Sie sind auf Seite 1von 702

Proceedings

2009

XXVI National CME in Surgery:


SURGERY UPDATE 2009
Department of Surgery,
Maulana Azad Medical College, New Delhi

Foreword
The National Continuing Medical Education Programme in Surgery organized by the
department of Surgery, Maulana Azad Medical College, New Delhi was introduced twenty
six years ago as a weekend programme to update the knowledge of surgeons. Since then it
has blossomed into a six day academic exercise eagerly looked forward to by the surgeons
all over the country and has established itself as the gold standard for Continuing Medical
Education Programmes. This is the only surgical CME that has been organized continuously
for twenty six years. The proceedings, comprising of lectures delivered during the update in
a text form were first introduced and published in 1998 and have become an integral part of
the update since then. This year also it gives us great pleasure to present a book on the
PROCEEDINGS OF THE XXVI NATIONAL CONTINUING MEDICAL EDUCATION
PROGRAMME IN SURGERY, similar to previous years.
Every surgical disorder in the scientific programme has been chosen carefully in the context
of its importance to the attending delegates. All the authors are well- recognized authorities
with a vast personal clinical experience on the particular subject they were chosen to
elaborate. As will be evident from the written texts, they have contributed a very
comprehensive account of the respective topics and are also to be commended for
submitting the latest references at the end of each chapter for ready referral. The quality of
their text reflects their involvement in our programme. A sincere effort has been made to
format the book in a uniform manner without any effort to edit the text provided by the
contributors.
This years programme is a full day comprehensive CME on selected topics of particular
interest to the postgraduate. Emphasis is on subjects with more bearing on their clinical
application. Every years Proceedings can be considered one part of the trilogy of books
which will cover nearly the whole course for the postgraduate student over a three year
period.
We sincerely thank the contributors for their effort. We also wish to thank all the colleagues
in the department for their encouragement and guidance in making this project possible. Our
sincere thanks are also due to the resident staff who worked for procuring, proof reading and
formatting the text. Finally, we must emphasize the contribution of the delegates who have
always given an overwhelming response to our endeavor of bringing out the written text of
our CME programme over the years. We sincerely hope that the Proceedings will meet the
stiff demands of the delegates and serve as a nodal point of learning for the postgraduates.

Dir. Prof. V.K.Ramteke


HOD, Surgery, MAMC & LN Hospital
& Organizing Chairman
SURGERY UPDATE 2009

Prof. A.K. Sarda


Organizing Secretary
SURGERY UPDATE 2009

Index
1. Abdominal tuberculosis Manoj Andley
2. Ulcerative colitis surgical aspects Sandeep Saluja, Saleem Naik
3. Premalignant lesions of the bowel Shaji Thomas
4. Current trends in colon cancer P.N. Agarwal, Gaurav Thami
5. Neonatal intestinal obstruction Satish K. Aggarwal
6. Emergency management in patients with intestinal obstruction
7. Pathophysiology of acute intestinal obstruction Vivek Agrawal, M. K. Joshi
8. Radiological Evaluation of Intestinal Obstruction in Adults Anjali Prakash
9. Complications of intestinal obstruction Nikhil Talwar
10. Advances in the Management of intestinal obstruction in adults Rajdeep Singh
11. Thoracic outlet syndrome Chintamani
12. Vascular grafts Saket Aggarwal
13. Superior mediastinal syndrome Ravi Kanan
14. Vasular surgery (conventional & endovascular) for PVD Sanjay Tyagi
15. Diabetic foot Rajiv Parakh
16. Recent Advances in the Management of chronic arterial insufficiency Pawanindra Lal
17. Critical limb ischemia Arun Gupta
18. Lower limb amputations and rehabilitation Sumit Sural
19. Recent Advances in varicose veins N. S. Hadke, Pankaj K. Garg
20. Deep venous thrombosis Kumud Rai
21. Venous ulcers A. K. Kakar, Pankaj Garg
22. Evaluation of lower extremity veins Rashmi Dixit
23. Carcinoma gall bladder Ravi Kant, Bina Ravi
24. Hepatocellular carcinoma Durgatosh Pandey, Karthikeyan Senniappan, Naveen Sharma
25. Biliary strictures P. K. Mishra, R. Rajesh
26. Choledochal cyst Vijay Arora
27. Causes, presentation and surgical management of obstructive jaundice
Rajneesh K. Singh, Jayanth Rajagopala Reddy, Pankaj Sihag

28. Imaging of obstructive jaundice Poonam Narang


29. Modern imaging in patients with obstructive jaundice
30. Endoscopic management of obstructive jaundice
31. Recent Advances in the Management of biliary calculi Sushanto Neogi
32. Portal hypertension P. Khanduri
33. Cirrhotic and Non cirrhotic portal hypertension
34. Radiological investigations for portal hypertension Pankaj Tyagi
35. Non surgical management of portal hypertension
36. Surgical management of portal hypertension

37. Retroperitoneal tumours Sanjay Gupta


38. Acute kidney injury in surgical patients: Its management and renal replacement
therapy Rajiv Kohli
39. Varicocele A. K. Sarda
40. Radiological investigations: conventional and advanced in haematuria due to
diseases of the lower urinary tract Alpana Manchanda
41. Recent advances in management of bladder cancer Kim Mammen, Viju J Abraham, S
Ahmad, A Tuli, Y Ghosh

42. Current management of urinary bladder cancer S. K. Jain


43. Radiotherapy in carcinoma urinary bladder Arun K. Rathi, Vikash Kumar
44. Urolithiasia: clinical features and complications V. K. Ramteke, Vivek Wadhwa
45. Imaging of urinary calculi Anju Garg
46. Medical management of urinary calculi N. P. Singh
47. Invasive and non-invasive management of urinary calculi
48. Management strategies for cystitis K. M. Singh
49. Pyonephrosis and perinephric abscess Deepak Ghuliani
50. Paraneoplastic syndromes Anjali Mishra, M. Sabaretnam
51. Retrosternal goiters Amit Agarwal, Pooja Ramakant, Gyan Chand
52. Medullary thyroid cancer
53. Multiple endocrine neoplasia Gaurav Agarwal, Dhalapathy Sadacharan
54. Thyroidal Radioiodide Uptake (RAIU): Diagnostic use
55. Hot solitary thyroid nodule T. K. Thusoo
56. Cold STN - an enigma D. Bhatnagar
57. Multinodular goiter A. K. Kakar, Animesh Singh
58. ATA management guidelines for patients with thyroid nodules
59. Follicular cell malignacies - Work-up of a case K. D. Varma
60. Guidelines for surgical management of WDTC K. D. Varma
61. Recent advances in management of WDTC Chander Bhushan Singh
62. Role of Nuclear Medicine in Diagnosis and Followup of WDTC Ravi Kashyap, Abhinav
Jaimini

63. Complications of thyroid surgery A. K. Sarda


64. Gangrene A. K. Sarda
65. Gas gangrene V. K. Ramteke, Naresh Rao
66. Prostate cancer Madhu S. Agrawal, Himanshu Yadav, Prashant Lavania

Contributors

Abdominal tuberculosis

Advances in the management of intestinal


obstruction in adults
Dr. Rajdeep Singh

Dr. Manoj Andley


Professor of Surgery,
Departmentof Surgery,
LHMC & SK Hospital,
New Delhi

Assistant Professor of Surgery,


Maulana Azad Medical College
& assoc. Lok Nayak Hospital,
New Delhi

Ulcerative colitis surgical aspects


Dr. Sandeep Saluja

Thoracic outlet syndrome


Dr. Chintamani

Asstt. Professor of GI Surgery,


Govind Ballabh Pant Hospital,
New Delhi

Dir. Professor of Surgery,


Maulana Azad Medical College
& assoc. Lok Nayak Hospital,
New Delhi

Premalignant lesions of the bowel


Dr. Shaji Thomas

Vascular grafts
Dr. Saket Aggarwal

Professor of Surgery,
LHMC & SK Hospital,
New Delhi

Assistant Professor,
CTVS, GBP Hospital,
New Delhi

Neonatal intestinal obstruction


Dr. Satish K. Aggarwal

Superior mediastinal syndrome


Dr. Ravi Kanan

Professor of Pediatric Surgery,


Maulana Azad Medical College
& assoc. Lok Nayak Hospital,
New Delhi

Oncological Surgeon,
Silchar,
Assam

Current trends in colon cancer


Dr. P. N. Agarwal

Vascular surgery for PVD


Dr. Sanjay Tyagi

Professor of Surgery,
Maulana Azad Medical College
& assoc. Lok Nayak Hospital,
New Delhi

Professor & Head of Cardiology, Govind Ballabh


Pant Hospital, New Delhi
Diabetic foot
Dr. Rajiv Parakh

Pathophysiology of acute intestinal obstruction


Dr. Vivek Agrawal

Chairman,
Department of Vascular Surgery,
Sir Ganga Ram Hospital,
New Delhi

Professor of Surgery,
UCMS and GTB Hospital,
New Delhi

Recent Advances in the Management of chronic


arterial insufficiency
Dr. Pawanindra Lal

Radiological evaluation of intestinal obstruction in


adults
Dr. Anjali Prakash

Professor of Surgery,
MAM College & Lok Nayak Hospital,
New Delhi

Professor of Radiology,
Maulana Azad Medical College
& Lok Nayak Hospital, New Delhi

Critical limb ischaemia


Dr. Arun Gupta

Complications of intestinal obstruction


Dr. Nikhil Talwar

Professor of Surgery,
UCMS & GTB Hospital,
New Delhi

Specialist, Department of Surgery,


Lok Nayak Hospital,
New Delhi

Lower limb amputations & rehabilitation


Dr. Sumit Sural

Causes, presentation and surgical management of


obstructive jaundice
Dr. Rajneesh K. Singh

Professor of Orthopaedics,
MAM College & Lok Nayak Hospital,
New Delhi

Associate Professor of G.I.Surgery,


S.G.P.G.I., Lucknow

Recent advances in varicose veins


Dr. N. S. Hadke

Imaging of obstructive jaundice


Dr. Poonam Narang

Professor of Surgery,
Maulana Azad Medical College
& assoc. Lok Nayak Hospital,
New Delhi

Professor of Radiology,
Govind Ballabh Pant Hospital,
New Delhi
Portal hypertension
Dr. Prakash Khanduri

Deep venous thrombosis


Dr. Kumud Rai

Head of Surgery,
St. Stephens Hospital,
New Delhi

Director, Vascular Surgery,


Max Heart & Vascular Institute,
New Delhi

Radiological investigations for portal hypertension


Dr. Pankaj Tyagi

Venous ulcers
Multinodular goiter
Dr. A. K. Kakar

Associate Professor,
Gastroenterology,
PGIMER, RML Hospital
New Delhi

Dir. Professor of Surgery,


MAM College & Lok Nayak Hospital,
New Delhi

Recent advances in the management of biliary


calculi
Dr. Sushanto Neogi

Evaluation of lower limb veins


Dr. Rashmi Dixit
Professor of Radiology,
MAM College & Lok Nayak Hospital,
New Delhi

Assistant Professor of Surgery,


Maulana Azad Medical College
& assoc. Lok Nayak Hospital,
New Delhi

Carcinoma gall bladder


Dr. Ravi Kant

Retroperitoneal tumours
Dr. Sanjay Gupta

Formerly Professor of Surgery,


Maulana Azad Medical College
& assoc. Lok Nayak Hospital,
New Delhi

Professor of Surgery,
UCMS & GTB Hospital,
New Delhi

Hepaatocellular carcinoma
Dr. Durgatosh Pandey

Acute kidney injury in surgical patients: Its


management and renal replacement therapy
Dr. Rajiv Kohli

Assistant Professor of Surgical Oncology, Institute


of Medical Sciences, Banaras Hindu University,
Varanasi

Consultant, Dialysis Unit,


Lok Nayak Hospital,
New Delhi

Biliary strictures
Dr. P. K. Mishra

Varicocele
Complications of thyroid surgery
Gangrene
Dr. A. K. Sarda

Associate Professor,
G.I. Surgery,
Govind Ballabh Pant Hospital,
New Delhi

Professor of Surgery,
MAM College & Lok Nayak Hospital,
New Delhi

Choledochal cyst
Dr. Vijay Arora

Radiological investigations: conventional and


advanced in haematuria due to diseases of the
lower urinary tract
Dr. Alpana Manchanda

Surgeon Incharge, Colorectal Clinic & Chairman,


Department of General Surgery, Sir Ganga Ram
Hospital, New Delhi

Professor of Radiology,
MAM College & Lok Nayak Hospital, New Delhi
6

Recent advances in the management of bladder


cancer
Dr. Kim Mammen

Retrosternal goitres
Dr. Amit Agarwal
Additional Professor,
Endocrine Surgery,
S.G.P.G.I.,
Lucknow

Professor & Head of Urology, Christian Medical


College & Hospital, Ludhiana
Current management of urinary bladder cancer
Dr. Sudhir K. Jain

Multiple endocrine neoplasia


Dr. Gaurav Agarwal

Professor of Surgery,
MAM College & Lok Nayak Hospital,
New Delhi

Additional Professor,
Endocrine Surgery,
S.G.P.G.I.,
Lucknow

Radiotherapy in carcinoma urinary bladder


Dr. Arun K. Rathi

Hot solitary thyroid nodule


Dr. T. K. Thusoo

Professor of Radiotherapy,
Maulana Azad Medical College
& assoc. Lok Nayak Hospital,
New Delhi

Director,
Dept. of General & Endocrine Surgery, Max
Healthcare,
New Delhi

Urolithiasis: clinical features and complications


Gas gangrene
Dr. V. K. Ramteke

Cold STN an enigma


Dr. Dinesh Bhatnagar

Dir. Professor & Head of Surgery,


Maulana Azad Medical College
& assoc. Lok Nayak Hospital,
New Delhi

Professor & Head of Surgery,


Vardhman Mahavir Medical College
& Safdarjung Hospital,
New Delhi

Imaging of urinary calculi


Dr. Anju Garg

Follicular cell malignacies - Work-up of a case


Guidelines for surgical management of WDTC
Dr. K. D. Varma

Professor of Radiology,
MAM College & Lok Nayak Hospital,
New Delhi

ex-Prof & Head, Deptt. of Surgery & Chief, Div. of


Endocrine Surgery and applied Nuclear Med., cum
Medical Suptd. in Chief, King George Medical
College & Hospitals;
presently, visiting Professor,
Vivekanand Institute of Medical Sciences,
Lucknow

Medical management of urinary calculi


Dr. N. P. Singh
Professor of Medicine,
Maulana Azad Medical College,
& assoc. Lok Nayak Hospital,
New Delhi

Recent advances in management of WDTC


Dr. Chander Bhushan Singh

Pyonephrosis and perinephric abscess


Dr. Deepak Ghuliani

Assistant Professor of Surgery,


Maulana Azad Medical College
& assoc. Lok Nayak Hospital,
New Delhi

Assistant Professor of Surgery,


Maulana Azad Medical College,
& assoc. Lok Nayak Hospital,
New Delhi

Role of Nuclear Medicine in Diagnosis and Follow


up of WDTC
Dr. Ravi Kashyap

Paraneoplastic syndrome
Dr. Anjali Mishra

Head, Division of Nuclear Medicine & Medical


Informatics and Additional Director,
INMAS,
Delhi

Assistant Professor,
Endocrine Surgery,
S.G.P.G.I.,
Lucknow

Carcinoma prostate
Dr. M.S. Agrawal
Formerly Professor of Urology,
SN Medical College, Agra
Presently, Consultant Urologist, Agra

Abdominal Tuberculosis
Manoj Andley
Definition
The term abdominal tuberculosis refers to tuberculous infection of the gastrointestinal tract,
mesenteric lymph nodes, peritoneum and omentum, and of solid organs related to the gastrointestinal
tract such as the liver and spleen. Other forms of intra- abdominal tuberculosis, such as of the kidney,
urinary tract and genital organs, constitute a different entity and will not be discussed in this section.

Various pathological forms of abdominal tuberculosis


I. Peritoneal tuberculosisacute or chronic
A. Tuberculosis of the peritoneumchronic form
(i) Wet or ascitic type:
Generalized
Localized (loculated)
(ii) Dry or fibrous type:
Adhesive type
Plastic type
Miliary nodule type
B. Tuberculosis of peritoneal folds and contents
Mesenteric adenitis
Mesenteric cysts
Mesenteric abscesses
Bowel adhesions
Rolled-up omentum
II. Gastrointestinal tuberculosis
Ulcerative
Hypertrophic or hyperplastic
Sclerotic or fibrotic
III. Tuberculosisof solid viscera (e.g. liver and spleen)

Epidemiology
Starting from the mid-1980s a resurgence of tuberculosis occurred, due to a large extent to the
epidemic of acquired immune deficiency disease .Intestinal tuberculosis is seen more frequently in
people of poor socioeconomic circumstances. Its incidence is higher in patients with
caseopneumonic and advanced lung disease than in those with fibrotic lesions and early disease.

The frequency of extrapulmonary tuberculosis has increased, largely an influence of human


immunodeficiency virus (HIV) infection; over 50 per cent of individuals with HIV and tuberculosis
develop extrapulmonary disease compared to 10 to 15 per cent in those without HIV. Finally,
there is a marked increase in the emergence of multidrug-resistant M. tuberculosis organisms, a
cause of much concern for the global control of tuberculosis.

Microbiology
Mycobacterium tuberculosis is responsible for nearly all cases of abdominal tuberculosis. Other
pathogenic organisms such as M. bovis have been largely eliminated by public-health measures
and are rarely encountered today. Several other atypical or anonymous mycobacteria whose
pathogenicity is not yet established have been identified.

Routes of infection and pathogenesis


Mycobacterium tuberculosis spreads to the abdomen by several routes. Ingestion of contaminated
food may cause primary intestinal tuberculosis; this route of infection has decreased in recent
years. Secondary intestinal disease arises from swallowed sputum containing tuberculous bacilli; it
is influenced by the virulence and quantity of the bacilli, and by host resistance to the infection.
The peritoneum, mesenteric nodes, and the intestine may become infected during the bacteraemic
phase that may follow primary pulmonary tuberculosis. Mycobacteria may also spread from
diseased adjacent organs, such as the fallopian tubes. When the intestines become infected by
lymphatic spread from the mesenteric lymph nodes, the nodal disease is considered as the
primary site and intestinal involvement is secondary. This conclusion is supported by the
observation that the earliest intestinal lesions are found in the submucosal layer, while the
overlying mucosa is normal. In addition, more advanced abnormalities such as caseation necrosis
are found in the mesenteric nodes rather than in the intestine. The bacteria may also be
disseminated in the bile, since they are sequestrated and excreted from granulomas in the liver.

Sites of intestinal involvement


The terminal ileum and ileocaecal junction are involved most frequently. The other regions affected
in order of decreasing frequency are: colon, jejunum, rectum and anal canal, duodenum, stomach,
and oesophagus. The site of predilection is dictated by factors such as the abundance of lymphoid
tissue, the rate of absorption of the intestinal contents, prolonged stasis, which provides longer
time of contact with the mucosa, and the digestive activity of the intestinal contents.

PATHOLOGY
Intestinal tuberculosis
Ulcerative lesions
Tuberculous intestinal ulcers are usually deep and are transversely placed in the direction of the
lymphatics. Multiple ulcers may be seen, most often in the terminal ileum. Disease progression is
associated with the appearance of an inflammatory mass around the bowel. The diseased part of
9

the gut becomes thickened and the serosal surface is studded with tubercles. There is often a
marked increase in mesenteric fat, with fat wrapping around the bowel loops. The regional nodes
become enlarged and may caseate, leading to mesenteric abscess formation. Bowel perforation is
rare, and is usually confined by the perilesional inflammatory mass.
Hyperplastic lesions
In the hyperplastic form of intestinal tuberculosis, a fibroblastic reaction occurs in the submucosa
and subserosa, resulting in marked thickening of the bowel wall; this, together with involvement of
the adjacent mesentery, lymph nodes, and the omentum, results in the formation of a mass lesion.
Hyperplastic lesions are believed to be the result of reduced bacterial virulence and increased host
resistance.
Sclerotic lesions
The sclerotic variety is associated with strictures of the intestine, typically described as 'napkin-ring
strictures', which may be single or multiple. When multiple, the strictures may occur in a short
segment of the bowel or over the entire length of the intestine. Enteroliths can form proximal to the
stricture. In some patients a combination of the different pathological forms may be seen.

Peritoneal tuberculosis
Acute peritonitis
Acute tuberculous peritonitis is extremely rare and is encountered under the following
circumstances: in the miliary phase of the disease, on perforation of intestinal disease, and with
local dissemination from a ruptured, caseating mesenteric lymph node.
Chronic peritonitis
The chronic form of tuberculous peritonitis is much more common and typically presents as
ascites. The fluid is usually clear and straw coloured, but may be sanguinous. Peritoneal
adhesions that range from thin and flimsy to dense and thick may occur. In the presence of
adhesions the ascitic fluid may become loculated, presenting as a localized cyst. The
characteristic lesions are miliary nodules. When the nodules increase in size and coalesce, plastic
adhesions develop, which may completely obliterate the peritoneal cavity, forming an abdominal
cocoon that may encase the intestines. The omentum thickens to form a transversely placed
mass, the so-called rolled-up omentum.

HISTOPATHOLOGY
The typical histological feature of tuberculosis is the caseating granuloma, which may become large
and confluent; these are seen in all diseased areas including the bowel, mesenteric nodes, and
peritoneum. The granulomas have a peripheral zone of lymphocytes, plasma cells, and Langhans
giant cells with a central area of necrosis. Healing of the granulomas is associated with mucosal
regeneration.

10

CLINICAL FEATURES
Abdominal tuberculosis is seen most frequently in patients between the ages of 30 and 50 years.
Females outnumber males by 2:1. The onset of illness is usually insidious, and the initial
symptoms are often vague and non-specific; this is particularly true of peritoneal tuberculosis. As
the disease progresses the individual may develop fever, which is present in two-thirds of the
patients, night sweats, malaise, weakness, anorexia, and weight loss. The appearance of specific
symptoms depends upon the predominant site of involvement.
Peritoneal tuberculosis: Tuberculous peritonitis usually presents with ascites. Less frequently,
fluid collection is mild but the fibrotic component is more prominent, resulting in thickening of
the peritoneum with adhesions, fluid loculation, and the classic 'doughy feel' of the
abdomen. Patients with peritoneal tuberculosis, especially women, often have coexisting
tuberculosis of the pelvic organs, since the genital tract is frequently the portal of entry of the
tubercle bacillus. This point is worth remembering, since a good pelvic examination and
endometrial biopsy may provide the simplest method of confirming the diagnosis.

