposed. The inci­
dence of disease associated with Rhodococcus equi, how­
ever, varies. On some farms R. equi pneumonia is rare,
while on others clinical disease occurs enzootically,
even though the organism can be cultured from the soil
of both. This incongruity is likely to be a result of dif�
ferences in the type of soil, climate, prevalence of dusty
conditions, stocking rate, and intensity of management
that exist between farms, as well as differences in viru­
lence among resident strains of the organism. Virulent
strains of R. equi are characterized by the presence of a
15 or 17.5 kDa virulence-associated protein (VapA) on
the cell membrane. Farms which have clinical disease
due to R. equi are usually endemic premises for VapA
strains of the organism, while farms having little inci­
dence of disease are infected less heavily with the viru­
lent organism. This protein is encoded for by an 85 or
90-kilobase plasmid. Though long recognized as an
identifying marker for virulent strains, it has recently
been shown conclusively that this plasmid is in fact a vir­
ulence factor for the organism. The presence of the
plasmid is essential for intracellular replication within
macrophages and subsequent development of disease.
The organism dwells and replicates within phagosomes
after being phagocytized by macrophages, preventing
(by an unknown mechanism) the usual fusion of the
phagosome with a lysosome. Macrophages thus infected
do not undergo the respiratory burst associated with the
lysosomal enzymatic activation which mediates intracel­
lular killing. Infection of macrophage cells by R. equi
eventually causes the degeneration and death of the
immune cell, possibly by inappropriate lysosomal rup­
ture and degranulation into the cytoplasm. Neutrophil
cells of both foals and adult horses function as effective
phagocytes, and can effectively process and destroy R.
equi.

Inoculation of foals occurs via either the respiratory
route, following inhalation of aerosolized particles, or
the oral route, via ingestion. In dusty conditions, bacte­
ria present in the soil and feces become aerosolized, serv­
ing as the direct source of exposure and pulmonary
infection for foals. Colonization of the bowel by
RJwdococcus. equi occurs when foals ingest infected soil
or forage, are coprophagous, or swallow expectorated,
bacteria-laden sputum. R. equi pneumonia is also preva­
lent in areas with grass pasture and little or no dust or
exposed soil. In these circumstances, feces from adult
horses serving as passive carriers may be an important
source of exposure for foals. In adult horses, ingestion
results in passive passage of the organism through the
intestinal tract, with resultant deposition of the bac­
terium back into the environment. In immunologically
naive foals, however, the organism thrives and replicates,
resulting in significant amplification of bacterial num­
bers in the environment and enhanced risk to other
young stock if manure produced by infected foals is not
promptly removed. During the optimal environmental
conditions that prevail during summer months, R. equi
numbers in contaminated soil can multiply by ten-thou­
sand-fold in 2 weeks, such that 1 gram of soil could
theoretically contain millions of virulent organisms.
CLINICAL SIGNS
The clinical picture of pulmonary disease mediated by
Rhodowccus equi has been well described. Young foals
aged 1-6 months are typically affected. Foals in this age
category are particularly susceptible to infection
because they are in an immunologic stage of waning
maternal antibody. Most foals reach this age with its
characteristic antibody 'trough' when warmer tempera­
tures and dusty conditions are beginning to prevail,
increasing the aerosolization of bacteria. Foals often
present with an apparently acute onset of clinical dis­
ease characterized by
• fever
• tachypnea
• depression.
However the actual onset and early development of
lesions in lung tissue is insidious and clinically silent.
The disease process and degree of pulmonary involve­
ment are typically well advanced by the time clinical
signs are evident and a diagnosis is made. The incuba­
tion period may vary. In one study virulent organisms
sprayed into the trachea of healthy foals resulted in the
development of fever in 11-16 days. Evaluation of the
thorax with radiography or ultrasound usually demon­
strates the presence of cavitary lesions representing a
DIARRHEA IN THE FOAL 27
multifocal, abscessing pattern of bronchopneumonia.
The perihilar regions, and the cranial and cranioventral
areas of the lungs tend to be most severely affected, and
the hilar lymph nodes are often involved. In some cases
a more atypical interstitial pneumonia may occur.
In addition to pulmonary disease, extrapulmonary
manifestations of infection may be observed, including
• mesenteric lymphadenitis
• ulcerative colitis
• immune-mediated polysynovitis
• uveitis and keratoconjunctivitis
• osteomyelitis
• septic synovitis
• cutaneous pyogranulomas.
Of these extrapulmonary lesions, enteric disease
(ulcerative colitis and mesenteric lymphadenitis) is the
most common. Ulcerative colitis and/or mesenteric
lymphadenitis were present concurrently with pneumo­
nia in 50 per cent of foals with Rhodococcus equi infection
in one survey. Any of the extrapulmonary manifesta­
tions of disease may precede signs of pneumonia, but
once such clinical signs are observed, further evaluation
will usually document the presence of underlying and
concurrent pulmonary disease.
Intestinal colonization by Rhodococcus equi may
include several manifestations. Enterocolitis in the
form of diffuse infiltration of the lamina propria and
submucosa by infected macrophages and multinucleate
giant cells occurs. Affected segments have grossly thick­
ened, corrugated mucosa with multiple, irregularly
shaped, well-demarcated foci of necrosis and crateri­
form ulcers, from 0.5-4 cm in diameter. Histologically,
the granulomatous infiltrate can be seen to fill the lam­
ina propria, distort villi, and displace intestinal glands
and crypts. These areas of granulomatous infiltrate are
associated with those areas of the lamina propria and
submucosa that are associated with lymphoid follicles.
Cecal, colonic, and mesenteric lymph nodes may also
become enlarged and firm. Foals with enteric infections
commonly demonstrate the following clinical signs
• diarrhea
• fever
• variable weight loss.
In some cases cellular obstruction of the lymph
nodes and lymphatic vessels leads to ascites; affected
foals will show chronic weight loss and appear unthrifty
and potbellied in addition to producing diarrhea.
Although R. equi can be cultured from the stool of many
foals or horses, documentation of increasing R. equi
numbers in the feces, over the normal background
numbers present, may be helpful in identifYing
clinically affected foals.
503
27 GASTROINTESTINAL DISEASE IN THE FOAL
In the intestinal form of infection, it is likely that
Rhodococcus equi utilizes the specialized microfold cells
in the intestinal wall as a route of entry to
macrophages in Peyer's patches and discrete lymphoid
follicles diffusely distributed along the intestinal tract.
These microfold cells, or M-cells, are interspersed
among the villous enterocytes, and function as anti­
gen-presenting cells, delivering lumenal antigen to
immune cells in the submucosa and lamina propria
for processing. Once the bacteria are ensconced
within the phagosomes, they travel with the
macrophage and may subsequently access lymph
nodes in the mesentery of the small intestine, cecum,
and large colon, causing enlargement and abscessa­
tion of these nodes. They may also enter the lacteal
and lymph vessels, eventually gaining access to the cir­
culation via the thoracic duct. The bacteria can then
become hematogenously distributed, resulting in
abscessation at random sites. Such abscesses often
develop in the peritoneal cavity, but in horses and in
other species, including humans, R. equi abscesses
have been reported in a variety of locations. In
humans, the organism has caused disease in both
immunocompetent and immunocompromised individ­
uals, though it occurs more commonly in patients with
dysfunctional cell-mediated immunity such as HIV
patients and transplant recipients. Respiratory tract
disease, including chronic, granulomatous pneumonia
and extrapulmonary infections such as mediastinitis, is
the most common disease manifestation in humans,
but thyroid abscesses, post-injection gluteal abscesses,
renal abscesses, and a variety of other affected body
sites have all been reported. Only about 30 per cent of
humans with R. equi infections report any contact with
herbivores or soil where herbivores have been.
TREATMENT AND PREVENTION
Diarrhea is the primary presenting sign in foals with
abdominal lymphadenitis or colitis. Diarrhea may also
develop as a complication of antimicrobial treatment
with erythromycin and rifampin. The erythromycin/
rifampin combination is the anti-rhodococcal treat­
ment regimen of choice, because of
• the drugs' lipophilic properties, permitting good
penetration across abscess walls and into the
intracellular space of macrophages
• the synergistic action of the two agents combined.
Disruption of colon microflora is thought to cause
the diarrhea in affected foals, necessitating (in some
cases) adjustment of erythromycin doses to a lower
rate in the recommended dose range or temporary dis-
504
continuation of the drugs for 24-48 hours. In some
cases the diarrhea will be self-limiting and will not
necessitate any alteration in dosing. Occasionally treat­
ment with different antimicrobial drugs is necessary.
Hyperthermia is another complication occasionally
encountered in foals being administered ery­
thromycin. The problem occurs most frequently in
very hot weather when the thermoregulatory mecha­
nisms are already challenged to a maximum in a pneu­
monic foal.
Successful management of farms with an enzootic
Rhodococcus equi presence must address the issues of pro­
phylactic measures for the disease, early identification
of affected foals, and effective therapy of ill foals.
Immune prophylaxis is an active area of research, and
much remains to be elucidated and understood. For
instance, administration of hyperimmune serum to
young foals has been shown to reduce the incidence
and mortality of Rhodococcus equi pneumonia on
enzootic premises but is not effective at treating estab­
lished disease. Vaccination of mares and their foals with
a preparation of VapA protein extract was not protec­
tive for clinical disease and may have enhanced the like­
lihood of R. equi pneumonia in the foals. Preventative
measures that are known to be effective, however,
include
• prompt removal and composting of manure from
infected foals
• rotating pastures to decrease erosion of pasture into
dusty paddocks
• segregation of ill foals from the general population.
These measures effectively reduce the numbers of
the infective organism in the environment, reducing
the immune challenge to the at-risk population of foals
in their immunologically vulnerable phase.
Equine cryptosporidial
diarrhea
NO Cohen
INTRODUCTION
Diarrhea is a common and often serious disease of foals.
Protozoal diarrhea in foals caused by the coccidian par­
asite Cryptosporidium parvum is being increasingly recog­
nized. The purpose of this chapter is to review the
epidemiology, clinical signs, diagnosis, treatment, and
prevention of C. parvum infection in horses.

LIFE CYCLE AND TRANSMISSION
Infection of foals occurs by ingestion of the infective,
sporulated oocysts. These excyst in the small intestine
and attach to the epithelium in a location described as
intracellular but extracytoplasmic. Amplification
occurs both through asexual and sexual multiplica­
tion. Oocysts are formed that are capable of autoinfec­
tion prior to excretion (thin-walled oocysts) or that
are immediately infectious when shed in feces (thick­
walled oocysts) . Transmission occurs either via the
fecal-oral route or by ingestion of contaminated food
or water. Sources of infection for horses are unknown
but, as for people, contaminated municipal water may
be important. Conflicting evidence exists as to
whether mares are the source of infection for foals,
however, in the author's experience mares are not the
source of infection for foals. In Texas cattle do not
appear to be an important source of infection for
horses.
EPIDEMIOLOGY
Prevalence
Prevalence varies with the method of detection used
and the population studied. Infection among clinically
normal, mature horses is rare (approximately 0-5 % ) .
Prevalence a t breeding farms may b e higher, particu­
larly among foals. Prevalence is higher among foals with
diarrhea than among clinically normal foals, and preva­
lence may approach 1 00 per cent among diarrheic foals
at farms during an outbreak.
Signalment
Foals are at increased risk of infection, particularly
those from 1-4 weeks of age, however diarrhea associ­
ated with Cryptosporidium parvum may be seen in foals
younger or older than this.
The time from infection to shedding oocysts for
cryptosporidial diarrhea in foals is unknown. Most foals
shedding cryptosporidial oocysts have been older than
5 days of age. Although cryptosporidial diarrhea has
been described in foals with diarrhea observed at 2 days
of age, cryptosporidial infection should be ranked
lower in the differential diagnosis for diarrhea of a 2-
day-old foal than in that of a foal aged 5-10 days.
Cryptosporidial infection and diarrhea are rare in
mature horses. Evidence of predisposition by sex or
breed does not exist, although most epidemiological
studies of equine cryptosporidiosis have been con­
ducted in groups of mares and foals.
DIARRHEA IN THE FOAL 27
Immune status
Immunocompromised foals, such as those with severe
combined immunodeficiency disease, are at increased
risk. However, immunocompetent foals can also
develop cryptosporidial diarrhea. Although the disease
will generally be more severe among immunocompro­
mised foals, severe or fatal diarrhea can occur in
immunocompetent foals.
Farm epidemics
Some farms experience epidemics of cryptosporidial
diarrhea. Recurrence during ensuing years is rare. A
high density of foals, a municipal water source, foaling
in stalls (versus pasture) , and poor hygiene may be risk
factors for infection and disease.
CLINICAL SIGNS
Clinical signs in foals vary with age and immune status
and are usually limited to the gastrointestinal tract and
related organs. Diarrhea associated with cryptosporidial
infection is more prevalent during the first 3-4 weeks of
life, but older foals, weanlings, and yearlings can be
affected. Among immunocompromised foals with com­
bined immunodeficiency, signs are often severe and
can progress rapidly. In these foals sites other than the
small intestine may be infected including the stomach,
common bile duct, colon, and major pancreatic ducts.
Among immunocompetent foals, clinical signs associ­
ated with cryptosporidial infection will vary from absent
to fatal diarrhea. Inapparently infected foals may repre­
sent a source of infection for other foals. The severity of
signs may be related to agent factors (inoculum size, vir­
ulence) , host factors (age, immunocompetence) , and
environmental factors (water source, housing prac­
tices) . In older foals (i.e. 3-6 months) the diarrhea may
be more chronic and can persist until foals are 9-12
months of age. In all infected foals concurrent infection
with other putative enteropathogens (Salmonella spp.,
rotavirus, coronavirus, adenovirus) may be observed.
DIAGNOSIS
Ante-mortem diagnosis of cryptosporidial infection is
generally based on detection of oocysts in the feces.
Fecal samples should be submitted as fresh material or
in recommended preservative ( 1 0 % formalin or
sodium acetate-acetic acid-formalin) . Oocysts can be
detected using either concentration or staining tech­
niques. Concentration of oocysts may be accomplished
by flotation or sedimentation. Regardless of technique,
505
27 GASTROINTESTINAL DISEASE IN THE FOAL
distinguishing oocysts from yeast is an important diag­
nostic issue.
In veterinary diagnostic laboratories, three tech­
niques are commonly used
• flotation of oocysts
• acid-fast staining of oocysts
• detection of oocysts using an immunofluorescence
assay (IFA) .
Sedimentation techniques are rarely used in veteri­
nary diagnostic laboratories. Of the flotation tech­
niques used, flotation in Sheather's sugar solution is
most common. Prompt processing is important because
oocysts collapse and lose their spherical shape when left
in Sheather's sugar solution.
Acid-fast staining of fecal specimens is widely used
for detection of Cryptosporidium parvum. The technique
is simple and staining kits are commercially available.
The organisms appear as red spheres (4-6 mm in diam­
eter) against a dark, counter-stained background, while
yeast generally do not appear red (Plate 27.2) . The
technique has relatively poor specificity making it a
poor choice for a screening test. However, it is useful
clinically as a diagnostic test because of its good sensi­
tivity, availability, and low cost.
The IFA test has relatively low sensitivity but excel­
lent specificity. A commercial immunofluorescence
assay is available (Meridian Diagnostics Inc., Cincinnati,
OH) that simultaneously detects cryptosporidial and
giardial organisms. The high cost relative to staining
techniques and specialized microscopic equipment
needed are limitations of the IFA. To date, reliable
enzyme-linked immunosorbent assays have not been
developed and validated for detecting Cryptosporidium
parvum in samples from horses. Flow cytometric meth­
ods are more sensitive than IFA or acid-fast staining, but
are not widely available.
The pattern of oocyst shedding by foals is variable in
duration (from days to many weeks) and can be inter­
mittent. Shedding may be antecedent, concurrent, or
subsequent to the onset of diarrhea. Because of the vari­
able duration and the intermittent pattern of shedding,
multiple samples (at least three) should be submitted
for detecting Cryptosporidium parvum in feces from foals.
It may be easier to detect oocysts in unformed feces
than in formed feces.
TREATMENT
Although over 1 20 different treatments have been
tested in a variety of animals, to date no specific
chemotherapy or immunotherapy has been proven to
be convincingly effective for treating Cryptosporidium
506
parvum in people and other mammals, and none has
been evaluated in a controlled clinical trial among
foals. Those treatments that may have greatest potential
for use in foals include paromomycin and bovine
colostrum.
Paromomycin is an expensive aminoglycoside antibi­
otic that is poorly absorbed from the gastrointestinal
tract. Paromomycin reduced the duration and severity
of diarrhea and eliminated oocyst shedding in neonatal
calves experimentally infected with Cryptosporidium
parvum. Paromomycin was effective in treating a cat
with cryptosporidiosis. Doses used in calves have ranged
from 50-100 mg/kg administered orally once or twice
daily. No data exist for the use of this drug in foals.
Adverse effects of paromomycin in humans include
diarrhea, nausea, and abdominal cramps. As for all
other agents used to treat cryptosporidial infection,
experimental and clinical evidence also exists indicat­
ing a lack of effectiveness of paromomycin. No antibi­
otic approved for use in horses has been demonstrated
to be effective in the treatment of cryptosporidial
diarrhea.
Hyperimmune bovine colostrum has been used with
varying success as a means of prophylaxis and therapy of
cryptosporidiosis in animals and patients with AIDS. A
factor limiting the use of hyperimmune bovine
colostrum is its availability. Pooled bovine colostrum,
however, is more readily available. Pooled bovine
colostrum from non-immunized animals also may be
protective in controlling cryptosporidiosis; non­
immunoglobulin factors in the colostrum may provide
protection. Use of hyperimmune or pooled bovine
colostrum has not been uniformly successful. The ben­
efits of administration of colostrum or hyperimmune
colostrum to foals, regardless of their age, with cryp­
tosporidiosis is unknown.
Treatment of foals with severe combined immuno­
deficiency is likely to be unsuccessful. In immunocom­
petent foals, infection is often subclinical or mild and
self-limiting; in these foals no treatment or supportive
care is needed. In more severely affected foals further
treatment may be necessary.
CONTROL AND PREVENTION
The prevention and control of cryptosporidiosis can be
difficult. Currently, immunization effective at prevent­
ing cryptosporidiosis in horses and foals is lacking.
Although some chemotherapeutic agents have shown
preventive potential, the cost-effectiveness of such pro­
phylaxis is often a limiting factor. Oocysts shed in feces
are infective, extremely resistant to environmental fac­
tors, and can survive for months if not exposed to