Gastrointestinal tuberculosis: The most common presentation in patients with disease of the
gastro-intestinal tract is abdominal pain. The pain may be dull and vague, but when colicky it
suggests intestinal obstruction. In such patients the pain is often exacerbated by eating and
relieved by vomiting, but only transiently as it soon recurs. Diarrhoea is another common
symptom in patients with intestinal involvement. The stools may be watery, small in amount,
and mixed with blood when the disease affects predominantly the colon. In primary smallbowel disease the stools are large in amount, foul smelling, and resemble those seen in
patients with malabsorption. Other symptoms include flatulence, nausea, altered bowel
habit, and borborygmi. Abdominal distension suggests the presence of ascites or persistent
subacute intestinal obstruction. Typical duodenal ulcer-like pain may occur when the
duodenum

is

involved.Other

symptoms

may

include

weight

loss,fever,anorexia,

amenorrhoea and pulmonary symptoms.

Physical examination
Patients with chronic abdominal tuberculosis are often malnourished and anaemic. In some the
abdomen may be completely normal on examination, but most demonstrate some abnormal
findings. There may be visible peristalsis and the distended bowel loops can be palpated. The
abdomen may show diffuse distension and tenderness, or the signs may be more localized,
usually in the right lower quadrant. An ileocaecal mass may be felt in the right iliac fossa or
higher up in the right lumbar region. A 'doughy' abdomen suggesting peritoneal disease has
become less common in recent years. A rolled-up omentum, when present, is felt as a
transversely place mass in the epigastric region. Loculated ascites, mesenteric cysts, and
mesenteric abscesses present as cystic masses.

11

Patients with ascites may have shifting dullness and a fluid thrill. In patients with large-bowel
disease a diffusely thickened and tender colon may be felt. Other findings include
hepatosplenomegaly, pelvic abnormalities mimicking gynaecological tumours, and features of
gastric-outlet obstruction due to direct involvement of the stomach or extrinsic compression of
the duodenum by enlarged mesenteric lymph nodes. Rectal examination may reveal anal
fistulas, fissures, or stricture.

Complications: Intestinal obstruction and malabsorption are the most frequent complications.
Much less common are bowel perforation and massive gastrointestinal haemorrhage.
Perforation is usually confined, owing to the presence of surrounding adhesions; as a result,
signs of free perforation of the bowel are rarely seen. Acute bleeding from the rectum or
haematemesis are rare, but can occasionally be severe and life threatening. Fistulas, both
internal between adjacent bowel loops or with other hollow organs (uterus, vagina), and
external to the skin, are described but are rare.

DIAGNOSIS
Since the discovery of the tubercle bacillus it has been possible to make a precise diagnosis of
tuberculosis. However, in patients with abdominal tuberculosis the causative organism is often difficult
to identify and the diagnosis is generally made by indirect methods.

Laboratory tests
The most common abnormality on routine blood tests is an elevated erythrocyte sedimentation
rate, found in over 90 per cent of patients. Other abnormalities include varying degrees of anaemia
and leucopenia with relative lymphocytosis. A positive tuberculin skin test (Mantoux test) is an
excellent screening test in non-endemic countries, but is of little use in endemic countries because
of high rates of positivity in healthy individuals and in those who have received the bacillus
CalmetteGurin (BCG) inoculation.
Analysis of ascitic fluid
Routine tests
The ascitic fluid has a high white blood-cell count, with a predominantly lymphocytic response.
3

A total white-cell count of 500/mm or more has a sensitivity of 81 per cent, a specificity of
48 per cent, and a diagnostic accuracy of 46 per cent for tuberculosis. If a high count is
associated with a predominantly non-polymorphonuclear response, the specificity and
accuracy improve to 82 per cent and 78 per cent, respectively. The diagnostic usefulness of
the white-cell count is reduced in the presence of coexisting conditions such as cirrhosis and
HIV infection, both of which are associated with an increased incidence of abdominal
tuberculosis. In patients with cirrhosis and AIDS the response of white cells is poor and the
total white blood-cell count is often within the normal range.

12

Another characteristic of tuberculous ascites is high total protein, usually 2.5 g/dl or more, and
the serum/ascitic fluid albumin gradient (SAAG) is less than 1.1. However, high total protein is
seen in several conditions, and the sensitivity, specificity, and diagnostic accuracy of this test
for tuberculosis are only 65, 78, and 74 per cent, respectively. As with the white blood-cell
count, the protein content of ascitic fluid in cirrhotic patients with peritoneal tuberculosis is
significantly lower; the concentration is less than 2.5 g/dl in 30 to 50 per cent of patients, and
the SAAG is highly variable. Other biochemical tests, such as lactate dehydrogenase
(elevated to over 90 units/l), low pH, and an ascitic fluid:blood glucose ratio of less than 0.96,
are usually positive in tuberculous ascites, but these tests are non-specific and of little
diagnostic value.

Adenosine deaminase: Lately, adenosine deaminase (ADA) in ascitic fluid has received much
attention. ADA is an enzyme present in several cell types including macrophages,
lymphocytes, and erythrocytes. Its concentration in body fluids correlates with the number and
degree of stimulation of lymphocytes, and is a marker of host immune response. Several
studies have shown that ADA activity is an extremely useful diagnostic test for tuberculous
ascites, with specificity and sensitivity of over 95 per cent. However, in the presence of
cirrhosis, seen in more than 50 per cent of patients with peritoneal tuberculosis in the West,
the sensitivity of ADA drops to 30 per cent; this is related to the abnormal T-lymphocyte
activation and proliferation in those with cirrhosis. For similar reasons, ADA activity is likely to
be less useful in HIV-positive patients, limiting the effectiveness of this test in subgroups of
patients who are highly susceptible to tuberculosis. However, in those without these
predisposing conditions, ADA is extremely useful and should be a first-line investigation,
obviating the need for more invasive and expensive diagnostic tests. Another test that may
-lymphocytes) in the ascitic fluid.

Bacterial isolation and culture: Positive identification of M. tuberculosis provides the definitive
diagnosis of tuberculosis. Acid-fast smears prepared from ascitic fluid have an extremely low
yield, with positive results in fewer than 5 per cent of patients. Culture of ascitic fluid for M.
tuberculosis is more useful and is positive in 20 to 45 per cent of patients. An important
disadvantage of culture is that the results take 4 to 6 weeks, which severely limits the clinical
usefulness of the test. While awaiting the results of culture, antituberculosis treatment should
be started, which can be modified later based on drug-sensitivity findings.

Laparoscopy and peritoneal biopsy: Blind needle biopsy of the peritoneum can be performed in the
presence of ascites using special needles (Abrams' or Cope's). Most workers note a low
complication rate, but fatality has been reported. The main risk of blind biopsy is bowel perforation,
particularly in patients with adhesions between bowel loops and the anterior abdominal wall. Open
biopsy of parietal peritoneum under local anaesthesia is much safer. A less traumatic and more
useful approach is to obtain targeted biopsy specimens from diseased areas such as enlarged
13

lymph nodes under ultrasonographic or computed tomographic (CT) guidance. The single most
sensitive diagnostic test is laparoscopic examination of the peritoneum. The peritoneal lining loses
its smooth, glistening appearance and becomes rough, irregular and dull. The characteristic
finding, as described above, is the presence of miliary tubercles. In addition, fibrous adhesions
ranging from tiny filaments to thick bands may be seen. Ascitic fluid, if present, should be sent for
biochemical analysis and culture. Targeted biopsy specimens should be obtained, preferably from
the miliary tubercles. Peritoneal biopsy should be performed even if peritoneal nodules are not
seen; histological examination shows caseating granulomas in nearly 90 per cent of patients. The
combination of the distinctive visual and histological appearances accurately identifies nearly all
patients. However, positive identification of M. tuberculosis histologically or by culture is made in
only one-half of the patients. The complication rate of laparoscopy is low (less than 5 per cent) but
care should be taken in the presence of adhesions. This procedure is especially rewarding in
patients with AIDS and cirrhosis, because of a much broader differential diagnosis of ascites and
the poor sensitivity of the other tests.

Imaging studies
Plain radiographs: may show calcification of the mesenteric lymph nodes and calcified
granulomas in the spleen, liver or pancreas, but these findings do not imply active disease.
Patients in intestinal obstruction may show dilated bowel loops and airfluid levels. An
abnormal chest radiograph indicating pulmonary tuberculosis helps in the differential diagnosis
but is seen in fewer than 50 per cent of patients with gastrointestinal disease.
Ultrasonography: Several ultrasonographic findings have been described. The peritoneum
assumes a thickened, irregular, echo-poor, sheet-like or nodular appearance. Ultrasound is
very sensitive in detecting small quantities of fluid. Because of their small size, peritoneal
nodules are rarely detected, but are better visualized in the presence of ascites and appear as
tiny, echo-poor deposits. A characteristic finding is the presence of alternating echogenic and
echo-free layers produced by the bowel wall, the serosa, and the adjacent bowel loop with
interloop fluid collections; this is termed the 'club sandwich' appearance. In addition, isolated or
matted enlarged lymph nodes, with hypoechoic or anechoic centres caused by caseation
necrosis, may be seen.
Computed tomography: Similar findings as noted on ultrasound, but with better definition and
resolution, are seen with the CT scan. The ascitic fluid has high-density appearances because
of its elevated protein content. The thickening and nodularity of the peritoneum and mesentery
can be more easily identified with CT than ultrasonography. In patients with intestinal disease
there is thickening of the bowel wall and of the ileocaecal valve. The ultrasound and CT
findings, although fairly characteristic, are not pathognomonic of abdominal tuberculosis.
Similar appearances can be seen in other diseases such as lymphoma, metastatic carcinoma,
peritoneal mesothelioma, and pseudomyxoma peritonei.
Barium studies: Barium studies provide useful information on the extent and severity of the
intestinal disease. The earliest abnormalities include altered bowel motility, and irregularity and
14

thickening of the mucosal folds. Barium swallow may show compression of the oesophagus by
a mediastinal node, with or without mucosal ulceration. In patients with more advanced
disease, mucosal ulcers, deformity of the bowel lumen, and stricture formation are noted.
Rarely, sinus tracts and fistulas may be seen. Thickening of the ileocaecal valve, a wide-open
valve accompanied by narrowing of the terminal ileum (Fleischner sign), and a fibrotic terminal
ileum opening into a contracted caecum (Sterlin sign) are characteristic of intestinal
tuberculosis.
Enteroclysis (small-bowel enema) is generally considered the ideal method of assessing the
small bowel. This technique involves passing a tube into the distal duodenum, which greatly
reduces enthusiasm for the test, both by the radiologist and the patient. Most radiologists
therefore prefer the use of small-bowel series. The regular 20 per cent wt/vol barium mixture
has a high density, which often prevents proper examination of overlapping bowel loops. Lowdensity barium preparations (13 per cent wt/vol) containing methylcellulose have been
introduced in the belief that they permit better dispersion of a barium that is less prone to
flocculation and has greater transradiancy, allowing a 'see-through' effect with good
visualization of overlying loops. Whether these preparations are indeed better remains to be
confirmed. For the large bowel the study of choice is aircontrast barium enema.

Overall, barium studies have a low sensitivity and are abnormal in only about 60 per cent of
patients with endoscopically proven disease. A rapid transit and lack of barium retention may
occur in inflamed segments of the small bowel, resulting in false-negative results. Moreover, the
barium abnormalities are non-specific and can be mimicked by other conditions such as
Crohn's disease and lymphoma.

Endoscopy with biopsy


Fibreoptic endoscopes have made it possible to visualize directly the gastrointestinal tract. The
ileocaecal region can be accessed easily by colonoscopy, and the use of enteroscopes allows
examination of the proximal small bowel. The usual endoscopic findings are mucosal ulcerations,
nodularity, deformity, narrowing, and stricture of the bowel. Rarely, there is diffuse disease of the
colon with hyperaemia and friability of the mucosa, mimicking ulcerative colitis. The endoscopic
abnormalities in tuberculosis can be mistaken for Crohn's disease. Ulcers seen in tuberculosis are
usually transversely located and have sharply defined margins with the surrounding mucosa
showing erythema, while in Crohn's disease the ulcers are serpiginous, often longitudinal, with a
relatively normal surrounding mucosa.

15

Features differentiating intestinal tuberculosis from Crohn's disease


Features

Tuberculosis

Crohn's disease

Intestinal ulcers

Transverse; any location

Longitudinal; mesenteric border

Serosal miliary nodules Numerous

Rare

Perforation

Confined and rare

Rare

Fibrosis

Common

Uncommon

Stricture

Short (< 3 cm)

Usually long

Abscess and fistulas

Uncommon

Common

Granulomas

Many, large, well defined Few

Caseation

Usually present

Submucosa

Oedematous and widened Reduced or obliterated

Hyalinization

Common

Absent

Rare

Biopsy specimens obtained at endoscopy show granulomas and epithelioid cells in 40 to 74 per
cent of patients with intestinal tuberculosis. However, confirmatory findings of caseation necrosis
are present in only 8 to 21 per cent, acid-fast bacilli are observed infrequently, and positive
cultures are obtained in only 6 to 40 per cent of patients. Although endoscopy provides a definitive
diagnosis in only about one-third of the patients, it is very useful in excluding other conditions such
as lymphoma, carcinoma, and caecal amoeboma.

Serological studies
Because of the difficulty in identifying M. tuberculosis in tissue material, a sensitive and specific
serological test should be very helpful. Infection with M. tuberculosis stimulates a cell-mediated as
well as a humoral immune response. The tuberculin skin test is a manifestation of the cellmediated immune response. Serological tests based on the detection of specific antibodies to M.
tuberculosis have been under investigation for several years. Mycobacterium tuberculosis has a
complex structure and contains numerous antigens that cross-react with each other as well as with
antigens of other mycobacterial species. Enzyme-linked immunosorbent assays based on the use
of one of several bacterial antigenic preparations are commercially available, but they provide
sensitivity, specificity, and diagnostic accuracy of only 80 per cent, and moreover are unable to
identify clearly (a) active disease from dormant infection, (b) M. tuberculosis infection from other
mycobacterial infections, and (c) individuals with previous BCG inoculation.

Polymerase chain reaction


The low positive identification rate for M. tuberculosis in intestinal tuberculosis is related to the
presence of small numbers of organisms in the tissues. By amplifying tiny quantities of DNA and
RNA, the polymerase chain reaction is thus ideally suited for this condition. The technique has
been used in a variety of clinical specimens including sputum, cerebrospinal fluid, pleural and
16

peritoneal fluids, and biopsy tissues, with sensitivity, specificity and positive predictivity of 85, 99,
and 95 per cent, respectively. Based on studies with pulmonary secretions, the polymerase chain
reaction can detect as few as 50 organisms per reaction, which is at least fivefold below the lower
limit of detection by culture. The technique has also been successfully used on endoscopically
obtained biopsy specimens but much more work is required before it can be recommended for
routine use.

TREATMENT
Medical treatment
The treatment of abdominal tuberculosis is primarily medical. Since acid-fast bacilli and caseation
necrosis are seen in a minority of patients, and culture results take several weeks, empirical
antituberculous chemotherapy should be initiated in every patient with suspected tuberculosis.
Different regimens of antituberculosis chemotherapy
Regimens

Drugs

I. Standard therapy

Streptomycin 1520 mg/kg per day IM


Ethambutol

Dosage form

25 mg/kg per day


2 weeks
15 mg/kg/day
1218 months

Isoniazid

710 mg/kg per day


1218 months

Rifampicin

10 mg/kg per day


6 months

II. Short-term therapy*

Pyrazinamide 1.5 g/day 2 months


Isoniazid

300 mg/day 6 months

Rifampicin

450 mg/day 6 months

III. Directly observed therapy* Pyrazinamide 1.5 g/day 2 months


Isoniazid

300 mg/day 2 months


600 mg/BIW 4 months

Rifampicin

450 mg/day 2 months


600 mg/BIW 4 months

IM, intramuscular; BIW, twice weekly.


* In high-resistance areas a fourth drug, ethambutol 25 mg/kg per day 2 months or streptomycin
0.75 g/day intramuscular 2 months, is added.

17

Standard therapy: Until recently, the usual antituberculous treatment consisted of streptomycin
(1520 mg/kg body wt) intramuscularly daily for 2 months, isoniazid (710 mg/kg) orally daily
for 12 to 18 months, and rifampicin (10 mg/kg) orally daily or ethambutol (25 mg/kg for 2 weeks,
followed by 15 mg/kg) orally daily for 12 to 18 months.

Short-term therapy: The current guidelines put forward by the World Health Organization and the
United States Centers for Disease Control recommend a much shorter course of therapy. The
initial treatment consists of a three-drug regimen of isoniazid (300 mg), rifampicin (450 mg), and
pyrazinamide (1.5 g) in countries where the resistance rate to isoniazid is below 4 per cent. In
countries with higher drug-resistance rates, a fourth drug is added, ethambutol (25 mg/kg) or
streptomycin (1 g). All drugs are administered daily for 2 months, after which the patient is
switched to two drugs: isoniazid 300 mg/day and rifampicin 450 mg/day for 4 months.

Directly observed therapy: If facilities for directly observed therapy are available, initial treatment
is the same as in short-term therapy, but after 2 months patients are started on a twice-a-week
regimen consisting of isoniazid (600 mg/day) and rifampicin (600 mg/day) for 4 months. Thus,
the total length of treatment for both short-term and directly observed therapies is 6 months.

Comment
Although these guidelines are based on studies in pulmonary tuberculosis, there is no evidence
that patients with abdominal tuberculosis require longer therapy. Patients should be monitored
every 4 to 6 weeks for drug-related side-effects. Isoniazid should be discontinued if the liver
enzymes (alanine and aspartate amino-transferases) increase threefold over baseline. It is
advisable to administer pyridoxine hydrochloride (510 mg/day) to all patients to prevent isoniazidinduced peripheral neuropathy. If a coexisting open pulmonary lesion is present, the patient should
be isolated for 2 weeks. If not, the patient may be treated at home.

Response to treatment
The clinical response to treatment is excellent. Systemic symptoms such as fever, malaise, and
weight loss subside in a few weeks. Mucosal abnormalities take longer, but follow-up barium
studies and endoscopy demonstrate regression of the lesions in most individuals. The majority of
patients (approx. 70 per cent) with symptoms of subacute bowel obstruction and evidence of
intestinal stricture show complete resolution of the radiological abnormality.

Antituberculosis-drug resistance
Multidrug-resistant M tuberculosis received little attention until the early 1990s when several
outbreaks were reported in patients with HIV. In 1994, the World Health Organization initiated
global surveillance for antituberculosis-drug resistance in 35 countries and results of the first
4 years (19941997) of this project were recently published. Among patients with no prior
18

treatment, a median of 9.9 per cent (range 241 per cent) were resistant to at least one drug and
multidrug resistance was seen in 1.4 per cent (014.4 per cent). The resistance rates to individual
drugs were: isoniazid 7.3 per cent, streptomycin 6.5 per cent, rifampicin 1.8 per cent, and
ethambutol 1 per cent. Much higher rates of drug resistance were observed in patients with history
of previous antituberculous treatment.
Drug resistance is a major threat to tuberculosis control programmes worldwide. Patients with
resistant strains are less likely to be cured, and the treatment is more expensive and more toxic
than in those with susceptible organisms. Multidrug resistance occurs more frequently in noncompliant patients, in the presence of HIV infection, and in malnourished individuals. The current
emphasis is to create more facilities for directly observed therapy. Studies show that unsupervised
treatment has a drug-completion rate of only 25 to 50 per cent, while directly observed therapy
results in 85 to 90 per cent cure, with relapse rates of only 5 per cent.

Use of corticosteroids
Studies in the 1980s suggested that concomitant use of corticosteroids might decrease the
incidence of adhesions and intestinal obstruction by reducing the deposition of fibrous tissue.
However, the role of corticosteroids in abdominal tuberculosis is uncertain, since no controlled,
randomized trials have been performed. The routine use of steroids is therefore not recommended.

ROLE OF SURGERY
Indications: Surgery is reserved for mechanical complications of tuberculosis or when medical
therapy fails. Emergency surgery is indicated in the presence of acute complications such as
free perforation of the bowel and severe intestinal haemorrhage. The most common indication
for surgery is intestinal obstruction secondary to stricture formation. In these patients, unless
there is complete obstruction, conservative management is advocated. If symptoms persist,
elective surgery is performed at a later stage, with significantly less morbidity. Predictors for
surgical intervention are long strictures (12 cm or more in length) and multiple areas of
involvement. Other indications for surgery are bowel adhesions, intra-abdominal abscess due
to a confined perforation, mesenteric abscess, and internal or external fistulas. Surgery is also
appropriate if the diagnosis is in doubt and when malignancy cannot be ruled out with
reasonable accuracy.

Surgical procedures: Patients presenting with acute bowel perforation should be treated by
resection of the involved segment and primary anastomosis. Simple closure of perforation is
followed by a high incidence of reperforation and fistula formation. Drainage tubes are not
recommended and, if used, should be removed early because of increased risk of
abdominocutaneous fistulas if they are left in place for more than 7 days.

Surgical techniques for patients with bowel obstruction have evolved over time. At one time,
bypass procedures such as ileotransverse colostomy and enteroenterostomy were practised
19

commonly, but have now been abandoned because of complications such as blind-loop
syndrome, malabsorption, and perforation. Similarly, radical bowel resection and extensive
dissection of mesenteric lymph nodes have fallen out of favour because of complications,
including the development of short-bowel syndrome. The order of the day is minimal surgery.
The procedure of choice for an ileocaecal massis limited resection with 5-cm margins from
visibly abnormal tissue in place of the standard right hemicolectomy. Segmental bowel
resection has become rare and is only performed if multiple strictures are located in close
proximity. Most surgeons prefer stricturoplasty for lesions involving the small bowel. Other
procedures advocated are ileocaecoplasty and coloplasty for ileocaecal and colonic strictures,
respectively.

Approach to intestinal adhesions: Intestinal adhesions require a meticulous surgical approach.


In addition to releasing the adhesions, enteric stenting has been found useful in preventing
adhesive bowel obstruction. Patients with florid sepsis may be treated by laparostomy, followed
by secondary abdominal closure once the sepsis is controlled; this prevents recurrent
adhesions and reduces postoperative morbidity and mortality. Patients with enterocutaneous
fistulas are treated by resection of the fistulous tract, drainage of any intra-abdominal abscess,
and intestinal anastomosis. A multicentre, prospective, randomized trial has shown that the
interposition of a barrier film for a sufficient length of time between diseased areas of intestine
contributes to adhesion-free healing. Seprafilm and Interceed are a few of the commercially
available barrier films proved to be effective. Some of these patients may need stenting in
addition to barrier-film placement.

SPECIFIC FORMS OF TUBERCULOSIS


Appendiceal: Tuberculosis of the appendix is reported in 0.1 to 3 per cent of patients with
tuberculosis. Isolated tuberculosis of the appendix is rare. Appendectomy followed by
antituberculosis chemotherapy is the treatment of choice.