extremes of temperature or desiccation. Oocysts can be
killed by steam, 1 0 % formalin, 5% ammonia, and undi­
luted commercial bleach, although prolonged expo­
sure is necessary which can be difficult to achieve. Good
sanitation may help by decreasing the oocyst burden in
the foals' environment. Specific sanitation strategies
would include providing uncontaminated water, rigor­
ous cleaning (preferably with steam) and disinfecting
foaling stalls, removing all the bedding, and isolating
diarrheic foals.
ZOONOTIC CONSIDERATIONS
Ingestion of oocysts in people can cause gastrointestinal
disease in immunocompetent and immunosuppressed
people. People working with animals, including farmers
and veterinarians, are considered to be at increased
risk. Cryptosporidiosis has occurred in veterinary stu­
dents exposed to infected calves and foals. Efforts to
minimize transmission in persons handling infected
foals should include instruction regarding, and rigor­
ous attention to, hygiene, protective clothing (possibly
to include face mask, gloves, gown or coveralls, and
boots) , and efforts to disinfect contaminated areas.
Persons with primary or acquired immunodeficiency
should not be exposed to foals with diarrhea in which a
diagnosis of cryptosporidiosis is possible. Because of the
low prevalence of infection, mature horses do not
appear to be an important source of environmental
contamination.
Diarrhea - other causes
JF Freestone
ANTIBIOTIC-INDUCED DIARRHEA
Antibiotic-induced diarrhea occurs because of the inhi­
bition of the normal anaerobic bacterial flora and the
secondary proliferation of pathological bacteria. In
adult horses antibiotic-induced colitis is generally
severe and can rapidly be fatal. In foals antibiotic­
induced diarrhea is generally mild and will often
resolve quickly once the antibiotics are discontinued.
Diarrhea can be induced by a number of antibiotics.
Some antibiotics will cause a problem only in certain
regions and this is probably a reflection of differences
in the normal intestinal bacterial flora. In foals the
antibiotic most commonly associated with diarrhea is
erythromycin. Erythromycin is widely used in combina-
DIARRHEA IN THE FOAL 27
tion with rifampin for the treatment of Rhodococcus equi
infections. Diarrhea that develops in a foal on ery­
thromycin will generally resolve 48 hours after the
antibiotic is discontinued. Often the foal needs to con­
tinue receiving antibiotics for the R equi infection.
Trimethoprim sulfamethoxazole and rifampin can be
used when problems of either hyperthermia or diar­
rhea have developed secondary to the use of ery­
thromycin. R equi infections have resolved in response
to this antibiotic combination.
SEPTICEMIA
Diarrhea is a common clinical sign in the septicemic
foal. Septicemia usually develops in the first 7 days of
life. Foals may be normal at birth, become infected and
then deteriorate, or be born septicemic with weakness
and inability to stand and nurse. The common clinical
signs in the septicemic foal initially are lethargy, depres­
sion, and failure to nurse, followed by diarrhea. The
common bacteria implicated in neonatal septicemia are
Escherichia coli, Actinobacillus spp., Klebsiella pneumoniae,
and Streptococcus spp. The basis for treatment of these
foals is antibiotics to kill the infectious agent with sup­
porting medical therapy and nursing care for the
neonate.
Another foal diarrhea syndrome which has not been
widely reported has been termed 'fetal diarrhea'. The
newborn foal with fetal diarrhea will be born covered in
liquid yellow-brown feces. These foals are infected in
utero, and there may be an accompanying placentitis.
The amniotic fluid is contaminated with feces and the
foal is subject to aspiration pneumonia. These foals are
generally septicemic and may appear healthy and
robust at birth but will often be unable to stand and will
then rapidly deteriorate. Other foals born with fetal
diarrhea will progress normally and it is assumed these
foals develop diarrhea shortly prior to birth and have
limited exposure to the severely contaminated environ­
ment. All foals born with evidence of fetal diarrhea
should be treated with broad spectrum antibiotics and
closely monitored for signs of deterioration.
NUTRITIONAL CAUSES OF DIARRHEA
Nutritional causes of diarrhea in foals have been associ­
ated with overfeeding, use of milk replacers, and a rapid
change in diet from mare's milk to milk replacers (e.g.
orphaned foals) . In foals deprived of mares colostrum
and milk for 48 hours because of the possibility of
neonatal isoerythrolysis, and supplemented with milk
replacer, it is common for a self-limiting diarrhea to
507
27 GASTROINTESTINAL DISEASE IN THE FOAL
develop. Foals with these forms of diarrhea remain clin­
ically normal.
Lactase deficiency and lactose intolerance have both
been reported in foals. These are both are unusual
causes of diarrhea. Lactase deficiency can be evaluated
by use of an oral lactose tolerance test.
Ingestion of sand and dirt by foals can also cause
diarrhea secondary to local irritation of the lining of the
gastrointestinal tract. Diagnosis can be made by exam­
ining the feces for sand or in severe cases using abdom­
inal radiography. Treatment with orally administered
methyl cellulose may be effective in removing the sand
and dirt.
EQUINE HERPESVIRUS
__�_�_Wil*�I#lI**WA"'�»lIi!lfW"_;{'"",'��ty"'*'_'lli
Foals infected in utero with equine herpesvirus may
develop diarrhea although it is not the predominant
clinical sign in these foals. Often the infected foal will
appear normal at birth but will fail to stand and nurse
and then progressively deteriorate, developing severe
respiratory distress terminally. These foals are treated
and supported as septicemic foals, although treatment
is generally unsuccessful. A definitive diagnosis is made
on histopathological changes in the lung, liver, and the
Iymphoreticular tissues at necropsy.
CANDIDIASIS
Candida albicans is a commensal organism of the
mucous membranes and gastrointestinal tract.
Superficial infections have been reported in foals.
Systemic candidiasis is rare and generally occurs in foals
treated with prolonged broad spectrum antibiotics for
septicemia. Immunocompromised foals are also predis­
posed to candidiasis.
Diarrhea has been reported in foals with systemic
candidiasis, but this is considered an unusual cause. As
these foals are often immunocompromised or have
been treated long term with antibiotics, the diarrhea
may not be directly due to the Candida infection.
PARASITES
Strongyloides westeri
Strongyloides westeri is a questionable cause of diarrhea in
young foals. Transmission occurs by ingestion of infec­
tive larvae from the mare's milk or via skin penetration.
The pre-patent period is 8-14 days. Attempts to estab-
508
lish a clear association between infective larvae and the
induction of diarrhea have been unsuccessful.
Treatment of mares on the day of parturition with iver­
mectin was unsuccessful in blocking vertical transmis­
sion. Treating foals with ivermectin or oxibendazole is
effective.
Strongyle infections
Equine strongylosis occurs secondary to mixed infec­
tions with large strongyles and cyathostomes (small
strongyles) . These mixed infections cause gastrointesti­
nal tract irritation and clinical signs of intermittent soft
feces, but can also cause persistent diarrhea in foals.
The severity of the clinical signs is related to the parasite
load. Foals grazing pasture containing high levels of
strongyle eggs, or immunologically naive foals with a
good worming history that are subsequently exposed to
strongyle infections are at risk of developing clinical
signs of strongyle parasitism. These clinical signs
include lethargy, depression, decreased weight gain, a
rough hair coat, and diarrhea. Treatment with iver­
mectin is effective in controlling these mixed infec­
tions.
Proliferative enteropathy in
foals
J-P Lavoie and R Drolet
Proliferative enteropathy is a transmissible enteric dis­
ease affecting a number of mammalian species, notably
pigs. It has a worldwide distribution and its causal agent
has been recently identified and classified as Lawsonia
intracellularis, an obligate intracellular bacterium.
CLINICAL PRESENTATION
The disease has been described sporadically in horses,
either as isolated cases or as outbreaks in breeding
farms. Foals 4-7 months of age appear most suscepti­
ble to the disease. Common clinical signs include
depression, rapid and severe weight loss, subcutaneous
edema, diarrhea, and colic. Extremely poor body con­
dition with a rough hair-coat and a pot-bellied appear­
ance are common findings in affected foals. The
disease may lead to death within a few days or cause
chronic growth retardation. Concomitant respiratory
tract infection and intestinal parasitism are also found
in some foals.
 DIARRHEA IN THE FOAL 27

CLINICAL PATHOLOGY

Hypoproteinemia is the most consistent laboratory find­

ing. Other commonly observed abnormalities include
transient leukocytosis, anemia, increased creatine
kinase, hypocalcemia, hypochloremia, and hypona­
tremia.

DIFFERENTIAL DIAGNOSIS

The clinical signs presented by foals with proliferative

enteropathy resemble those associated with common
gastrointestinal diseases caused by parasites, infections
caused by Salmonella spp., Clostridium spp., and
Rhodococcus equi, or sand impactions. However, these
conditions are unlikely to cause outbreaks of disease
characterized by weight loss, diarrhea, colic, and severe
hypoproteinemia in foals of this age group.

DIAGNOSIS

Post-mortem diagnosis of proliferative enteropathy is
based on identifying the characteristic intracellular bac­
teria within the apical cytoplasm of proliferating crypt
epithelial cells of the intestinal mucosa, using a silver
stain (Figure 27.2 ) . The severe hyperplasia of the
intestinal crypts often causes a grossly detectable thick­
ening of the mucosa of the distal small intestine.
Polymerase chain reaction analysis and immunohisto­
chemistry confirm the presence of Lawsonia intracellu­
laris in intestinal tissue. Isolation of the organism is not
a practical means of diagnosis as it cannot yet be culti­
vated in conventional cell-free media and the technique
is available in only a few research institutions.
Ante-mortem diagnosis of proliferative enteropathy
is based on clinical signs, hypoproteinemia, and the
exclusion of common enteric infections. The presence
of the organisms can be detected using polymerase
chain reaction analysis of fecal samples. Although spe­
cific, to date this technique has revealed a low sensitivity
in horses. The use of serology for the diagnosis of
Lawsonia intracellularis infection in a small number of
foals suggests that this technique may be promising.
Figure 27.2 Intestinal crypts from a foal with proliferative
enteropathy. Numerous bacteria are agglomerated withi n
the apical cytoplasm o f the crypt enterocytes (arrow
heads). Warthi n Starry silver stain.
be required in some foals. Foals with severe hypopro­
teinemia may benefit from administration of plasma
intravenously.
OUTCOME
Without appropriate antimicrobial therapy the disease
may lead to death. However a rapid improvement
« 24-48 h) in attitude, appetite, weight gain, and colic
signs or diarrhea may be observed in foals following
administration of erythromycin and/or rifampin. The
increase in plasma protein concentration lags com­
pared to the improvement noted on other parameters
during therapy.

THERAPY
Erythromycin estolate (25 mg/kg p.o. q. 6-8 h) alone
or combined with rifampin (7 mg/kg p.o. q. 12 h) for a
minimum of 21 days is effective in controlling the dis­
ease. Additional symptomatic treatment such as antimi­
crobial, anti-ulcer therapy and parenteral feeding may
BIBLIOGRAPHY
Foal heat d iarrhea
Becht] L, Semrad S D ( 1 986) Gastrointestinal diseases of
foals. Compo Cont. Educ. Pract. Vet. 8 ( 7 ) : S367-S374.
Masri M D, Merritt A M, Gronwall R, Burrows C F ( 1 986)
Fecal composition in foal heat diarrhea. Equine Vet. J
1 8 (4) :301- 6.

509
27 GASTROINTESTINAL DISEASE IN THE FOAL
Viral d iarrhea
Cohen N ( 1 997) Diarrheal diseases of foals. In: Current
Therapy in Equine Medicine 4th edn, N Robinson (ed. ) , W B
Saunders, Philadelphia, p. 631.
Fenger C ( 1 998) Neonatal and perinatal diseases. In: Equine
Internal Medicine, S Reed and W Bayly (eds). W B
Saunders, Philadelphia, pp. 962-3.
Smith B ( 1996) Diarrhea. In: Large Animal Internal Medicine
2nd edn, B P Smith (ed. ) . C V Mosby, St Louis, pp . 1l9-123 .
Salmonellosis in the foal
Clarke R C, Gyles C L ( 1993) Salmonella. In: Pathogenesis oj
Bacterial Injections in Animals, 2nd edn, C L Gyles and C 0
Thoen (eds). Iowa State University Press, Ames, lA,
pp. 133-53.
Jones S L, Spier SJ ( 1 998) Inflammatory diseases of the large
intestine causing diarrhea. In: Equine Internal Medicine.
S M Reed and W M Bayly (eds) . Philadelphia,
W B Saunders, Philadelphia, pp. 663-7.
Kowalski J ]. Bacterial and mycotic infections. In: Equine
Internal Medicine. S M Reed and W M Bayly (eds ) .
Philadelphia, W B Saunders, Philadelphia, p p . 68-70.
Madigan J E ( 199 1 ) Neonatal salmonellosis. In: Manual oJ
Equine Neonatal Medicine, 2ndedn , J E Madigan (ed. ) . Live
Oak Publishing, Woodland, CA; pp. 133-5.
Madigan J E ( 1 995) Diarrhea in neonatal foals. In: Large
Animal internal Medicine, 2nd edn, B P Smith (ed . ) . Mosby
Year Book, St Louis, MO; pp. 391-4.
Spier S J ( 1993) Salmonellosis. Vet. Clin. N. Am. Equine Pract.;
9:2 385-7.
Vaala W E ( 1 996) Failure of passive-transfer: diagnosis,
treatment and prevention. In: Proceedings oj Equine Stud
Medicine. Post Graduate Foundation of Veterinary Science,
University of Sydney, Sydney, Australia; pp. 3 1-8.
Vaala W E ( 1 996) Neonatal foal diarrhea. In: Proceedings oj
Equine Stud Medicine. Post Graduate Foundation of
Veterinary Science, University of Sydney, Sydney,
Australia; pp. 133-5.
Vaala W E ( 1 996) Neonatal septicemia. In: Proceedings oJEquine
Stud Medicine. Post Graduate Foundation of Veterinary
Science. University of Sydney, Sydney, Australia; pp. 21 1-18.
Clostridial enterocolitis i n foals
East L M, Savage CJ, Traub-DargatzJ L et at. ( 1 998)
Enterocolitis associated with Clostridium perJringens
infection in neonatal foals: 54 cases ( 1 988-1997) . J Am.
Vet. Med. Assoc. 2 1 2 ( 1 1 ) : 1 751-6.
Meer R R, Songer J G ( 1997) Multiplex polymerase chain
reaction assay for genotyping Clostridium perJringens. Am.J
Vet. Res. 58(7):702-5.
Netherwood T, Binns M, Townsend H et at. ( 1998) The
Clostridium perfringens enterotoxin from equine isolates; its
characterization, sequence and role in foal diarrhea.
Epidemiol. Inject. 120:193-200.
Rhodococcus equi as an agent of intestinal
disease
Anzai T et at. ( 1 997) Comparison of tracheal aspiration with
other tests for diagnosis of Rhodococcus equi pneumonia in
foals. Vet. Microbiol. 56(3-4 ) : 335-45.
Barton M D, Hughes K L ( 1 984) Ecology of Rhodococcus equi.
Vet. Microbioi.; 9:65-76.
510
Brumbaugh G W, Davis L E , Thurman J C , et al. ( 1990)
Influence of Rhodococcus equi o n the respiratory burst of
resident alveolar macrophages from adult horses. Am. J
Vet. Res.; 5 1 : 766-71 .
Giguere S , PrescottJ F ( 1 997) Strategies for the control of
Rhodococcus equi infections on enzootic farms. Proc. Am.
Assoc. Equine Pract.; (43) :65-70.
Hondalus M K ( 1 997) Rhodococcus equi: Pathogenesis and
virulence. Proc. Am. Assoc. Equine Pract. ; 43:71-8.
PrescottJ F, Hoffman A M ( 1 993) Rhodococcus equi, Vet. Clin.
N. Am. Equine Pract.; 9 (2) :375-84.
PrescottJ F et al. ( 1 996) Use of a virulence-associated protein
based ELISA for Rhodococcus equi serology in horses. Equine
Vet.J 28(5) : 344-9.
Takai S et al. ( 1 986) Quantitative fecal culture for early
diagnosis of Corynebacterium (Rhodococcus) equi enteritis in
foals. Can. J Vet. Res.; 50 (4) :479-84.
Tizard I ( 1 996) Immunity at body surfaces. In: Veterinary
Immunology 5th edn, I R Tizard ( ed . ) . W B Saunders,
Philadelphia, pp. 254-55.
Zink M C, YagerJ A, Smart N L ( 1 986) Corynebacterium equi
infections in horses, 1958-1984: a review of 1 3 1 cases. Can.
J Vet. Res. 27:213.
Zink M C, Yager J A, Prescott J F et al. ( 1 987) Electron
microscopic investigation of intracellular events after
ingestion of Rhodococcus equi by foal alveolar macrophages.
Vet. Microbiol.; 14:295-305.
Equine cryptosporidial d iarrhea
Cohen N D, Snowden K ( 1 996) Cryptosporidial diarrhea in
foals. Comp. Cont. Educ. Pract. Vet. 18:298-306.
Cole D J, Cohen N D, Snowden K, Smith R ( 1 998) Prevalence
and risk factors for fecal shedding of Cryptosporidium
parvum oocysts in horses. J Am. Vet. Med. Assoc.
2 1 3: 1 296-1 302.
Cole D j, Snowden K, Cohen N D , Smith R ( 1 999) Detection
of Cryptosporidium parvum in horses: thresholds of acid-fast
stain, immunofluorescence assay, and flow cytometry. J
Clin. Microbiol. 37.
Xiao L, Herd R P ( 1 994) Review of equine Cryptosporidium
infection. Equine Vet. J 26:9-13.
Diarrhea - other causes
BechtJ L, Semrad S D ( 1 986) Gastrointestinal diseases of
foals. Compo Cont. Educ. Pract. Vet. 8:S367-S374.
Klei T R ( 1986) Other parasites - recent advances. Vet. Clin.
N. Am. Equine Pract. 2: 329-36.
Martens RJ, Malone P S, Brust D M ( 1985) Oral lactose
tolerance test in foals: techniques and normal values. Am.
J Vet. Res. 46: 2 1 63-6.
McClure JJ, AddisonJ D, Miller R 1 ( 1 985)
Immunodeficiency manifested by oral candidiasis and
bacterial septicemia in foals. J Am. Vet. Med. Assoc.
186: 1 1 95-7.
Reilly L K, Palmer J E ( 1994) Systemic candidiasis in four
foals. J Am. Vet. Med. Assoc. 205:464-6.
Thamsborg S M, Leifsson P S, Grondahl C, Larsen M, Nansen
P ( 1 998) Impact of mixed strongyle infections in foals
after one month on pasture. Equine Vet. J 30:240-5.
Proliferative enteropathy in foals
Duhamel G E, Wheeldon E B ( 1 982) Intestinal adenomatosis
in a foal. Vet. Patho!.; 19:447-9.

Frank N, Fishman C E, Gebhart C] et al. ( 1 998) Lawsonia
intmcellularis proliferative enteropathy in a weanling foal.
Equine Vet. ]; 30:549-52.
Lavoie .J P, Parsons D, Drolet R ( 1 998) Proliferative
enteropathy in foals: a cause of colic, diarrhea and
protein-losing enteropathy. Proc. Am. Assoc. Equine Pract.
44:1 34-5.
DIARRHEA IN THE FOAL 27
McOrist S, Gebhart C], Boid R et al. ( 1 995) Characterization
of Lawsonia intmcellularis gen. nov., sp. nov., the obligately
intracellular bacterium of porcine proliferative
enteropathy. Int. ] Syst. Bacteriol; 45:820-5.
Williams N M, Harrison L R, Gebhart C] ( 1 996) Proliferative
enteropathy in a foal caused by Lawsonia intmcellularis-like
bacterium . ] Vet. Diag. Invest; 8:254-6.
51 1
 26
Diseases of the rectum and anus in the
foal

EM Santschi

Atresia recti and ani supply to a portion of the gut, leading to ischemic local
necrosis. However the cause of the vascular insult is
unknown.

INTRODUCTION

Atresia recti and ani are rare conditions of neonatal

foals. Foals affected with atresia recti and ani initially
nllrse well but cannot pass meconium normally. The
ingestion of food causes fluid and gas to accumulate
and the intestine becomes distended causing colic.
EPIDEMIOLOGY
Ag e
Atresia recti and ani are congenital conditions, there­
fore clinical signs of colic and bloating in foals with this
condition are only seen within 48 hours of birth.
CLINICAL SIGNS
Atresia ani is easily diagnosed as there is no visible anus.
Foals affected with atresia ani usually show signs of
abdominal pain and progressive abdominal distention
within 48 hours of birth. Some foals with atresia ani
have either a rectovaginal fistula or rectourethral fistu­
lae, so small amounts of feces may be passed through
the vulvae or penis. Foals with atresia recti may have an
anus, but digital palpation will reveal a blind pouch and
no feces. Caudal abdominal radiographs may help
delineate the extent of atresias. Elevating the foal's
hindquarters will cause gas to fill the terminal patent
gut and the caudal blind pouch can be determined.

Gender and genetics

Atresia recti and ani are rare conditions and no genetic
predisposition has been noted.
ETIOLOGY
Atresia recti and ani probably have different, and as yet
unknown, causes. Atresia ani occurs when the anal
membrane persists - during normal embryologic devel­
opment the anal membrane breaks down resulting in a
caudal opening in the terminal portion of the fetal gut.
The most commonly accepted cause of intestinal atre­
sias, including atresia recti, is a congenital loss of blood
PATHOLOGY
Gross pathology
For atresia ani there is no anus and there is haired skin
where the anus should be. There may be a communica­
tion between the urethra and rectum. For atresia recti
there is a discontinuity between the anus and terminal
small colon.
DIAGNOSIS
These conditions are diagnosed by clinical signs.