Anal canal: Patients with tuberculosis of the anal canal may present with multiple fistulas, fissures, or
perianal abscesses. Treatment consists of drainage of the abscess combined with antituberculous
chemotherapy.

Gastric: Involvement of the stomach is rare, occurring in 0.3 to 2.3 per cent of patients with
pulmonary tuberculosis. The rarity of this location is related to several factors including the
resistance of the gastric mucosa to infection, the lack of lymphoid tissue in the stomach, and the
constant flow of contents through the stomach. Tuberculosis of the stomach presents as an
ulcerative, granulomatous, or fibrosing lesion; the last two types may result in gastric-outlet
obstruction. At endoscopy, the lesion may be mistaken for peptic ulcer disease, gastric carcinoma,
or gastric sarcoidosis. Similar appearances are also seen in syphilis of the stomach. The diagnosis
may be confirmed on endoscopic biopsy specimens.
20

Antituberculous chemotherapy should be initiated in all patients; this is curative in most, especially
those with ulcerative lesions, which can be confirmed on repeat endoscopy and biopsy. Surgical
intervention is required if gastric-outlet obstruction persists despite treatment. The usual surgical
approach is a partial gastric resection such as a Billroth gastrectomy or a sleeve resection. Gastric
cancer presents in a similar fashion, and both tuberculosis and cancer may coexist in the same
patient. Therefore, if there is any doubt about the diagnosis, it is best to proceed with frozensection biopsy followed by surgical resection if indicated.

Liver and spleen: Hepatic tuberculosis has become exceedingly rare these days. The diagnosis is
usually made accidentally during exploratory laparotomy or at autopsy in immunocompromised
patients. The lesions typically are granulomas, with or without central caseating necrosis, calcified
masses, and biliary strictures. Tuberculous periportal lymph nodes may cause obstructive jaundice
by compressing the bile duct. Patients with hepatic tuberculosis usually have hepatomegaly, with
or without jaundice. Symptoms related to abdominal tuberculosis often overshadow those due to
liver disease. Liver enzymes, in particular serum alkaline phosphatase, are usually elevated.
Tuberculosis should be differentiated from other conditions associated with hepatic granulomas
such

as

leprosy,

sarcoidosis,

Hodgkin

disease,

brucellosis,

infectious

mononucleosis,

inflammatory bowel disease, drug-induced liver damage, and syphilis. Chronic active hepatitis may
also mimic tuberculosis of the liver. The treatment of hepatic tuberculosis is chemotherapy. It
should be remembered that most antituberculous drugs (except ethambutol) are hepatotoxic, and
may aggravate the liver damage and worsen the jaundice. These patients therefore should be kept
under close observation during antituberculous chemotherapy.

Splenic tuberculosis is also rare and may present as a splenic abscess or with hypersplenism.
The presence of multiple hypoechoic lesions on ultrasonography of the spleen in a HIV-positive
patient is highly suggestive of disseminated tuberculosis. The diagnosis is usually made following
surgical resection of the diseased spleen.

'Silent' tuberculosis: Subclinical or 'silent' abdominal tuberculosis is seen mainly in patients


belonging to upper socioeconomic groupings in the Third World countries. The onset of illness is
often precipitated by stressful conditions. The patients present with atypical symptoms, resulting in
frequent misdiagnosis. The response to short-term antituberculous drug therapy is excellent.

Abdominal Tuberculosis in childhood: Abdominal tuberculosis in children is seen most frequently


in immunosuppressed individuals and in those who have not been vaccinated with BCG. Clinically,
weight loss and malaise occur in 95 per cent of these children, followed by abdominal distension
(83 per cent), abdominal pain (79 per cent), and anaemia (76 per cent). Laboratory tests show
leucocytosis and an altered albumin:globulin ratio; pulmonary tuberculosis is see on the chest
radiograph. Imaging studies, including plain radiographs, ultrasonography, CT, and gastrointestinal
21

contrast studies, are helpful in localizing the defect. The diagnosis is confirmed on tissue obtained
by endoscopic biopsy or with echo- or CT-guided fine-needle aspiration; samples may be stained
by the ZiehlNielsen method for acid-fast bacilli, subjected to microbiological culture and drugsensitivity testing, and examined histopathologically. A short course of chemotherapy is an
effective and economical treatment, and is associated with minimal side-effects in children.

HIV and tuberculosis: Abdominal tuberculosis in HIV-infected patients is invariably a manifestation


of disseminated disease and results in significant mortality. Extrapulmonary tuberculosis is seen in
over 50 per cent of patients. Fever, weight loss, lymphadenopathy, and splenic abscesses are
seen more commonly in HIV-infected patients than in those without HIV infection.
The diagnostic techniques are the same as in uninfected individuals and include bacteriological
testing of body fluids, abdominal ultrasound and CT scanning combined with guided-needle
aspiration biopsies, barium examination, fibreoptic endoscopy, and laparoscopy. Serological tests
such as enzyme-linked immunosorbent assay lack sensitivity due to a poor humoral immune
response. Most patients respond well to conventional antituberculous drugs used in standard
doses. Some experts recommend a longer course of therapy (9 months). Despite treatment, a few
patients experience a downhill course, which may be due to drug resistance or the presence of
overwhelming infection.

PROGNOSIS
The prognosis of uncomplicated abdominal tuberculosis is good. Most patients respond well to
medical therapy and the outcome of surgical management of complications is generally good. Bowel
obstruction or perforation associated with plastic adhesions and the development of enterocutaneous
fistulas with intra-abdominal abscesses are associated with increased morbidity and poor prognosis.

GENERAL RECOMMENDATIONS
The main advance in the diagnostic approach to patients with suspected abdominal tuberculosis is
the use of endoscopy. Most patients with peritoneal tuberculosis can be diagnosed by laparoscopy,
since the peritoneal appearances are fairly distinctive and the histological yield is high. If this facility is
not available, adenosine deaminase in ascitic fluid should be assessed because of its high positive
predictive value for tuberculosis, especially in patients without coexisting cirrhosis or HIV infection. In
contrast to peritoneal tuberculosis, the diagnosis of gastrointestinal tuberculosis is more difficult. All
endoscopically accessible lesions should be biopsied and the specimens used for histology, staining
for acid-fast bacilli, and culture. Even if a positive diagnosis of tuberculosis is not made, diseases
such as carcinoma and lymphoma can be excluded. The next step in endemic countries is a
therapeutic trial with antituberculous drugs. The majority of patients, even those with strictures, show
a good response. In the West, where tuberculosis has made a major comeback, the main differential
diagnosis is with Crohn's disease, and the clinical, radiological, and histological features of the two
are often indistinguishable. Here, a specific diagnostic test for M. tuberculosis such as polymerase
chain reaction, may prove extremely helpful.
Index
22

Ulcerative Colitis: Surgical Aspects


Sundeep Singh Saluja, Saleem Naik
Ulcerative colitis (UC) is an inflammatory ulcerating disease of the mucosa of large intestine of
unknown cause. It varies in severity. It is an inflammatory bowel disease that can be cured by surgery.
Although primarily treated by medical management, one third of patients require surgical resection,
1

which most of them undergo within 10 years of initial diagnosis . Till late 1960s, surgical options were
limited to total proctocolectomy with Brooke ileostomy or subtotal colectomy with ileorectal
anastomosis. Later, two other surgical options were developed, continent reservoir ileostomy (kock
2

pouch) and ileal pouch anal anastomosis . The latter one revolutionized the surgical management of
UC and has become the procedure of choice.

INDICATIONS FOR SURGERY


Elective surgery
Approximately 70% of patients undergo surgery for chronic disease. Since there is no clear
demarcation for referring these cases, close consultation between surgeon, gastroenterologist and
patient is necessary to prevent excessive delay in surgical intervention which may affect the
surgical outcome with increased complication rates. The indications for elective surgery are:
a) Failure of medical treatment can be due to following reasons
i) Steroid resistant ulcerative colitis: Response to steroids has been variously defined,
but can be regarded as clinical improvement after treatment with high-dose oral steroids
(40-60 mg prednisone or equivalent) within 30 days, and in severe ulcerative colitis, clinical
3,4

improvement after treatment with high-dose intravenous steroids within 7-10 days .
Conversely, patients who fail to respond to steroids within these timeframes have been
defined as steroid-resistant. It constitutes 20-30% of patient undergoing surgery.
ii) Steroid dependent ulcerative colitis: Patients with ulcerative colitis who require several
courses of systemic steroids in order to achieve remission, but are followed by relapse of
symptoms during steroid tapering or soon after their discontinuation. This pattern of drug
response is known as steroid-dependency. Approximately 20-30 % patients are steroid
3

dependent .
iii) Steroid complicating ulcerative colitis: Complications of long term steroids like
diabetes mellitus, osteoporosis, cataract etc constitutes a subgroup, which require surgical
intervention.
Procedure: These patients may undergo either two-stage or three stage pouch procedure
depending upon their general condition.

b) Cancer or cancer prophylaxis: 10% patients of UC undergo surgery for cancer or


5

dysplasia . The independent risk factors identified include long duration of disease, presence of
pancolitis, associated primary sclerosing cholangitis and early onset of disease. The cumulative
6

probability is estimated to be 3%, 5% and 9% at 15, 20 and 25 years respectively or an


23

increase of 0.5-1% yearly after 8-10 years of duration . Hence, surveillance is recommended
after 8years in patients with pancolitis and 15 years in those with left sided colitis.
8

Procedure: depends on type of lesion

Low grade dysplasia, high grade dysplasia, dysplasia associated lesion or mass
(DALM) and obstructive lesion are treated with restorative proctocolectomy with IPAA.

Malignancy
a) Localized colon cancer: Restorative proctocolectomy, mucosal proctectomy with
IPPA
b) Colon cancer of uncertain stage: Staged colectomy with ileostomy and Hartmann
followed by IPAA (favourable pathology) or permanent ileostomy (unfavourable
pathology).
c) Metastatic or advanced colon cancer: Colectomy with permanent ileostomy and
Hartmann or ileorectal anastomosis.
d) High rectal cancer (early stage): Restorative proctocolectomy, mucosal proctectomy
with IPAA
e) High rectal cancer (advanced stage): Subtotal proctocolectomy with ileostomy with
low Hartmann closure of the rectum followed by adjuvant treatment. If no recurrence
till 2 years, then IPAA can be planned.
f)

Distal rectal cancer: Total proctocolectomy with permanent ileostomy

c) Debilitating extra-intestinal manifestations are very rare independent indication for


surgery. Progressively destructive pyoderma gangrenosum or Coombs positive hemolytic
anemia unresponsive to steroids may rarely necessitate colectomy. Primary sclerosing
cholangitis, ankylosing spondylitis and sacroileitis do not respond to colectomy, while arthritis
and skin lesions respond well.
Procedure: Restorative proctocolectomy, mucosal proctectomy with IPAA

d) Malnutrition and growth retardation are significant problem in pediatric patients which
1

may necessitate colectomy .


9

Emergency surgery

Approximately 20% patients require urgent or emergent surgery for acute complications.
a) Toxic colitis: failure to respond to intensive treatment (nil per oral, intravenous fluids,
10

parenteral steroids and antibiotics) for 3-5 days .


Procedure: subtotal colectomy with Hartmann/ mucous fistula and end ileostomy is procedure of
choice in these patients.

b) Toxic megacolon: It is a variant of toxic colitis with dilatation of colon (transverse colon
diameter 6 cm). Evidence of free perforation or generalized peritonitis is indication for immediate

24

surgery. Septicemia, failure to respond to medical management (24-72hrs) and major colonic
hemorrhage are indications for urgent surgery. Incidence of this complication has decreased.
Procedure: Decompressive blow hole transverse colostomy and diverting loop ileostomy followed
11

by colectomy was considered to be safest procedure in 1960s . With better medical management
(increased awareness and earlier diagnosis of toxic megacolon), recognition of need for early
surgery, better antibiotics and postoperative supportive measures, most of these patients are
12

managed with subtotal colectomy with ileostomy and mucous fistula .

c) Perforation peritonitis: is the most lethal complication and usually occurs in setting of toxic
megacolon. Signs and symptoms may be minimal in these patients as they are on high steroid
doses. Mortality may be as high as 50%.
Procedure: Best managed by subtotal colectomy with ileostomy and mucous fistula

d) Massive hemorrhage: accounts for 10% of all emergency colectomies for UC.
Procedure: Most patients are managed by subtotal colectomy with ileostomy and Hartmanns
procedure. Additional proctectomy is rarely required for stump bleeding.

SURGICAL OPTIONS
While selecting the procedure, following parameters are taken under consideration
i) Age
ii) General Condition
iii) Status of Continence
iv) Patients desire for continence
v) Presence of dysplasia/ carcinoma
vi) Emergency/elective operation
vii) Diagnostic uncertainty

Total Proctocolectomy and Brooke Ileostomy

13

Total proctocolectomy and Brooke ileostomy is the earliest operation performed for UC. It removes
all the diseased mucosa and eliminates the risk of future cancer. As for cure of disease, it still
remains the gold standard. Added advantages include, absence of functional problems associated
witth a ileal-anal pouch. Major drawback of this operation is permanent ileostomy that has poor
social acceptance and causes psychological trauma. It is mostly performed as an elective
procedure
Indications
a) Patients with poor sphincter tone
b) Old patients (> 60 years) who are not good candidates for IPPA
c) Lifestyle related contraindication: keeps away from toilet facility
d) UC with distal rectal cancer

25

Complications
i) Ileostomy related complications
ii) Pelvic dissection related: sepsis, hemorrhage, sexual and urinary dysfunction.
iii) Perineal wound related complications
Overall morbidity is 40%, 30% and 20% for emergency, urgent and elective cases.

Total Proctocolectomy with Continent Ileostomy (Kock pouch)

12,13

To reduce the esthetic appearance of the conventional ileostomy, a continent ileostomy was
developed from terminal ileum by Kock in 1969. This pouch provides internal storage for intestinal
contents and is attached to the abdominal wall with a flush ostomy opening. The patient empties
the pouch 4-6 times a day using a catheter, thereby eliminating the need for external appliance.
The operation was modified by addition of an intestinal nipple valve, using intusscepted ileum. The
procedure has not enjoyed widespread acceptance because of its intricate construction and
relatively high risk of valvular dysfunction, requiring one or more revision procedures. Satisfactory
14

long term function has been reported in two third of patients .


Indications
a) Patient already with permanent ileostomy and wishes to be continent
b) Patients who are poor candidates for IPAA and wish to be continent
c) Those with failed IPAA:
Contraindications
a) Obese patients
b) Psychological unstable patients
Complications
i) Valvular dysfunction: revision rate 20%
ii) Nonspecific reservoir ileitis 10%
iii) Pouch skin and pouch enteric fistula

Subtotal colectomy with ileostomy

15,16

It is the most common procedure in the emergency condition. The principle is to remove most of
the diseased colon and retain rectum for establishing continence later. This avoids the pelvic
dissection in emergency situation and its attendant complications. Patients can recover from the ill
effects of disease and steroid before definitive surgery is planned.
Indications
a) Emergency surgery in UC
b) Indeterminate colitis
c) Patients on long term steroids
d) Patients with significant malnutrition
Contraindication
a) haemodynamically unstable patients, especially toxic megacolon with sepsis

26

Hartmann Vs mucous fistula


Most patients do well with Hartmann procedure. If the bowel is friable then the mucous fistula should
be taken out to avoid pelvis sepsis.

Subtotal colectomy with ileorectal anastomosis

10

Ileorectal anastomosis at the time of subtotal colectomy converts the procedure into a definitive
one. The principle is to remove most of the diseased colon with maintaining anal continence.
Bowel frequency varies from 2-4/day with loose consistency. Another advantage is the pelvic
dissection is avoided in these patients. The major disadvantage of this procedure is that, it retains
rectum which is at risk for a) recurrence of disease b) malignancy (13- 20% after 20-30 years).
These patients require long term surveillance. The major complication is leak, which in elective
setting is <2%.
Indications
a) UC and advanced PSC with portal hypertension
b) UC with advanced colonic malignancy
c) Chronic UC with rectal sparing (rare)
Contraindications
a) During emergency setting as leak rate are high
b) Presence of perianal disease or rectal stricture

Restorative Proctocolectomy
Restorative proctocolectomy has become the procedure of choice for patients with ulcerative
colitis. The principle is to remove the whole of diseased colon and rectum with preservation of the
anal sphincter and hence maintain continence. A pouch is constructed from 2- 4 ileal loops which
increases stool holding capacity and thereby reduces the bowel movements.
Contraindications
a) Patients with poor sphincter tone
b) UC with distal rectal cancer
Relative contraindication
a) Patients > 60 years
b) Lifestyle related contraindication: keeps away from toilet facility

Technical considerations and controversies of IPAA

13,15

Pre operative preparation

Procedure is preceded by careful counseling. If possible, patient should talk to the previously
operated patients, to have realistic expectations.

Site of the ileostomy should be marked

Deep vein thrombosis prophylaxis

Bowel preparation is not given as it may precipitate acute attack.

Steroids should be continued preoperatively


27

Procedure (key points)


Colectomy starts with mobilization of right colon, followed by rest of the colon. Both flexures are
carefully brought down. Ileocolic trunk is preserved while middle colic is tied flush with superior
mesenteric vessels. The omentum is excised along with transverse colon by some as it reduces
17

adhesions in the postoperative period, while others retain it as it limits infection . Terminal
ileum is transected flush with the caecum. Rectal mobilization is carried out along with
mesorectum till the pelvic floor.

Hand sewn vs stapled: In hand sewn anastomosis, rectum is divided 3 cm above the dentate
line. Mucosectomy is carried above dentate line transanally. Ileal pouch is brought through the
rectal cuff and hand sewn anastomosis is completed circumferentially at dentate line. While in
stapled anastomosis rectum is divided 2 cm above the dentate line using linear stapler. The
pouch anal anastomosis is carried out using end to end circular stapler without any
mucosectomy.
Proponents of stapled anastomosis

18

It is technically easier and faster.

It maintains the transitional zone of anal mucosa which may improve neorectal sensation
and continence.

A finite risk of malignancy or disease recurrence still remains as all rectal mucosa is not
eliminated after mucosectomy.

Proponents of hand sewn anastomosis

As it removes the complete rectal mucosa therefore has minimal risk of flare up or
malignancy.

Mucosectomy does not affect the continence.

A recent metaanalysis of 4183 patients shows that stapled IPAA offered improved nocturnal
continence which was reflected in higher physiologic measurement. A risk of increased
19

incidence of dysplasia in stapled group was not statistically significant . Therefore stapled
IPAA is probably better choice except in patients with dysplasia or rectal cancer and patients
with extraintestinal manifestations.

Pouch design: To reduce the bowel frequency, rectum like reservoir was devised from ileum.
2

Parks and Nicholls (1978) described an ileal reservoir in S configuration using 3 loops .
20

Utsunomiya devised a simpler configuration (J pouch) using 2 loops . After a decade of


experimentation with various configuration of pouch (S, J, H and W), the J configuration has
been accepted as standard operative technique. Evidence suggests that pouch compliance
correlates with the length of the intestine used rather than actual design. 30-40 cm of the ileum
is required to achieve the optimal results.
28

Advantages of J pouch: easier to construct, better efficiency of evacuation and excellent fit into
the concavity of sacrum.
W and S pouch have longer length and can be used if J pouch is not reaching down. W pouch
has the poorest results in emptying.
13

Mobility of pouch : Pouch should reach 4-6cm below pubic symphysis without stretching.
Sometime the apex of the pouch may not comfortably reach down. It can occur in tall/obese
patients or in patients who have undergone previous surgeries.
Operative techniques employed to improve the mobility of the pouch are
a) Mobilization of the small bowel mesentery to the third part of duodenum
b) Transverse incisions of the peritoneal layers of the small bowel mesentery. Avoid any
excessive skeletonization of the blood vessels that may result in tearing of blood vessels.
c) Division of either distal ileocolic or branches of superior mesenteric arteries provided an
adequate supply is available through marginal vessels.
d) Preservation of middle colic and its right branch during vascular ligation of colon. The
mesentery of colon with its marginal artery proximal to this point is preserved. With this
maneuver both ileocolic and distal superior mesenteric artery are ligated.
e) Alternative pouch configuration S and W shaped pouch.

Diverting ileostomy: Proponents suggests using a temporary diverting loop ileostomy allows
fecal diversion during early weeks following surgery to allow ileal pouch and ileoanal
anastomosis heal, thereby significantly reduces the post operative complications like pelvic
sepsis and anastomotic dehiscence. The function of the anal sphincter is restored in the resting
phase. Opponents argue that incidence of small bowel obstruction increases with ileostomy. It
adds an extra procedure and thereby increases the hospital stay. It avoids disuse atrophy of
pouch and anal sphincter. Proximal ileostomy may obstruct the marginal artery and lead to
pouch ischemia. Evidence suggests that loop ileostomy may be omitted in selected cases
where patient is on low dose steroids, good general condition and nutritional status and had no
21

technical problems during surgery . Diverting ileostomy does not prevent leak but significantly
reduce complication flowing leak most importantly pelvic sepsis, which is the most important
independent prognostic factor, for pouch function.

Laparoscopic IPAA

22

: It is a difficult procedure involving all four quadrants of abdomen and quite

often a friable colon. Recent reports suggest laparoscopic IPAA is safe and feasible. Surgical
time is much longer than conventional surgery. It is possible in patients who had prior
colectomy. It has been shown to have less pain, adhesions, with improved cosmesis and
fertility rates and better quality of life.

29

Special considerations
Age: most patients undergoing pouch surgery are in thirties and forties. Earlier, age> 55 years was
considered as an absolute contraindication for pouch surgery. Now with increasing experience
older patients with good sphincter function are being offered pouch surgery. However,
increased incidence of nocturnal evacuation and incontinence occur in these patients.
Women: women with active ulcerative have reduced fertility as a result of disease activity and
23

extensive pelvic dissection and IPAA further decreases fecundicity . Therefore consideration
should be given to delayed proctectomy and IPAA reconstruction in child bearing age if it is
safe to do so. Pregnancy itself is safe and most of the patients are able to carry to term. One
third of patients experience transient disturbances in pouch function, mainly during third
trimester and three months following delivery. The type of delivery does not affect the pouch
13

function postpartum. Presence of ileal pouch does not mandate cesarean section .

Complications
Early
a) Small bowel obstruction is the most common complication. The frequency varies from 1126%

24-26

. Three fourths of patients are managed conservatively. The most common site of
27

obstruction is at the ileostomy . Other causes include adhesions, internal hernia, stenosis
and volvulus around the ileostomy.
b) Sepsis occurs in 3-15% patients

24-26

. Causes include a leak of the pouch or pouch anal

anastomosis and contamination of the peritoneal cavity at surgery. In the recent years
incidence of pelvic sepsis has come down.
c) Urinary retention
d) Hemorrhage, deep venous thrombosis and pulmonary embolism are other rare complications.

Late
a) Pouchitis is the most frequent late complication occurring in 10- 28% of patients

24-26

. It is

characterized by fever, abdominal pain and increased stool frequency and urgency with peak
incidence at 18 months after surgery. The key components are sign and symptoms,
endoscopic findings and histology. Most patients have intermittent symptoms and respond
well to metronidazole and ciprofloxacin. Some patients may experience chronic pouchitis that
may ultimately lead to pouch excision.
b) Pouch fistulas occur in 2-8-9.7 % of cases

24-26

. It usually occurs between pouch and perianal

skin or pouch and vagina. Factors that may predispose to these fistula include ischemia of
pouch, leak, inadvertent inclusion of vagina in the anastomotic suture line and crohns
disease. If the fistula occurs early after IPAA it is likely to be secondary to anastomotic leak.
Antibiotics, drainage of associated pelvic abscess and prolonged ileal diversion are required
to manage these patients. They may close spontaneously or persistent fistula may be treated
28

with advancement flaps or pouch reconstruction .

30

29

c) Pouch failure: it occurs in about 5-20% of patients . Causes of pouch failure include pelvic
sepsis, anastomotic stricture, fistula, pouchitis, poor functional result or crohns disease.
Pelvic sepsis and anastomotic failure are the main and often interrelated cause of pouch
30

31

failure . Pouch salvage surgery with reanastomosis may be successful in about 60% cases .

d) Sexual and urinary dysfunction

Long term functional results and quality of life


Functional results after IPAA improve during the first year. Initial frequency of 8-10 stools per day
improves to 4-6 stools per day at 1 year. Factors associated with slightly worse pouch function
include age greater than 50, presence of extra-intestinal manifestations, anastomotic strictures and
pouchitis. Overall patients are not bothered by minor degree of incontinence and 93% patients
24

reported an excellent quality of life . Several studies have shown better quality of life in patients
32

with IPAA than in medically treated patients or patients with TPC and permanent ileostomy .

Summary
Although since long, surgery is known to be potentially curative for ulcerative colitis, a fewer
patients opted for it. Surgical management of ulcerative colitis has changed since the development
of pouch procedure. However, it requires a lot of motivation from the patient to go through a long
period of convalescence. In specialized center, 80% patients are continent with frequency of 4-6
stools per day and good quality of life.

REFERENCES
1.

Becker JM. Surgical therapy for ulcerative colitis. Gastroenterology clinics of North America
1999;28:371-90.

2.

Parks AG, Nicholas R. Proctocolectomy without ileostomy for UC. BMJ 1978;2:85-88.

3.

Munkholm P, Langholz E, Davidsen M, Binder V. Frequency of glucocorticoid resistance and


dependency in Crohn's disease. Gut 1994; 35: 3602.

4.

Truelove SC, Jewell DP. Intensive intravenous regimen for severe attacks of ulcerative colitis. Lancet
1974; 303: 106770.

5.

Lavery IC. Cancer in mucosal ulcerative colitis. In: Jagelman DG editor. Mucosal Ulcerative colitis.
Mount Kisco NY, Futura, 1986: 177-88.

6.

Lennard-Jones JE, Melville DM, Morson BC, Ritchie JK, Williams CB. Precancer and cancer in
extensive ulcerative colitis: findings among 401 patients over 22 years. Gut. 1990;31:800-6.

7.

Munkholm P. Review article: the incidence and prevalence of colorectal cancer in inflammatory
bowel disease. Aliment Pharmacol Ther. 2003;18 Suppl 2:1-5.

8.

Stucchi AF, Aarons CB, Becker JM. Surgical approaches to cancer in patients who have
inflammatory bowel disease. Gastroenterol Clin North Am. 2006;35:641-73.

9.

Oakley JR. Management of toxic ulcerative colitis. Fazio VW, Church JM, Delany C. 2 ed.Current
therapy in colon and rectal surgery Mosby, 2005. St Louis 219-24

10. Blumberg D, Beck DE. Surgery for ulcerative colitis. Gastroenterol Clin North Am. 2002;1:219-35.

31

11. Turnbull RB, Hawk WA, Weakley FL. Surgical treatment of toxic megacolon: Ileostomy and

Colostomy to prepare patients for colectomy. Am J Surg 1971;122:325-31.


12. MRB Kieghley Acute fulminant colitis and emergency colectomy. MRB Keighley, NS Williams (eds)

Surgery of the anus rectum and colon Vol.2 WB saunders company Ltd, 1993. London 1379-97.
13. Mcmurrick PJ, Dozois RR. Chronic ulcerative colitis: Surgical options. Fazio VW, Church JM, Delany

C. 2 ed.Current therapy in colon and rectal surgery Mosby, 2005. St Louis 211-18
14. Lepist AH, Jrvinen HJ. Durability of Kock continent ileostomy. Dis Colon Rectum. 2003;46:925-

8.
15. Kelly KA, Dozios RR. Chronic ulcerative colitis. Kelly KA, Sarr MG, Hinder RA. 1 ed. Mayo Clinic

Gastrointestinal Surgery WB saunders, 2004 Pennsylvania 533-52


16. Hawley PR. Emergency surgery for ulcerative colitis. World J Surg. 1988;12:169-73.
17. Ambroze WL Jr, Wolff BG, Kelly KA, Beart RW Jr, Dozois RR, Ilstrup DM. Let sleeping dogs lie: role

of the omentum in the ileal pouch-anal anastomosis procedure. Dis Colon Rectum. 1991;34:563-5.
18. Gemlo BT, Belmonte C, Wiltz O, Madoff RD. Functional assessment of ileal pouch-anal anastomotic

techniques. Am J Surg. 1995;169:137-42


19.

Lovegrove RE, Constantinides VA, Heriot AG, Athanasiou T, Darzi A, Remzi FH, Nicholls RJ, Fazio
VW, Tekkis PP. A comparison of hand-sewn versus stapled ileal pouch anal anastomosis (IPAA)
following proctocolectomy: a meta-analysis of 4183 patients. Ann Surg. 2006;244:18-26.

20. Utsunomiya J, Iwama T, Imajo M et al. Total colectomy, mucosal proctectomy, and ileoanal

anastomosis. Dis Colon Rectum.1980 Oct;23(7):459-66.


21. Larson

DW,

Pemberton

JH.

Current

concepts

and

controversies

in

surgery

for

IBD.

Gastroenterology. 2004;126:1611-9.
22. Simon T, Orangio G, Ambroze W, Schertzer M, Armstrong D. Laparoscopic-assisted bowel resection

in pediatric/adolescent inflammatory bowel disease: laparoscopic bowel resection in children. Dis


Colon Rectum. 2003;46:1325-31.
23. McGuire BB, Brannigan AE, O'Connell PR. Ileal pouch-anal anastomosis. Br J Surg. 2007;94:812-23.
24. Fazio VW, Ziv Y, Church JM et al. Ileal pouch-anal anastomosis complications and function in 1005

patients. Ann Surg 1995;222:120-8.


25. Marcello PW, Roberts PL, Schoetz DJ et al. Long term results of the ileoanal pouch procedure. Arch

Surg 1993;36:1105-11.
26. Wexner SD, Wong WD, Rothenberger DA et al. The ileoanal reservoir Am J Surg 1990;159:178-85.
27. Marcello PW, Roberts PL, Schoetz DJ et al. Obstruction after ileal pouch-anal anastomosis: A

preventable complication? Dis Colon Rectum 1993;36:1105-11.


28. Whitlow CB, Opelka FG, Gathright JB et al. Treatment of colorectal and ileoanal anastomotic sinuses.

Dis Colon Rectum 1997;40:760-3


29. Fazio VW, Tekkis PP, Remzi F et al. quantification of risk for pouch failure and life expectancy of

ileoanal pouch. Ann Surg 2003;238:605-17


30. Olangunju A, Korsgen S, Keighley MRB. Pouch salvage: long term outcome. Dis Colon Rectum

1997;40:548-52
31. Galandiuk S, Scott NA, Dozios RR et al. Ileal Pouch anal anastomosis; Reoperation for pouch related

complications. Ann Surg 1990;212:446-54


32. Pemberton JH, Philiphs SF, Reddy RR et al. Quality of life after Brooke ileostomy and ileal pouch

anal anastomosis. Ann Surg 1989;209:62-628

Index
32

Premalignant Lesions of the Bowel


Shaji Thomas
SMALL BOWEL
Malignant tumors of the small bowel are extremely rare. They manifest vague and nonspecific
symptoms and present significant diagnostic and therapeutic challenges to the cancer surgeon. The
most common subtypes are adenocarcinoma (24% - 44%), carcinoid (20% - 42%), lymphoma (12% 27%), and gastrointestinal stromal tumor (7% - 9%).

Table 1: Genetic and Environmental conditions that predispose to cancer of the small bowel.
Condition

Histology

Familial adenomatous polyposis

Adenocarcinoma

Hereditary

Adenocarcinoma

nonpolyposis

colon

cancer
Crohns disease

Adenocarcinoma

Peutz-Jeghers

Adenocarcinoma,
hamartomas

Gardners syndrome

Adenocarcinoma, desmoid

Celiac disease

Adenocarcinoma, lymphoma

Neurofibromatosis

Paraganglioma

AIDS

Lymphoma

History of other primary cancer

Adenocarcinoma, carcinoid

Small intestinal adenocarcinomas are believed to arise from preexisting adenomas through a
sequential accumulation of genetic abnormalities similar to that described for pathogenesis of
colorectal cancer.

1. Familial adenomatous polyposis (FAP). Patients have multiple adenomas in the colon, and if
untreated, have a 100% relative risk of developing colon cancer. They are also at risk for
development of adenomas and adenocarcinomas of the small intestine, mainly in the
periampullary duodenum. Periampullary adenocarcinoma is one of the leading causes of death in
patients with FAP who have undergone total colonic resection.

2. Hereditary nonpolyposis colorectal cancer (HNPCC). They have a lifetime risk of 1% - 4% of


small bowel cancer. Small bowel tumors may often be the presenting tumor in these patients and
occur at a very young age (below 30 years of age).
3. Crohns disease. Tumors occurred 2 decades earlier (av age 48 yrs), and usually in those
patients with long-standing Crohns disease of greater than 10 years. These associated tumors
appeared more common in the ileum, unlike sporadic adenocarcinomas which are most common
in the duodenum.
33

4. Celiac disease. 13% adenocarcinoma and 39% lymphomas were found associated with celiac
disease. Lymphomas arising in the setting of celiac disease are referred to as enteropathyassociated T-cell lymphoma (EATL).

5. Peutz-Jeghers. Rare autosomal dominant disease. Characterized by multiple hamartomatous


like polyps of the small bowel and pigmentation of skin and mucous membranes. Present with
obstruction, bleeding and small bowel intussusception. The relative risk of developing small bowel
cancer is approximately 18-fold greater than the general population.

6. Other primary cancers. Greater than 8-fold increased risk of having a second primary
malignancy in patients with small bowel adenocarcinoma. Similarly, risk of small bowel
malignancy was increased in cancers of the colon, rectum, ampulla of Vater, pancreas, uterus
ovary, prostate, thyroid, skin and soft tissue sarcomas.

COLON AND RECTUM

Risk factors for colorectal cancer


1. Age. 90% occur in people over the age of 50 years. Can develop earlier, so symptoms of
significant change in bowel habits, rectal bleeding, melena, unexplained anemia, or weight loss
require a thorough evaluation.
2. Hereditary risk factors. While 80% of colorectal cancers occur sporadically, 20% will have a
known family history of colorectal cancer. Assays currently exist to detect the most common
defects in the APC gene and in mismatch repair genes.

3. Environmental and dietary factors. Cancers more common in populations consuming diets
high in animal fat and low in fibre. Obesity and sedentary lifestyle increase cancer-related
mortality.

4. Inflammatory bowel disease. Increased risk in patients with long-standing colitis from
inflammatory bowel disease. Duration and extent of colitis correlate with risk. In ulcerative (and
Crohns) pancolitis, risk of carcinoma is 2% after 10 years, 8% after 20 years, and 18% after 30
years. Screening colonoscopies and random biopsies are recommended annually after 8 years
of disease for pancolitis, and after 12 to 15 years of disease for patients with left sided colitis.

5. Other risk factors. Cigarette smoking.

34

Genetic defects
Mutations may cause activation of oncogenes (K-ras) and/or inactivation of tumor-suppressor
genes (APC, DCC [deleted in colorectal carcinoma], p53). Colorectal carcinoma is thought to
develop from adenomatous polyps by accumulation of these mutations.
The APC gene is a tumor-suppressor gene. Mutations in both alleles are necessary to initiate
polyp formation. APC inactivation alone does not result in a carcinoma. It sets the stage for
accumulation of genetic damage that results in malignancy. Additional mutations that are
involved are activation of the K-ras oncogene, and loss of tumor-suppressor genes DCC and
p53.
K-ras is classified as a proto-oncogene because mutation of only one allele will perturb the cell
cycle. Mutation of K-ras results in uncontrolled cell division.
DCC is a tumor-suppressor gene and loss of both alleles is required for malignant degeneration.
DCC mutations are present in more than 70% of colorectal carcinomas.
Mutations in tumor-suppressor gene p53 are present in 75% of colorectal cancers.

Adenoma-Carcinoma sequence
A localized lesion projecting above the surrounding mucosa is a polyp. Majority of colorectal
carcinomas evolve from adenomatous polyps; this sequence of events is the adenoma-carcinoma
sequence. There is a high risk of colorectal cancer development in individuals whose adenomas
are not removed. Adenomas greater than 1 cm in size have a 15% chance of progressing to
carcinoma during a 10-year period.

Polypectomy decreases colorectal cancer risk. Besides

adenomatous polyps, polyps associated with ulcerative colitis also have a markedly increased risk
of colorectal carcinoma.

Polyps
1. Neoplastic polyps. (tubular adenoma, villous adenoma, tubulovillous adenomas):
Dysplastic lesions occurring in upto 25% of population above 50 years of age. Risk of
malignant degeneration related to both size and type of polyp. Tubular adenomas are
associated with malignancy in only 5% of cases, but villous adenomas may harbor cancer in
upto 40%, and tubulovillous in about 22%. Although most neoplastic polyps do not evolve to
cancer, most colorectal cancers originate as a polyp. Secondary prevention strategies eliminate
colorectal cancer by targeting the neoplastic polyp for removal before malignancy develops.
Polyps may be pedunculated or sessile. Pedunculated polyps can be removed by colonoscopic
snare excision, but sessile polyps may have to be removed by saline lift and piecemeal
excision.

35

2. Hamartomatous polyps. (Juvenile polyps)


Characteristic polyps of childhood and are not usually premalignant. Gross appearance is
identical to adenomatous polyps and must be treated by polypectomy.
i.

Familial juvenile polyposis. Autosomal dominant. Hundreds of polyps in colon and


rectum. May degenerate to adenomas and carcinoma. Annual screening should begin at
age of 10 and 12 years. If rectum is relatively spared, then total abdominal colectomy with
ileorectal anastamosis and close surveillance of retained rectum. If rectum is involved,
total proctocolectomy with ileal pouch-anal reconstruction.

ii.

Peutz-Jeghers syndrome. Hamartomatous polyposis of the small intestine, and to a


lesser extent, of the colon and rectum. Associated characteristic melanin spots of lips and
buccal mucosa. No significant risk of malignant degeneration, however, carcinoma may
occasionally develop. Surgery only for symptoms of obstruction or bleeding. Screening
with baseline colonoscopy and upper endoscopy at 20 years and annual flexible
sigmoidoscopy thereafter.

iii.

Cronkite-Canada syndrome. Gastrointestinal polyposis associated with alopecia,


cutaneous pigmentation, atrophy of fingernails and toenails, diarrhea, vomiting,
malabsorption, and protein-losing enteropathy. Most patients die of this disease. Surgery
only for complications like obstruction.

iv.

Cowdens syndrome. Autosomal dominant disorder. Hamartomas of all embryonal cell


layers. Facial trichilemmomas, breast cancer, thyroid disease, gastrointestinal polyps.
Patients should be screened for cancers. Treatment based upon symptoms.

3. Inflammatory polyps. (Pseudopolyps)


Usually associated with inflammatory bowel disease, but can also occur with amebic colitis,
ischemic colitis, and schistosomal colitis. Lesions are not premalignant, but cannot be
distinguished from adenomatous polyps and should be removed. Polyposis maybe extensive
and may mimic familial adenomatous polyposis.

4. Hyperplastic polyps.
Small lesions. Extremely common. How hyperplasia without dysplasia. Not premalignant, but
cannot be distinguished from adenomatous polyps and are therefore often removed. Large
hyperplastic polyps (> 2 cm) may harbor foci of adenomatous tissue and dysplasia, and have a
slight risk of malignant degeneration.

Inherited colorectal carcinoma


1. Familial Adenomatous Polyposis.
Rare autosomal dominant condition due to a mutation in the APC gene. Of patients with FAP,
APC mutation testing is positive in 75% of cases. Upto 25% will present without other
affected family members. Presents with hundreds to thousands of adenomatous colonic

36

polyps shortly after puberty. Lifetime risk of colorectal cancer approaches 100% by age 50
years.
Screening is by flexible sigmoidoscopy of first-degree relatives of FAP patients beginning at
age 10-15 years. Today, APC gene testing may be used to screen family members. If APC
testing is positive in a relative of a patient with a known APC mutation, annual flexible
sigmoidoscopy beginning at age 10-15 years is done till polyps are identified. If APC testing
of patient is negative, the relative can be screened starting at age 50 years as per average
risk guidelines. If APC testing is refused / unknown, annual flexible sigmoidoscopy
beginning at age 10-15 years is performed till age 24 years, then every 2 years till age 34
years, every 3 years till age 44 years, then every 3-5 years.
FAP patients are also at risk for development of adenomas anywhere in the gastrointestinal
tract, particularly in the duodenum in the periampullary region. Upper GI endoscopy is
recommended for surveillance every 1 to 3 years beginning at age 25 to 30 years.
Once FAP is diagnosed, treatment is surgical and is affected by age of patient, presence and
severity of symptoms, extent of rectal polyposis, and presence and location of cancer or
desmoid tumors. Three operative procedures can be considered: total proctocolectomy with
either an end ileostomy or continent ileostomy; total abdominal colectomy with ileorectal
anastomosis; and restorative proctocolectomy with ileal pouch-anal anastomosis.
FAP maybe associated with extraintestinal manifestations such as congenital hypertrophy of
retinal pigmented epithelium, desmoid tumors, epidermoid cysts, mandibular osteomas
(Gardners syndrome), and central nervous system tumors (Turcots syndrome).

2. Attenuated FAP
Variant of FAP associated with mutations in the APC gene in 60% of patients. Patients
present later in life with fewer polyps (usually 10-100), dominantly located in the right colon.
Colorectal carcinoma develops in 50% of these patients, but occurs later (average age 50
years). Patients are also at risk for duodenal polyposis.
When APC mutation is positive, genetic counseling and testing used to screen at-risk family
members. If family mutation is unknown, screening colonoscopy is recommended beginning
at age 13-15 years, then every 4 years till age 28 years, and then every 3 years.
Patients are candidates for total abdominal colectomy with ileorectal anastomosis.
3. Hereditary Nonpolyposis Colon Cancer (HNPCC or Lynchs Syndrome)
More common than FAP. Inherited in an autosomal dominant pattern. The genetic defects
arise from errors in mismatch repair.
Characterized by development of colorectal carcinoma at an early age (average age 40-45
years). 70% of affected individuals will develop colorectal cancer. These cancers are more
common in proximal colon and have better prognosis than sporadic cancer. They also have
a 40% risk of synchronous or metachronous colorectal cancer.

37

They may be associated with extracolonic malignancies including endometrial (40% lifetime
risk), ovarian, pancreas, stomach, small bowel, biliary, and urinary tract carcinomas.
Diagnosis is made based upon family history. The Amsterdam criteria for clinical diagnosis of
HNPCC are three affected relatives with histologically verified adenocarcinoma of the large
bowel (one must be a first degree relative of one of the others) in two successive
generations of a family with one patient diagnosed before age 50 years. Presence of other
HNPCC related cancers should raise suspicion of this syndrome.
Screening colonoscopy is recommended annually for at-risk individuals beginning at age 2025 Years or 10 years younger than the youngest age at diagnosis in the family. Annual
transvaginal ultrasound or endometrial aspiration biopsy is also recommended.
Total colectomy with ileorectal anastomosis with follow-up annual proctoscopy is
recommended once adenomas or carcinoma is diagnosed or prophylactically. Prophylactic
hysterectomy and bilateral salpingo-oophorectomy considered in women who have
completed childbearing.

4. Familial colorectal cancer.


Nonsyndromic familial colorectal cancer accounts for 10-15% of patients with colorectal
cancer.
The lifetime risk of colorectal cancer in patient with no family history of this disease is around
6%; this increases to 12% if one first-degree relative is affected, and to 35% if two firstdegree relatives are affected. Age of onset before 50 years is associated with higher
incidence in family members.
Screening colonoscopy recommended every 5 years beginning at age 40 years, or 10 years
before the age of the earliest diagnosed patient in the family.

Guidelines for screening for average risk population (asymptomatic, no family history of colorectal
cancer, no personal history of polyps or colorectal carcinoma, no familial syndrome)

Screening beginning at age 50 years.

Recommended procedures include yearly FOBT (fecal occult blood testing), flexible
sigmoidoscopy every 5 years, FOBT and flexible sigmoidoscopy in combination, air-contrast
barium enema every 5 years, or colonoscopy every 10 years.

Index

38

Current Trends in Colon Cancer


PN Agarwal, Gaurav Thami
Introduction
Colorectal cancer ranks as the third most common malignancy in United States and represents
1

second most leading cause of cancer related mortality . The life time risk of developing colorectal
carcinoma in average risk population (no family history) is approximately 6% and increases with
2

positive family history of the disease . Colon cancer is three times more common than rectal cancer.
Colorectal cancer occurs in hereditary, sporadic and familial forms.

AJCC PATHOLOGICAL TNM STAGING


TX Primary tumor cannot be assessed
T0 No evidence of primary tumor
Tis Carcinoma in situ: intraepithelial or invasion of lamina propria*
T1 Tumor invades submucosa
T2 Tumor invades muscularis propria
T3 Tumor invades through the muscularis propria into the subserosa, or into nonperitonealized pericolic or perirectal tissues
T4 Tumor directly invades other organs or structures, and/or perforates visceral peritoneum**
Regional lymph nodes (N)
NX Regional lymph nodes cannot be assessed
N0 No regional lymph node metastasis
N1 Metastasis in one to three regional lymph nodes
N2 Metastasis in four or more regional lymph nodes

Stage grouping
Stage 0 Tis
Stage I T1,2
Stage II T3,4
Stage III Any T
Stage IV Any T

Distant metastasis (M)

N0
N0
N0
N1,2
Any N

M0
M0
M0
M0
M1

MX Distant metastasis cannot be assessed


M0 No distant metastasis
M1 Distant metastasis
*Note: Tis includes cancer cells confined within the glandular basement membrane (intraepithelial) or lamina propria (intramucosal)
with no extension through the muscularis mucosae into the submucosa.
**Note: Direct invasion in T4 includes invasion of other segments of the colorectum by way of the serosa; or into vagina/prostate in
the rectum.