491
26 GASTROINTESTINAL DISEASE IN THE FOAL
TREATMENT
Treatment of atresia ani requires surgical anastomosis
of the terminal rectum and the skin, and closure of any
urethral or vaginal fistulae. Surgery can be performed
under general anesthesia or under sedation and
epidural anesthesia. A 2.0 x 1.0 cm elliptical incision
(long axis oriented vertically) is made where the anus
should be, and the terminal rectum is retracted cau­
dally. The terminal rectum is opened and sutured to
the skin. It is helpful to first suture the rectum using
four equally spaced interrupted sutures and then filling
in between them with interrupted sutures.
Closure of urethral or vaginal fistulae with the rec­
tum requires dissection of the border of the fistulae and
492
a two-layer closure. The mucosa of the fistula is
removed and the submucosal tissues sutured together.
The rectal mucosa is then closed separately.
There is little information about correction of atresia
recti. Surgical correction (via rectal pull through) is dif­
ficult because of the inaccessibility of the blind-ended
segments in the pelvic cavity. Permanent colostomy
might be an option for salvage.
BIBLIOGRAPHY
Benamou A E, Blikslager A T, Sellon D C (1995) Intestinal
atresia in foals. Compo Cont. Educ. Pract. Vet. 17:1510-16.
 28
Hepatic diseases in foals

Portosystemic shunts Only five cases of congenital portosystemic vascular

anomalies have been reported in horses, of these five
cases
LA Fortier
• two were classified as single extrahepatic
• one as multiple extrahepatic
INTRODUCTION
• one as single intrahepatic
• one was designated as an arteriovenous anomaly.
Portosystemic shunts (PSS) are anomalies of the porto­
systemic circulation that allow direct communication A presumptive diagnosis of PSS is based on history, clin­
between the portal circulation and a systemic vein such ical signs, and blood tests, while a definitive diagnosis
as the vena cava. The shunting vessel(s) circumvents requires hepatic scintigraphy or positive-contrast por­
portal blood from entering the hepatic circulation and tography. Medical management may provide temporary
being cleared of toxic metabolites by the liver. relief from the signs of hepatic encephalopathy.
Portosystemic shunts are classified as However, without surgical ligation of the shunt vessel(s)
progressive deterioration occurs.
• congenital or acquired
• intrahepatic or extrahepatic
• single or multiple.
PATHOPHYSIOLOGY
This chapter primarily addresses congenital PSS,
although the fundamental pathophysiology and med­ Portosystemic shunts divert portal blood away from the
ical management described applies to acquired shunts liver thereby allowing noxious substances such as
as well. ammonia, mercaptans, short-chain fatty acids, and false
Intrahepatic shunts represent a failure of the neurotransmitters that are normally cleared by the liver
ductus venosus to close normally 2-3 days following to remain in the systemic circulation, resulting in
birth. Embryologically the ductus venosus provides a hepatic encephalopathy. Ammonia has been widely
direct communication between the left umbilical vein suggested as the major neurotoxin of hepatic disease.
and the caudal vena cava. In the neonate, when the Hyperammonemia emerges from decreased hepatic
ductus venosus fails to close, portal blood drains into conversion of ammonia to urea and is a characteristic
the left hepatic vein just prior to entering the caudal sign of PSS in horses. Ammonia exert� its toxic effects
vena cava. Congenital extrahepatic shunts most com­ on neuronal cell membranes and impairs neurotrans­
monly originate from the portal vein but may also mission through competing with potassium and subse­
originate from the left gastric vein, splenic vein, quently inhibiting the sodium-potassium-dependent
cranial or caudal mesenteric vein, or gastroduodenal adenosine triphosphatase. Portal blood comprises
vein, and typically empty in the caudal vena cava or 75-80 per cent of total hepatic blood flow and 50 per
azygous vein. cent of hepatic oxygen supply. Portal blood therefore

51 3
28 GASTROINTESTINAL DISEASE IN THE FOAL
determines the environment of the hepatocyte through
its hormone, nutrient, and oxygen content. Shunting of
portal blood from the liver results in liver atrophy due
to the lack of hepatic blood flow and concurrent
decreased supply of hepatotrophic factors such as
insulin and glucagon.
Poikilocytosis (erythrocyte malformation) and
microcytosis with normochromic erythrocytes are com­
mon findings on blood laboratory results in foals with
PSS. The cause of poikilocytosis in PSS remains unde­
fined and the microcytosis is believed to result from
metabolic toxins interfering with iron uptake and
metabolism or disrupting erythrocyte membrane
integrity. Neither poikilocytosis nor microcytosis are
specific for PSS, however, they are considered indicative
of serious hepatobiliary disease
CLINICAL SIGNS
The signalment for foals with PSS is inconsistent.
Belgian, Thoroughbred, Quarter horse, and Arabian
foals presented for a wide variety of clinical signs
between the ages of 2 weeks and 11 months. The pre­
senting history and clinical signs may include
1. small body size for age
2. episodic signs of hepatic encephalopathy including
• disorientation
• seizures
• stupor
• head pressing
• circling
• undirected aggression
• apparent cortical blindness
• non-responsiveness to auditory stimuli
• coma.
Neurologically, all reported cases had normal proprio­
ceptive responses and in the cases with apparent corti­
cal blindness, pupillary light reflexes were assessed as
normal. Differential diagnoses based on clinical signs
typically include PSS, bacterial or viral meningitis, and
idiopathic cerebral edema. A definitive diagnosis is
based on clinical laboratory data and positive-contrast
portography or hepatic scintigraphy.
DIAGNOSIS
In addition to a thorough physical and neurological
examination, blood should be submitted for routine
hematologic and serum biochemistry tests, and deter­
mination of serum concentrations of blood ammonium
and bile acids. Foals with PSS are typically microcytic
514
and normochromic with normal hematocrit and total
protein values (Table 28.1). There may be a mild
mature neutrophilia present, consistent with a stress
leukogram. Poikilocytosis is typically noted on red
blood cell morphology as mild to moderate.
Serum biochemistry values are typically within nor­
mal limits, including serum gamma glutamyl trans­
ferase and blood urea nitrogen concentrations, with the
possible exceptions of increased total bilirubin concen­
trations and hypoglycemia. In all reported cases of PSS
in foals, blood ammonia and total serum bile acid con­
centrations have been increased over normal values.
Increased concentrations of total serum bile acids and
blood ammonia, with normal hepatic enzyme concen­
trations in foals, should be considered indicative of con­
genital portosystemic vascular anomalies (Table 28.1).
Blood ammonia concentrations are typically at least sev­
enfold greater than age-matched controls and are con­
sidered a more definitive indicator of congenital PSS in
foals than increased total serum bile acid concentra­
tions. Correct handling of blood samples for blood
ammonia concentration determination is critical to
obtain reliable, diagnostic results. Blood samples from
the patient and an age and species-matched control
should be collected and transported on ice for immedi­
ate evaluation. Freezing or storage of plasma is discour­
aged as it may result in spuriously high or low values.
Pre- and postprandial determination of serum bile acid
values, while valuable in dogs and cats in the diagnosis
of PSS, are of little value in foals due to the physiology
and anatomy of the alimentary canal, particularly the
absence of a gallbladder.
Diagnostic test Abnormalities noted with
P55
hemogram microcytosis, poikilocytosis
serum biochemistry :thyperbilirubinemia,
panel hypoglycemia
blood ammonia usually increased more than
7 x normal
serum bile acids increased
cerebrospinal fluid* :t increased nucleated cell
count, red blood cell count,
and total protein
:t indicates all these conditions are present
* following seizures

Positive-contrast portography remains the diagnostic
technique of choice for shunt confirmation and loca­
tion. The surgical approach for access to the portal cir­
culation may be made through either a ventral midline
celiotomy or through a right flank incision. If shunt lig­
ation is to be performed during the same anesthetic
procedure as the contrast portogram, then a right flank
approach is recommended since this is the preferred
approach for shunt ligation (see Treatment, Operative
techniques) . Foals have a relative straight-branching
mesenteric venous pattern, allowing catheters to be
readily advanced within the cranial mesenteric vein and
potentially into the portal vein or shunt. An iodinated
contrast agent such as Renografin-76 is injected as
needed (typically 50-80 ml) to opacify the portal
venous system and abdominal radiographs are obtained
during the last few seconds of positive-contrast injec­
tion. If a shunt cannot be identified by positive-contrast
portography, a liver biopsy should be obtained to look
for hepatic dysplasia or microvascular shunting, this has
been reported in dogs but has not been recognized in
foals. The hepatic histologic abnormalities observed in
hepatic dysplasia are similar, and possibly indistinguish­
able from those observed in animals with PSS.
Fluoroscopically assisted portography is typically unre­
warding in foals due to the depth of their abdomens.
Hepatic scintigraphy is useful for shunt confirmation
but provides no information on shunt location and is
therefore also a less rewarding technique than positive­
contrast portography.
Additional diagnostic tests that may be beneficial
include abdominal ultrasound and cerebrospinal fluid
evaluation. Abdominal ultrasonography may identify
the PSS, however, a positive-contrast portogram should
still be performed preoperatively to confirm the ultra­
sound findings and determine the pattern and direc­
tion of portal blood flow. Cerebrospinal fluid analysis in
foals with PSS should be normal or reveal a slightly
increased total nucleated cell count, a mildly increased
total protein concentration, and an elevated red blood
cell count, consistent with trauma, but not indicative of
myelitis.
TREATMENT
Preoperative management
If anesthesia, portography, and surgical ligation of the
shunt are being considered, medical management of
the hepatic encephalopathy must be obtained before
anesthesia and surgery are attempted. Gaining manage­
ment of the hepatic encephalopathy may require sev­
eral days of intense medical therapy. Extreme caution
HEPATIC DISEASES IN FOALS 28
should be exercised when handling foals exhibiting
signs of hepatic encephalopathy. The frequent stum­
bling and undirected aggression may be harmful not
only to the people handling the foal, but to the foal as
well, necessitating a well-padded stall and possibly heavy
sedation. To control seizures and aggressive behavior,
tranquilizers, particularly benzodiazepines, and barbi­
turates should be administered cautiously, starting at
half of the recommended dose, since animals with PSS
are very susceptible to their depressive effects. In the
preoperative period, medical management should
be directed toward reducing encephalopathic toxins.
Medications should be judiciously chosen to include
those that do not require or interfere with hepatic
metabolism. The drugs of choice for ulcer prophylaxis
medication should be ranitidine or famotidine, because
unlike cimetidine, they are excreted primarily by the
kidneys and do not interfere with hepatic metabolism
of drugs. Metronidazole is frequently used in small
animals to reduce the number of ammonia-producing
bacteria in the colon, and if administered should be
given at half the recommended dose as it is metabolized
primarily in the liver and peripheral neuropathies have
been reported after its administration in humans with
PSS. Intravenous administration of dimethyl sulfoxide
should be avoided as it is an effective carrier molecule
and could increase the transport of encephalopathic
toxins from the alimentary canal into the brain. Foals
should be maintained on a low protein diet to reduce
ammonia production, while maintaining their energy
and fluid requirements. Lactated Ringer's solution
should not be administered to severely affected animals
because it may induce alkalosis and worsen the
encephalopathy. Oral administration of lactulose
and/or neomycin should be considered. Lactulose is a
synthetic disaccharide which bypasses small intestinal
digestion. In the colon it acts as a cathartic and lowers
the fecal pH thereby inhibiting ammonia generation by
fecal bacteria.
Operative techniques
In foals affected with PSS, anesthesia may be poorly
tolerated because of the severe metabolic effects of the
disease. The use of tranquilizers, especially benzodi­
azepines, and barbiturates for anesthetic induction or
sedation should be avoided if possible because, as noted
above, animals with PSS are very susceptible to their
depressive effects. Mask or nasal intubation for induc­
tion using oxygen and isoflurane offers a relatively safe
anesthetic protocol. During surgery, the foal should be
kept warm and supported with intravenous fluids con­
taining glucose. All personnel involved in the anesthe­
sia, contrast portogram, and surgical ligation should be
515
28 GASTROINTESTINAL DISEASE IN THE FOAL
aware of the added risks and it should be stressed that
anesthetic and surgical times be kept to an absolute
minimum.
The preferred surgical approach for PSS ligation in
foals is a large right paracostal incision with an 18th rib
resection. This approach is superior to a ventral median
celiotomy to provide adequate exposure where the
depth of the abdomen and volume of small and large
intestines preclude adequate exposure to the portal cir­
culation. A thorough understanding of portal vascular
anatomy is paramount for shunt identification. A patent
ductus venosus represents the most difficult PSS to
identify and ligate. Most are located in the left or
central hepatic divisions and may be managed by left
hepatic vein attenuation which is technically easier than
intracaval techniques or intraparenchymal dissection,
particularly in the depth of an equine foal abdomen.
Mter the shunt is located, a catheter is placed in a
jejunal vessel to facilitate measuring portal pressures
during shunt ligation. If shunt ligation is performed
during the same anesthetic procedure as the positive­
contrast portogram, the same jejunal catheter may be
used for contrast injection and portal pressure moni­
toring. The catheter is connected to a water manometer
or pressure transducer and the shunt is ligated with
non-absorbable suture while the portal pressure is mon­
itored and abdominal viscera are observed for signs of
cyanosis and congestion. Cellophane banding instead
of suture ligation for shunt attenuation should be con­
sidered so that progressive and partial attenuation of
the shunt vessel is possible while monitoring the portal
pressure and abdominal viscera for signs of portal
hypertension. In dogs there was no difference in clini­
cal outcome between those cases where partial shunt
attenuation was performed to avoid portal hyperten­
sion, versus complete occlusion of the shunt vessel.
There are no data on normal portal vascular pressures
in foals. Until more information is available regarding
PSS ligation in foals, it would seem reasonable to follow
the guidelines set out for small animals which caution
that portal hypertension develops when portal pres­
sures increase more than 10 cmH20 over baseline
values or when visceral congestion is visible during or
after shunt ligation.
Postoperative management
Postsurgical care consists of intensive supportive care
similar to that described for preoperative management
in addition to monitoring wound healing and observing
for portal hypertension. Portal hypertension is charac­
terized by
• ileus
• shock
51 6
• bloody diarrhea
• abdominal pain.
Foals may still require treatment for hepatic
encephalopathy and should be maintained on a low
protein diet until complete resolution of clinical signs.
Postoperative blood ammonia and serum bile acid con­
centrations are usually monitored for signs of improve­
ment. However, in small animals, there is no correlation
between declining blood ammonia or total serum bile
acids and resolution of clinical signs. Blood ammonia
and serum bile acid values may never return to normal,
this is most likely the result of permanent hepatic
parenchymal abnormalities.
OUTCOME AND PROGNOSIS
Surgical mortality in foals with congenital PSS is high
with only one successful case of PSS ligation reported in
the literature. Interestingly, two out of five reported
cases of foals with PSS were full blooded Belgians, with
one case occurring in a Thoroughbred, one an Arabian,
and one a Quarter horse. The heritability of PSS in
horses is unknown but there is accumulating evidence
that these anomalies are inherited in certain purebred
dogs and cats. With so few cases of PSS reported in foals,
it is not possible to determine heritability, but this pos­
sibility should be kept in mind and discussed with the
foal's owners prior to surgical correction. The mortality
associated with surgical correction of PSS should
decrease with early diagnosis, surgical attenuation of
the shunt through a right flank approach instead of
a ventral midline celiotomy, and most importantly,
appropriate and aggressive preoperative and postopera­
tive management.
Tyzzer's disease
WV Bernard
Tyzzer's disease is an acute, fulminate bacterial hepati­
tis, myocarditis and! or colitis. The disease has been
reported in foals from 7-92 days of age. The causative
organism, Clostridium piliformis, is a filamentous bac­
terium (Plate 28.1). The disease occurs sporadically,
however has been reported in outbreaks and is
endemic in certain geographic locations. The route of
infection is thought to be via ingested feces. Soil is
contaminated by infected individuals or possibly
rodents.

CLINICAL SIGNS
Clinical signs of Tyzzer's disease include
• sudden death
• depression
• anorexia
• coma/stupor
• seizures
• hyper- or hypothermia
• icterus
• petechiation
• abdominal pain
• diarrhea.
Clinical signs can be variable, however the overwhelm­
ing nature of the clinical presentation is the acute and
rapidly progressive course of the disease. Tyzzer's dis­
ease should be a primary differential diagnosis for a foal
that, having had no history of illness, is suddenly found
dead. Clinical diagnosis of C. pilifarmis can be challeng­
ing as the signs are non-specific and severe, often
including central nervous system signs and septic shock
with cardiovascular collapse. Foals may present in a
coma/stupor or exhibit seizures. Physical examination
identifies variable signs of sepsis and cardiovascular
shock. Icterus of mucous membranes is variable, as the
acute nature of the disease may not have resulted in a
significant hyperbilirubinemia. Petechiation and high
fevers may be present. Abdominal pain and/or hemor­
rhagic enterocolitis can be associated. The abdominal
pain is likely to be secondary to colitis or acute swelling
of the liver capsule. Myocarditis is an occasional finding
on necropsy associated with this disease.
DIAGNOSIS
Ante-mortem diagnosis is difficult as there is no rapid
definitive diagnostic test. Signalments with appropriate
age classification, acute onset, and associated clinical
signs should suggest Tyzzer's as a possibility. Liver
biopsy with appropriate histopathology can be diagnos­
tic but the long time course involved makes biopsy of
little use in therapy unless immediate impression
smears can be evaluated. Serum or plasma liver
enzymes (AST, SDH, and GGT) are moderately to
markedly elevated, with increases dependent upon the
time course of the disease. Affected foals are often
severely acidotic and hypoglycemic. Although these lab­
oratory parameters are not specific, severe acidosis and
hypoglycemia alone should suggest pursuit of a diagno­
sis of hepatic disease. Blood cultures should be per­
formed but are rarely diagnostic. Polymerase chain
reaction (PCR) testing is currently being evaluated.
HEPATIC DISEASES IN FOALS 28
Gross necropsy identifies typical white spots in the
hepatic parenchyma. Histopathology confirms a diag­
nosis of Tyzzer's disease. Warthin Starry stains identifY
filamentous bacteria in affected tissue (Plate 28.1).
Routine bacterial culture techniques are unrewarding.
TREATMENT
Successful treatment of a definitively diagnosed case of
Tyzzer's disease has not been reported in the literature.
Emergency therapy with appropriate fluid volume, dex­
trose, and bicarbonate replacement therapy will vary
depending on cardiovascular status and interference
with intermediary metabolism. Routine therapy for sep­
tic shock should be provided. The lack of antibiotic sen­
sitivity testing necessitates a choice of broad spectrum
antimicrobial therapy. High doses of intravenous peni­
cillin in combination with an aminoglycoside or other
broad spectrum intravenous therapy are appropriate
choices.
Congenital disorders
JE Adolf
BILIARY ATRESIA
There have been two reported cases of biliary atresia in
foals; one foal with extrahepatic atresia and one foal
with histopathologic evidence of both extrahepatic and
intrahepatic atresia. Both foals were presented to the
veterinary hospitals at approximately one month of age
for clinical signs including
• lethargy
• anorexia
• failure to thrive
• recurring high fever
• colic
• polydipsia
• polyuria
• icterus.
Serum biochemistry of one of the foals suggested bil­
iary obstruction, as evidenced by extremely increased
values of bilirubin (conjugated and imconjugated),
alkaline phosphatase, and gamma glutamyl transferase
(GGT). Hepatocellular disease was also suspected based
on an increased sorbitol dehydrogenase (SDH). Ante­
mortem diagnoses were not made in either foal, and
both underwent a post-mortem examination. The livers
517
28 GASTROINTESTINAL DISEASE IN THE FOAL
were enlarged and firm on gross examination. The
entrance of the bile duct into the duodenum was absent
in one foal, and although the extrahepatic bile duct
appeared grossly normal in the other foal, its patency
was not assessed. Histologic abnormalities noted in
both livers included extensive bile duct proliferation,
cholestasis characterized by bile-distended canaliculi,
severe fibrosis, hepatocyte degeneration, and a com­
plete lack of bile ducts within the remaining portal
triads.
Although the exact pathogenesis is not known, sev­
eral theories have stemmed from the human literature.
These include
• congenital absence (either from lumen destruction
or duct underdevelopment)
• a deficit in bile flow in utero
• excretion of a biliary toxin
• postnatal destruction secondary to a chronic
cholangiohepatitis.
In both foal reports, the authors hypothesized that
the biliary atresia was a congenital anomaly. In the
future, when biliary atresia is suspected, hepatobiliary
scintigraphy, as well as a liver biopsy, could be
attempted as ante-mortem diagnostic tools, as this was
successful in diagnosing a 21-day-old lamb with biliary
atresia.
SEROUS CYSTS
Serous cysts are occasionally encountered on the
diaphragmatic surface of the liver in foals. They are usu­
ally small and multiple, although they can be large and
solitary. Their origin is unknown but they could be
serosal inclusion cysts, part of a congenital biliary
abnormality or they could be of endodermal origin. On
most occasions these cysts are encountered incidentally
on necropsy.
Neoplastic conditions
JE Adolf
There have only been two reports regarding hepatic
neoplasia in foals. The first report was a mixed hamar­
toma in a late-term aborted fetus. Histological findings
included
• atypical hepatocytes (large hepatocyte-like cells with
eccentric nuclei and voluminous cytoplasm)
• abnormal biliary ducts
51 8
• fibroblastic-fibrocytic interstitial tissue
• a lack of structural organization.
The second report was of a hepatoblastoma of a full­
term, stillborn foal. On gross pathologic examination,
the liver contained numerous, light tan masses, that
were lobulated with necrotic centers on cross section.
The tumor had metastasized to the thoracic cavity, as
evidenced by enlarged tracheobronchial lymph nodes.
Histopathologically there were two distinct epithelial
cell types within the liver nodules: fetal and embryonal
cell types, with the latter cell type predominating. The
architecture of the tracheobronchial lymph nodes was
obliterated by infiltration of embryonal-type cells. This
is the only reported case of hepatoblastoma in a foal.
Hepatoblastomas have been reported in a fetus, a wean­
ling, yearlings and young adults. Erythrocytosis is a fea­
ture of many cases.
Infectious processes
_�_.i
JE Adolf and TJ Divers
BACTERIAL ORIGIN
Septicemia and/or endotoxemia
Bacterial septicemia is a common condition in foals
during the neonatal period. Manifestations of sep­
ticemia range from pneumonia, enteritis, and poly­
arthritis, to death from septic shock and multiple
system organ failure. The liver can be affected in sep­
ticemia by a variety of pathophysiologic mechanisms. A
relatively common finding in septic foals is the presence
of icterus, characterized by hyperbilirubinemia (pri­
marily unconjugated) without elevations in other liver
parameters or evidence of intravascular hemolysis. The
underlying etiology for the hyperbilirubinemia is
unknown, but possible etiologies include intestinal sta­
sis (secondary to septicemia) and increased resorption
of bilirubin, liver immaturity, damage to erythrocytes,
lack of nutritional intake, intrahepatic cholestasis, or an
isolated defect in bilirubin excretion. This hyperbiliru­
binemia is generally mild to moderate and resolves if
the septicemia is successfully treated. Mild hyperbiliru­
binemia can also be found in healthy equine neonates.
In addition, increased liver enzyme values other than
bilirubin (alkaline phosphatase, GGT, and SDH) can be
elevated in normal neonatal foals.
Septicemia can lead to bacterial hepatitis via
hematogenous inoculation. Common bacterial isolates
from foals with sepsis include the gram-negative

bacteria EScherichia coli, Actinobacillus equuli, Klebsiella
pneumoniae, Enterobacter spp., and Salmonella spp., as
well as the gram-positive bacteria Streptococcus spp. and
Staphylococcus spp. A. equuli in particular has been
known to cause hepatitis and nephritis, characterized
by multifocal abscessation. Clinical signs associated with
bacterial hepatitis are similar to those signs commonly
seen in septic foals and include
• weakness
• depression
• decreased to absent suckle reflex
• icterus.
If the hepatitis is severe enough to cause extensive
hepatic necrosis and subsequent hepatic failure, then
other signs associated with hepatic encephalopathy may
be present (i.e. seizures) . The bilirubin and hepatocellu­
lar enzymes will be increased in these cases and
histopathologic findings would include leukocytic infil­
trate (primarily neutrophils) in the periportal tissue and
sinusoids, Kupffer cell hypertrophy and hyperplasia,
degeneration of hepatocytes, and focal areas of hepatic
necrosis. Treatment should encompass general support­
ive care, as in any intensive care neonate, and antibiotic
therapy (either broad spectrum or preferably those indi­
cated via culture and sensitivity) . If hepatic encephalopa­
thy is present, then other treatments are indicated (see
Chapter 19). The prognosis depends on a variety of
factors such as the bacterial agent involved, evidence of
multisystem involvement, and the severity of the hepatitis.
There have been a select number of cases of undiag­
nosed severe, acute hepatitis seen in 3-week to 3-month­
old foals, that have resembled Tyzzer's disease. Some
foals were outside the age range for Tyzzer's disease and
therefore were felt to have another type of hepatitis.
Clinical signs noted were
• high fever
• recumbency
• shock
• icterus.
Hematology and serum biochemistry were suggestive of
septicemia and/or endotoxemia (leukopenia, neutro­
penia, degenerative left shift) , as well as hepatitis
(increased liver enzymes and bilirubin) . Liver biopsies
for histopathology and culture were not performed
because of the presence of thrombocytopenia or other
coagulation abnormalities. The foals were treated with
supportive care (fluids, oxygen therapy, anti-inflamma­
tory therapy) and antibiotics. Because the foals subse­
quently recovered definitive diagnoses were not made.
Finally, the liver can be most severely affected by sep­
tic and/or endotoxic shock conditions, that can then
lead to fulminant hepatic failure and death. The hepatic
HEPATIC DISEASES IN FOALS 28
system, as well as the cardiovascular, pulmonary, and
renal systems, are the target organs most commonly rec­
ognized as being affected in shock conditions. The bio­
chemical and immunological events that take place in
septic and/or endotoxic shock are numerous and com­
plex; only a brief overview related to the liver will be dis­
cussed here (see also Chapter 11) . During severe septic
or endotoxic states, a large number of vasoactive medi­
ators and hormones are involved in altering the hemo­
dynamic system (i.e. interleukins, prostaglandins, tumor
necrosis factor, complement, oxygen free radicals, nitric
oxide, glucocorticoids, opioids) . This exaggerated res­
ponse to sepsis and/or endotoxemia is otherwise known
as the systemic inflammatory response syndrome (SIRS) .
The hemodynamic changes that occur in SIRS include
• increased cardiac output (initially)
• reduced peripheral vascular resistance (which leads
to hypotension)
• narrowed arterial-venous oxygen differences
• lactic acidemia
• increased vascular permeability.
SIRS and its profound systemic effects lead to defective
cellular mitochondrial function and specific visceral
microcirculatory defects. The final outcome is
decreased hepatic oxygenation.
Decreased hepatic oxygenation leads to hepatocellu­
lar damage, this is characterized microscopically by vac­
uolation of hepatocytes with swelling of mitochondria
and endoplasmic reticulum, increased lipid accumula­
tion, Kupffer cell vacuolation, and dilation of the bile
ducts. With widespread hepatic damage liver function is
impaired. If this impairment is accompanied by the dys­
function of other organ systems, the condition is known
as multiple organ dysfunction syndrome (MODS).
Diffuse hepatic necrosis and hepatocellular apoptosis
with subsequent hepatic failure can occur secondary
to the aforementioned hepatocellular changes. When
hepatic failure is coupled with the failure of other
organ systems, then the term multiple organ failure
(MOF) is used. In human patients, the incidence of
MOF in association with septicemia is 30 per cent. In
foals, the incidence of MOF has not been reported. The
treatment for septic and/or endotoxic foals with sec­
ondary hepatitis and hepatic necrosis could include
• appropriate antibiotic therapy
• fluids
• oxygen therapy
• dimethyl sulfoxide (DMSO), for its anti-oxidant and
anti-inflammatory properties
• acetylcysteine, a glutathione donor, used for its anti­
oxidant properties
• non-steroidal anti-inflammatory drugs
51 9
28 GASTROINTESTINAL DISEASE IN THE FOAL
The reader is referred elsewhere for a more compre­
hensive description of the treatments of endotoxic
shock (see Chapter 11) and liver failure (see Chapter
19). The prognosis for foals affected with septic and/ or
endotoxic shock with secondary liver involvement is
guarded to grave, due to the fact that MODS or MOF is
likely to be present as well.
Ascending infection
Cholangiohepatitis can occur in foals secondary to an
ascending bacterial infection. There are two primary
locations for the origin of infection
1. the umbilical vein
2. the hepaticoduodenal junction, where the common
hepatic duct enters the duodenum.
The umbilicus can serve as a portal of entry for bacter­
ial pathogens. Most foals with an umbilical infection are
less than 8 weeks old and there may be an association
between a patent urachus and infection. Not all
affected foals will have a palpable abnormality of the
umbilicus since the infection can reside internally.
Although the urachus is the most common structure of
the umbilicus to become infected, the umbilical vein
can be involved as well. If this occurs, then the infection
can ascend into the hepatic parenchyma. In one report,
four out of eight foals with an infected umbilical vein
developed an ascending hepatitis. Diagnosis is based
primarily on ultrasonographic findings, but also
includes umbilical palpation, laboratory data (complete
blood count (CBC) and liver enzymes), and bacterial
cultures (umbilical, blood and/or another septic
focus). Treatment consists of antibiotic therapy and, in
some cases, surgical marsupialization of the infected
umbilical vein to the ventral abdominal wall. Surgical
removal of the entire umbilical vein has been attempted,
but is not preferred, because of the likelihood of hem­
orrhage from the liver during the procedure.
Cholangiohepatitis, originating from the hepatico­
duodenal region, can be a sequela of gastroduodenal
ulceration in foals. Duodenal strictures may occur sec­
ondary to duodenal ulceration, these could then cause
cholangiohepatitis through two mechanisms. If the
stricture occurs at the hepaticoduodenal area, then bile
duct obstruction and ascending cholangiohepatitis can
follow. A stricture that occurs aborad to the bile duct
opening can cause bile stasis, reflux of ingesta into the
bile duct, and an ascending infection that extends to
the liver. The former condition, with complete bile duct
obstruction, warrants a very poor prognosis. Diagnosis
is based on clinical signs associated with gastroduodenal
ulcers and obstructive disease (lethargy, decreased
interest in nursing, diarrhea, bruxism, colic, nasogastric
520
reflux), endoscopic and radiographic evidence of out­
flow obstruction, and laboratory evidence of liver
involvement (increased liver enzymes, icterus).
Treatment involves surgery, where the duodenal stric­
ture can be bypassed, and anti-ulcer and antibiotic
therapies. Reported surgical options include gastro­
jejunostomy and duodenojejunostomy, and if the bile
duct is completely obstructed, then a hepaticojejunos­
tomy can be performed. If a needle aspirate or liver
biopsy is taken at the time of surgery, it could support a
diagnosis of cholangiohepatitis (portal hepatitis, biliary
hyperplasia). If surgery is successful, and normal bile
flow is restored, the liver enzymes will decline over time,
indicating a resolution of the cholangiohepatitis.
Except for one reported foal with peri-duodenal absces­
sation and secondary biliary obstruction, reported post­
operative complications were not related to continued
hepatic disease.
VIRAL DISEASES
Equine herpesvirus type-1 (EHV-1)
EHV-l is a well-known cause of abortion and stillbirths
in the equine. In some cases, a live foal is produced,
which is either premature or full term. In the majority
of cases, neonatal EHV-l infections are fatal, although
there are two reported cases of neonatal foals with con­
firmed EHV-l viremia that survived. Common clinical
presentations for foals born infected with EHV-l
include
• weakness
• inability to stand unassisted
• failure to nurse
• depression.
Findings on physical examination may include
• icterus
• tachycardia
• tachypnea
• dyspnea.
A fundic examination may reveal dark red optic discs
and irregularly dilated vessels. Complete blood count
values can be profoundly abnormal, including leukope­
nia, neutropenia, and lymphopenia. Biochemical analy­
sis may reveal hyperbilirubinemia and elevated liver
enzymes, but these are uncommon findings. If bone
marrow of an affected foal was collected, it might show
severe toxic changes in the myeloid scores, a depletion
of myeloid elements, and a left shift within the myeloid
line. The clinical course will usually deteriorate rapidly
and may be accompanied by signs of respiratory distress

and/or failure (persistent hypoxemia, hypercapnia).
The foals usually die within 3-5 days. Typical post­
mortem examination findings include
• moderate to severe multifocal necrotizing hepatitis
• moderate to severe necrotizing bronchiolitis and
bronchopneumonia
• focal or massive necrosis in the lymphoreticular
organs.
The demonstration of intranuclear inclusion bodies in
affected organs such as the liver and lung is pathogno­
monic for EHV-I infection. Definitive diagnosis is based
on virus isolation (blood, tissues), immunohistochemi­
cal or fluorescent antibody staining (hemolymphatic
organs, liver, lung, etc.) and/or polymerase chain reac­
tion (peR) testing (tissues, amniotic fluid). Treatment
for EHV-l has recently been attempted using acyclovir
at doses of 8-16 mg/kg p.o. t.i.d. In this report two out
of three treated foals survived, and survival may have
been influenced by the administration of acyclovir.
Cytomegalovirus
Equine herpesvirus type-2 is a cytomegalovirus that is of
questionable significance in its pathogenicity. There
has been one report of a foal that had diffuse hepatic
necrosis and cellular pigmentation without the pres­
ence of inclusion bodies on post-mortem examination,
that was attributed to cytomegalovirus infection.
PARASITIC DISEASES
Large strongyles
Both Strongylus edentatus and S. equinus larvae can pene­
trate the wall of the cecum and subsequently inoculate
the liver. S. equinus larvae migrate through the liver
capsule, causing hemorrhagic, fibrinous inflammation,
and then penetrate the bile duct, where fibrosis can
occur secondarily. S. edentatus larvae will reach the liver
through the portal circulation and then migrate
through the liver, leaving small white foci to be appreci­
ated grossly. Diagnosis is based on clinical evidence of
parasitism (failure to thrive, rough hair coat, debility),
clinicopathologic evidence of hepatitis (increased liver
enzymes) and if performed, histopathologic evidence
of hepatitis (inflammatory infiltrate, possible fibrosis,
possible larvae identification within a core of necrotic
eosinophils). Due to the long pre-patent period of S.
edentatus and S. equinus (8-11 months), a fecal worm
egg count will most likely be negative in affected foals.
Treatment should consist of larvicidal anthelmintic reg­
imens, including ivermectin, moxidectin (not for use in
foals < 4 months of age), fenbendazole (10 mg/kg for
HEPATIC DISEASES IN FOALS 28
5 days or 50 mg/kg for 3 days) or thiabendazole
(440 mg/kg once).
Ascarids
Parascaris equorum larvae will penetrate the small intesti­
nal wall and migrate to the liver as part of the migratory
life cycle. The migration of larvae through the liver can
cause focal hemorrhages and small, white, nodular
lesions. Microscopically, lesions are characterized by
inflammatory infiltrate (predominately lymphocytes
and eosinophils) around the portal triads, and fibrosis.
The diagnostic findings are similar to those mentioned
for strongylosis, except that with a shorter pre-patent
period (l 0-12 weeks), a fecal flotation is more likely to
be positive for ascarid eggs. Treatment consists of larvi­
cidal anthelmintics, such as moxidectin (not for use in
foals < 4 months of age) or fenbendazole at 10 mg/kg
for 3 days. Ivermectin at a regular dose (0.2 mg/kg) is
not effective against the ascarid larvae.
Flukes
Although liver flukes (Fasciola hepatica) are a rare occur­
rence in the equine, there have been reports of natural
and experimental infections in adult horses and foals. F.
hepatica infections may be clinically inapparent or may
be associated with clinical signs such as lethargy, poor
hair coat quality, and exercise intolerance. Diagnosis
is based on a fecal examination and/or necropsy,
although not all infections appear to be patent.
Treatment consists of fasciolicides, such as triclabenda­
zole, carbon tetrachloride or oxyclozanide.
OTHER INFECTIOUS CONDITIONS
Leptospirosis
Leptospirosis is a spirochete infection that can lead to
equine abortions, stillbirths, or premature live births.
Necropsies performed on aborted fetuses or stillborn
foals often reveal an enlarged, pale liver and icterus.
Histopathologic findings are quite characteristic,
including hepatocellular dissociation, mixed leukocytic
infiltration of portal triads and giant cell hepatopathy.
Originally, the cause of giant cell hepatopathy was not
known, but was subsequently identified in cases of lep­
tospirosis. There have been no reports of hepatic dis­
ease in live foals infected with leptospirosis. Diagnosis
following an abortion or stillbirth is made by bacterial
cultures and fluorescent antibody testing of representa­
tive organs and characteristic histopathologic lesions,
with a possibility of identifying the spirochete on micro­
scopic samples.
521
28 GASTROINTESTINAL DISEASE IN THE FOAL
Ehrlichia ristic;;
Ehrlichia risticii, the causative agent of equine monocytic
ehrlichiosis or Potomac horse fever (see Chapter 20),
has recently been recognized as an abortifacient.
Experimentally and naturally infected mares tend to
abort at around 7 months gestation. Histopathologic
findings on the aborted fetuses have been consistent,
including
• lymphohistiocytic enterocolitis
• hepatitis
• myocarditis
• lymphoid hyperplasia.
Diagnosis is based on the characteristic microscopic
lesions, isolation of E. risticii from fetal tissues and
serum titers from infected mares suggestive of infec­
tion. There have not been any reported cases of live
foals born from dams infected during gestation.
Toxic disorders
EX
JE Adolf and TJ Divers
IRON TOXICITY
In 1983, various reports from around the United States
indicated an emerging cause of toxic hepatopathy in
foals. The cases were subsequently linked to the
administration of an oral proprietary nutritional paste
containing viable primary cultures and fermentation
products as well as vitamins and iron (as ferrous
fumarate). Experimental reproductions of the disease
found that the iron in the oral supplement was the toxic
principal. Affected neonatal foals were all given the
paste shortly after birth and began to show clinical signs
within 2-5 days. Only those foals that received the paste
before ingesting colostrum appeared to be affected.
The predominant clinical signs were
• depression
• marked icterus
• ataxia
• aimless wandering
• colic
• convulsions.
Marked elevations in liver enzymes, primarily GGT,
alkaline phosphatase, and bilirubin, were noted on
serum biochemical analyses. Some foals also had
elevated SDH and aspartate aminotransferase (AST)
values. Other clinicopathologic abnormalities indica­
tive of hepatic failure included hyperammonemia, high
522
aromatic to branch chain amino acid ratio, and pro­
longed prothrombin time and partial thromboplastin
time. Except for two foals in one experimental report,
all foals died after exhibiting ante-mortem signs of
hepatic encephalopathy (seizures, head pressing, and
coma). Pathologic findings were similar among affected
foals
• gross liver atrophy
• hepatocyte necrosis
• prominent bile duct proliferation
• occasional periportal fibrosis.
Many foals also demonstrated Alzheimer type II cells
within cerebral tissue (found in, cases of hepatic
encephalopathy), multifocal, acute catarrhal to hemor­
rhagic enteritis, lymphoid necrosis, and renal cortical
necrosis. The oral paste was taken off the market shortly
after these cases were reported.
NSAIO TOXICITY
Non-steroidal anti-inflammatory drugs (NSAIDs) are
known occasionally to cause hepatotoxicosis in
humans, and this has been infrequently reported in
horses. To date, no cases have been reported in foals,
although the author has seen two foals at the veterinary
hospital with rising liver enzymes (SDH, GGT, alkaline
phosphatase) while they were receiving oral carprofen.
Liver enzymes decreased after discontinuation of the
carprofen and no long-term adverse effects were noted.
Carprofen in particular has been associated with hepa­
tocellular toxicosis in dogs. NSAID-related hepatotoxic­
ity is believed to be an idiosyncratic reaction in people
and dogs, except for acetaminophen and aspirin, which
cause time and dose-dependent hepatic disease.
Despite the absence of reported NSAID-induced hepa­
totoxicity in foals, the monitoring of liver enzymes
in foals receiving NSAIDs, especially carprofen, is
warranted.
OTHER HEPATOTOXINS
�����----------------------
With the exception of iron toxicity, reports of hepato­
toxins in foals, especially plant and chemical toxins, are
rare. However, there are many substances that are
potential hepatotoxins in horses (see Chapter 19), an
abbreviated list is given here.
Common drugs include
• carbon tetrachloride
• tetracycline
• erythromycin
 HEPATIC DISEASES IN FOALS 28

• rifampin In the most recent report, amino acid profiles revealed

• phenobarbital increased serum ornithine and glutamate and
• copper increased urine orotic acid concentrations, similar to
• glucocorticoids the HHH syndrome. All of the described cases are
• anabolic steroids deceased - they either died or were euthanized due to
• diazepam treatment failure and clinical deterioration.
• Hz blockers.

Hepatotoxic plants include PORTAL VEIN THROMBOSIS

• pyrrolizidine alkaloid-containing plants
A portal vein thrombosis was seen in a 6-week-old thor­
• alsike clover
• blue-green algae oughbred with Streptococcus zooepidemicus cellulitis and
• lantana. pneumonia and Rhodococcus equi polyarthritis and pneu­
monia. Based on the hematology and serum biochem­
Chemical substances include istry, bacteriologic findings, and the presence of an
umbilical abscess, the thrombosis was presumably sec­
• tannic acid
ondary to a septic process. The thrombus (see Figure
• phenols
28.1) occupied 90 per cent of the portal vein, as well as
• phosphorus
the primary intrahepatic portal vein branches. The liver
• mycotoxins.
parenchyma appeared normal ultrasonographically,
The type of liver damage induced by these substances but histopathologic examination revealed diffuse hepa­
will dictate any observed liver enzyme abnormalities tocellular atrophy and poorly developed vascular pro­
(i.e. cholestatic versus hepatocellular enzyme derange­ files. Liver enzyme abnormalities were present - GGT,
ments) . So, for any foal with unexplained liver enzyme SDH, and alkaline phosphatase were elevated.
elevations, hepatotoxicosis secondary to drugs, plants, Treatment was aimed at the septic process and included
or other chemical substances, should be considered antibiotics and anti-inflammatory drugs. Repeat ultra­
and investigated. sound examinations demonstrated a recannulization of
the portal vein and the development of hyper echogenic
foci in the liver parenchyma. As the thrombus resolved,
the liver enzymes declined. Despite the presence of
Other liver diseases abnormal echogenic foci in the liver, no permanent
liver function abnormalities were detected. Portal vein
JE Adolf and TJ Divers

HYPERAMMONEMIA IN MORGANS

There have been two reports of persistent hyperam­

monemia leading to signs of hepatic failure in Morgan
weanlings and yearlings. Clinical signs, such as weight
loss, depression, and other signs associated with hepatic
encephalopathy, were noted soon after weaning. Blood
tests demonstrated elevations in liver enzymes and
blood ammonia levels (typically >300 Jlg/ml) . In
addition, some cases experienced hemolytic crises.
Histopathologic findings in the liver were variable and
included lymphocytic-plasmacytic periportal hepatitis,
portal fibrosis, bile duct hyperplasia, karyomegaly, and
cytomegaly. Although the exact etiology of this disease
is unknown it may be caused by an inherited defect in
ammonia metabolism. The disease has some similarities Figure 28.1 A hyper-echoic thrombus can be seen within
to an inherited disorder in humans, known as hyper­ the lumen of the portal vein of a Thoroughbred foal. The
ornithinemia, hyperammonemia and homocitrullinuria thrombus appears to have some mineralization and is cast­
(HHH) syndrome. In both equine reports there were ing an acoustic shadow. The liver parenchyma appears
pedigree similarities suggesting a genetic component. normal on the sonogram.