According to DUKE classification, tumors were classified as A, B, or C, with stage A indicating tumor restricted to, but not
through, the bowel wall; stage B indicating penetration through the bowel wall; and stage C indicating spread to local-regional
lymph nodes.

Dukes subsequently modified his staging system, first dividing stage C into C1 (local lymph nodes involved) and C2 (lymph
nodes at the point of ligature involved) and later adding a fourth stage (subsequently known as stage D) for distant metastasis.

Kirklin et al divided Dukes' stage A into a more restricted stage A (mucosal and submucosal involvement only) and a new B1,
which involved (but did not fully penetrate) the muscularis propria. The old stage B became B2.

Astler and Coller addressed the issue of depth of tumor penetration in patients with positive lymph nodes, breaking stage C
into stages C1 (node-positive with primary tumor confined to the bowel wall) and C2 (node-positive with tumor penetrating the
full thickness of bowel wall).

Prognostic factorsIt includes

Stage of the tumor

Margins (negative proximal/ distal/ tangential or radial margins)

Degree of differentiation.

Vascular invasion
39

Lymphatic invasion

DNA content /Aneuploidy/ Proliferative index

Bowel perforation at the time of surgery.

Experience of Surgeon and surgical technique is one of the most important


prognostic factor in a patient of colon cancer.

DIAGNOSTIC EVALUATION
The aim of investigative workup of a patient with colon cancer is to assess the large bowel with regard
to the primary lesion, concomitant lesions and other potential underlying colonic disease; exclude the
metastatic disease at the time of initial presentation and perform the routine preoperative assessment
for surgery.

The importance of a good history and a careful physical examination cannot be

overstressed.
Double contrast Barium enema (DCBE) and Colonoscopy
DCBE and colonoscopy are the modalities that are used for establishing the diagnosis of colon
cancer.
Barium enema gives good anatomic and topographic information that not only may be sufficient
to diagnose a polyp or carcinoma but also demonstrates the site and configuration of the
lesion, and the presence or absence of diverticulosis. The air insufflated after the barium
shows clearly the mucosal destruction from an ulcerated carcinoma or the mucosal coating of
both adenomatous polyps and polypoid carcinomas. The technique of DCBE is limited by its
lack of sensitivity for small polyps (<1 cm in diameter) and for areas within the rectosigmoid,
hepatic, and splenic flexures, where large bowel loops may overlap making a single lumen
difficult to identify. DCBE is nontherapeutic, provides no tissue diagnosis and may miss flat
mucosal lesions that might represent a synchronous lesion.
Colonoscopy enables the visualization of the entire colon, allows for biopsy or removal of any
suspicious lesions and is considered the gold standard for evaluating the colonic pathology.
It enables a more detailed study of the mucosa, visualizing lesions of less than 0.5 cm. The
principal advantage over radiology is that lesions can be biopsied, or removed by snare
cautery if they prove to be adenomatous polyps or a small polypoid carcinoma. The
complication rate following colonoscopy is very low, with a much less than 1% incidence of a
bowel perforation. However, there are some limitations to the technique. There is a 25% risk
of smaller lesions escaping detection and an estimated 10% incidence that the caecum might
not be reached for technical reasons. As a general rule, all patients with colorectal cancer
should have a preoperative colonoscopy or atleast a double-contrast barium enema if the
facilities of colonoscopy do not exist. The sensitivity of DCBE for detection of polyps <1 cm is
very low when compared with colonoscopy. The early experience with this modality suggests
that the sensitivity for identifying lesions of more than 1 cm varies from 83 to 100% and the
specificity is greater than 90%.

[11]

The sensitivity for polyps of more than 1 cm ranges from 75

to 100%.

40

Ultrasonography and computed tomography: Once the diagnosis of carcinoma of the colon or
rectum has been made, additional investigations are necessary to plan and organize treatment.
The liver is the most common site for metastasis, followed by lung, retroperitoneum, ovary,
peritoneal cavity, and, rarely, adrenal glands. Ultrasonography is very operator dependent, tends
to vary in quality and is therefore not very useful in colon ca. staging .

Abdominal computed tomography (CT): The rationale for obtaining a preoperative CT scan is to
assess the local effects of the tumor, ( e.g identify any adjacent organ invasion) and to look for
metastatic disease elsewhere in the peritoneal cavity, such as liver metastases deep in the
parenchyma that might not be otherwise noted at laparotomy. It can also serve as a baseline
for follow-up imaging studies. It provides better discrimination for smaller hepatic lesions and can
distinguish angiomas from metastases as small as 1.0 cm in diameter after contrast
enhancement. CT also provides more information about lymphadenopathy, detects small
volumes of ascites, ovarian enlargement, and hydronephrosis from retroperitoneal spread.A
'baseline' CT of the abdomen should always be done in all patients with colon cancer.

CT Colonography (Virtual Colonoscopy): Virtual colonoscopy (VC) is an emerging radiographic


technique that involves reconstruction of three-dimensional images of the colon from the twodimensional data obtained by a spiral CT scanner. The images can be displayed so that the
entire bowel is seen from the outside, similar to that obtained by a double contrast barium
enema, and from within the lumen. Bowel preparation is required; however, the technique is less
invasive, no sedation is required, and patient acceptance of this technique is high . However, VC
lacks the advantage of colonoscopy of direct access to colonic tissue for biopsies or other
intervention. Several prospective studies of VC versus colonoscopy have demonstrated mixed
3

results in terms of specificity, sensitivity and interobserver error .Virtual colonoscopy has yet to
gain general acceptance as a colorectal cancer screening tool.

A Chest X-ray in two planes is commonly sufficient in order to rule out extra hepatic metastases
although the yield of this test is relatively low. A CT scan of the chest may be needed to
characterize any suspicious lesion on chest x-ray.

PET scan: PET Scan is an imaging modality that is based on the detection of 2-flouro 2deoxyglucose (FDG) in the tumor cells.PET scan is particularly useful to detect the recurrence
following surgery. It can readily differentiate the post operative scar tissue or post radiation
changes from local recurrence of tumor. Various studies reported the sensitivity of PET scan to
4

detect local recurrence up to 90% . Though PET can provide important information however, its
role following curative treatment is evolving and cannot be recommended as a standard of care
at present.

41

Carcinoembryonic Antigen: An elevated preoperative CEA level is prognostic factor for cancer
recurrence. Patients in whom the elevated CEA fails to normalize after a potentially curative
operation are at particularly high risk of recurrence. Several authors have presented evidence
indicating that CEA is an independent prognostic factor. Given the prognostic significance of the
preoperative CEA, it is recommended that all patients undergoing operation for colorectal cancer
should have a serum CEA done prior to operation.
General workup of patient involves a battery of investigations for preoperative assessment which
includes complete haemogram, LFTs, KFTs, electrolytes and ECG.

TREATMENT
Surgery forms the mainstay of the treatment for the patients of colorectal cancer.
A. Aims of surgery include- Tumor resection with negative margins (proximal/ distal )
- Adequate lymph node dissection which is achieved by proximal ligation of blood vessels
at their origin. According to the recommendation of CAP(College of American
Pathologists), minimum of 12-14 lymph nodes should be isolated from surgical specimen
for proper N staging.
- Restoration of intestinal continuity by anastomosis.

B. Do all patients need to undergo surgery?


- Patients with definitive chances of cure (stage I/ II/ III)
- Patients of advanced disease (incurable distant metastasis) with symptomatic primary
e.g. obstruction , bleeding, perforation.

Preoperative Bowel Preparation: Mechanical bowel cleansing and antibiotic prophylaxis have been
used as an integral part of the preoperative management in colorectal surgery. The procedure of
preparing the bowel before surgery involves two factors: purging the fecal contents (mechanical
preparation) and administration of antibiotics effective against colonic bacteria. Tradition has held
that an unprepared colon (i.e., one that contains intraluminal feces) poses an unacceptably high
rate of failure of the anastomosis to heal. However, since the colonocytes receive nutrition from
intraluminal free fatty acids produced by fermentation from colonic bacteria, there are concerns
that purging might actually be detrimental to the healing of a colonic anastomosis. The most
commonly used regimens include polyethylene glycol (PEG) solutions or sodium phosphate. PEG
solutions require patients to drink a large volume and may cause bloating, nausea and vomiting.
Sodium phosphate solutions are generally better tolerated, but are more likely to cause fluid and
electrolyte abnormalities.

Various studied have found both PEG and sodium phosphate are

equally efficacious in bowel cleansing

5,6,7,8

. Antibiotic use in colorectal surgery is a well-established

practice that reduces infectious complications. Elective colorectal cases are classified as cleancontaminated and, as such, benefit from routine single-dose administration of parenteral antibiotics
30 minutes before incision. There is evidence to show that when operative times are prolonged,
42

additional doses at 4-hour intervals reduce wound infection. When the operation is completed,
postoperative administration of antibiotics for a clean-contaminated case such as a routine
segmental resection does not further reduce infectious complications and may promote
Clostridium difficile colitis. Antibiotics active against both aerobes and anaerobes are ideal:
second- or third-generation cephalosporins alone, or combination of a fluoroquinolone plus
metronidazole or clindamycin is typical.

While performing the colonic resection for malignancy, the proximal and distal margin of 5cm was
advocated earlier. However, in the present era it has been found that distal margin of 2 cm is
sufficient in cases of well and moderately differentiated tumors. Distal margin of 5cm is still
advocated in cases of poorly differentiated tumors.

Standard Resections of the Colon


Tumor

Resection

Description of Extent

Major Blood Vessel

Location
Cecum

Safety
margin

Right

Terminal ileum to mid

Ileocolic artery, Right colic

hemicolectomy

transverse colon, right

artery, Right branch of

flexure included

mid colic artery

Ascending

Right

Terminal ileum to mid

Ileocolic artery, Right colic

colon

hemicolectomy

transverse colon, right

artery, Right branch of

flexure included

mid colic artery

Hepatic

Extended right

Terminal ileum to

Ileocolic artery, Right colic

flexure

hemicolectomy

descending colon (distal

artery, Mid colic artery

5 cm

5 cm

5 cm

to left flexure)
Transverse

Extended right

Terminal ileum to

Ileocolic artery, Right colic

colon

hemicolectomy

descending colon (distal

artery, Mid colic artery

5 cm

to left flexure)
(Transverse

Transverse colon

Mid colic artery

colon resection)

(including both flexures)

Splenic

Extended left

Right flexure to

Mid colic artery, Left colic

flexure

hemicolectomy

rectosigmoid colon

artery, Inferior mesenteric

(sigmoid, beginning of

artery

5 cm

rectum)
Descending

Left

Left flexure to sigmoid

Inferior mesenteric artery,

colon

hemicolectomy

colon (beginning of

Left branch of mid colic

rectum)

artery

Sigmoid

Rectosigmoid

Descending colon to

Superior hemorrhoidal

colon

resection

rectum

artery, Inferior mesenteric


artery

43

5 cm

5 cm

Anastomotic techniques
The strongest layer of the bowel is the submucosa, which must be included in all deeply placed

sutures. The material with which the anastomosis is made does not seem to be of critical
importance.
Colocolic anastomoses were, until fairly recently, fashioned in two layers, an outer seromuscular

layer with a non-absorbable suture and an inner, absorbable suture layer. The outer layer was
usually interrupted, while the inner layer was often a continuous suture. Randomized studies
have demonstrated that a single layer of interrupted, full-thickness suture is as good or better.
Diverting stomas do not reduce the leakage rate, but perhaps reduce the morbidity and mortality
of such leaks.
Stapling instruments are now widely used to perform anastomosis. Construction of a side-to-side

anastomosis using linear stapling devices is suitable if the bowel can be delivered on to the
abdominal wall. End-to-end anastomosis using a circular stapler is most useful for low pelvic
anastomoses. The instruments may shorten operating time but they are much more expensive
than sutures. Controlled studies do not show any convincing differences in leakage rates
between hand-sutured and stapled anastomoses, provided the surgeon is equally competent
with either technique. Selection of method is one of surgeon preference and economics.

Laparoscopic Colon Resection: Laparoscopic surgery has become a particularly important addition
to the armamentarium of the surgical oncologist. For many decades colonic resection for
malignancy was performed by conventional open technique. First report of laparoscopic assisted
colectomy was published by Jacobs et al in 1991.

There are several potential advantages for laparoscopic approaches to the surgical management
of colon cancer. Length of incision, patient recovery time, and return to bowel function are often
cited as justification for a laparoscopic approach. The improved visualization resulting from
magnification allows one to perform much more intricate and careful dissection during laparoscopic
surgery. The technical difficulties faced during laparoscopic resection of the colon relate to the size
of the specimen being removed and the need to perform an anastomosis. These difficulties can
be overcome through careful placement of incisions for specimen removal as well as a judicious
use of stapling devices to perform the anastomosis.

A number of studies looking at the relative risks and benefits of the laparoscopic resection of colon
9,10,11,12

cancer have been performed or are ongoing

.The Clinical Outcomes of Surgical Therapy

(COST) trial examined both the oncologic outcomes with respect to disease-free and overall
survival as well as the impact of laparoscopic versus open surgery on patient recovery, pain
management, and time to return of bowel function. An initial report on quality of life showed only a
modest short-term benefit for laparoscopic resection versus a conventional open procedure but the
44

overall results of the trial with respect to oncologic outcomes demonstrated equivalence between
the laparoscopic and open approach.

Limitations

Intraoperative tumor localization early ca may not be detected from serosal surface during
laparoscopic approach, so accurate localization is important to avoid resection of wrong
segment of colon. Methods used/employed to identify tumor site include colonoscopic tattooing
/intraoperative endoscopy.

Tumor deposits /implants at port sites. Various techniques have been advocated to decrease
the port site recurrences. e.g. evacuation of pneumoperitoeum through trocars, extraction of
specimen in plastic bags, treatment of extraction incision and port site incision with povidone
iodine solution.

Learning curve- minimum of 30-50 cases for benign or metastatic disease have been
recommended before attempting laparoscopic resection of curable colorectal carcinoma by
many associations. Hand assisted techniques may also be used as an alternative to straight
laparoscopic techniques.

ADJUVANT CHEMOTHERAPY
Rationale: Surgical resection forms the mainstay of treatment for patients with stage II and III colon
cancer. There is a significant risk of residual micrometastatic disease in these patients at a volume
that is beneath the levels of clinical detectability. The role of adjuvant therapy is to eradicate this
microscopic metastatic disease.

Indications
1. All patients with Stage III disease (node positive disease)
The overall disease free survival at 5 years for patients of stage III disease with surgery has
been found to be equal to 50% . However, it has been found that disease free survival with
chemotherapy increases up to 70-78% at 4 years. Therefore, adjuvant chemotherapy has been
strongly recommended for patients of stage III disease.

2. Stage II colon carcinoma


Patients of stage II colon cancer with one or more of the risk factors have a poorer prognosis
and a prognosis closer to patients with stage III disease. Therefore, adjuvant chemotherapy is
recommended in stage II patients with any one of the following adverse prognostic factors

Poorly differentiated histology.

Inadequate lymph node sampling

Bowel perforation/obstructing cancer.

Perivascular invasion.
45

Chemotherapy Regimens
National Surgical Adjuvant Breast and Bowel Project (NSABP) C-01 trial (surgery alone, BCG, or
chemotherapy regimen of semustine , vincristine , and fluorouracil ) was the first to demonstrate
that postoperative chemotherapy could result in a survival advantage after resection of locally
advanced colon cancer. There was no statistically significant differences between the BCG and
surgery-only groups; however, the group treated with MOF had a significantly better disease-free
and overall survival than the control group.
In 1990, the National Cancer Institute established adjuvant chemotherapy as the standard of care for
patients with node-positive resected colon cancer on the basis of the results of intergroup
0035(surgery vs 5-FU/Levamisole) trial. The overall disease free survival with surgery was 44% as
13

compared with 61% of patients who received 5-FU and levamisole .


Further trials were done using 5-FU/Leucovorin combination. The NSABP C-04 study concluded that
no additional advantage was gained by addition of levamisole to 5-FU/LV.

On the basis of all these trials it has been concluded that 5-flourouracil forms basic component of all
the chemotherapeutic regimens. 5-FU is a prodrug that is enzymatically activated to its active
phosphorylted form. Leucovorin (folinic acid) accentuates the effect of 5-FU and therefore is
commonly used along with it in many regimens. Toxicity includes myelosuprresion and GI side
effects such as diarrhea and mucositis. Following are the commonly used regimens of 5-FU/LV
chemotherapy:

Mayo clinic regimen Bolus 5-FU 425 mg/m +LV 20 mg/m

day 1 through day 5 every 4-5

weeks.

Rosewell park regimen 5-FU 500 mg/m + LV 500 mg/m weekly for 6 weeks.

De Gramont regimen LV 200 mg/m i.v. over 2 hours followed by 5-FU 400 mg/m i.v. bolus

followed by 22 hour infusion of 5-FU 600 mg/m day 1 -2 every 2 weeks.

Patient receiving infusional 5-FU + lecuovorin had a superior tumor response rate and improved
median disease free survival as compared to those receiving bolus 5-FU + Leucovorin. Infusional 5FU regimen is recommended over bolus regimen.

Oral Fluoropyrimidine Therapies: Two oral 5-FU prodrugs, capecitabine and uracil/tegafur
(UFT), have demonstrated efficacy in metastatic disease that is comparable to the Mayo clinic
schedule of parenteral 5-FU/leucovorin. Both of these agents have

been studied in the

adjuvant setting in comparison to Mayo Clinic 5-FU .Disease-free survival in the capecitabine
group has been found to be equivalent to of the 5-FU-plus-leucovorin group and capecitabine
resulted in significantly fewer adverse events than Mayo Clinic bolus 5-FU/leucovorin . This
trial demonstrates that capecitabine is a reasonable oral alternative to intravenous 5-FU plus
leucovorin in the adjuvant treatment of colon cancer. But as 5-FU/leucovorin alone is no longer

46

the standard postsurgical adjuvant treatment for colon cancer, therefore, the role of
capecitabine in the management of colon cancer remains limited at this time.

The NSABP C-06 trial assessed the use of oral uracil/tegafur (UFT) plus oral leucovorin in the
treatment of stage II and III colon cancer. There were no significant differences in disease-free
or overall survival between the treatment groups. The combination of oral UFT+LV is an
acceptable alternative to parenteral 5-FU/leucovorin.

The major side effects associated with capecitabine include diarrhea and plantar palmar
erythrodysesthesia (hand foot syndrome).

Oxaliplatin and Irinotecan-Based Combination Therapies: Clinical trials have established that
the antitumor activity of combinations of either irinotecan plus 5-FU/leucovorin or oxaliplatin
plus 5-FU/leucovorin is superior to that of 5-FU/leucovorin alone.

Oxaliplatin is a third generation platinum compound of di-aminocyclohexane family and acts by


blocking DNA replication and transcription. Its administration is associated with neurotoxicity
which may be manifested as paraesthesias and dysesthesisas of hands, feet, peri-oral region
and throat.

Oxaleplatin plus biweekly infusional 5-FU/leucovorin was evaluated in the MOSAIC trial. The
patients were randomized to the LV5FU2 regimen, a biweekly infusional and bolus 5FU/leucovorin regimen, or the FOLFOX 4 regimen, which is LV5FU2 plus oxaliplatin on day 1
.The 3-year disease-free survival was superior in the FOLFOX 4 group. Overall diease free
survival improved from 66% to 72% for stage III patients .The 3-year disease-free survival for
the stage II patients was 84% in the control arm and 87% in the FOLFOX 4 arm. Neuropathy
was the major side effect experienced with FOLFOX .

Irinotecan is semisynthetic derivative of campothecin ( plant alkaloid) . It inhibits topoisomerase


-1enzyme that aids in DNA uncoiling for replication and transcription. The side effects of
irinotecan includes neutropenia and diarrhea.
2

Folfox-4: Oxaliplatin 85mg/m over 2 hours, leucovorin 200mg/m followed by 5-FU bolus
2

400mg/m followed by infusional 5-FU 600mg/m over 22 hours. Oxaliplatin is administered


on day 1 only whereas all other drugs are given on day 1 and day 2. Cycle is repeated every
14 days.
2

Modified Folfox-6: Oxaliplatin 85smg/m + leucovorin 400mg/m over 2 hours followed by 52

FU bolus 400mg/m followed by infusional 5-FU 2400-3000mg/m over 46-48 hours. Cycle is
repeated every 14 days.

47

Monoclonal Antibodies: Bevacizumab and Cetuximab are the two monoclonal antibodies being
used for treatment of stage IV patients.It hs been shown in many trials that addition of
bevacizumab to standard chemotherapy regimen improves the response rate, rate of tumor
progression and increases the median survival by almost 5 months in patients with stage IV
disease. Bevacizumb is a monoclonal antibody against vascular endothelial growth factor (VEGF).

Side effects include hypertension requiring treatment in upto 10% patients, gastrointestinal
perforation, arterial thrombosis. It interferes with wound healing and therefore should be started
after complete healing of wound.

Cetuximab is a monoclonal antibody against epidermal growth factor (EGFR). It has demonstrated
high degree of antitumor activity in colorectal cancer patients whose tumor have progressed
despite standard chemotherapy. However no randomized trials have been done to evaluate
the effect of cetuximab on survival and its clinical use in first line treatment of metastatic
disease should be considered as investigational

General Guidelines

At the very least, 5-FU based regimen should always be administered in all patients with stage
III colon cancer and selected patients of stage II colon cancer with adverse prognostic factors
as described earlier for a period of six months.

The FOLFOX schedule is now the most widely used and accepted adjuvant therapy. Modified
FOLFOX -6 regimen is routinely used in patients with stage II and stage III disease.

Oral capecitabine or oral UFT/leucovorin are acceptable oral alternatives if only 5-FU/LV
regimen is being considered for treatment in patients with stage II and stage III disease.

Either of the FOLFOX/FOLFIRI (5FU/LV/Irinotecan) can be used for treatment of patients with
Stage IV disease. Bevacizumab may be added to any of the above regimens with equal
efficacy, has been found to increase median survival by about 5 months but at same time
increases the treatment cost.