523
28 GASTROINTESTINAL DISEASE IN THE FOAL
thrombosis has been well described in humans and
occasionally occurs in horses. Affected adult horses
tend to exhibit signs of hepatic encephalopathy, but the
aforementioned foal and one other foal that the author
(TJ Divers) treated with this condition did not. This dis­
crepancy may be related to the fact that foals have much
smaller colons, and are therefore less likely to overpro­
duce ammonia. Affected animals may also exhibit diar­
rhea, because of portal hypertension secondary to the
thrombosis.
NEONATAL ISOERYTHROLYSIS
Rarely, a foal develops significant liver disease (continu­
ally elevating GGT) and dysfunction (rising direct
bilirubin) while being treated for neonatal isoerythroly­
sis (NI). This is more often a problem in foals requiring
multiple blood transfusions. The exact cause of the liver
disease/dysfunction is unknown, but may involve
hypoxic damage, hemochromatosis, and biliary hyper­
plasia from excessive bilirubin secretion (bilirubin
secretion in bile is the rate-limiting step in bilirubin
metabolism/excretion). Most of the foals do eventually
recover from both the NI and liver disease so relatively
few necropsies are available to collect further informa­
tion regarding this condition.
PERINATAL ASPHYXIA
Perinatal asphyxia most commonly affects the neuro­
logic system, but hepatic damage can also occur follow­
ing a hypoxic insult. Although hepatic damage in this
context has not been specifically reported in foals, peri­
natal asphyxia is not an uncommon occurrence in
equine neonates and therefore hypoxic-induced liver
damage is possible. As in humans, icterus and liver
enzyme elevations would be present if there was suffi­
cient liver damage. Treatment would include support­
ive care (i.e. oxygen therapy) and addressing the needs
of any other affected organ system.
BIBLIOGRAPHY
Portosystemic shunts
Beech], Dubielzig R, Bester R (1977) Portal vein anomaly
and hepatic encephalopathy in a horse.]. Am. Vet. Med.
Assoc. 170(2) :164-6.
Birchard S], Sherding R G (1992) Feline portosystemic
shunts. Compend. Cont. Educ. 14(10):1295-300.
Buonanno A M, Carlson G P, Kantrowitz F (1998) Clinical
and diagnostic features of a portosystemic shunt in a foal.
]. Am. Vet. Med. Assoc. 192:387-90.
524
Center S A, Magne M L (1990) Historical, physical
examination, and clinicopathologic features of
portosystemic vascular anolamies in the dog and cat.
Semin. Vet. Med. Surg. (Sm. Anim.) 5:83-99.
Fortier L A, Fubini S L, Flanders] A, Divers T] (1996) The
diagnosis and surgical correction of congenital
portosystemicvascular anomalies in two calves and two
foals. Vet. Surg. 25:154-60.
Lawrence D, Bellah] R, Diaz R (1992) Results of surgical
management of portosystemic shunts in dogs: 20 cases
(1985-1990 ) . ]. Am. Vet. Assoc. 201(11) :1750-3.
Lindsay W A, Ryder] K, Beck K A, McGuirk S M (1998)
Hepatic encephalopathy caused by a portacaval shunt in a
foal. Vet. Med. 83:798-805.
Mathews K, Gofton N (1987) Congenital extrahepatic
portosystemic shunt occlusion in the dog: Gross
observations during surgical correction.]' Am. Anim. Hosp.
Assoc. 24:387-94.
Olgilvie G K, Engelking L R, Anwer M S (1985) Effects of
plasma sample storage on blood ammonia, bilirubin, and
urea nitrogen concentrations: Cats and horses. Am.]. Vet.
Res. 46:2619-22.
Youmans K R, Hunt G B (1999) Experimental evaluation of
four methods of progressive venous attenuation in dogs.
Vet. Surg. 28:38-47.
Tyzzer's disease
Williams N E (1998) Tyzzer's disease. Equine Disease Quarterly
6:4-5.
Divers T D (1997) Tyzzer's disease. In Current Therapy in
Equine Medicine 4th edn. N F Robinson (ed.) . W B
Saunders, Philadelphia, pp. 218-9.
Congenital disorders
Biliary atresia
Van der Leur R] T, Kroneman] (1982) Biliary atresia in a
foal. Equine Vet.]. 14: 91-3.
Serous cysts
Kelly W R (1993) The liver and biliary system. In Pathology of
Domestic Animals, K V F ]ubb, P C Kennedy and N Palmer
(eds ) . Harcourt-Brace]ovanovich Publishers, San Diego,
pp. 319-406.
Neoplastic conditions
Roperto F, Galati P (1984) Mixed hamartoma of the liver in
an equine foetus. Equine Vet.]' 16:218-20.
Neu S M (1993) Hepatoblastoma in an equine fetus.]. Vet.
Diagn. Invest. 5:634-7.
Infectious processes
Septicemia and/or endotoxemia
Hawthorne T B (1990) Neonatal hyperbilirubinemia. In
Equine Clinical Neonatology, A M Koterba, W H Drummond
and P C Kosch (eds ) . Lea and Febiger, Philadelphia, pp.
589-601.
Miller D], Keeton G R, Webber B L, et al. (1976) Jaundice in
severe bacterial infection. Gastroenterology 71:94-7.

Fahrlander H, Huber F, Gloor F ( 1 964) Intrahepatic
retention of bile in severe bacterial infections.
Gastroenterology 47:590-9.
Gossett K A, French D D ( 1 984) Effect of age on liver enzyme
activities in serum of healthy quarter horses. Am.]. Vet.
Res. 45: 354-6.
Paradis M R ( 1 994) Update of neonatal septicemia. Vet. Clin.
N. Am. Equine Pract. 10: 1 09-35.
Fly D E ( 1 988) Multiple system organ failure. Surg. Clin. N.
Am. 68:1 07-22.
Gullo A ( 1 999) Sepsis and organ dysfunction/failure. An
overview. Mineroa Anestesiol. 65:529-40.
Ascending infection
Reef V B, Collatos C, Spencer P A, et a!. ( 1 989) Clinical,
ultrasonograpbic, and surgical findings in foals with
umbilical remnant infections . ]. Am. 11et. Med. Assoc.
195:69-72.
Campbell-Thompson M L, Brown M P, Slone D E, et al.
( 1 986) Gastroenterotomy for treatment of gastroduodenal
ulcer disease in 14 foals. ] Am. 11et. Med. Assoc. 1 88:840-4.
Orsini J A, Donawick W J ( 1989) Hepaticojejunostomy for
treatment of common bepatic duct obstructions associated
with duodenal stenosis in two foals. Vet. Surg. 1 8:34-8.
Equine herpesvirus Type- 1
Murray M J , Piero F,Jeffrey S C, et al. ( 1 998) Neonatal equine
herpesvirus Type I infection on a thoroughbred breeding
farm. ] Vet. Intern. Med. 1 2:36-41 .
Perkins G, Ainsworth D M , Erb H N , et al. ( 1 999) Clinical,
haematological and biochemical findings in foals with
equine herpesvirus-l infection compared with septic and
premature foals. Equine Vet. ] 3 1 :422-6.
Golenz M R, Madigan J E, Zinki J ( 1 995) A comparison of the
clinical, clinicopathological and bone marrow
characteristics of foals with equine herpes and neonatal
septicemia. In Proceedings Annu Am Coli Vet Intern Med
Forum 585-7.
Cytomegalovirus
Rossdale P D ( 1 972) Modern concepts of neonatal diseases in
foals. Equine 11et.] 4: 1 1 7-28.
Large strongyles and ascarids
Uhlinger C A ( 1 996) Parasite control programs. In Large
Animal internal Medicine, B P Smith (ed. ) . Mosby-Year
Book, Philadelphia, pp. 1 685-710.
Flukes
Owen J M ( 1 977) Liver fluke infection in horses and ponies.
Equine Vet.] 9:29-3 1 .
HEPATIC DISEASES I N FOALS 28
Leptospirosis
Poonacha K B, Donahue J M, Giles R C, et al. Leptospirosis in
equine fetuses, stillborn foals and placentas. Vet. Patho!.
30:362-9.
Ehrlichia risticii
Long M T, Goetz T E, Kakoma I, et al. ( 1 995) Evaluation of
fetal infection and abortion in pregnant ponies
experimentally infected with Ehrlichia risticii. Am.] 11et.
Res. 56: 1 307-16.
Toxic disorders
Iron toxicity
Divers T J, Warner A, Vaala W E, et al. ( 1 983) Toxic hepatic
failure in newborn foals. ] Am. 11et. Med. Assoc.
183:1407-1 3.
Mullaney T P, Brown C M ( 1 988) Iron toxicity in neonatal
foals. Equine Vet. ]. 20: 1 1 9-24.
NSAID toxicity
Lewis J H ( 1 984) Hepatic toxicity of nonsteroidal anti­
inflammatory drugs. Clin. Pharmacol. Ther. 3 : 1 28-38.
MacPhail C M, Lappin M R, Meyer D J, et al. ( 1 998)
Hepatocellular toxicosis associated with administration
of carprofen in 21 dogs . ]. Am. Vet. Med. Assoc.
2 1 2 : 1 895-9 0 1 .
Other hepatotoxins
Pearson E G ( 1 996) Other hepatotoxins. In Large Animal
Internal Medicine, B P Smith (ed . ) . Mosby-Year Book,
Philadelphia, pp. 930-3.
Other liver diseases
Hyperammonemia in Morgans
Divers T J, Tennant B C, Murray M J , et al. ( 1 994) Unusual
cases of liver disease in Morgan foals. Gastroent. 11iewpoint
2:6.
McConnico RS, Duckett W M , Wood P A ( 1 997) Persistent
hyperammonemia in two related Morgan weanlings. ]. 11et.
Intern. Med. 1 1 :264-6.
Perinatal asphyxia
Saili A, Saina M S, Gathwala G, et al. ( 1 990) Liver dysfunction
in severe birth asphyxia. Ind. Pediatr. 27: 1 291 .
525
Index

Abdomen Adhesions 209-211 atresia ani 492

auscultation 4,110 experimental modeling 210 atresia coli 488
physical examination 4 in foals 466,483 cecal bypass 271
Abdominal abscesses 330-332 gut viability and 164,165,166-167 end-to-end 175,176
Abdominal closure 181-184,187 incidence 209 functional 180,181
Abdominal distention 317-322 in intestinal obstruction 104,105,259, end-to-side 176,177
Cushing's disease 322 264 general considerations 172-175
distention colic 317-319 pathophysiology 104,105,209-210, hand-sewn 175-176,177-178
fecaliths 462 259,264 impaction at 215-216
fetal hydrops 321 prevention 210-211 purse-string 170,178
foals 451 surgical protocol 210 revisions/complications 185-187
differential diagnosis and evaluation sutures and 168,170,172,180-181 enlargement 186
459-462 treatment 211 leaking 185
hemoperitoneum 321 ultrasonography 30,31 rotation 174
ileocolonic aganglionosis 461 Adipose tissues 395 side-to-side 176,177-179,255-256
ileus 320 Aeromonas spp. 423 stapled 176,178-179,180,181
intestinal atresia 461 AfIatoxins 384,420 see also Sutures
intestinal obstruction/impaction Age determination 70-71 Anatomic system, dental nomenclature
319-320,462 Airway, after anesthesia 154-155 69-70
meconium retention 460-461 Albumin:globulin (A:G) ratio 12 Anatomy
peritonitis 321,462 Albumin levels 11 in laparoscopic examination 47-48
pneumoperitoneum 320 Alfalfa 196,295-296,299,300,418,419 rectal palpation of normal horse 7-8
potential causes 317 Alkaline phosphatase 12,386,387,388, ultrasonographic 26-28
uroperitoneum 321,461-462 389,391,398 in videolaparoscopy 45-46
ventral body wall hernias and prepubic Alkaloid intoxication 389-391 Anemia 11
tendon rupture 321-322 Allopurinol 194 Anesthesia, general
Abdominal drainage and lavage 328-329 Alopecia 378 colic surgery 145-155
Abdominal pain see Pain Alpha2 agonists blood tests and 152
Abdominal quadrants, palpation 159-161 in anesthesia 147 cardiovascular system and 146,
Abdominocentesis 13-16 -induced arrhythmias 234,236 150-151,152,153
chronic and recurrent colic 342 postoperative pain relief 207-208 complications 152-154,219-222
in foals 15-16,453 Alpha fetoprotein 393 depth of anesthesia 150
abdominal distention 460 Alsike clover 393 drugs used 147-150
bowel wall perforation 453, 460 Altrenogest 351,352 induction 147
decision for surgery 467 Aluminium hydroxide 243 monitoring patients 150-152
hemoperitoneum 333 Alveolar periostitis 74,75-76 preparation of patient 146-147
instrumen ts 13 Alzheimer type II cells 382,385,522 pulmonary system and 145-146,
in peritonitis 325-326 Ameloblastomas 73,79 151-152,154-155
ultrasonography and 15,16 Aminocaproic acid 218,334,359 recovery 154-155
Abortion 355,412,414,520,521,522 Amitraz 280,420 pregnant mare and 351
colic and 351,352,354 Ammonia toxicity see Hyperammonemia Anesthesia, local
Acepromazine (acetylpromazine) 24 119, Amsinckia intermedia 389 laparoscopy 46,48-49
121,124,148,359 Amylase activity 349 Anisognathism 69
N-Acetylcysteine 194-195 Analgesia Anoplocephala magna 54
Acid-base balance 12 in colic 119-122,124 Anoplocephala perjoliata 53,54, 57,259,274
abdominal pain and 138-140 dosages and efficacy 119 Anorectal abscesses 331
expected abnormalities 138 gastric decompression 120 Anorectal lymphadenopathy 314
in distributive shock 202-203 narcotics 121 Antacids 243,244,473,474
hyperlipemia and 398-399 NSAIDs 120 Anthelmintics
Acorns 419,423 sedatives 120-121 in chronic diarrhea 431
Acremonium coenophialum 422-423 spasmolytics 121-122 control programs 56,58-60
Actinobacillus lignieresii 78 walking 120 cyathostomosis 435
Acupuncture 206 during transport 133 precipitation of disease 433
Acute abdomen foals 464-465 grass sickness and 343-344
prognosis 141-142 in grass sickness 348 resistance 54,56,59,60,435
rectal examination 112-119 in peritonitis 328 side effects 58
Adamantinomas 73 postoperative pain 206-208,209 treatments 57-58
Adenocarcinoma 337 Anastomosis 172-181,255 see also specific agents

527
INDEX

Anti-arrhythmic therapy 236-237 Autotransfusion 334,359 hyperlipemia and 394,395

Antibiotic-induced diarrhea 410,411, AV block,profound 236 post-parturient,cecal perforation 274
412,423,507 Avocado toxicity 419 recurrent volvulus 291-292
Antibiotic tberapy Azotemia 138, 373 Brotizolam 348
abdominal abscesses 331-332 Bruxism 471
biliary tract disease 388 Bacteria Buccal mucosal flaps 85-86,87
chronic diarrbea 431 peritoneal fluid analysis 18 Bull's eye sign 29,30,456,457,482
clostridial disease 410-411,412,501 see also specific diseases Butorphanol 24,47,119,121, 148,154
distributive shock 203 Bacteroides fragilis 75-76 postoperative pain 206,207,208
endotoxemia 195 Barium enema 459-460 Calcium 235
periradicular disease 75-76 Bermuda grass 259 post-anesthetic myopathy and 222
peritonitis 328 Berteroa incana 423 see also Hypercalcemia,Hypocalcemia
post-anestbesia myopathy/neuropathy Bethanecol 124,213-214,244,246 Calcium borogluconate 140,405-406,419
and 220 Bezoars 302-303 Calcium gluconate 154
postoperative colitis 232 Bicarbonate estimation 12, 123,154,203, Cancer cachexia 374-375
preoperative 141 463-464 Candidiasis 508
salmonellosis 408,409,499 Bile acids 383, 391 Cantharidin toxicosis 417-419
thrombophlebitis 137 Bile duct hyperplasia 387 Capillary refill time (CRT) 3-4,110
Anticoagulant therapy 226-227 Bile fluid leakage 19 Capnograph 151
Antidiarrbeal agents 435-436 Bile salt therapy 388 Carbohydrates
Anti-endotoxin therapy 123,193,203, Biliary atresia 517-518 absorption tests 20-21,379
213,230 Biliary calculi 386-389 fermentation and dental disease 74
Antifreezes 421 Biliary tract disease 386-389 soluble,in grain overload 421-422
Antihistamines 422 Bilirubin levels 382,383, 384,387 Carbon tetrachloride 521
Anti-inflammatory agents Biochemistry Carboxymethylcellulose 159, 161,
adhesions and 210 hyperlipemia 397-398 210-211,271
in distributive shock 203 parameters 11-12 Cardiac arrhythmias
ileus and 213 parasite-associated diseases 57 in foals 464
in peritonitis 328 in peritonitis 326-327 postoperative 232-237
Antimesenteric enterotomy 295 Biopsy aftercare and prognosis 237
Antimesenteric teniotomy 295 chronic diarrhea and 430 anti-arrhythmic treatment 236-237
Antioxidant status 221 endoscopic 26 electrocardiography 232
Antithrombin III activity 223-224,227 laparoscopic 44,48 electrolyte status and 234-236
Arabian borses 295,350 in malabsorption syndromes 379 pathogenesis 234
Arachidonic acid metabolism 104,147, see also specific sites prevalence and significance 232-234
192 Bismuth subsalicylate 195,406,431 Cardiac output,in anesthesia 151
Arsenic intoxication 420 Bismuth,synthetic 412 Cardiogenic shock 198
Arterial oxygen levels 145 Bite plate 72,73 Cardiovascular function
Arterial rupture,at parturition 357-359 Blister beetles 417-418,419 in colic 146
Arteritis,mesenteric 55,262,436-437 Blood flow,viability and 166,167-168 anesthesia and 146,150-151,152,
A.carids 521 Blood pressure 153
biology and lifecycle 54 in anesthesia 150-151, 152-153,153 foals 451
control programs 59 arterial rupture,parturition 358, 359 small intestinal obstruction 253
egg survival 53 in hypovolemic shock 199-200 fluid therapy 123
fecal tests 57,521 Blood substitutes 202 Caslick procedure 353
ill thrift 56 Blood tests,anesthesia and 152 Castor bean plant 420
impaction 56, 262,481-482 Blood transfusions 202,218,333-334,359 Castration 17,327,331,332,477
pathogenesis 55,521 Blood volume 199 Cathartics 281,486
treatment 58,521 Blue-green algae 419 Catheters 134-137
Ascites 320, 503 Body condition score 367-368 complications 135,137,226
Aspartate aminotransferase 220, 221-222, Body weight balance 367 considerations 134-135
383,387,390,392 Bone scintigraphy 34-36 guidelines for use 226
Aspergillosis 424 Borborygmi 4 management 137,226
A.lpergillus spp. 378,384,423,424 Bots 60 during transport 132-133
Asphyxia,perinatal 524 Botulism 64 materials 132
Aspiration pneumonia 64,79,89,92,507 Bougienage 93 replacement 136
Aspirin 207,226,422 Bowel sounds 4,110, 206 treatment of thrombophlebitis 137,226
Astragulus spp. 420 Bowel wall biopsy 342,372,380 types 135-136
Atipamazole 234,236 Bradydysrhythmias 232,234,236 Cecal acidosis 275-276
Atracurium 150 Breath hydrogen tests 38 Cecal bypass 271
Atresia ani 461, 491-492 Brood mare Cecal content transfer 431
Atresia coli 461, 486-489 abdominal pain in pregnancy (non­ Cecal distention 268-269
Atresia recti 461,491-492 colic) 356-357 Cecal impaction 269-272
Atrial fibrillation 234 colic 351-361 clinical signs and diagnosis 269-270
Atropine 121-122,150,236,420 general considerations 351-352 epidemiology and etiology 269
Aural fistulae 73 non-pregnant mare 352-353 prognosis and prevention 271-272
Auscultation 4, 110 parturient mare 357-361 treatment 270-271
colic 254 pregnant mare 351-352,353-357 Cecal infarction 276
foals 451-452 copulation injuries 305,353 Cecal intussusceptions 272-274
Auto suturing device 42,43 hemiperitoneum 332,333 Cecal perforation 271,274-275

528
 INDEX

Cecal trocarization 268-269 weight loss 369-370 small intestinal 249-266

Cecal tympany 268-269,319 see also Acid-base balance, epidemiology 250-251
Cecocecal intussusceptions 30,272-274, Biochemistry, Electrolyte balance, outcome and prognosis 483-484
436 Fluid balance, Hematology postoperative management and
Cecocolic intussusceptions 30, 55, Clostridial diarrhea 13,410-412 complications 483
272-274,436 clinical signs and clinical pathology risk factors 250-251
Cecum 411,500 see also specific disorders
anatomy and function 267-268 diagnosis 411-412,500-501 spasmodic 125
rectal examination 8,114-115 etiopathology 410-411,499-500 surgery for 145-188
Celiotomy in foals 456,499-502 anesthesia 145-155
in colic, indications for 129-132 prognosis 501 closure of abdomen 181-184
postoperative colic, ultrasonography treatment and prevention 412,501-502 evaluation of gut viability 164-168
33-34 Clostridium difficile 230-231,410-412,500, exploration of abdomen 158-164
repeat 184-187 501 repeat laparotomy 184-187
acute 185-186 antibiotic-associated infection 124 surgical approaches 155-158
decision-making 184-185 Clostridium peifringens 258,261,410,411, techniques 168-181
delayed 186-187 412,499-502 ultrasonography
surgical procedure and revisions Clostridium piliformis 516-517 indications for 29
185-187 CNS signs, in Theiler's disease 381-384 postoperative 33-34
techniques Coagulation status Colic, clinical evaluation 107-144
flank, through 17th or 18th rib adhesions and 209-210 clinical pathology 132,466-467
157-158 endotoxin and 104,191-192 clinical signs 107-109
other approaches 158 liver disease and 382 decision for surgery 129-132, 465-467
paralumbar flank 157-158 normal 223 decision to refer 126-129
ventral midline 155-156,356 salmonellosis 408 false (non-gastrointestinal) colics
ventral paramedian 156-157 see also Thrombophlebitis 118-119
Cellophane banding 516 Coccidiosis 60 fecal production 128
Cellulitis, catheter-related 135,136,137 Cockspur hawthorn fruit 280 geographical location 127
Cellulose digestion 267-268 Codeine phosphate 57,431,435-436 management and deworming history
Central nervous system 'wind-up' 205 Colic 127
Central venous catheter 132 acute, decision to refer 126-129 medical history 127
Central venous pressure 151 cecal diseases 267-278,see also specific pain severity 127,130
Cerebral edema 382 disorders peritoneal fluid analysis 131
Charcoal, activated 195,406,409,419, chronic and recurrent physical examination 109-112,
420,431 causes 339,340 129-131,466
Chemotherapy 338 defined 338-339 abdominocentesis III
Chenodeoxycholic acid 423 differential diagnosis 338-343 clinical examination 109-110
Chloral hydrate 207 investigation 339-343 heart rate 110,129-130
Chlorambucil 338 congenital defects 477-480 history 109,466
Chloramphenicol 412 distention 317-319 jugular vein filling 110
Chlorhexidine-impregnated catheters 135 clinical signs and diagnosis 318 mucous membranes 110
Choke 67,89 treatment 318-319 nasogastric intubation 110-111,
Cholangiocarcinoma 389,393 foals 477-484 130-131
Cholangiohepatitis 386-388,520 large colon diseases 279-298,485-490, rectal examination I l l , 112-119,
Choledocholithomy 388 see also 130
Choledocholiths 386 specific conditions rectal temperature 109-110,129-130
Cholelithiasis 386 medical therapies 119-125 respiratory rate 110,129-130
Chronic obstructive pulmonary disease aims 119 ultrasonography I l l, 131
(COPD) 376 analgesia 119-122,124 progression of colic 127
Chyloabdomen 479-480 anti-endotoxin therapy 123 response to medical therapy 128,
Chyloperitoneum 19 anti-inflammatory 123 131-132
Chylous effusions 19 cardiovascular support 123 signalment 127
Cimetidine 243,244,245 fluid therapy 122-123 Colitis
Cirrhosis, chronic hepatic 394 intestinal motility alterations 123-125 chronic idiopathic 437
Cisapride 124,214-215,348,465 laxatives 122 granulomatous 443
Cisplatin 248 walking 120 parasite-associated 54-55,57
Citrobacter spp. 387 parasitic infection postoperative 230-232
Cleft palate 79-87 cyathostome 436 prevention 231-232
acquired 65,66,80,81 mild strongyle-associated 55 segmental eosinophilic 296-297
clinical signs 81 tapeworm-associated 56,58 ultrasonography 32,456,457
etiology and pathophysiology 80 treatment 57,58 see alw Equine right dorsal colitis
investigation and diagnosis 81-82 preoperative preparation 140-141 Colloid therapy 139,140,201,405
prevention 87 preparation for referral transport Colon
prognosis 86 132-134 exteriorization 162-164
treatment 82-86 risk factors 101-103 rectal palpation 8
complications 86-87 farm management factors 102 resection length and viability 173
Clenbuterol354 medical history 101-102 ultrasonography, foals 456,457
Clinical pathology 11 preventative medicine factors 102 see also Large colon, Small colon
chronic and recurrent colic 341-342 signalment 101 Colonic biopsy 167
neoplasia 336 weather 102-103 Colonic ulceration. NSAlD toxicosis 416

529
INDEX

Colopexy 291-292 Dental abscess 35 strongylosis 436-437

Colostomy 310-312 Dental anatomy 69
Colostrum 449,499,507 Dental caries 74
bovine 506 Dental cysts 73
Combined immunodeficiency syndrome Dental disease 69-77
(eID) 350 developmental disorders 72-77
Compartment syndrome 221,222 infectious 74-76
Conduction block 221,222 signs 71-72
Copper levels 357 Dental eruption time 70
Coronary bands, dermatitis 391 Dental nomenclature 69-70
Corticosteroids 57,193,210,334,338, Dental scintigraphy 34-36
379,392,435 Dental tumors 73
Creatine kinase activity 220,221-222 Dentigerous cysts 73
Crypt enterocytes, proliferating 509 Depression 108, 382, 387
Cryptosporidial diarrhea 504-507 Dermatitis 391,406
zoonotic considerations 507 Desflurane 149
CryjJtosporidium spp. 60,350,504-507 Dessicated feed 245,246
Crystalloid therapy 138-140,192, Detomidine 24,47,119, 121,206,207,
201-202,359,405 208,234
Cushing's disease 322 Dexamethasone 193, 236,379,392
Cyathostomes Dextrans 192,211
anthelmintic resistance 54,59,60 Diabetes mellitus 349-350
biology and lifecycle 54 Diaphragmatic hernia 261,480
clinical features 55-56 Diaphragm, displaced 245, 246
control programs 58-60 Diarrhea
diarrhea 56,57 hemorrhagic, clostridial 412
intussusceptiollS 55,272,274 infectious, postoperative colitis
investigation 56--57 230-232
clinical history 56 recurrent 56,436
fecal test� 56--57 Diarrhea, acute 405-425
hematology/biochemistry 57 aspergillosis 424
pathogenesis 54-55 bacterial infections 423
treatment 57,58 clostridial, in adult horses 410-412
weight loss 55-56 deranged intestinal motility 423
Cyalhostomosis 432-436 drug-induced 415-417,423
clinical signs 55,434 grain overload 421-422
diagnosis 434-435 NSAID toxicity 415-417
epidemiology 434 principles of treatment 405-406
etiology and pathogenesis 432-433 oral rehydration 406
malabsorption and 372-373 toxic colitides 417-421
treatment 58,435-436 cantharidin toxicosis 417-419
weight loss and 372-373 toxicities 422-423
Cyclooxygenase inhibition 192,206--207 see also Potomac horse fever,
Cyclophosphamide 338 Salmonellosis
Cyproheptadine 322 Diarrhea, chronic 427-446
Cystotomy, laparoscopic 45 chronic inflammatory bowel disease
Cytokine response 103-104,191,193-194 437
Cytology, peritoneal fluid 16,17,18, 19,20 clinical signs 427-428
Cytomegalovirus 521 defined 427
Cytosine arabinoside 338 differential diagnosis 428
Cytotoxins 407,410,411,496 Eimeria leukarti 444
equine right dorsal colitis 438-442
Dantrolene 222 evaluation 428-430
Database, on-line 422 general principles of treatment
Decompression 430-432
cecal 268-269 giardiasis 444
foals 465 hepatic disease 444
gastric 120,206, 246,247 histoplasmosis 443
ileus and 213 idiopathic 443
Decompression tract 159 intestinal fibrosis 444
Deglutition 63-64 intestinal lymphangiectasia 444
compromised 65-67 intestinal neoplasia 437
Dehiscence 182,197,216,217,311 intestinal tuberculosis 443
Dehydration larval cyathostomosis see
abdominal pain and 138-140 Cyathostomosis
acute diarrhea 405-406 Neospora caninum 443
in anesthesia 152-153 other causes 442-444
clinical parameters 12 peritonitis 444
estimation of 138 salmonellosis (chronic) 443
fluid therapy see Fluid therapy sand enteropathy 437-438
Trichomonas equi 444
Diarrhea in foals 493-511
antibiotic-induced 507
candidiasis 508
clostridial enterocolitis 499-502
cryptosporidial 504-507
equine herpesvirus 508
fetal 507
foal heat 493
nutritional causes 507-508
proliferative enteropathy 508-509
Rhodococcus equi 502-504
salmonellosis 495-499
septicemia 507
strongyle infection 508
Strongyloides westeri 508
viral 493-495
Diazepam 24, 148,348
Digestible energy (DE) input 399-400
Dimercaprol 420
Dioctahedral smectite 412
Dioctyl sodium succinate 122,246,281,
423
Dipyrone 119, 120,207
Disinfection procedures 232
Disseminated intravascular coagulation
(DIC) 195-196,382
Distention see Abdominal distention,
specific sites
Distributive shock 198
clinical findings 201
pathophysiology 200
treatment 202-203
Disuse atrophy 311
DMSO (dimethylsulfoxide) 133-134,153,
194,195,222,388
Dobutamine 153
Dog-sitting position 109
Domperidone 124
Donkeys, hepatic disease 389, 396,397,
398,399,400
Dopamine 153,192
Doppler techniques 166--167
Draft breeds 221-222
Drainage, peritoneal 229
Draining tract 182
Draschia megastoma 476
Dry sickness (mal seco) 251,343
Duodenal perforation 472
Duodenal stricture 458
Duodenal ulceration 470,471,472
Duodenitis 471
Duodenoscopy 24,25-26
Duodenum
anatomy 249
in endoscopy 25-26
Dysautonomia 67,343
Dyserythropoiesis 370
Dysmasesis 74
Dysphagia 63-67
compromised deglutition 65-67
defined 63
diagnosis 64-65
normal deglutition 63-64
post-laryngoplasty 66
weight loss and 371
Ear teeth 73
ECN, equine-clinicians' network 93

530
 INDEX

Edrophonium 150 Endotoxemic shock see Distributive shock Escherichia coli 314,387
Ehrlichia nsticii 412-414,415,522 Endotoxin 191 Esophageal cysts, intramural 67,96
FimPria leukarti 60,273, 444,482 Endotoxin response 191-192,200,519 Esophageal disorders 89-98
Elt'ctrocardiography 150-151,232-234 End-tidal carbon dioxide 151 clinical signs 89
Electrolyte balance 12 End-tidal concentration of anesthetic 150 diagnosis 89-90
acutt' diarrhea 405-406 Enema 305,459-460,486 general surgical considerations 90-92
cardiac automaticity and 234-236 Enrofloxacin 408 complications/ prognosis 96--97
chronic diarrhea 429 Enteral formulations 399-400 incisional closure 91-92
/,)als 454 Enteritis surgical approaches 91
hyperlipemia and 398-399 anterior 257-258, 261 see also specific disorders
peritonitis 326--327 atypical 494 Esophageal diverticulum 93, 95
Electrolyte therapy eosinophilic 32,36 Esophageal fistula 95
abdominal pain and 138-140 in foals 455,456, 457,499-502 Esophageal impaction 67,89
expected abnormalities 138 granulomatous 377,443 Esophageal neoplasia 67,96,247-248
ill anesthesia 152-1.�3,154 hemorrhagic 500 Esophageal obstruction 89,92-93
chronic diarrhea 430 lymphocytic-plasmacytic 33,36,372, Esophageal peristalsis 63-64
in colic 122-123 378,379 Esophageal phase of glutition 63-64,
")als 463-464 rectal examination 114 66-- 6 7
Elephant on a tub posture 345 scintigraphy 36 Esophageal replacement 94
ELISA 231,494, 495 ultrasonography 32,33 Esophageal resection 94
Eltmac 120, 192,207 Enterobacter spp. 387 Esophageal rupture 67,93
Emaciation 368 Enterocentesis 13-14, 17,19 Esophageal stricture 67,93-95
Iff alw Weight loss Enterocolitis Esophageal tone 5
Emollit'nts 281 granulomatous 378 Esophageal ulceration 416
Encephalopathy Rhodococcus equi infection 503 Esophagitis 471, 472
primary hyperammonemia 384-386 Enterocutaneous fistula 478 Esophagomyotomy 94
Theiler's disease 381-384 Enterolithiasis 293-296 Esophagoplasty 94
Endoscopy 21-26 clinical signs and diagnosis 293-294, Esophagoscopy 23-24,24,65,90
cleft palate 81-82 299-300 Esophagotomy 92-93,94-95
duodenal ulceration 471 complications 295 Esophagus
dysphagia 64-65 large colon 293-296 anatomy and physiology 89,91
equipment 21-23,26 postoperative care 295 congenital abnormalities 96
filals 453 prevention and recurrence 295-296, fenestration of cicatrix 94-95
gastric squamous cell carcinoma 247, 248 300 muscular patch grafting 94
gastric ulceration 242-243, 245 small colon 299-300 physical examination 89-90
gastroduodenal ulceration 472-473 surgery 294-295,300 radiography 90
procedures 23-26 Enteroliths 295,299 Estrogens, conjugated 359
adult horses 24 Enterotomy Estrus 352,493
biopsy 26 gut viability and 165-166 Evacuation, large colon 290
duodenum 25-26 intestinal preparation 172 Exercise-related colic 242, 3.';3
esophagus 24 site 172, 173 Exercise therapy 120,206,260, 286,319,
foals 23, 24 see also Sutures 329, 357
stomach 24-25 Enterotoxins 410,411,496,500 Exteriorization of viscera 161-164
see also Laparoscopy Eosinophilia 11 Eyeball, in anesthesia 150
Endotoxemia Eosinophilic infiltrates, chronic 377-378, Eyes, examination 452
coagulopathy and 223-224,22.� 379
hepatic infection in foals 518-520 Ephedrine 153 Facial paralysis 65
intestinal obstruction 103-104 Epicauta spp. 417-418,419 Famotidine 192
laminitis and 229,230 Epidural anesthesia 307, 308,313 Fasciola hepatica 521
management during transport 133-134 Epiglottal entrapment 66 Fasting, effects 196
pathophysiology 103-104,191-192 Epiglottic retroversion 87 Fecal analysis 12-13,56--57,370,411-412,
peritoneal fluid analysis and 18 Epiploic foramen entrapment 260 429-430
postoperative 192-196 Epsom salts 122 in rectal examination 6
in pregnant mare 351-352 Equine infectious enterocolitis see Fecal blood 13
salmonellosis 407,408,409, 496--497, Potomac horse fever Fecal cultures 13,497-498,499,500-501
498-499 Equine monocytic ehrlichiosis see Fecal egg reduction count tests (FERCT)
treatment principles 192-196 Potomac horse fever 59-60
antibiotics 195 Equine right dorsal colitis 438-442 Fecal impaction 301-302
anti-inflammatory therapy 123 cause 439 see also Grass sickness
biological products 192-193 clinical pathology 439-440 Fecaliths 302,303,462
disseminated intravascular clinical signs and diagnosis 439-440 Fecal worm egg count (FWEC) 12,56-- 57,
coagulation and 195-196 progression and prognosis 442 60,437
endotoxin nentralization 123,193 treattnent 440-442 Feed see Nutrition, Nutritional support
fluid/ electrolytes 192 Erythroctye parameters 11 Feed impactions, in pregnancy 353-354
free radical scavengers 194-195 Erythrocytophagia 18, 19 Fenbendazole 58, 435
ga.trointestinal tract fimction and 195 Erythrocytosis 518 Fescue grasses 422-423
glucocorticoids 193 Erythromycin Festuca spp. 422-423
NSAIDs 192 clostridial diarrhea 124,410-411,412, Fetal diarrhea 507
prevention of laminitis 195 507 Fetal hydrops 321
TNF, and 193-194 as prokinetic 124,214,465 Fever 129-130,374,391,411,414

531
INDEX
Fiberoptic endoscopy 21,22
Fibrin activity
adhesions and 105,209-210
in distributive shock 200
in hypovolemic shock 199
in liver disease 382
normal 223
in peritonitis 323,324
Fibrosis, intestinal 444,471-472
Flatulent colic see Colic, distention
Flexor tenotomy, deep digital 230
Flotation techniques 506
Fluid balance 12
Fluid therapy
abdominal pain and 138-140,
463-464
expected abnormalities 138
cecal impaction 270
colic 122-123
diarrhea
acute 405-406
chronic 430
viral 494-495
distributive shock 202-203
during transport 132-133
endotoxemia 192
foals 463-464
hepatoencephalopathy 383-384
hyperlipemia and 398-399
hypovolemic shock 201-202,334,
:�58-359
intestinal impaction 139,140,280-281
peritonitis 327
salmonellosis 408-409,499
Flunixin meglumine
in distributive shock 203
in endotoxemia 123,192,195
pain relief 119,120
postoperative pain 206,207,208
Fluoroscence studies 65,166-167, 168
Foaling see Parturition
Foals
abdominocentesis 15-16
antibiotic-induced diarrhea 410,411,
412
an ti-ulcer medication 192
cecal perforation 274
colicky pregnant mare and 351-352
diarrhea see Diarrhea in foals
endoscopy 23,24,26
gastric ulceration see Gastric ulceration
in foals
hepatic diseases see Hepatic diseases in
foals
intestinal atresia 304
iron overload 393,522
large and small colon disease and colic
485-490
medical therapy of pain 463-465
analgesics 464-465
decompression 465
fluid therapy 463-464
nutrition 464
prokinetics 465
pancreatitis, acute 350
parasite infections, ill thrift 56
peritoneal fluid 16-17, 19,323,454
salmonellosis 408,409,495-499
small intestinal disease and colic
477-484
532
stomach diseases
abscesses 476
endoparasitism 475-476
gastroduodenal ulceration 469-475
ulcer syndromes 470-472
Foals, clinical evaluation 449-468
abdominal distention, differential
diagnosis 459-462
abdominocentesis 453,460
clinicopathological data 453-454,
466-467
endoscopy 453
history 449-450, 459, 466
nasogastric intubation 452, 460
physical examination 450-453, 459,
466
radiography 452,457-458,459-460,
467
rectal examination 451
sedation 24,452
signalment 450
surgical decision re colic 465-467
ultrasonography 28,29,452-453,
454-457,459-460,467
Foreign bodies
impaction 280
oral cavity 65,66,78
small colon obstruction 300-301
Formalin 359
Fourth branchial arch defects 66
Free fatty acids 395
Free radicals 194,195
Frog supports 422
Frusemide 155
Functional residual capacity 145
Fungal enterocolitis 378, 379
Fungal toxins 251,384,420
Fungi, predacious 59
Furosemide 192
Galvayne's groove 71
Gamma glutamyl transferase (GGT) 383,
386,387,389,390,391,398
Gasterophilus spp. 60,475-476
Gastric abscess 476
Gas tric acid secretion 470
Gastric decompression 120,206,246,
247
Gastric dilation 246-247
Gastric emptying 480
impaired 244, 471-472
Gastric erosions 244,470
Gastric impaction 245-246
Gastric lavage 417, 465
Gastric lesions, stress-induced 471
Gastric mucosal biopsies 26
Gastric outlet obstruction/pseudo-
obstruction 471-472,480
Gastric perforation see Gastric rupture
Gastric reflux, nutritional support and
197
Gastric rupture 247,318,472
Gastric squamous cell carcinoma
247-248,337
Gastric ulceration 241-245
clinical signs 242
diagnosis 242-243
epidemiology 242
etiopathogenesis 241-242,416
NSAID toxicosis 416
prevention 244
treatment 243-244,245,417
Gastric ulceration, foals 389,469-475,
480
clinical signs 472
diagnosis 472-473
etiopathogenesis 469-470
prevention 475
treatment 473-475
ulcer syndromes 470-472
gastric outlet obstruction/pseudo-
obstruction 471-472
perforation 472
silent 470-471
stress-induced gastric lesions 471
sudden onset severe 471
Gastrin 241
Gastroduodenal bypass surgery 475
Gastrointestinal neoplasia 334-338,437
investigation 335-336
presentation and clinical signs 33.�,
374-375
prevalence and etiology 335
treatment and prognosis 338
types and sites 334-335
Gastrointestinal tympany 317-319
Gastroscopy 21,22,23,24-25,26
foals 453
Gastrosplenic ligament 260
Giant cell hepatopathy 521
Giardiasis 444
Gingivitis 74,75
Globulins 11-12
Glottic protection, compromised 66
Glucocorticoids 193
Glucose absorption tests 20-21, 336, 350,
372,379
Glucose therapy, in hyperlipemia 399,
400
Glycopyrrolate 150,236
Grain overload 421-422
Granulosa-theca cell tumor 353
Grass sickness 67,251,343-348
clinical pathology and pathology 346
clinical signs 344-346, 347
diagnosis 256-257,346-347
epidemiology and etiology 343-344
risk factors 251
treatment 347-348
Guaifenesin 148
Habronema spp. 60,476
Halothane 149,152
Hamartoma, mixed 518
Head
edema 136,137
physical examination 3-4
Healing, incisions 181,196
Heart auscultation 4
Heart disease, chronic 375
Heart failure 375
Heart rate 4,110,130,450-451
Helicobacter spp. 470
Hemangiosarcoma 332
Hematology
chronic diarrhea 429
parameters 11
parasite-associated diseases 57
peritonitis 326-327
weight loss 369-370