ADJUVANT RADIATION THERAPY


The routine use of adjuvant postoperative radiation therapy in colon cancer remains
investigational. However, adjuvant radiation can be used in following subset of patients with colon
cancer. These include patients with close or positive resection margins, resection of T4 colon
cancers adherent to structures or tissues which cannot be fully resected. e.g hepatic flexure
tumors with duodenal invasion, sigmoid cancers with invasion into pelvic structures.

These

cancers have high local failure rates and can be considered for combined-modality therapy,
including 5-FU based chemotherapy plus concurrent radiation to the tumor bed.
48

GENE THERAPY
Several aspects of colorectal cancer make the disease a potential target for gene therapy
approaches. Multiple trials of different gene therapy approaches including virus directed enzyme
prodrug therapy, immunogenic manipulation, gene correlation have all been initiated. Major
therapeutic benefits from the gene therapy has yet to realized and the role of these approaches
remains highly investigational at this time.

Follow-Up after management of Colon Cancer is aimed to identify the local-regional or distant
recurrence that is potentially curable by surgery as well as to identify any second primary tumor in
these patients. A reasonable follow up of patients following treatment would include

Clinical examination of the patient at 3 monthly intervals.

CEA measurements every 3 months.

Annual CT scan of the chest and abdomen for the first 3 years.

Colonoscopy should be performed at 3 years following the resection .If there is no evidence of
recurrence it should be repeated every 5 years.

If a rising serum CEA is detected on two consecutive measurements in the absence of imageable
disease by CT scan, a PET scan should be done this time.

FUTURE DIRECTIONS
Portal Vein Infusion: Hepatic metastases derive their blood supply primarily from the hepatic artery.
However, tumors less than 5 mm in diameter obtain substantial portions of their blood supply from
both the hepatic and portal circulations. Delivery of chemotherapy directly into the portal vein
would appear to be a reasonable maneuver in the adjuvant treatment of colorectal cancer as the
liver is the most common extraregional site of metastases.

A modest, albeit statistically significant, advantage in disease-free survival (74% vs. 64% at 4
14

years) was demonstrated for the group receiving intraportal chemotherapy in NSABP-02 trial . At
present, intraportal adjuvant chemotherapy should remain limited to clinical investigations.

Intraperitoneal Chemotherapy: The peritoneal cavity is drained by portal lymphatics into the portal
vein. Intraperitoneal chemotherapy therefore delivers high concentrations of drug to the portal
circulation without the need for portal vein canalization. In addition, extremely high concentrations
of chemotherapy can be given directly onto the peritoneal surfaces, thereby increasing local
cytotoxicity. The high first-pass hepatic clearances of floxuridine and 5-FU make these drugs good
agents for intraperitoneal administration. However, the efficacy has not been proven by many
studies.

The role of vaccine therapy and active specific immunotherapy for treatment of resected colon cancer
remains highly investigational in the present era.
49

REFERENCES
1.
2.

Landis S.H., Murray T., Bolden S., Wingo P.A.: Cancer statistics, 1999. CA Cancer J. Clin. 1999; 49:8.
In: Ries L.A., Kosary C.L., Kankey B.F., et

al ed. SEER

Cancer

Statistics

Review

19731995,

Bethesda, MD: National Cancer Institute; 1998. 112.


3.

Fletcher J.G., Johnson C.D.: Computed tomographic colonography: Current and future status for
colorectal cancer screening. Semin. Roentgenol. 2000; 35:385.

4.

Libutti SK, Alexander HR, Jr., Choyke P, et al. A prospective study of 2-[18F] fluoro-2-deoxy-Dglucose/positron emission tomography scan, 99mTc-labeled arcitumomab (CEA-scan), and blind
second-look laparotomy for detecting colon cancer recurrence in patients with increasing
carcinoembryonic antigen levels. Ann Surg Oncol 2001;8(10):779.

5.

Cohen SM, Wexner SD, Binderow SR, et al: Prospective, randomized, endoscopic-blinded trial
comparing precolonoscopy bowel cleansing methods. Dis Colon Rectum 1994; 37:689-696.

6.

Frommer D: Cleansing ability and tolerance of three bowel preparations for colonoscopy. Dis Colon
Rectum 1997; 40:100-104.

7.

Poon CM, Lee DW, Mak SK, et al: Two liters of polyethylene glycol-electrolyte lavage solution versus
sodium phosphate as bowel cleansing regimen for colonoscopy: A prospective randomized
controlled trial. Endoscopy 2002; 34:560-563.

8.

Vanner SJ, MacDonald PH, Paterson WG, et al: A randomized prospective trial comparing oral
sodium phosphate with standard polyethylene glycol-based lavage solution (Golytely) in the
preparation of patients for colonoscopy. Am J Gastroenterol 1990; 85:422-427.

9.

Patankar SK, Larach SW, Ferrara A, et al. Prospective comparison of laparoscopic vs. open
resections for colorectal adenocarcinoma over a ten-year period. Dis Colon Rectum 2003;46(5):601.

10. Lauter DM, Lau ST, Lanzafame K. Combined laparoscopic-assisted right hemicolectomy and low

anterior resection for synchronous colorectal carcinomas. Surg Endosc 2003.


11. Weeks JC, Nelson H, Gelber S, et al. Short-term quality-of-life outcomes following

laparoscopic-

assisted colectomy vs open colectomy for colon cancer: a randomized trial. JAMA 2002;287(3):321.
12. A comparison of laparoscopically assisted and open colectomy for colon cancer. N Engl J Med

2004;350(20):2050.
13.

NIH consensus conference. Adjuvant therapy for patients with colon and rectal cancer.

JAMA

1990;264(11):1444.
14. Wolmark N, Rockette H, Wickerman DL, et al. Adjuvant therapy of Dukes' A, B, and C

adenocarcinoma of the colon with portal vein fluorouracil hepatic infusion: preliminary results of
National Surgical Adjuvant Breast and Bowel Project Protocol C-02. J Clin Oncol 1990;8:1466.

Index

50

Neonatal Intestinal Obstruction


Satish Kumar Aggarwal
A constellation of conditions causing bowel obstruction at different levels and by different mechanisms
can present with similar clinical features in the neonatal period. Most of them are not dire
emergencies and can be operated as planned acute after fluid resuscitation and radiological
diagnostic work up. Malrotation with midgut volvulus is a fire brigade emergency requiring urgent
laparotomy to untwist the bowel in order to save it from catastrophic necrosis. While most cases have
congenital mechanical obstruction, such as atresia or stenosis, functional obstruction is not rare.
Congenital functional obstruction classically occurs in Hirschsprungs disease. Many cases with
systemic sepsis present with ileus that may mimic mechanical obstruction. Neonatal Necrotising
Enterocolitis is a rapidly progressive condition in the preterm, and may result in bowel loss due to
inflammation, ischemia and necrosis. This chapter aims to describe the common cause of neonatal
congenital obstruction, their clinical features, radiological investigations, general principles of
management and specific operative treatment.

Common causes of Neonatal intestinal obstruction:


1. Duodenal atresia (post ampullary)
2. Jejuno ileal atresia
3. Malrotation with or without volvulus (more common with volvulus)
4. Hirschsprungs disease (functional obstruction)
5. Meconium disease of infancy (Meconium ileus, Meconium peritonitis, cystic Meconium
peritonitis, small left colon syndrome, Meconium plug syndrome.)
Uncommon causes
1. Pyloric atresia
2. Annular pancreas causing duodenal obstruction (undistinguishable from duodenal atresia)
3. Duodenal web with a hole causing partial duodenal obstruction
4. Windsock abnormality duodenal diaphragm getting stretched into distal gut with chronic
duodenal obstruction.
5. Pre ampullary duodenal atresia (non bilious vomiting with double bubble)
6. Colonic atresia
7. Rectal atresia
8. Milk curd obstruction
Other important causes not traditionally included in NIO
1. Oesophageal atresia
2. Anorectal malformations
3. Obstructed inguinal hernias
4. Congenital pyloric stenosis
5. Neonatal intussusception

51

Medical / systemic causes: NEC, Systemic sepsis, neonatal appendicitis

Generalities on clinical presentation


At birth the abdomen of a child is not distended and there is no gas in the bowel. Gas is ingested
as the child breathes and gradually fills the intestines over the next 24 hours. Bile stained vomiting
and abdominal distension are the key features of neonatal intestinal obstruction.
Bile stained vomiting (green vomiting) is always considered surgical unless proved
otherwise. It should not be confused with small vomits of yellow fluid which is common and
insignificant. Obstructed bile is green.
Timing and degree of distension varies depending on the cause. Proximal small bowel
obstructions such as duodenal and jejunal atresia present with early vomiting but minimal
distension. Ileal and colonic atresia present with gradual distension over one to two days
and late vomiting. Distension at birth should arouse suspicion of congenital mass lesions
(duplications, lymphangioma, large teratomas) or Meconium disease of infancy especially
Giant Cystic Meconium Peritonitis.
Passage of meconium. Most term neonates pass the first Meconium within 24 hours of birth.
Delay should arouse the suspicion of Hirschsprungs disease. Most case of intestinal
atresia do pass some Meconium for a few days (gut distal to atresia produces intestinal
juice).
General condition, feeding and systemic signs: Most babies born with congenital bowel
obstruction are otherwise healthy, active and systemically well. They will also accept first
few feeds well only to develop vomiting and abdominal distension later. If a child is
systemically ill with sepsis, he or she may develop features of intestinal obstruction due to
gut involvement secondarily. In that case the systemic signs will precede intestinal
symptom.

A baby who was born normal and healthy and took feeds well but develops bilious vomiting on the
third or fourth day and becomes limp and pale suddenly is most likely to have acute volvulus because
of malrotation. Examination will reveal shock and pallor with minimal abdominal signs. Plain
abdominal film may show paucity of distal gas with few proximal loops. This is the most feared entity
and although an upper GI contrast study is indicated, there may not be enough time. It is a fire
brigade emergency, requires quick fluid resuscitation and a prompt laparotomy to de-twist the small
bowel. At times laparotomy is a part of ongoing resuscitation. Failure to act quickly may result in
ischemic loss of the entire small bowel with dreaded consequences of short bowel syndrome.

IMAGING
Plain x ray of the abdomen is the most important imaging tool. It should be done in supine
position AP view. Erect view is unnecessary and distressing to the neonate. Some generalities about
the X-ray findings are as follows:

52

1. Plain X- ray is actually a contrast X ray, air being the contrast. At birth there is no air in the gut.
As the child starts breathing the air is ingested and travels across the intestines. In about an
hour it should reach the jejunum and in 24 hrs the rectum. So timing of x ray is important.
Distal ileal atresia may not become evident on X- ray in the first few hours of life. Timing of
X- ray is of utmost importance in Anorectal malformations, where it should be performed
after 24 hours.

2.

It is not possible to differentiate between small and large bowel loops in a neonate on plain
film. A loop more than 1 cm in size is considered dilated. Normal bowel gas pattern in a
neonate is that of the entire abdomen filled with bowel loops, but of normal size. Loops
localized to a particular area, fixed loop on serial films, and dilated loops indicate
abnormality.

3. Presence of gas in rectum rules out proximal atresia. Stenosis however, still remains a
possibility. Different conditions can be diagnosed on plain film:

Only distended stomach and no gas distal pyloric atresia

Distended stomach and proximal duodenum (classical double bubble) Duodenal


atresia. The dimple in between two bubbles is because of the pyloric contraction.

Proximal few bowel loops seen and no distal loops Upper small bowel atresia / jejunal
atresia.

Many distended loops suggests some form of distal obstruction:


Ileal atresia: many distended loops. Step ladder pattern, many levels on lateral
view.
Dilated proximal loops, soap bubble appearance and paucity of distal gas: Meconium ileus
Picture of Meconium ileus with calcification- Meconium peritonitis.
Too many dilated loops with distended abdomen and gas filled loops reaching the
periphery: Hirschsprungs disease / colonic atresia.

4. Free gas on supine film: It is not necessary to get an erect film to pick up free gas. Large
amount of free gas is expected in common conditions like gastric perforation or colonic
perforations. This can be seen as Foot ball sign on a supine film. The gas collects in the
central abdomen and gets distributed on either side of the falciform ligament, which shows
as an oblique shadow in the centre of a big blob of gas (American Football), hence the
name.
The liver shadow will not be dense because of the overlying air.
Wriggler sign: Gas on both sides of the bowel wall (intra-luminal and free extra-luminal)
makes the bowel wall very bright and sharply defined. This is referred to as Wriggler sign.
Scrotal gas: Especially in preterm babies because of patent processus Vaginalis.

53

Small amount of free gas (as expected in NEC) may be missed on supine film. For this cross
table view in left lateral decubitus position is taken. The child lies in lateral position on his left
side, X-ray plate is kept against the back and the beam comes from the front. Small triangular
pockets of free air will be seen opposite the abdominal wall flanked by bowel loops. Free air
may also be seen between the right edge of the liver and the right lateral abdominal wall.

5. Cross table lateral view in prone position: the child lies in prone position for two or three
minutes with the pelvis elevated by 45 degrees on a soft wedge. X-ray plate is kept along
the left or right thigh perpendicular to the table; X-ray beam comes from across the table,
centered over the greater trochanter. So a dead lateral view is taken. This view is of
importance in suspected Hirschsprung's disease and Anorectal malformations. In the prone
position with pelvis elevated the gas rises in the rectum. If X ray shows rectal gas it almost
rules out Hirschsprung's disease. In Anorectal malformations the distance between the
rectal gas and the skin is measured. If it is less than one cm, a primary perineal Anoplasty
operation can be done. If more than one cm, colostomy should be done and definitive repair
deferred for few weeks.

6. Invertogram: The child is put in upside down position for two to three minutes before taking a
lateral view with a purpose to know the type of Anorectal malformation high or low. It
becomes very uncomfortable for the child, invites aspiration if there is associated tracheoesophageal fistula (association of ARM, oesophageal atresia and duodenal atresia triple
atresia is well known). Therefore, it has now become obsolete in favor of cross table prone
lateral film.

7. Plain X-ray in NEC: In NEC X-ray findings are best interpreted on serial x rays. Fixed loop at
12 hour interval, small amount of free gas, intra-mural gas, portal venous gas etc are the
features of NEC on plain film.

8. X- Ray in peritonitis. Normally the fat line in neonates is well appreciated in plain film because
of the good interface being provided by pre-peritoneal fat that separates the anterior
abdominal wall from the peritoneal cavity. In peritonitis this plain is lost due to peritoneal
inflammation. So hazy fat line, inability to clearly see the Psoas shadow and renal shadow
indicate peritoneal inflammation.
Large amount of free gas is seen with rectal/ colonic perforation, gastric perforation, isolated
ileal perforation (cardiac patients, pre term, and right to left shunts, on indomethacin for
PDA).

Contrast studies: Upper GI and lower GI contrast studies are indicated in certain situations to help in
the diagnosis and sometimes in the management also. Which study to do depends on clinical
suspicion and plain film findings. If upper bowel obstruction is suspected upper GI contrast is
54

indicated. If lower GI obstruction is suspected contrast enema is needed. If there is too much gas
on plain film a contrast enema will be helpful and vise versa. Water soluble non ionic contrast
material should be used. Conray being highly osmolar can cause sudden fluid shifts into the bowel
lumen leading to circulatory insufficiency. However, Conray or Gastrograffin should be used for
therapeutic contrast enema for Meconium ileus and small left colon syndrome.
Upper GI series: Contrast is injected through the nasogastric tube and serial films taken. The
most important indication is to confirm or exclude malrotation in a neonate presenting with
bile stained vomiting. Normal location of the duodeno-jejunal junction (DJ) is above and to
the left of trans-pyloric plane. Any abnormality in the location of DJ means malrotation
irrespective of other findings. In a case of malrotation with volvulus one may see cork screw
appearance of proximal jejunal loops in addition to an abnormally located DJ. One more
possible use of upper GI series is in partial upper small bowel obstruction such as jejunal
stenosis, band obstruction, and internal herniation. In such cases the presentation is usually
not in the neonatal period but a few weeks after birth.
Lower GI study (contrast enema). It is performed under antibiotic cover (triple antibiotic shot
before the procedure). Initial contrast is always water soluble non ionic. Dye is injected per
rectum till the dilated loops are filled in. If the dye reaches the dilated loops it rules out
atresia. In suspected Meconium ileus there will be micro colon (colonic diameter less than 1
cm). The differential diagnosis of micro colon is:
1. Meconium ileus and its variants
2. Total colonic aganglionosis: rounded splenic flexure
3. Distal ileal atresia: dye fails to reach dilated segment.

Appearance of soap bubble appearance on plain film and micro colon in contrast enema
calls for therapeutic enema with gastrograffin. Gastrograffin will dissolve the thick
tenacious Meconium from the terminal ileum which will be passed per rectum relieving
the obstruction. Enema may have to be repeated several times for the first few days to
completely relieve the obstruction. Care should be taken to hydrate the patient well so
that fluid disturbances do not occur. Being osmolar in nature the dye withdraws fluid into
the lumen to dissolve the Meconium thus causing fluid deficit in the intravascular
compartment.
In suspected Hirschsprungs disease the contrast enema should be performed with the help
of a non-lubricated end opening plain tube ( Not Foley catheter) placed in the distal
rectum just about a cm from the anal verge. Dye is injected slowly under fluoroscopic
guidance to see the filling of collapsed rectum followed by appearance of a funnel
shaped dilatation (transition zone) and finally the dilated segment of proximal colon.
Lateral views are taken. On visualization of the transition zone further dye is not injected.
Demonstration of an unmistakable transition zone should end the procedure there being
no requirement for a delayed film. In doubtful cases a 24 hr film is taken to see clearance
55

of the dye. HD can be diagnosed on contrast enema by a transition zone (classically at


recto sigmoid, sometimes long segment and rarely total colonic). It is a myth that the
transition zone disappears after bowel washout, per rectal examination and in neonates.
In the authors experience transition zone is as evident is neonates as in three months
old managed with bowel washouts three times a day for three months. Ultra-short
segment HD can not be diagnosed by contrast enema and requires ano-rectal
manometry. Contraction of external sphincter causes distal rectum to funnel down. This
is normal and should not be mistaken for transition zone.

Ultrasound: It has limited role or evaluation of neonatal obstructions. In suspected malrotation it is


used to see the relationship of the superior mesenteric artery (SMA) and the SMV. Normally the
SMV is to the right of SMA (same as IVC and aorta). In malrotation this is reversed. One can also
see cork screw appearance of jejunal loops in volvulus. Cystic and solid masses can be assessed
with ultrasound. A child with distension a t birth is a good indication for ultrasound. Rarely neonatal
appendicitis and intussusception can be picked up.

PRINCIPLES OF MANAGEMENT

Put the child under warmer cot. Monitor SpO2, temperature and pulse.

Birth history and sequence of events.

Pass NG tube and aspirate contents. Leave it on free drainage. Do this first thing after a
focused physical examination.

Establish IV access and start fluid resuscitation with 20 ml/kg bolus of normal saline. Up to
three boluses may be required. Continue with maintenance fluids usually N/5 in 5% Dextrose.
100ml/kg/day. Replace NG losses by normal saline every 6 hours

Monitor serum Na and K. urine output. Send blood sample for Hematocrit, counts, urea,
electrolytes.

Start broad spectrum antibiotics.

Once hemodynamically stable, obtain a plain abdominal film in AP view and decide if further
contrast study is required.

Laparotomy should be planned after adequate resuscitation and diagnostic workup. It is not a dire
emergency unless you are suspecting volvulus of the mid gut.

Standard right supra umblical

transverse incision is given. Operation will depend on the findings. Table I shows the operative
treatment of different conditions.

Duodenal obstruction: Congenital duodenal obstruction can occur because of atresia (common),
stenosis, perforate or imperforate webs and extrinsic compression by bands or duplication cysts.
Annular pancreas can cause a total or partial obstruction and may be indistinguishable from
atresia.

56

Duodenal atresia occurs in 1 per 5000 live births. 25 % have Down syndrome. In 80% cases the
obstruction is distal to the ampulla of Vater resulting in bilious vomiting. In 20 % it is pre
ampullary. The etiology is thought to be failure of recanalisation of the gut from embryonic solid
cord stage. Most cases have a clear discontinuity including the serosa but occasionally there
may be a membrane inside the lumen causing obstruction with no breach in the serosal
continuity. Rarely the membrane can have a hole in the centre (referred to as diaphragm with
hole) causing partial obstruction. Prenatal diagnosis is possible by ultrasonography which
shows polyhydramnios and dilated stomach and duodenum. Since associated congenital
cardiac and Down syndrome are not infrequent, prenatal diagnosis becomes important to
facilitate parental decision regarding medical termination of pregnancy. Presentation after birth
in cases of atresia is with early onset bile attained vomiting, high gastric aspirates, and
electrolyte imbalance. Distension is usually not there but a distended stomach may be evident
before passing a NG tube. Plain film is diagnostic (double bubble). You may have to inject 30 40 ml of air in the stomach to visualize the double bubble. At times upper GI contrast study is
required to exclude malrotation, evaluate partial duodenal obstruction. Diagnostic work up
should include echocardiography, abdominal ultrasound and a genetic consultation for Down
syndrome. Treatment for atresia and annular pancreas is Duodenoduodenostomy. Since there
is gross lumen disparity between the proximal segment and the distal segment, a diamond
shaped anastomosis is ideal. At times the proximal limb requires tapering to correct gross
disparity. Post operatively it takes some days before the motility of the duodenum is restored
and feeds can be started. Membranous type lesion is treated by excision of the membrane.
Windsock anomaly resulting from a web requires expertise and experience because the level of
origin of the web may be much proximal to the level of change in the caliber. Prognosis is good
if Down syndrome is not associated.
Partial or chronic duodenal obstruction may present beyond neonatal period. An upper GI study
is almost always indicated.

Jejunoileal atresia: Jejunoileal atresia is caused by a mesenteric vascular accident in the intrauterine
life. It is classified as follows:
Type I:

Membranous no outward discontinuity but lumen obstructed.

Type II:

Interrupted. There is a fibrous cord separating the two ends.

Type III A: There is a mesenteric defect also in the shape of V. (most common)
Type III B: Apple peel atresia. Single vessel supplying the distal small bowel with retrograde
flow from right colic vessels. Distal gut spiraling around the vessel like an apple peel
or Christmas tree.
Type IV: Multiple atresias.

The more proximal the lesion, the earlier and more prominent the bilious vomiting and electrolyte
disturbances, and lesser the amount of air on plain film. If there is proximal obstruction decision
for surgery could be taken based on plain X-ray but if distal ileal lesion is suggested on plain x
57

ray a contrast enema may be required to differentiate atresia from Meconium ileus,
Hirschsprungs disease, colonic atresia. In distal ileal atresia the dye will not reach the dilated
segment and there will be micro colon.
Treatment is by resection of the atresia and end to end anastomosis. Fine suture material should
be used such as 6/0 PDS. The author uses single layer extra mucosal anastomosis. A segment
of proximal dilated and distal atretic bowel should be resected with the atresia because it is
thought that these segments lack normal myo-electric properties. End to back anastomosis
should be avoided to help bowel motility. Prognosis is good if excessive bowel is not resected.