Hematoma
at parturition 357,358,359
intramural 303
laparoscopic aspiration 46
post-ovulation 352-353
rupture 358
subscapular splenic 44
Hemiperitoneum 321
Hemochromatosis 393-394
Hemodynamic disturbances,and
transport 133-134
Hemoglobin concentration I I
Hemoperitoneum 18,19,201,332-334
Hemorrhage
at parturition 357-359
fecal examination 429,430
hematology profile 11
hypovolemic shock and 199,200-201,
202
incisional 216-217,218
intra-abdominal 216-217,218
liver failure and 382
treatment 217-218
Hemorrhagic diathesis 196
Hemorrhagic shock see Hypovolemic
shock
Hemostasis 223
Heparin therapy 196,203,210, 227,328,
329,400
complications 227
Hepatic abscess 44,45
Hepatic diseases 381-386,389-401
acute, with failure 381-384
chronic active hepatitis 391-392
chronic liver failure 392-394
chronic, weight loss and 373
hyperlipemia 394-401
primary hyperammonemia 384-386
pyrrolizidine alkaloid intoxication
389-391
right hepatic lobe atrophy 394
Sfe also specific conditions
Hepatic diseases in foals 513-525
ascending infection 520
biliary atresia 517-518
hyperammonemia in Morgans 523
leptospirosis 521
neonatal isoerythrolysis 524
neoplasia 518
parasitic 521
perinatal asphyxia 524
portal vein thrombosis 523-524
portosystemic shunts 513-516
septicemia/endotoxemia 518-520
serous cysts 518
toxic disorders 522-523
Tyzzer's disease 516-517
Hepatic enzyme activity 383, 384,386,
387,389,390,391,392
neoplasia and 393
Hepatic enzymes
in hyperlipemia 398
Hepatic fibrosis 386,387,521
Hepatic neoplasia 388-389,393
in foals 518
metastatic 393,518
Hepatic scintigraphy 37-38
Hepatitis
chronic active 391-392
serum see Theiler's disease
Hepatoblastoma 518
Hepatocellular carcinoma 393
Hepatoencephalopathy
bacterial infection and 519
cholangiohepatitis 387,388
clinical signs and diagnosis 382-383
iron toxicity 522
in portosystemic shunts 513,514, 515,
516
therapy and prognosis 383-384
Hepatoliths 386
Hepatotoxins 384, 389-391, 522-523
Herniation
internal 260-261
post-<:eliotomy 34
Herniorrhaphy 218-219
Herpesvirus, equine 508,520-521
Hetastarch 192
HHH syndrome 385-386,523
Histoplasma spp. 378, 423,443
Histoplasmosis 443
Hooks, of teeth 71,76
Hormone sensitive lipase (HSL) 395-396,
400
Hyaluronan 211
Hydrochloric acid secretion 241-242
Hydroxyethyl starch 139,140
Hyoid apparatus disease 65-66
Hyoscine 122
Hyperalgesia 205
Hyperammonemia 382,384-386,387,388
in Morgans 385-386,523
portosystemic shunts 513-514
Hyperbilirubinemia 384
Hypercalcemia 235
Hypercapnia 146, 152
Hypercoagulability 223-224
Hyperfibrinogenemia 370
Hyperglobulinemia 370,372
Hyperimmune products 123,133,193,
203
Hyperinsulinemia 350
Hyperkalemia 235,462,464
Hyperkalemic periodic paralysis (HYPP)
220-221,405
Hyperlipemia 350,394-401
associated diseases 395
clinical signs and diagnosis 396-398
epidemiology 394-395
pathogenesis and pathology 395-396,
398
prognosis and prevention 400-401
treatment 398-400
Hyperlipidemia 397, 400
Hypermetabolic syndrome, post­
anesthetic 221
Hyperproteinemia 370
Hyperthermia 504,507
malignant 220
post-anesthetic 221
Hypoalbuminemia 11,372,373,431,433
Hypobiosis 433
Hypocalcemia 154,235,406,418,
439-440
Hypoglossal nerve injuries 65
Hypoglycemia 350
Hypokalemia 154,235,464
Hypomagnesemia 235
Hypoproteinemia 370,430-431,433,439,
440
INDEX
Hypotension 152-153,221
Hypotensive shock 123
Hypoventilation 152
Hypovolemia
in anesthesia 152-153
management during transport 132-133
Hypovolemic shock 198
arterial rupture at parturition 358-359
clinical findings 200-201
fluid therapy 123,334
pathophysiology 199-200
treatment 201-202,463
Hypoxia
in anesthesia 146,152
Ileac arteries, external, rupture 357,358
Ileal biopsy 256-257,342
Ileal bypass 197-198
Ileal impaction 113-114,257,258-259
Ileocecal intussusception 29-30,114,186
Ileocecal ligament 250,267
Ileocecostomy 255
Ileocolonic aganglionosis 304,461,487,
488-489
Ileocolostomy 273,274
Ileum
anatomy 250
muscular hypertrophy 259
obstructive conditions 254, 255
rectal palpation 8,113-114
vascular supply 186
Ileus 211-215,262,320
anti-inflammatory anti-endotoxin drugs
213
clinical signs 212
definition and incidence 211
diagnosis 212
in foals 455,456,457,465
medical therapy 123-125
nasogastric decompression 213
nutritional support and 197
pathophysiology 212
prognosis 215
prokinetic agents 213-215,465
supportive therapy 212-213
treatment 195
III thrift, parasite-associated 56
Immunofluorescence assays 414,506
Immunoglobulin therapy 123,192-193
Impaction see specific sites and
conditions
Inappetance 197,348
Incision
protection during recovery 183-184
strength layer 182,183
Incisional closure 181-182
Incisional complications 181-182,
216-219
clinical signs 216-217
predisposing factors 216
treatment 217-219
Incisional drainage 182,217,218
Incisional hemorrhage 216-217,218
Incisional hernias 182,217, 218-219,
322
Incisional infections 33-34, 182,217,218
Incisor caps 73-74
Incisor profile 71
Infiltrative bowel disease 30,32-33,372
malabsorption and 377-378
533
INDEX
Inflammatory bowel disease
chronic (CIBD) 372,377-378,379,437
Inflammatory diseases
parasite-associated 54-55,57
scintigraphy 36-37
ultrasonography 30,32-33
Inflammatory response
adhesions and 209-210
hematology profile 11
peritoneal fluid analysis and 18
in peritonitis 323-324
in salmonellosis 496
weight loss and 369-370
Infundibular disease/necrosis 74
Ingesta
prehension 63
reduction pre-laparoscopy 46
Inguinal hernias 261,477-478
rectal examination 114
reduction 452,477
ruptured 478
ultrasonography 29, 30
Inguinal rings, palpation 8
Inspiratory time:expiratory time (I:E) 152
Insufflation 17, 24-25,26,41-42, 44,
46-47,48
Insulin
resistance 396,400
secretion 349,350
therapy 235, 350,464
Insulin-dependent diabetes mellitus
349-350
Intensive care plan 190-191
see also Postoperative treatment and
complications
Interstitium:crypt (I:C) ratio 167
Intestinal abscesses 483
Intestinal absorption, normal 379
Intestinal alkaline phosphatase 12
Intestinal atresia 304,461
Intestinal clamps 175,177
Intestinal content, evacuation 173
Intestinal diverticulae 262
Intestinal flora
antibiotic disruption 231
modification 406,431,432,502
Intestinal obstruction
exteriorization, algorithm 162, 163
pathophysiology 103-105
adhesion formation 105
endotoxemia 103-104
intestinal distention ID3
intestinal ischemia 103
motility disturbances 104-105
reperfusion injury 104,105
Intestinal protectants and absorbants 431,
442
Intestinal wall thickening 32,456,457
Intra-abdominal foraminae 260
Intralumenal pressure, viability and 167,
168
. Intrapalatal cysts 66
Intussusceptions
foals 462,482
rectal examination 114
rectal prolapse repair 313-314
repair of rectal tear 309
small intestinal 261-262
ultrasonography 29-30,456,457
see also specific sites
534
Intussusceptum 262
Intussuscipiens 261
Iodochlorohydroxyquin 432
Iron toxicity 393-394,522
Ischemia 18,103
Isoflurane 149, 152
Isoniazid 443
Isosthenuria 373
Isoxsuprine 354,422
Ispaghula husk 438
Ivermectin
in control programs 59
therapeutic regimens 58,60,435
Jejunocecostomy 255
Jejunojejunal intussusception 114
Jejunum, anatomy 249-250
Jugular vein filling 110
Jugular vein thrombosis 406
Kaolin and pectin 406, 431
Ketamine, in anesthesia 147-148,149,
154
Ketoprofen 119,120, 192,207
Kidney biopsy 48
Kidney disease, chronic 373-374
Klein grass 393
Lactase deficiency 508
Lactate dehydrogenase 220,221,228,
229, 383,392,398
Lactated Ringer's solution 201-202
Lactation 395,400
Lactic acidosis 275,399
Lactobacillus spp. 406,431, 502
Lactose intolerance 508
Lactose tolerance test 21
Lactulose 388
Lameness, chronic 371
Laminitis 229-230
clinical signs 230
defined 229
diagnosis 230
endotoxemia and 195
pathophysiology 229,421
postoperative 229-230
Potomac horse fever and 413,414,415
prevention and treatment 194,195,
230, 406,422
Lausoprazole 243
Laparoscopy 41-50
biopsy 44, 48
colic, chronic and recurrent 342-343
complications 44,49
defined 41
effects on peritoneal fluid 17
equipment 41-43
indications for 44-46
in peritonitis 327
surgical procedures 46-49
presurgical preparation 46-47
standing approach 46,47-48
ventral abdominal approach 48-49
Laparotomy see Celiotomy
Large colon
anatomy 284-285
colic-associated diseases in foals
485-490
decompression 292-293
impaction at anastomosis 215-216
laparoscopic evaluation 44,45
non-strangulating infarction 293
primary tympany 292-293
rectal examination 115-117
resection, nutritional support and
197-198
retroflexion, at laparoscopy 45
strangulating lesion 291
trocarization 292-293
viability 164,165,167-168
Large colon displacement 284-288,360
left dorsal (LDDC) 285-289
clinical signs 285-288
rectal examination 115-116
treatment 286-287
ultrasonography 30,31
non-strangulated 285-288
right dorsal (RDDC) 287-288
rectal examination 114-115,117
Large colon impactions 279-282
clinical signs and diagnosis 280,283
epidemiology and etiology 279-280,
283
outcome and prevention 282,284
sand impaction 282-284
treatment 280-282,283-284
Large intestinal obstruction
radiography 458-459
ultrasonography 30, 31,32, 33
Large intestine
exteriorization 162-164
malabsorption syndromes 372-373,376
Larval cyathostomosis see Cyathostomosis
Lavage
esophageal 92
gastric 417, 465
peritoneal 229
retrograde 300,301,302,303
Lawsonia intracellularis 508,509
Laxatives 122,231,281,438,486
Lazaroids 194
Leaky membranes 138, 139,140
Leiomyoma 338
Leiomyosarcoma 338
Leptospirosis 521
Lethal white syndrome 304,461,487,
488-489
Leukocytes
parameters 11
radiolabelled 36-37,417,440
Leukocytosis II, 369-370
Leukoencephalomalacia 384
Leukopenia 11
Levamisole 58
Lidocaine (lignocaine) 124,207,208,
215, 236-237
Linea alba incision 156
Lingual paralysis 65
Linoleic acid 442
Linseed oil 420
Lipase activity 349
Lipemia, gross 397
Lipid-derived mediators 103-104,191,
192
Lipid metabolism 395-396
normalization of 400
see also Hyperlipemia
Lip lesions 65
Lipoma, pedunculated 29, 30,32,
259-260,303-304,336-337
Lipoprotein lipase (LPL) 395,396,400

Lipoproteins, very low density (VLDL)
395, 396, 400
Liquid diets 197
Lithotripsy 388
Liver biopsy 382, 383, 387, 390, 391, 392,
515
procedure 10-11, 48
Liver failure 387
plant toxins 389
potential causes 392-394
undetermined cause 392
Liver flukes 521
Loperamide 406, 431
Louw's theory 461
Lung tumors 375
Lymphangiectasia, intestinal 444
Lymphosarcoma 33, 66-67, 320, 337, 338
weight loss and 372, 374-375, 378, 379
Magnesium 235
Magnesium oxide 243
Magnesium sulfate 122, 140, 235, 236,
237, 419
Malabsorption
carbohydrate absorption tests 20-21
large intestinal 372-373
small intestinal 372
total/partial 379
weight loss and 372-373
Malabsorption syndromes 376-380
causes 377-378
alimentary lymphosarcoma 378
chronic inflammatory bowel disease
377-378
enteric infections 378
small intestinal resection 377
clinical signs and diagnosis 378
treatment 379-380
Maldigestion, weight loss and 371-373
Malignant hyperthermia 220
Malocclusions 76-77
Malpractice action 308
Mal seco 251, 343
Management
cleaning procedures 232
clostridial diarrhea 412
factors in weight loss 368-369
gastric ulceration and 242, 244
parasite-associated disease 54, 56,
58--60
practices predisposing to colic 102
right dorsal colitis 441
salmonellosis 409-410, 499
Mandibular brachygnathia 72-73
Mandibular symphysiotomy 82-84, 86-87
Maniacal behavior 382, 383, 387, 388
Mares see Brood mare
Martingale, elastic 94
Masseter myopathy 221
Mastication 63
Matrix metalloproteinases 229
Maxillary brachygnathia 72-73
Mean arterial pressure (MAP) 359
Meckel's diverticulum 478-479
impacted 260-261
Meconium 460
Meconium impaction 482, 485, 486
diagnosis 457, 458, 487, 489
Meconium passage, normal 485
Meconium retention 460-461, 485-486
Megaesophagus 67, 96
Melanomas 19, 44, 45
Melena 13
Mercury toxicity 78, 420
Mesenteric abscesses 331, 332, 483
Mesenteric arteritis 55, 262, 436-437
Mesenteric defects, congenital 479
Mesenteric lipoma 336-337
Mesenteric lymphadenopathy 378
Mesenteric lymph node biopsy 342, 372,
380
Mesenteric resection 173-174, 175
Mesenteric stalk, palpation 7-8
Mesh placement 219
Mesocolic rupture 303
Mesodiverticular bands 260, 478-479
Mesothelioma 320
Mesperidine 148
Metabolic acidosis 12
in colic 153-154, 154
in distributive shock 202-203
Metoclopramide 123-124, 214, 465
Metronidazole 232, 412, 442
Microangiopathic hemolytic anemia 382
Microcytosis 514
Microfold cells (M-<:ells) 504
Midazolam 148
Migrating myoelectric complex (MMC)
211-212
Milk replacements 507-508
Mineral oil
in colic 122
in peritoneal fluid analysis 18-19
Minimal alveolar concentration (MAC)
149, 150
Misoprostol 243, 244, 417, 423, 441
Mittelschmerz 352
Modified Triadan System 70
Monocytosis 11
Morgans 303, 381, 385-386, 523
Morphine 119, 121, 148, 208
Motility
abnormal, medical therapy 123-125
bowel sounds 4
disturbances
acute diarrhea 423
cecal impaction and 269
intestinal obstruction 104-105
modification in chronic diarrhea 431
normal physiology 211-212
ultrasonography 32
Motility enhancers see Prokinetic agen t�
Motor neuron disease 376
Mouth
disorders of 78-79
physical examination 4, 78
Moxidectin
control programs 59
therapeutic regimens 58, 60, 435
toxicity 58, 435
Mucosal disease, esophageal 93
Mucosal protectant 473, 474
Mucosal ulcers 378
Mucosa-periosteal sliding flap 85
Mucous membranes 3-4, 201
colic and 110
toxic line 1 10
Multiple organ dysfunction syndrome
(MODS) 200, 201, 519
Multiple organ failure (MOF) 519
INDEX
Multisystemic eosinophilic
epitheliotrophic disease 378
Muscle atrophy 376
Muscle fiber necrosis 220
Muscle weakness, overall 220
Mustard plant toxicity 423
Mycobacterial infection, intestinal 377,
378, 423, 443
Mycobacterium spp. 423, 443
Mycosis 64
Mycotoxicosis 384
Mycotoxins 251, 384, 420
Myeloencephalitis 376
Myocarditis, immune-mediated 236
Myonecrosis 221
Myopathy, post-anesthetic 2 19-222
pathogenesis 220
prevention and prognosis 222
therapy 222
Naloxone 334, 359
Narcotic analgesics 121
Nasal edema 137
Nasogastric intubation 4-6
in colic 110-111, 130-131, 253
in endotoxemia 195
foals 452, 460
management during transport 134
procedure 4-6
Nasopharyngeal cicatrization 66
Necrotizing enterocolitis 483
Necrotizing hepatitis 521
Neomycin 423
Neonatal isoerythrolysis 524
Neonates
abdominal distention 460-462
normal parameters 449, 450-451
Neoplasia see Gastrointestinal neoplasia
and specific tumors
Neospora caninum 443
Neostigmine 123, 2 14, 281-282, 465, 495
Nephrosplenic entrapment see Large
colon displacement, left dorsal
Nephrosplenic ligament, palpation 7
Neurofibroma 338
Neurological disease 376
Neurological signs, alkaloid intoxication
390
Neurolomuscular disease 376
Neuromuscular blockade 150
Neuropathy, post-anesthetic 219-222
pathogenesis 220
prognosis and prevention 222
therapy 222
Neurotoxins 382
Neutropenia 1 1
Neutrophilia 369-370
Neutrophils
in peritoneal fluid 16, 17, 18, 19
in reperfusion injury 104, 105
Nitric oxide 105, 195, 200, 471
Nitroglycerine cream 195, 409, 422
Nitrous oxide 150
Nociceptors 204-205, 208
Non-esterified fatty acid (NEFA) 395-396,
397,399, 400
Non-strangulating infarction
large colon 55, 58, 293
small colon 304
small intestine 55, 58, 262
535
INDEX

Norepinephrine 153 Pain pathogenesis 54-55

NSAJDs (non-steroidal anti-inflammatory acute abdominal, prognosis 141-142 treatment
drugs) classification of severity 107-108, anthelmintic aspects 57-58
adhesions and 210 205-206 symptomatic aspects 57
cecal perforation and 274 clinical signs 107-108 see also specific parasites and diseases
colic 120 colic Parasympatholytic drugs 150, 307, 308
endotoxemia 192 chronic and recurrent 339, 340-341 Parenteral nutrition 197
hepatic toxicity 522 decision for surgery 130 foals 464
postoperative pain 206-207 decision to refer 127 Parietal hernia 261
toxicity 415-417 small intestinal obstruction 253 Parrot mouth 72
acute overdose 417 management during transport 133 Partial pressure of carbon diol'<ide
mechanisms 415-416 mechanisms of 107, 204-205 (paCO,) 152
right dorsal colitis 438-442 meconium retention 486 Partial pressure of oxygen (PaO,) 152
treatment 417 medical therapy in foals 463-465 Partial thromboplastin time (PTI) 382,
Nuclear scintigraphy see Scintigraphy analgesics 464-465 383, 387
Nutrition decompression 465 Parturition
assessment of 368-369 fluid therapy 463-464 colic and 357-361
needs 369 nutrition 464 effects on peritoneal fluid 18
Nutritional support prokinetics 465 gastrointestinal complications 360
alier surgery 196-198 ovulation-related 340, 352 PCR 230, 231, 408, 411, 413, 414, 509
long-term care 197-198 parietal 107, 205 Pelvic cavity, palpation 159-161
in chronic diarrhea 432 parturition 357 Pelvic flexure
foals with abdominal pain 464 persistent low-grade 371 colotomy 167
in grass sickness 347-348 postoperative 204-209 enterotomy 287, 294-295
hyperlipemia 399-400 clinical signs 205-206 exteriorization 162, 163, 164
right dorsal colitis 441 diagnosis 206 rectal examination 8, 115, 116, 117
Nutrition-induced diarrhea 507-508 neuroanatomy and pathophysiology Penrose drains 175, 177
204-205 Pentazocine 119, 121, 148
Oat stones 302-303 treatment 206-209 Pentoxirylline
Obstruction see Intestinal obstruction, referred 107, 205 endotoxemia 133, 134, 194, 195, 203,
specific sites visceral 107, 119-122, 124, 205 415
Obstructive shock 198 weight loss and 371 hypovolemia 359
Odontomas 73, 79 Palate Pepsin 241, 242
Oleander, toxicity 420 anatomy, embryology and physiology Pergolide 322
Oligodontia 73 79-80 Periapical abscess 75
Omental hernia 16, 453 see also Cleft palate, Soft palate Periapical osteitis 74, 75-76
Omeprazole 192, 243, 244, 245 Palpation Perineal injuries 360
Oocyst" cryptosporidial 505-506, 507 abdominal quadrants and pelvic cavity Periodontal disease 35, 36, 74-75
Opioids 148, 208 159-161 Peripheral nerve injuries 220
Oral cavity foals 451-452 Periradicular disease 74, 75-76
disorders of mouth 78-79 rectal. normal horse 7-8 Perirectal abscesses 308, 314
see also Cleft palate, Dental disease, Soft rectal tears and 305, 307 Peritoneal effusion, ultrasonography
palate transrectal, and videolaparoscopy 457
Oral examination 64, 81-82 45-46 Peritoneal fluid
Oral glucose absorption tests 20-21, 336, Palpebral reflex 150 analysis 16-20
350, 372, 379 Pancreas, anatomy and function 348-349 abdominal surgery, effects 17
Oral lactose tolerance test 21 Pancreatic diseases 348-350 ascites 320
Oral tumors 79 chronic 349-350 bowel rupture 18, 19
Organophosphates 59, 60, 420-421 Pancreatic fluid 349 chyloabdomen 479
Oropharyngeal lesions/tumors 66 Pancreatitis in colic 111, 131
Orotracheal tube 154-155 acute 350 contaminated samples 15, 17
Ossifying periostitis, chronic 74, chronic eosinophilic 349 disease effects 18-20
75-76 Panicum coloratum 393 enterocentesis effects 17
Ovarian tumors 353 Paracentesis see Abdominocentesis fat in 18-19
Overbite 72, 73 Paradoxical acidosis 154 hypovolemic shock 201
Ovetjet deformity 72, 76 Paralytic ileus 258 laparoscopy effects 44
Overo lethal white syndrome 304, 461, Paranoplocephala mammillana 54 in malabsorption 372
487, 488-489 Parascaris equorum see Ascarids neoplasia 336
Oxfendazole 58 Parasite infections 53-60 parturition effects 18
Oxyclozanide 521 clinical features of disease entities in peritonitis 325-326
Oxygen saturation, viability and 166, 167, 55-56, 60, 273, 276, 475-476 postoperative peritonitis 228-229
168 control programs 58-60 small intestinal obstruction 253
Oxygen therapy 154, 155, 203, 359 features 53-54 in weight loss 370, 372
Oxytetracycline 415 abundance of larvae/ eggs in normal characteristics 16-17, 322-323,
Oxytocin 361 environment 53 349
Oxyuris equi 60 occurrence of disease 53-54 foals 16-17, 19, 323, 454
parasite biology 54 see also Abdominocentesis
Pacemaker activity 249, 250, 268 parasite burden 54 Peritoneum
Packed cell volume (PCV) 11 investigations 56-57 anatomy and physiology 322-323
in colic 112 minor 60 ultrasonography, foals 457