Malrotation with or without volvulus: This is an embryonic abnormality that makes the embryonic
midgut prone to twist in a clockwise manner around the superior mesenteric vessels due to a very
narrow base of the mesentery. It results from an embryonic failure of rotation and fixation of the
midgut during 8-12 week of intrauterine life. During early embryogenesis the small bowel grows
rapidly and extrude into the extra embryonic coelome. During 8-12 week it returns back to the
abdominal cavity and rotates anticlockwise along the axis of SMA. The DJ flexure rotates 270
degree to rest above and to the left of pylorus. The root of mesentery elongates so that the
Ileocaecal junction lies in the right iliac fossa the root of mesentery stretches from DJ to ICJ.
Failure of this process of rotation and fixation results in abnormal location of DJ, juxtaposition of
duodenum and caecum close to each other and no length of the mesentery. A band (Ladd band)
runs from the retroperitoneum across the caecum and duodenum at the third part of the
duodenum.

Clinical features may be due to volvulus of the small bowel around SMA (most common and most
dreaded) or chronic duodenal obstruction due to Ladd bands or due to an intrinsic duodenal
stenosis.
Volvulus of the midgut occurs most frequently within the first week of life with sudden onset of bile
vomiting on 3-5 th day. Rapid deterioration occurs because of gut ischemia and the child may
present in shock. A quick resuscitation should be followed by an upper GI study if the child is
resuscitable. Many a time laparotomy is required urgently as part of resuscitation. The key to
surgery is the root of the mesentery. The volved gut is untwisted anticlockwise (usually two and
a half turns). Mesentery is widened and Ladd band is divided. The gut is positioned in the
position of non rotation i.e. the DJ lies to the right with duodenum straight, whole small bowel
on right, whole large bowel on left with the caecum in the left upper abdomen. Inversion
appendicectomy may be performed to avoid diagnostic difficulty and delay in treatment of a
future appendicitis (due to changed location). Laparoscopic approach to malrotation is also
possible.

Meconium ileus: It is characterized by retention of thick and tenacious Meconium in the distal small
bowel causing total obstruction. Pancreatic deficiency and cystic fibrosis are known to be
associated in about 80%. Meconium ileus occurs in 15 % cases of cystic fibrosis. Clinically the
58

child is distended at birth, bowel loops may be palpable filled with thick Meconium and bile
stained vomiting sets in. Due to mixing of air and Meconium the X ray shows a soap bubble
appearance. Digital rectal examination is difficult as the small rectal caliber does not allow insertion
of the finger. The child may pass some pellets of Meconium. Contrast enema shows micro colon.
The dye refluxes into the ileum showing Meconium pellets. Gastrograffin enema may be
therapeutic as described earlier. 50% patients do not respond to Gastrograffin enema. In them and
in complicated cases - Meconium peritonitis, post natal perforation, an urgent laparotomy is
performed. Necrotic and grossly dilated Meconium filled bowel resected, Meconium is washed and
anastomosis is performed with a venting stoma (Distal venting stoma- Bishop Koop, proximal
venting stoma- Santuli). Post operative irrigations with N Acetyl Cystine are given through the
venting stoma and through the rectum. Sweat chloride and genetic tests are done for evaluation of
cystic fibrosis. Once the bowel function becomes normal the venting stoma can be closed.
Hirschsprungs disease in the newborn
HD can present in the neonatal period in different ways:
1. Failure to pass Meconium within 24 hours. Most common presentation. Gradually abdominal
distension occurs. Plain X ray shows many gas filled loops all over the abdomen. Prone cross
table lateral view shows no rectal gas. Diagnosis is made by contrast enema which shows
typical transition zone. Suction rectal biopsy may provide the most definitive diagnosis but
requires expert pathologist. Typically in the biopsy on histochemistry the AChE activity is
raised, ganglion cells are absent and nerve bundles are hypertrophied. Suction biopsy is
easy, can be done without anesthesia but the tissue obtained is only mucosa and sub
mucosa. Absence of ganglion cells in the mucosal plexus means absence in all other areas
also. But it requires expert and experienced pathologist. Full thickness rectal biopsy provides
good tissue including the smooth muscle layers, hence easy for the pathologist. But it requires
GA and also may induce a little bit of scarring to make the definitive operation a little more
difficult. A good compromise (practiced by the author) is to take a punch biopsy without
anesthesia. The author uses the 3 mm laparoscopic biopsy forceps to obtain biopsy at 2 cm
from anal verge. The tissue obtained consists of mucosa, submucosa and a part of the
muscle.
For management the baby is put on rectal washouts twice or thrice daily to help rectal
clearance. Oral feeds are given. Child is sent home on washouts which are given by the
parents. At 6-8 weeks when the child has shown satisfactory growth a definitive pull through
operation is performed. The author favors a laparoscopic assisted trans-anal pull through at
about 6-8 weeks. No covering colostomy is required.
Requiring suppository or enema to pass Meconium

2.

Full blown small bowel obstruction with bilious vomiting, distension and failed passage of
Meconium. Often difficult to differentiated from ileal atresia. This presentation is usually seen
in total colonic aganglionosis. Contrast enema is helpful in diagnosis. Requires urgent
59

laparotomy and stoma creation at the transition zone. Definitive pull through is performed few
months later.

Condition
Duodenal
atresia

Jejunal atresia

Ileal atresia

Onset and
clinical features
Within few hours
after birth, bile
vomiting, no
distension

Imaging

Treatment

Remarks

Double
bubble on
plain film

Duodenoduodenostomy
(diamond shaped
anastomosis)

Within 24 hours
Bilious vomiting,
gradual
distension.
Meconeum
passed
24-48 hours,
progressive
distension, late
vomiting, may
pass encomium

Few dilated
bowel loops

Resection of atresia
and end to end
anastomosis

Etiology: failure of
canalization
25% have Down
syndrome.
DD: annular
pancreas, duodenal
stenosis, duodenal
diaphragm.
Etiology: intrauterine
vascular accident.

Many dilated
loops with
levels on
plain film.
Micro colon
on contrast
enema
Soap bubble
appearance
on plain film
Micro colon
on contrast
enema
No rectal gas
on cross
table prone X
ray
Transition
zone on
contrast
enema

Resection of atresia
and end to end
anastomosis

Resect about 5 cm
on either side of
atresia (poor
myoelectric property)
and to eliminate
lumen disparity.

Gastrograffin enema
May require laparotomy
for Bishop Koop or
Santuli procedure.

Investigate for cystic


fibrosis
Exclude HD by rectal
biopsy
My require repeated
gastrograffin enema
Rectal biopsy
diagnostic
Atypical presentation
likely in total colonic
aganglionosis.
Other operations:
Duhamel, Swenson,
Boley Scott Soave

Plain film non


contributory,
abnormal
location of DJ
on upper GI
contrast
study

Urgent Ladds
procedure

Meconium
ileus

Almost
immediately after
birth, distension
and bilious
vomiting.

Hirschsprungs
disease

No Meconium in
24 hours, gradual
soft distension,
no vomiting
despite massive
distension
(distension
because of
colonic dilatation)
3-5 days. Sudden
onset bile vomit,
rapid
deterioration to
shock.

Malrotation
with midgut
volvulus

Index
60

Rectal irrigations
(washouts) for 6-8
weeks
Laparoscopic assisted
Trans anal pull through
at 6-8 weeks

In 90% cases
volvulus occurs
within the first month
of life.
May also present
with recurrent
chronic duodenal
obstruction.

Emergency management of obstruction


From Scheins Commonsense Emergency Abdominal Surgery 2nd edition
SMALL BOWEL OBSTRUCTION
By far, the most common causes of small bowel obstruction (SBO) are postoperative adhesions and
hernias. Other, uncommon mechanical etiologies are bolus obstruction (e.g. bezoar), malignant or
inflammatory (e.g. Crohns disease) or intussusception.

The Dilemma
A significant number of SBO patients respond to conservative (non-operative) treatment. But
persevering with conservative management in SBO may delay the recognition of compromised
(strangulated) bowel, leading to excessive morbidity and mortality. Clearly, your challenge is to
resolve the following issues:
Which patients need an urgent laparotomy for impending or established bowel strangulation?
And when is initial, conservative treatment appropriate and safe?
Once instituted, how long should conservative treatment be continued before an operation is
deemed necessary? In other words, how to omit an operation without risking intestinal
compromise?

Terminology.

Simple obstruction: the bowel is blocked, compressed or kinked, but its vascular supply is
not threatened.

Strangulation-obstruction: the vascular supply to the segment of obstructed bowel is


compromised.

Closed-loop obstruction: a segment of bowel is obstructed at a proximal and distal point.


Commonly, the involved bowel is strangulated.

Understanding the terms partialversus completeobstruction is crucial to the planning of treatment.


These terms are based on plain abdomen radiographic findings.

Partial obstruction: there is gas seen in the colon, in addition to the small bowel distention
with fluid levels.

Complete obstruction: no gas seen in the colon.

Most episodes of partial SBO will resolve without an operation, while the majority of patients
presenting with a complete obstruction will require one.

Clinical Features
The three important clinical manifestations of SBO are colicky abdominal pain, vomiting and
abdominal distension. Constipation and absence of flatus is a relatively late symptom of SBO. The

61

pattern of these features depends on the site, cause and duration of the obstruction. For example,
in high obstruction, vomiting is prominent while pain and distension are absent or mild; as the level
of obstruction descends, the crampy pain becomes more marked. In distal SBO, distension is the
outstanding symptom with vomiting appearing later.
Feculent vomiting is the hallmark of long-standing, distal, complete SBO and is characteristic of
massive bacterial overgrowth proximal to the obstruction (Remember the main bulk of feces is
made of bacteria). It is a poor prognostic sign the more thick and smelly the nasogastric aspirate,
the less chance there is that the obstruction will resolve spontaneously.
The essential radiographic features seen on supine and erect abdominal X-rays are: gaseous
distension of the bowel proximal to the obstruction, presence of fluid levels and, in complete SBO,
absence of gas distal to the obstruction. The presence of parallel striations (caused by the valvulae
conniventes) running transversely, right across the lumen, are characteristic of distended small
bowel. Colonic gas shadows lack this pattern.

Is There a Strangulation?
The answer to this question is crucial if positive, not only is an operation compulsory, but it also
needs to be performed promptly. The most important feature of strangulation is continuous pain.
Signs of peritoneal irritation (guarding, rebound tenderness) may be present but remember that:

Dead bowel can be present with a relatively innocent abdomen.

Signs of peritoneal irritation are rarely useful in differentiating simple obstruction from
strangulation because they may also be found in simpleSBO when the distension is severe.
Dilated loops of intestine are tender you must surely have seen internists poking
aggressively into distended abdomens and diagnosing peritonitis?

Remember: no isolated clinical feature or laboratory finding present or absent can exclude or
confirm that the intestine is strangulating or dead. Do not wait for fever, leukocytosis or acidosis to
diagnose ischemic bowel because when all these systemic signs are present the intestine is
already dead!
Never forget that a common cause of strangulated bowel is an external hernia. The suspicion of
strangulation must make you examine, or rather re-examine more carefully, the five external
hernial orifices: two inguinal, two femoral and one umbilical.

MANAGEMENT
Fluid and Electrolytes: SBO results in significant losses (or sequestration) of extracellular fluid and
electrolytes, which have to be replaced intravenously. The aggressiveness of fluid management
and hemodynamic monitoring depend on the condition of the individual patient. The fluid of choice
is Ringers lactate. The charting of urine output in a catheterized patient is the minimal monitoring
necessary. Even patients scheduled for urgent laparotomy for strangulation require adequate preoperative resuscitation. Patients with SBO sometimes have intra-abdominal hypertension, which

62

may falsely raise their cardiac filling pressures (CVP, wedge). These patients require all the more
aggressive fluid administration to maintain adequate cardiac output.

Nasogastric Aspiration: A large NG tube (at least 18F in diameter) is needed. The NG tube has both
therapeutic and diagnostic functions. It controls vomiting, but its main aim is to decompress the
dilated stomach and consequently the gut proximal to the obstruction, which overflows back into
the stomach. In a simple obstruction, decompression of the obstructed bowel results rapidly in
pain relief and alleviates the distension. Essentially, the segment of intestine proximal to the
obstruction and distal to the gastroesophageal junction behaves like a closed loop
decompression of the stomach with a nasogastric tube converts it to a simple obstruction. In
strangulation or closed-loop obstruction, the pain persists despite nasogastric aspiration.
There is no advantage in connecting the NG tube to a suction apparatus; drainage by gravity is as
effective and more physiological. Long naso-intestinal tubes are a gimmick with unproven
benefits requiring cumbersome manipulations and causing delay when operation is necessary.

When to Operate?
An hour or two of fluid replenishment is compulsory in the management of every patient. Re-assess
your resuscitated patient: what is the pattern of pain now? Is there improvement on abdominal reexamination?
Immediate operation is required in a minority of patients: those who did not improve, those who
experience continuous pain, or those with significant abdominal tenderness. Here abdominal Xrays usually show a complete obstruction. The probability of strangulation is high. Book them for
an emergency operation.
An initial non-operative approach is often possible because most patients improve at first on the
drip-and-suck regimen. It would be safe to bet, at this stage, that patients with radiological partial
obstruction will eventually escape surgery, whereas those with complete obstruction will eventually
visit the operating room.

But how long is it safe to continue with conservative management? Some surgeons would abort
the conservative trial at 24 hours if the patient fails to open up, because of the nagging concern
about strangulation even in a benign-looking abdomen. Others are prepared to persevere, up to 5
days, in a carefully monitored patient. In the absence of an immediate indication for operation, we
favor the use of an oral water-soluble contrast medium (e.g.Gastrografin) as soon as the diagnosis
of SBO is made. Gastrografin, a hyperosmolar agent that promotes intestinal hurry, plays two
roles: diagnostic-prognostic and therapeutic.
The Gastrografin Challenge
After the initial gastric decompression, 100 ml Gastrografin are instilled via the NG tube, which is
then clamped for 2 hours. After 46 hours, a simple plain abdominal X-ray is obtained. This is not
a formal radiological study under fluoroscopy. Make sure that your patient does not get barium.
63

Presence of contrast in the large bowel proves that the obstruction is partial. In most of these
instances, the Gastrografin is passed per rectum as well. In partial SBO, Gastrografin is
often therapeutic as it expedites the resolution of the obstructing episode.
On the other hand, failure of Gastrografin to reach the colon within 6 hours indicates a
complete obstruction. The probability of spontaneous resolution after a failed Gastrografin
challenge is very low; most of these patients will require surgery anyway so why not
operate on them now?
Another sign of failed Gastrografin challenge is the failure of Gastrografin to leave the
stomach and enter the small bowel. It signifies a significant backpressure in the obstructed
bowel and the need for an immediate operation.
So if we admit a patient during evening hours with suspected adhesive SBO, and without features
mandating an immediate operation, we perform the Gastrografin challenge, and if by the morning
the contrast has not reached the colon we would operate. Of course the results of the Gastrografin
challenge test should be correlated with the whole clinical picture. Note that Gastrografin may pass
across a chronic small bowel narrowing. Thus, for the obstructive episode to be considered
resolved the abdominal symptoms and signs should disappear as well.

Additional Investigations
Clinical examination and plain abdominal radiographs, complemented by a Gastrografin challenge are
sufficient to allow us to reach the correct decision in the majority of patients. Is additional imaging
necessary or useful?

Ultrasonography has been reported by enthusiasts to define accurately the site of obstruction and
establish whether strangulation is present. It requires access to an expert, which most institutions
lack.
Oral and IV contrast-enhanced CT has been shown to accurately define the level of obstruction and
identify a strangulated bowel segment. This, however, does not mean that CT is usually
necessary. CT should be resorted to selectively in the following scenarios:

History of abdominal malignancy. A CT finding of diffuse carcinomatosis with or without


ascites could imply that symptomatic management is the correct option.

Virgin abdomen (see below).

Clinical picture not consistent with the usual partial adhesive SBO. Paralytic ileus may be
easily confused with a partial SBO. There is air in the large bowel, the Gastrografin goes
through but the patient remains symptomatic; fever and/or leukocytosis may be present. CT
will document the underlying responsible cause for the paralytic ileus (e.g. acute appendicitis
or diverticulitis).

Antibiotics: In animal models of SBO, systemic antibiotics delay intestinal compromise and decrease
mortality. In clinical practice, there is no need for antibiotics in patients treated conservatively, and
we operate whenever the suspicion of intestinal compromise is entertained. A single pre-operative
64

dose of antibiotics is administered prophylactically; no postoperative antibiotics are necessary


even if bowel resection has been performed. The only indication for postoperative therapeutic
administration would be long-standing bowel gangrene with established intra-abdominal infection.

The Conduct of the Operation

Carefully avoid iatrogenic enterotomies with their associated postoperative morbidity. Finding
your way into the peritoneal cavity may take time, but be patient for this is the longest part of
the procedure. The rest is usually simpler.

Find a loop of collapsed small bowel and follow it proximally. It will lead you to the point of
obstruction just distal to the dilated obstructed intestine. Now deal with the cause of
obstruction, be it a simple band or a bowel kink. Mobilize the involved bowel segment using
sharp and blunt dissection with traction applied on the two structures to be separated.

Resect only non-viable bowel or when the obstructed segment is impossible to be freed.
Frequently, an ischemic-looking loop of bowel is dusky after being released. Do not rush to
resect; cover the bowel with a warm, wet laparotomy pad and wait patiently; it will usually pink
up within 10 minutes. If not, it requires resection.

Concentrate on the loop which is responsible for the obstruction; there is no need to free the
whole intestine by dividing all the remaining innocent adhesions. This maneuver may be
cosmetically appealing, but adhesions lysed today will re-form tomorrow. As aptly stated by
Timothy Fabian: Lysis of all small bowel adhesions is not required because I believe that the
bowel is locked in the open

position by these chronic adhesions.

Occasionally, multiple points of obstruction appear to be present with no clear area of


demarcation between dilated and collapsed bowel. This is more common in patients after
multiple operations for SBO or those with early postoperative SBO. In this situation the whole
length of the gut has to be unraveled.

How to Manage an Iatrogenic Intestinal Injury during Adhesiolysis?


Transmural enterotomies should be repaired. We recommend a running, one-layered,
absorbable, monofilament technique. Superficial serosal tears should be left alone. Areas
where the mucosa pouts through the defect should be repaired with a running monofilament
seromuscular suture.

Decompress or Not?
Attempting decompression of the proximal distended bowel represents a double-edged sword.
On the one hand, excessive bowel distension impedes abdominal closure and contributes to
postoperative intra-abdominal hypertension with its well-known deleterious physiological
consequences. On the other hand, bowel decompression may contribute to postoperative ileus
and even cause peritoneal contamination. Most would decompress the distended bowel by
gently milking its contents towards the stomach, from where it is sucked by the anesthetist. Milk
65

the bowel very gently with your index and middle fingers, as obstructed bowel is thin-walled and
very easily injured. Do not pull too hard on the mesentery. Palpate the stomach from time to
time; if full, gently squeeze and shake it to restore patency of the NG tube. For a distal SBO,
you may also milk the small bowel contents towards the collapsed colon. Be that as it may,
open decompression through an enterotomy is unwise, given the risk of gross contamination.
Needle decompression is not effective, as enteric juices are abnormally viscous. Obviously,
open decompression should be performed if bowel is being resected insert a pool sucker or
a large sump drain connected to the suction through the proximal line of bowel transection and
accordion the bowel onto your suction device.
Before closing, run the bowel again for missed enterotomies. Check for hemostasis, as
extensive adhesiolysis leaves large oozing raw areas; intra-peritoneal blood promotes ileus,
infection and more adhesion formation. Close the abdomen safely. SBO is a risk for wound
dehiscence and a classic for the M & M conference.
Laparoscopic Approach: Wouldnt it be nice to relieve the SBO laparoscopically? And indeed
laparoscopic lysis of the obstructing adhesions seems attractive because in many cases the cause
of SBO is a single fibrous band. Easier said than done! The collective published experience (and
that which is not published, which is more realistic) points to a higher risk of injury to the distended
and friable obstructed intestine during the laparoscopic operation. This, of course, translates to a
higher rate of septic complications and postoperative morbidity.
Should you wish to attempt laparoscopic approach do it selectively on the easier cases:

First episode of SBO

Abdomen not excessively distended

Patient stable and able to endure a prolonged pneumoperitoneum superimposed on an


already distended abdomen

The first port should be placed through an open approach and away from the old incision. Most
importantly: do not be obstinate and know when to abort before you create too many holes.

Special Circumstances
The Virgin Abdomen
The patient presents with clinical and radiological features of SBO but with no abdominal wall
scar of previous surgery. What to do? Evidence of a complete obstruction is of course an
indication for a laparotomy but what with partial SBO? As with the adhesive partial obstruction,
we recommend a Gastrografin challenge.
In an obstruction caused by an intraluminal bolus, be it parasites or dry fruits, Gastrografin may
disimpact the bowel. In these cases, we would recommend elective abdominal imaging to
exclude an underlying cause. Non-resolving partial obstruction despite the Gastrografin
challenge suggests a mechanical cause, such as a congenital band, an internal hernia,
malignancy, inflammation or even an impacted bezoar. Laparotomy usually uncovers a treatable
cause of obstruction. A pre-operative CT scan just to find out what were dealing with is not
66

mandatory and may only delay the operation without changing its indication. But when in doubt, if
readily available, and in the absence of clinical strangulation, it may be helpful.
Cecal carcinoma is a typical cause of distal SBO in the virgin (or non-virgin) abdomen. The
clinical presentation is commonly gradual and smoldering. Gastrografin may pass through
into the cecum. In this case a CT would be diagnostic.
SBO due to previously undiagnosed but suspected Crohns disease is an exception; here a CT
may be very suggestive indicating continued conservative therapy.

Intussusception: Although common in pediatric patients is a very rare cause of SBO in adults. In
adults the leading point is usually organic (e.g. neoplasm, inflammatory lesions), and seldom
idiopathic as in children. Patients with small bowel or ileo-colic intussusception present with
non-specific features of SBO (in a virgin abdomen) necessitating operative treatment. A
specific pre-operative diagnosis can be obtained with ultrasound or CT, showing the multiple
concentric ring sign (bowel within bowel), but wont change what you need to do operate
and resect the involved segment of bowel. Although controversial, some would attempt
reduction of intussusception when there are no external signs of ischemia or malignancy and
if after reduction no leading point is found (i.e., idiopathic intussusception) one could leave the
bowel alone.