536

Peritonitis 321. 322-330
acute 325. 326
bile 3RR
chemical 462
chronic 325. 326-327
classification and etiology 323. 324
clinical signs 324-325
copulation-induced 353
in foals 462
gastric rupture 472
investigation and diagnosis 325-327
medical treatment 327-330
pathophysiology 323-324
peracute 325. 326
peritoneal fluid analysis 18. 1 9
postoperative 227-229
causes 227-228
clinical signs and diagnosis 228-229
treatment 229
prognosis 330
signalment and history 324
surgical treatment 329-330
ultrasonography 32. 457
Pethidine 1 1 9 . 121
Pharyngeal cysts 66
Pharyngeal hemiplegia 64
Pharyngeal neoplasia 66
Pharyngeal paralysis 64. 66
Pharyngeal phase of deglutition 63. 66
Pharyngeal stripping wave 63
Pharyngeal swallow reflexes 63
Phenothiazines 59. 121
Phenoxybenzamine 406. 431
Phenylbutazone 1 1 9. 120. 192. 195. 207.
230
toxicity 120. 207. 274. 4 1 7
see also Equine right dorsal colitis
Phenylephrine 153. 154-155. 286. 287
Photodocumentation 42
Photosensitivity 389. 390
pH. stomach contents 1 1 1
Physical examination 1-8
auscultation 4
general observations 3
head 3-4
history 3
thorax and abdomen 4
see also Nasogastric intubation. Rectal
examination; specific conditions
Phytoconglobates 302-303
Pink-rosewater diarrhea 495
Pinworm 60
Piperazines 59
Placenta. retained 36 1 . 414
Placentitis 507
Plank in the flank technique 356
Plant toxins 389. 393. 419-420
Plasma fibrinogen concentration 1 1
Plasmalyte 2 0I
Plasma therapy 123. 140. 192. 1 93. 203.
327. 430
Platelet plug formation 223
Pneumatosis intestinalis 483
Pneumoperitoneum 4 1 . 44. 47. 48. 320
Poikilocytosis 514
Polymyxin B 133. 193. 203. 406
Polyneuritis equi 376
Polyodontia 73
Polysaccharide storage myopathy 221 -222
Polyvinylpyrrolidone 211
Portal vein thrombosis 384. 523-524
Portography. positive-control 5 1 5
Portosystemic shunts 513-516
Positive end-expiratory pressure (PEEP)
152
Post-anesthetic airway obstruction 154
Postoperative treatment and
complications
abdominal adhesions 209-21 1
cardiac arrhythmias 232-237
colitis 230-232
foals 483
ileus 21 1-215
impaction at anastomosis 215-216
incisional complications 2 1 6-219
myopathy/neuropathy 2 1 9-222
nutritional support 196-198
immediate 196-197
long-term care 1 97-198
peritonitis 227-229
postoperative monitoring 189-191
protocols 190- 1 9 1
postoperative pain 204-209
postoperative shock and organ failure
1 98-204
thrombophlebitis 222-227
treatment of endotoxemia 1 9 1 - 1 96
Potassium supplements 1 40. 154. 235.
405. 464
Potomac horse fever 412-415
clinical signs and diagnosis 412-413.
414
epidemiology 413-414
treatment and prevention 4 1 5
Prednisolone 57. 193. 334
Prednisone 338. 392
Pregnancy
abdominal distention in 317. 321-322
abdominal pain (non-colic) 356-357
colic in 351 -352. 353-357
endotoxemia in 351 -352
hyperlipemia 396. 397. 400
see also Brood mare. Parturition
Prehension 371
Premolar caps 74
Prepubic tendon rupture 321 -322. 357
Preputial edema 378
Pressure bandages 217-218. 359
Pressure. intralumenal. and obstruction
103
Probiotics 406. 431. 502
Procainamide 236. 237
Progesterone 351-353
Prokinetic agents 2 1 3-215. 281 -282. 348.
465. 473. 474
Proliferative enteropathy 508-509
Propanol 236. 237
Propantheline bromide 307
Propofol 149
Propulsion. normal physiology 2 1 1 - 2 1 2
Propylene glycol 421
Protamine zinc insulin 350
Protein-losing enteropathies
cyathostomosis 433
weight loss and 372-373
Protein metabolism. abnormal hepatic
382
Prothrombin time (PT) 382. 383. 387
Proton pump 241
inhibitors 243. 244. 473, 474
INDEX
Pseudocysts 75
Psyllium. dry 438
Psyllium mucilloid 122, 283, 284. 438. 441
Ptosis. bilateral 345
Ptyalism 78. 471 . 472
Pulmonary disease. chronic 376
Pulmonary edema 155. 201
Pulmonary function
anesthesia and 146. 1 5 1 - 1 52. 154-155
in colic 145-146
Rhodococcus equi infection 503
Pulmonary hypertension 155
Pulmonary neoplasia 375
Pulpitis 74. 75
Pulse 3, 7. 8
Pulse oximetry 1 5 1 - 1 52, 168
Pulse rate 3
Pulsion (false) diverticulum 95, 262
Purse-string effect 170, 178
Pyrantel salts 54. 58. 59
Pyrrolizidine alkaloid intoxication
389-391
Quarter horses 1 40. 220-221 . 295. 303
Quassia amara 423
Quercus spp. (oak) 419. 423
Quidding 64. 371
Quinidine salts 234. 236. 237
Radiography
contrast studies 65. 90. 452. 457-458,
459-460. 467
dysphagia 65
enterolithiasis 294
esophagus 90
foals 452. 457-458. 459-460, 467
gastric impaction 245-246
gastroduodenal ulceration 472-473
Radiopharmaceuticals 34. 35
Ramifenazone 120
Ranitidine 243. 244, 245. 465
Reactive oxygen metabolites (ROM) 104.
105
Reactive oxygen species (ROS) 194
Rectal biopsy 9-10. 342. 372
Rectal examination 6-8
abdominocentesis and 1 3
applications 6
colic 1 1 1 . 1 12-1 1 9. 130. 253
chronic and recurrent 341
foals 451
in peritonitis 327
recognition of abnormalities
cecum 1 1 4-1 1 5
descending colon and rectum
1 1 7-1 18
large colon 1 15-1 1 7
small intestine 1 1 3-1 1 4
rectal tears and 305. 307
technique 6-8. 1 1 2-1 1 3
complications 7
lubrication 6
palpation of normal horse 7-8
videolaparoscopy and 45-46
Rectal liner 309-31 0
Rectal prolapse 312-313
Rectal prosthesis 309-3 1 0
Rectal tears 305-31 2
causes 305
classification 306-307
537
INDEX
Rectal tears - continued
clinical signs and diagnosis 307
prevention 307
prognosis 312
treatment
colostomy 310-312
definitive 308
immediate 307-308
primary repair 308-309
rectal liner, temporary 309-310
Rectal temperature 109-110
in colic 129-130
Rectum,anatomy 305-306
Rectus abdominus muscle,celiotomy
incisions 156, 157
Red cell count (RBC) I I
Red clover grass 420
Red worms see Cyathostomes,Strongyles,
large
Rehydration see Fluid therapy
Renal failure,weight loss and 373-374
Renal function,in hypovolemic shock
199-200
Renosplenic entrapment see Large colon
displacement,left dorsal
Renosplenic space,palpation 7
Reperfusion injury 104, 105, 201
Resection
length,and viability 167, 172-173, 377
nutritional support and 197-198
small intestine 255-256, 377
see also Sutures
Respiration,evaluation 4, 451
Respiratory rate J l O, 129-130, 152
foals 450-451
Restraint
anesthesia and 147
endoscopy 24
foals 450,452
nasogastric intubation 4-5
rectal examination 6
Reticuloendothelial system of liver,
scintigraphy 37-38
Retropharyngeal abscess/ neoplasia 66
Rhabdomyolysis,recurrent exertional 221
Rhinitis 346
Rhizoctonia leguminicola 420, 422-423
Rhodococcus equi 330, 332, 502-504
clinical signs 503-504
epidemiology and pathogenesis 502-503
treatment and prevention 504
Richter's hernia 261
Richter-type hernia 260
Ricinus communis 420
Rickettsiae see Potomac horse fever
Rolling 108, 109
therapeutic 286, 356
Romifidine 119, 121
Rotavirus diarrhea 493, 494, 495
R on T phenomenon 236, 237
Saline therapy 192,201-202
in abdominal pain 138-140
acute diarrhea 405,406
in colic 122,123
Salmonella spp. 495-496
postoperative colitis 230-231
in right dorsal colitis 439
serogroups 407
virulence factors 407, 496
538
Salmonella typhimurium DTl04 410 Small colon
Salmonellosis 406-410 enteroliths 299-300
chronic 443 fecal impaction 301-302
clinical signs and diagnosis 407-408, fecaliths, phytoconglobates and bezoars
496-- 498 302-303
control and prevention 409-410,499 foreign body obstruction 300-301
etiopathology 406-407 , 495-496 impaction at anastomosis 215-216
fecal culture 13, 498, 499 intestinal atresia 304
in foals 408, 409,495-499 intramural hematoma 303
prognosis 409 mesocolic rupture 303
risk factors and epidemiology 407 non-strangulating infarction 304
treatment 408-409,498-499 obstruction,ultrasonography 30, 32
Salt intoxication 421 rectal examination 117-118
Sand enteropathy 437-438 strangulating lesions 303-304
Sand impaction 282-284 trauma at parturition 360
clinical signs and diagnosis 15, 283 viability assessment 168
treatment 283-284 Small intestinal diverticulum 262
Scalding,perineal 493 Small intestinal entrapment,
Scin tigraphy 34-38 ultrasonography 29-30
dental 34-36 Small intestinal impaction,in foals
hepatic 37-38 481-482
inflammation and infection 36--3 7 Small intestinal intussusception; in foals
labeled white blood cells 36--37, 417, 440 482
techniques and agents 34, 35 Small intestinal lesions,ultrasonography
Scours,36-- hour 495 29-30
Scrotal hernias 477 Small intestinal obstruction
Seasonal malaise syndrome 373, 436 causes 258-262
Sedation clinical signs and diagnosis 253-254
endoscopy 24 foals,radiography 458
foals 24, 452 medical treatment 257-258
hepatoencephalopathy 383 pathophysiology 251-253
in pain relief 120-121 prognosis 263-264
rectal examination I l l ,112 rectal examination 113-114
rectal examination and 6 simple 251-252
standing laparoscopy 47 strangulating 252-253,261
Segmental eosinophilic colitis 296--2 97 surgical correction 254-257
Selenium 221, 222, 393 ultrasonography 29-30,32
toxicity 420 Small intestine
Senecio spp. 389, 390 anatomy and physiology 249-250
Septicemia 496, 497, 507, 518-520 causes of disease 258-262
Septic shock see Distributive shock colic
Seroconversion 414 clinical signs and diagnosis 253-254
Serology,tapeworm infection 53, 57 epidemiology 250-251
Serosal diverticulum 306 foals 477-484
Serosal irritation 159 medical,prognosis 263-264
Serous cysts 518 outcome and prognosis 262-263,
Serum alkaline phosphatase (SAP) 12 483-484
Serum hepatitis see Theiler's disease postoperative management and
Serum protein electrophoresis 57, 372, complications 483
429 risk factors 250-251
Severe combined immunodeficiency surgical,prognosis 262-263
(SCID) 505, 506 see also specific diseases
Sevoflurane 149, 152 edematous 456, 457
Shear mouth 77 exteriorization 161-162
Shock,postoperative 198-204 impaction at anastomosis 215
classification 198-199 malabsorption syndromes 372, 376--380
clinical findings 200-201 maldigestion 372
defined 198 resection
pathophysiology 199-200 anastomosis 255-257
perioperative monitoring 203-204 malabsorption and 377
treatment 201-203 nutritional support and 197-198
Short bowel syndrome 172 viability 164-167, 172-173 , 255
Shunt ligation 515, 516 ultrasonography,foals 4!15-457
Sialadenitis 78 Sodium chloride,as laxative 122
Silent ulcers 470-471 Sodium thiosulfate 420
Silver sulfadiazine 135, 406 Soft palate
Sin usitis 74 anatomy and physiology 79-80
Skin lesions 378 dorsal displacement (DDSP) 65, 66
Siaframine 420, 422-423 repair 85-86
Slurry feeds 197 see also Cleft palate
 INDEX

Sorbitol dehydrogenase 383,384,387, Surgery serodiagnosis 53,57

390,398
Sow mouth 72
Spasmolytics 121-122
Spirurid nematodes 476
Spleen,palpation 7
Splenic biopsy 48
Splenic puncture 14-15,17,18, 19
Squamous cell carcinoma
esophageal 67,96,247-248
gastric 247-248
oral cavity 79
Stallions 148,305,353 see also
Castration
Standardbreds 261,273,377
Standing flank celiotomy 46,47-48,355
Staphylococcus spp. 137
Staples/stapling 172,176,178-179,180,
181,183
Starch tolerance test 21
Stt'nt bandage 183-184
Step mouth 76
Stomach
anatomy and physiology 241-242,
469-470
contracture 472
diseases see specific conditions
endoscopy 24-25,26
radiography 458
ultrasonography 455
Stomach worms 476
Stomatitis 78
Strangulating lesions
large colon 291
peritoneal fluid analysis 18, 19,20
small colon 303-304
small intestine 252-253,260,261
Streptococcus bovis 229
Streptococcus equi 331
Streptococcus zooepidemicus 314
Slress
gastric lesions in foals 471
right dorsal colitis and 440,441
Strongyles,large
biology and lifecycle 54
clinical features of infection 55,56
control programs 58,59
hepatic disease 521
investigations 56-- 57
mixed infections see Strongylosis
pathogenesis 54-55
treatment 57
Strongyles,small see Cyathostomes
Strongyloides westeri 60,508
Strongylosis 436--437
clinical signs 56,436
diagnosis 437
diarrhea and 508
Strongylus edendatus 54,349,521
Strongylus equinus 54,349,521
Strongylus vulgaris 54,55,57,262,273,
436-437
Sub-epiglottic cysts 66
Succinyl choline 150
Sucralfate 192,243, 244,245,419,441
Sugar beet feeds 67,197
Sulfasalazine 442
Summer sores 60
Supraventricular arrhythmias 236, 237
Surface oximetry 166,167
colonic impactions 282
left dorsal displacement of large colon
286--287
pregnant mare and 351,355,356
Surgery,for colic 145-188,254-255,
263-264
anesthesia see Anesthesia,general
approaches to abdomen 155-158,254
flank celiotomy through 17th or
18th rib 157-158,287
other approaches 158
paralumbar flank celiotomy 157-158
preoperative preparation 155
ventral midline celiotomy 155-156,
356
ventral paramedian celiotomy
156--157
closure of abdomen 181-184
incisional protection 183-184
sutures 182-183
duration 263
evaluation of gut viability 164-168, 255
large intestine 164,165,167-168
small intestine 164-167
exploration of abdomen 158-164,254
detailed 159-161
exteriorization of viscera 161-164
initial 158-159
postoperative care see Postoperative
treatment and
complications
prognosis 263-264
repeat laparotomy 184-187
abdominal closure 187
decision 184-185
delayed 186--1 87
procedure and revisions 185-187
survival rates 263
techniques 168-181
anastomosis see Anastomosis
enterotomies 172
intestinal preparation 172
staples 172
sutures see Sutures
Sutures
adhesions and 180-181
auto suturing device 42,43
bite size 183
materials 168
closure of abdomen 182-183
strength 182-183
patterns 168-172, 172,183
sinuses 182,183,218
Swallowing 63-64
difficulties see Dysphagia
Sweating,effects of 138
Sympathomimetics 153
Systemic inflammatory response
syndrome (SIRS) 191-192,200,519
Table,laparoscopy 43,48-49
Tachydysrhythmias 153
Tapeworms
biology and lifecycle 54
colic 56,57,58
control programs 59
in ileal impaction 259
in intussusceptions 273
pathogenesis 54, 55
treatment 57,58
Technetium isotopes 34-37
Teeth
age determination 70-71
deviated 77
eruption time 70
exaggerated transverse ridges 77
retained deciduous 73
table angles 77
tall 76
see also Dental entries
Teflon catheters 135,136
Telazol, 149
Temperature
colic 129-130
indications 4
normal values 109-110
Temporomandibular joint disorders 65
Tension bands,dental 72-73
Tetanus antitoxin 381
Tetrazolium analysis 166--167
Theiler's disease 381-384
clinical signs and diagnosis 381-383
therapy 383-384
Thermodilution technique 151
Thiopental 148-149
Thoracic neoplasia 374,375,376
Thoracotomy 158
Thorax,physical examination 4
Thoroughbreds 221
Thrombophlebitis 137,222-227
clinical signs 224-225
defined 222
pathogenesis 223-224,226
prevention 226-- 227
septic 222,224,225,227
treatment 227
Thrombosis,catheter-related 135,136,
137
Thrombus formation 223
Thromoboembolic arteritis 262,436-- 437
Tiletamine-zolazepam 149
Tirilazad mesylate 194
TNF. 193-194
Tolazoline 147
Tongue lesions 65,66,78,87
Tonicity, determination 140
Tooth root abscess 35
Total nucleated cell count, peritoneal
fluid 16,17,18,19
Total plasma protein (TPP) 11
Total protein
in colic 112
peritoneal fluid 16,17,18,19
Toxic coli tides,and acute diarrhea
417-421
cantharidin toxicosis 417-419
see also Colitis,right dorsal,NSAlDs,
toxicity
Tracheoscopy 65
Traction (true) diverticulum 93,95
Training,videolaparoscopy 45-46
Tranquillizers 359
Transfaunation 431
Transhyoid pharyngotomy 82, 84-85,86,
87
Transport, preparation for 132-134
Trendelenberg position 43, 46,49
Trestle table appearance 108, 109

539
INDEX

Trichomonas equi 444
Trichostrongylus axei 476
Trichothecenes 420
Triclabendazole 521
Triglycerides 395, 396, 397-398, 399, 400,
479
Triodontophorus spp. 54
Tromethamine 154
Tuberculosis, intestinal 377, 378, 423, 443
Tympanitic colic see Colic, distention
Tympany, bowel sounds 4
Typhlectomy 158
Typhlotomy 270-271
Tyzzer's disease 5 1 6-51 7
Ultrasonography 26-34
abdominocentesis and 15, 16
biliary tract disease 387, 388
cecal intussusceptions 274
clinical indications for 29
colic 29, 1 3 1
chronic and recurrent 342
postoperative 33-34
small intestinal obstruction 253
foals 453-454, 454-457, 458, 459-460,
467
colon 457
peritoneum 457
small intestine 457
stomach 455
gastroduodenal ulceration, in foals
472-473
gut viability and 166-167
hemoperitoneum 333
hypovolemic shock 201
inflammatory and infiltrative diseases
30, 32-33
large intestinal lesions 30
in liver failure 392
normal anatomy in 26-28
in peritonitis 327
postoperative peritonitis 229
sand impaction 283
small intestinal lesions 29-30, 456, 457
technique and equipment 26
thrombophlebitis 224-225
transducers 26, 455
weight loss and 29
Umbilical hernias 261 , 452, 478, 479
strangulation 478
Umbilical infection 520
Urea levels 370, 373
Urea nitrogen, peritoneal fluid 16-17
Urine, red discoloration 382
Urogenital examination 327
Uroliths 45
Uroperitoneum 1 7, 321, 461-462
in foals 450, 454
Uterine artery rupture 357-359
Uterine contractions, normal 357
Uterine horn, inversion 360-361
Uterine prolapse 360-361
Uterine rupture 357, 360
Uterine torsion 354-356
Utero-ovarian artery rupture 357, 358
Uterus, dorsoretroflexion 354
Vaccines
Ehrlichia risticii 414, 4 1 5
mutant core polysaccharide 123
R. equi 504
rotavirus 495
Salmonella spp. 499
Vaginal injuries 353
Vascular hyporeactivity 200
Vasculitis, immune-mediated 391
Vasodilators, and laminitis 230
Venous admixture 145, 152, 155
Ventral body wall hernias 321-322
Ventral edema 3 1 7, 320, 321
Ventricular arrhythmias 232-234, 236,
237
Ventricular premature depolarizations
233
Ventricular tachycardia 232, 233-234,
236, 237
Vesicular stomatitis 78
Viability of gut 164-168, 172-173, 185,
255, 377
Video-endoscopy 21-22, 23
Video-fluoroscopy 65
Videolaparoscopy 42, 45-46, 48-49
Vincristine 338
Vinegar 296, 300, 384
Viral diarrhea 493-495
Viral diseases, hepatic 391 , 520-521
Virulence-associated protein A (VapA)
502
Vitamin A 197-198
Vitamin B 196, 197-198
Vitamin E 197-198, 221 , 222, 393
Vitelline duct and arteries 478-479
Volatile fatty acid (VFA) production
267-268
Volvulus
gut viability and 165, 167
large colon 288-290
at parturition 360
non-strangulated 289-290
prevention 291-292
rectal examination 1 1 6-1 1 7
strangulation 291
treatment 290, 291
small colon 303
small intestinal 29, 260, 261
foals 455, 456, 462, 480-481
Volvulus nodosus 261
Walking 120, 206, 329, 357
Water intake 102, 109, 279, 369
Wave mouth 76
Weakness
generalized 220-221
localized 220
overall muscle 220
Weather 102-103, 279
Weight loss 367-380
assessment of body condition 367-368
causes 368, 370-376
chronic inflammatory bowel diseases
372, 379
digestion and absorption problems
371-372, 376
heart disease, chronic 375
infection, low-grade chronic 374
kidney disease, chronic 373
liver disease, chronic 373
neoplasia 374-375
neurological! neuromuscular disease
376
persistent low-grade pain 371
prehension/swallowing difficulties 371
protein-losing enteropathies 373
pulmonary disease, chronic 376
clinical pathology 369-370
cyathostome-associated 55-56, 436
definition 367
differential diagnosis and evaluation
367-376
environmental factors 368-369
gastrointestinal neoplasia 335
nutrition, assessment of 368-369
in right dorsal colitis 439
ultrasonography, indications for 29
White cell count (WBC) 1 1 , 1 1 2
Wooden tongue 78
Wound healing 1 8 1 , 196
Wry nose 80
Xanthine metabolism 104, 105
Xylazine
abdominal pain relief 1 1 9, 120-121
in anesthesia 147-148, 154
in endoscopy 24
postoperative pain 206, 207, 208
sedation 47, 452
side effects 1 2 1
Xylose absorption test 2 1 , 372
Yohimbine 1 24, 147, 2 1 4
Zolazepam 1 49
Zoonotic considerations 410, 507
Z-plasty, double opposing 85

540