The Known Cancer Patient: A patient is admitted with SBO a year or two following an operation for
gastric or colonic cancer. You should first attempt to obtain information about the findings at
previous laparotomy. The more advanced the cancer then, the higher the probability that the
current obstruction is malignant. Clinically, cachexia, ascites or an abdominal mass suggests
diffuse carcinomatosis. These cases present a medical and ethical dilemma. On the one hand, one
wishes to relieve the obstruction and offer the patient a further spell of quality life. On the other
hand, one tries to spare a terminal patient an unnecessary operation. Each case should be
assessed on merit. In the absence of stigmata of advanced disease, surgery for complete
obstruction is justifiable. In many instances adhesions may be found; in others, a bowel segment
obstructed by local spread or metastases can be bypassed. When diffuse carcinomatosis is
suspected clinically or on CT scan, a reasonable option would be to insert a palliative, venting
percutaneous gastrostomy, allowing the patient to die peacefully at home or in a Hospice
environment.

Radiation Enteritis: Radiation treatment of abdominal or pelvic malignancies is not an uncommon


cause of SBO; this usually develops months or even years after irradiation. A relentless course of
multiple episodes of partial SBO, initially responding to conservative treatment but eventually
culminating in a complete obstruction, is characteristic. There is also the uncertainty about the
obstruction being malignant or adhesive in nature. One always hopes that it is adhesive, because
67

SBO due to radiation injury is bad news indeed. When forced to operate for complete obstruction,
one finds irradiated loops of bowel glued or welded together and onto adjacent structures. The
paper-thin bowel tears easily. Accidental enterotomies are frequent, difficult to repair, and
commonly result in postoperative fistulas. Short involved segments of bowel are best resected, but
when longer segments are encountered, usually stuck in the pelvis, it is safest to bail out with an
entero-enteric or entero-colic bypass. Postoperative short-bowel syndrome is common whatever
the procedure. Long-term prognosis is poor radiation enteritis is almost as bad as the
malignancy the radiation had attempted to control.

Recurrent Multiple Episodes of SBO: The patient is typically re-admitted every second month for
SBO and has undergone, in the past, multiple operations for this condition. How should he be
managed? We would treat him as any other patient presenting with adhesive SBO. Fortunately,
most such episodes are partial, and responsive to conservative treatment. When complete
obstruction develops, operative management is obviously necessary. Attempts at preventing
subsequent episodes with bowel or mesentery plication or long tube stenting are recommended by
some. The evidence in favor of such maneuvers is anecdotal at best. We do not practice them.
Occasionally a patient develops obstruction early in the aftermath of an operation for SBO: this is a
case par excellence for prolonged non-operative management, with the patient maintained on TPN
until adhesions mature and the obstruction resolves.

Gallstone Ileus: Gallstone ileus develops typically in elderly patients with longstanding cholelithiasis.
It is caused by a large gallstone eroding into an adjacent segment of bowel usually the
duodenum that then migrates distally, until stranded at the narrow ileum. Presentation is usually
vague as initially the stone may disimpact spontaneously causing intermittent episodes of partial
obstruction. You will never miss the diagnosis once you habitually and obsessively search for air in
the bile ducts on any plain abdominal X-ray you order. The air enters the bile duct via the enterocholecystic fistula created by the eroding gallstone. Treatment is operative and should be tailored
to the condition of the patient. In frail and sick patients deal only with the SBO: place an
enterotomy proximal to the stone and remove it and search for additional stones in the bowel
above you do not want to have to reoperate! In patients who are younger and reasonably fit and
well you may want to also deal with the cause of the problem the gallbladder. Perform a
cholecystectomy and close the duodenal defect.

Prognosis
Overall, about half the patients presenting with an adhesive SBO can be managed without an
operation. About half the patients will suffer subsequent episodes of SBO, irrespective of the
treatment surgical or conservative. The aim is therefore to operate only when necessary, but not to
delay a necessary operation.

68

COLONIC OBSTRUCTION
Malignant and Diverticular Colonic Obstruction
The four steps you should consider in the approach to patients with mechanical colonic obstruction
are:

Establish the exact diagnosis

Then, at operation

Decompress the colon

Resect the obstructing lesion

Decide whether there should be a primary anastomosis or a colostomy

Preoperative Diagnosis and Management


The clinical hallmark of colonic obstruction is significant abdominal distention associated with
recent onset of constipation and lack of flatus. The obstruction usually develops gradually over a
few days, sometimes on a background of a change in bowel habit. The usual site of the obstructing
carcinoma is in the sigmoid or left colon. The sigmoid is also the locus of any obstructing
diverticular mass. Right colonic lesions become obstructing only at the ileocecal region. Because
of the wide caliber of the rectum, rectal cancer very rarely presents with a complete obstruction.
Most of these patients are elderly and, because the obstruction may have affected them for
several days, they have not been eating and drinking properly, and so they are dehydrated. Make
a thorough examination of the abdomen. It is usually, but not invariably, grossly distended. Be
especially observant of signs of peritonitis, which may indicate a manifest or pending perforation of
the colon usually proximal to the obstructing lesion. The site of perforation may be a pre-existing
sigmoid or left colonic diverticulum, but more commonly it is in the right colon. The right colon and
cecum is the widest part of the bowel. It will also be the most distended part with the highest
tension of the bowel wall (Laplaces law), thus the most likely to perforate. When the ileocecal
valve is competent the small bowel will be only mildly distended while massive distension and
pressure affects the right colon. This pressure can tear the circular muscle layer or cause ischemic
necrosis with subsequent perforation. Tenderness of the abdomen on the right side may be a sign
of this development. If such tenderness is present and the abdominal X-ray shows a grossly
distended right colon (in excess of 10 cm) then operation must not be delayed beyond the
requirements of resuscitation.
Plain abdominal X-rays usually show a distended colon because the obstructing lesion is most often
in the left colon. When the obstruction is in the right colon, at the cecal area, it can sometimes be
difficult to differentiate between small bowel and large bowel obstruction. In long-standing left
colonic obstruction when the ileocecal valve is incompetent, the small bowel becomes dilated as
well. Severely dilated loops of fluid-filled small bowel may then obscure the distended colon a
picture that may be misinterpreted as partial small bowel obstruction. Regardless of the
appearances on plain X-rays you must positively confirm the diagnosis by additional investigation
and exclude pseudo-obstruction (see below).What you have to do is document the site of the
obstruction: this can be done either with colonoscopy or a contrast enema. Our bias is against
69

the use of barium in this situation and in favor of a water-soluble contrast such as Gastrografin.
The site of the obstruction, but not the cause, will usually be evident. At this stage obstruction is
obstruction the management is the same whether a carcinoma (common) or a diverticular mass
(rare) causes it. A pre-operative CT scan is not mandatory but will usually give the diagnosis.
When clinical and laboratory features are suggestive of carcinomatosis, or extensive hepatic
metastatic involvement, CT documentation of the advanced disease allows better planning of
treatment together with the patient and family. You do not want to operate on a jaundiced patient
whose liver is almost replaced with metastases for hell surely succumb to hepatic failure after the
operation.

Planning and Timing the Operation


In general, in the absence of signs of actual or impending compromise of the bowel wall there is no
reason for you to hurry with the operation. Daytime surgery, with all that it means in terms of the
surgical team and supportive personnel, is the better option for the patient and yourself. There is
plenty of time to prepare the patient for a definitive operation to relieve the obstruction. On the
other hand, should the patient have peritonitis, systemic inflammatory response syndrome (SIRS),
or free abdominal gas on abdominal imaging, an emergency operation is necessary. Antibiotic
treatment should be started and the time of the operation decided according to the progress of the
resuscitation-optimization.

Obviously, in patients with colonic obstruction bowel preparation is contraindicated. Any cleansing
solutions administrated from above will accumulate proximal to the obstruction further dilating the
obstructed colon and making your life more miserable during the operation. Some surgeons like to
administer enemas to clear the rectum and colon distal to the obstruction but these sections of the
bowel are usually empty. Do not forget to administer the usual dose of systemic antibiotic
prophylaxis just before the operation.

In general, the operation for acute colonic obstruction is a major procedure, often in a patient who
is old and fragile. Consequently the mortality and morbidity of these operations are significant. To
avoid complications and mortality you have to exercise your best judgment along the lines
presented below.

The Operation
A long midline incision is nearly always preferable. The findings of ascites, peritoneal seedlings,
omental cake, and hepatic metastases will immediately tell you that the battle has been lost and
the operation is merely palliative. If the obstruction is in the right colon there is usually not a lot of
bowel distension. Then, the operation is a rather straightforward right hemicolectomy with primary
anastomosis.
The left colon or the sigmoid, however, is the usual site of the obstruction. Here the proximal colon
is distended making the operation more difficult. First inspect the ascending colon to find out if
70

there are tears or necrosis due to the distension. If there are they can be of any stage from minor
to large with micro-perforation. The significance of the tears is that if they are extensive or necrotic
it may suggest that a subtotal colectomy is indicated. Otherwise proceed as follows:

Decompression. Because of the distended bowel it may be difficult to expose the lesion on
the left side and to manipulate the bowel. Sometimes it is better to make an enterotomy into
the terminal ileum and insert the suction device (poolsuction or a large sump drain) through
the hole to decompress the small bowel and also pass the device through the ileocaecal valve
to decompress the right colon. Close the hole transversely with a suture. It should now be
possible to expose the lesion that causes the obstruction. Often, in cases diagnosed and
treated early, the colonic distention is caused by gas and not fecal matter; it can be relieved
simply by inserting a large needle or angiocath connected to the suction tube,and tunneled
through the tenia coli.

Resection. Whether it is cancer or diverticulitis-sigmoiditis the principles of treatment are the


same. Mobilize the lesion the same way you would at an elective operation and resect it. If
you are accustomed to linear cutting staplers (TLC or GIA) this is one of the best instances to
use staplers. Transect the bowel on each side of the lesion and divide also the mesentery and
the segmental vessels with the linear stapler. You have resected the cause of the obstruction
with complete control of the bowel ends and no leakage. Now is the time to decide whether
the bowel ends should be joined or the proximal end should be brought out as a colostomy.

Do notice that it is considerably more difficult to operate on colonic obstruction than on a similar
elective case. You will need the extra hands of an assistant to achieve exposure and the decisions
are much more complex during the operation. It is advisable to do the operation together with a
colleague who can assist with the decisions. If it is a cancer operation it should be the correct
cancer resection not just an operation that relieves the obstruction. A simple bowel resection is
permissible only if the cancer is disseminated so the type of resection has no influence on the
prognosis of the cancer. In that situation a colostomy is usually the better option because it is safer
for the patient and has less risk of a new obstruction due to local recurrence of the tumor.

To Anastomose or Not?
The judgment process here is not much different from that considered after sigmoidectomy for
acute diverticulitis. What is different, however, is that here there is no associated peritonitis and
suppuration.

In essence after you have resected the lesion you are left with a few options:

End left (iliac) colostomy Hartmanns procedure

Primary colocolic or colorectal anastomosis

Subtotal colectomy with ileosigmoid anastomosis

71

If the cancer is situated in the transverse or descending colon it is often better to do a subtotal
colectomy and an ileosigmoid anastomosis. This usually means that empty or mildly distended
and well-perfused small bowel is joined to normal colon below the obstruction. Most patients
will manage an ileosigmoid anastomosis without incapacitating diarrhea and incontinence,
while an ileorectal anastomosis requires that the patient has had normal continence before the
current illness. For cancers of the sigmoid colon or rectosigmoid junction, a sigmoid
colectomy is adequate and a subtotal colectomy should be considered only if the ascending
colon is ischemic or perforated as mentioned above.

Some Controversies
The main dispute is the question of primary anastomosis and the means of obtaining that goal. It is
only a problem for left-sided obstructions. On-table bowel irrigation has been proposed as a
means of primary anastomosis between clean proximal colon and the rectum. The irrigation
prolongs the operation substantially and therefore represents negative damage control. An
alternative is the subtotal or total abdominal colectomy with anastomosis of the terminal
ileum to the sigmoid colon or rectum. This also is a bigger operation that takes longer. In a
large Scottish randomized trial comparing the two means (subtotal vs. segmental resection) of
obtaining a primary anastomosis there was no difference in survival or anastomotic healing with
either method. There are now several randomized trials of elective colonic resection with or without
mechanical bowel preparation. Again there was no difference in anastomotic healing. It may not be
entirely valid to extrapolate the results with residual feces of the elective colon to the massive
fecal load of the acute colon. It appears, however, that a primary anastomosis can be made safely
on the obstructed colon after decompression and removal of feces with suction and milking the
colonic end before joining it to the rectum. We, among others, make an anastomosis in an
unprepared bowel in selective cases.

Why bother with a primary anastomosis at all when it increases the operation time and
complexity of the operation? A Hartmann resection and colostomy is quicker and simpler. It
is not an all-or-nothing situation but the concerned surgeon will know that the Hartmann
resection is often the better choice if the patient is in bad general condition or if the cancer
cannot be radically removed. About half of the Hartman resections will never be reversed, often
for very good reasons. For the less experienced surgeon we suggest that the Hartmann
resection is always a valid option.

Is there any role for a decompressive colostomy without resection of the obstructing
lesion? This staged management was commonly used only a few decades ago, usually
consisting of a transverse colostomy which represented the first stage. Nowadays we would
reserve this option in two circumstances:

72

The critically ill patient who wont tolerate a major procedure; for example, a patient
developing an obstruction a week after a myocardial infarction. Here, a transverse
colostomy or even cecostomy under local anesthesia will alleviate the obstruction.

When there is pre-operative evidence of wide-spread malignant disease, as discussed


above.

The Colostomy
It should be understood that the creation of an emergency colostomy is potentially problematic. A
common problem is retraction due to inadequate mobilization of the bowel. It frequently causes
disruption of the mucocutaneous suture line in the early postoperative course, followed by
retraction of the bowel end to a subcutaneous position and progressive stenosis of the skin
orifice. Even retraction into the peritoneal cavity resulting in peritoneal soiling with feces
occasionally occurs. To be safe,make sure that the left colon has been mobilized up to and
sometimes including the splenic flexure. The closed proximal end should easily reach out
several centimeters beyond skin level and rest in that position without support. Do not settle for
anything less or you may make the patients remaining life an ordeal. The colostomy hole
through the rectus abdominis muscle will have to be larger than normal because of the bowel
distension. It is sometimes necessary to evacuate some of the gas and feces before the bowel
can be brought out. A simple rule of thumb is that when the colostomy hole is kept open with
retractors the bowel end should pass easily between them, and it will not pass if the retractors
are removed. There is no need to close the lateral gutter, or even to fix the bowel to the anterior
abdominal wall if it has been sufficiently mobilized. The mucocutaneous suture of the colon to
the skin with an absorbable suture is all that is needed.
You should choose either an anastomosis or a colostomy. The proximal protective ostomy for an
anastomosis is a hybrid of disputable value. Should the anastomosis break, the protective
colostomy is of little help because the colon was not clean and will leak all the residual feces
distal to the protective stoma. A reoperation becomes necessary anyway. There is no study that
proves that the ostomy prevents anastomotic failure.

Our Own Preferences


We believe that nowadays in most patients resection of the obstructing lesion and a primary
anastomosis can and should be achieved safely. For sigmoid lesions we opt for a sigmoidectomy
followed with a colorectal anastomosis; if the proximal colon is excessively loaded or appears
compromised we proceed with a subtotal colectomy and an ileorectal anastomosis. The latter is
also our preference for lesions in the proximal descending colon and the transverse colon. We
reserve the Hartmann procedure for high risk patients and those who appear poorly nourished .

Index

73

Pathophysiology of acute intestinal obstruction


Vivek Agrawal, Mohit Kumar Joshi
Introduction
Acute intestinal obstruction (AIO) is a common surgical emergency. Depending on the presence
or absence of bowel activity, it is classified as either dynamic or adynamic. Although there are
many causes of acute intestinal obstruction, the presentation is with following four classical
features:
1. Pain
2. Vomiting
3. Distension
4. Absolute constipation (obstipation)

Bowel obstruction results in alterations of the normal intestinal physiology. Despite the well known
changes viz., distension, decreased absorption, intraluminal hypersecretion, and alterations in
motility, the pathophysiology of bowel obstruction still remains incompletely understood. In addition
to these changes, neural and hormonal control mechanisms, endogenous bacterial flora, and the
innate immunity of the gut are also disrupted.
In the past, it was thought that a decrease in blood flow to the gut was responsible for most of the
pathophysiologic changes in bowel obstruction. More recent experimental work, however,
suggests that many of these changes occur due to an increase in blood flow that occurs during the
1

early phases of bowel obstruction due to intramural bowel inflammation. The clinical features of
bowel obstruction vary depending upon the site of obstruction. In proximal bowel obstruction the
main features are pain and vomiting, where as in distal obstruction the preliminary features are
pain and distension. Following complete evacuation of the fecal matter from the gut distal to the
site of obstruction, obstipation sets in.
Pain: Pain may be perceived in the upper, middle or lower abdomen (Monks zones of pain)
depending upon the site of obstruction viz., the foregut (T5-8), midgut (T9&10) or the hindgut
(T11&12). Pain arising from gut is perceived via autonomic innervation, and it is sensitive to
stretching, twisting, pulling and compression.

Vomiting: Vomiting leads to fluid and electrolyte disturbances. In proximal lesions it is projectile and
contains proximal bowel contents along with the ingested food material. In distal bowel obstruction
the contents are feculent due to exaggerated proliferation and fermentation of the intestinal
contents by the bacteria in the affected part of gut. The fluid and electrolyte imbalance as a result
of vomiting is further compounded by the distension of the involved segment of the gut due to
accumulation of considerable amount of fluid.

74

Pathophysiological changes in acute bowel obstruction


The pathophysiological changes that occur with AIO can be studied under following heads:
1. Intestinal distension
Although a constant feature of bowel obstruction, the mechanism underlying the intestinal
distension has not been elucidated completely. Most of the gas distending the small bowel
in early phases of obstruction accumulates from swallowed air. Other sources include:
fermentation of sugars, production of carbon dioxide by interaction of gastric acid and
bicarbonates in pancreatic and biliary secretions, and diffusion of oxygen and carbon
dioxide from the blood. Following dilatation and inflammation, activated neutrophils and
macrophages accumulate in the bowel wall due to increased blood flow to the gut, these
release reactive proteolytic enzymes, cytokines, and other locally active substances which
inhibit or damage the secretory and motor processes of the gut. The nitric oxide produced
during the process causes smooth muscle relaxation, further aggravating the distension and
inhibiting gut contractility. The normal intraluminal pressure of 2 to 4 cm of water rises to 8 to
10 cm of water in obstruction, which may reach 30 to 60 cm of water in closed loop
obstruction. The reactive oxygen radicals produced during these changes not only affect gut
motility but also its permeability.

During the first 12 hours of AIO, water and electrolytes accumulate within the lumen
secondary to a decrease in absorption. By 24 hours, accumulation occurs more rapidly due
to a further decrease in absorption and in addition to an increase in intestinal secretion
secondary to mucosal injury and increased permeability. Although the role of neural or
systemic humoral/hormonal mechanisms in aggravating distension remains likely, it is poorly
investigated. This decrease in the absorptive capacity of the gut with an increase in
intraluminal secretion leads to excessive fluid losses which can lead to dehydration.
Although the intestinal wall distal to the obstruction maintains normal function, the inability of
the luminal content to reach the unobstructed gut compounds the dehydration.

2. Intestinal Motility
In the early phase of bowel obstruction, intestinal contractile activity increases in an attempt
to propel intraluminal contents past the obstruction. Later, it diminishes secondary to
intestinal wall hypoxia and exaggerated intramural inflammation; however, the exact
2

mechanisms have not been completely elucidated. Some investigators have suggested that
the alterations in intestinal motility are secondary to a disruption of the normal autonomic,
parasympathetic (vagal) and sympathetic, splanchnic innervation.

It is also proposed that cells of Cajal, interstitial cells that affect gut motility transiently lose
their function while maintaining their viability in bowel obstruction. In obstruction, the
proximal bowel distends, with a complete loss of electrical slow waves which is generated
by the cells of Cajal. With relief of obstruction, these cells become functional once again,
75

and the slow waves return. It remains unclear whether this loss of function of the cells of
Cajal represents the primary cause of diminished gut motility or an epiphenomenon.

3. Circulatory Changes
Ischemia of the bowel wall can occur by several different mechanisms. Extrinsic
compression of the mesentery by adhesions, fibrosis, mass, twisting or a hernia defect,
extrinsic pressure on a segment of bowel (e.g., a fibrous band), or progressive distension in
the setting of a closed-loop obstruction can all cause vascular compromise or strangulation.
The consequences of vascular compromise are more disastrous in large bowel obstruction,
4

as in nearly a third of people ileocecal valve is competent , which functionally leads to


closed-loop obstruction between the competent ileocaecal valve and the site of obstruction
in the large bowel.

Progressive distension of the bowel lumen with a concomitant increase in intraluminal


pressure results in increased transmural pressure on capillary blood flow within the bowel
wall. In simple (nonclosed loop) obstruction, this occurs rarely, as the obstructed distended
bowel can decompress proximally. Severe intestinal distention, however, is self-perpetuating
and progressive, intensifying the peristaltic and secretory derangements and increasing the
risks of dehydration and progression to strangulating obstruction. Strangulating obstruction
is obstruction with compromised blood flow; it occurs in nearly 25% of patients with small5

bowel obstruction . It is usually associated with hernia, volvulus, and intussusception.


Strangulating obstruction can progress to infarction and gangrene in as little as 6 hours.
Venous obstruction occurs first, followed by arterial occlusion, resulting in rapid ischemia of
the bowel wall. The ischemic bowel becomes edematous and infarcts, leading to gangrene
and perforation. It is more common in cecum and ascending colon where the luminal
diameter is greatest and (by Laplace's law) the wall tension (and ischemia) is also
4,6

maximum . This makes large bowel obstruction more of a surgical emergency than small
bowel obstruction. With strangulation, there can also be blood loss into the infarcted bowel,
which together with the preexistent fluid loss leads to further hemodynamic instability,
exacerbating the already compromised blood flow of the intestinal wall.

4. Microbiological changes and Bacterial Translocation


The upper small intestine contains gram-positive facultative organisms in small
6

concentrations, usually <10 colonies/mL. More distally, the bacterial count increases in
8

concentration to about 10 colonies/mL in the distal ileum, with flora changing primarily to
coliforms and anaerobes. In the presence of obstruction, bacteria proliferate rapidly proximal
to the obstruction in direct proportion to the duration of obstruction, reaching a plateau of
9

10

10 10

colonies/mL after 1248 hours of obstruction.

1,7

The bowel distal to the obstruction

tends to maintain its usual bacterial flora until ileus sets in, following which there is
generalized bacterial proliferation. Toxins produced by these bacteria disrupt the mechanical
76

integrity of the gut mucosa. Once the gut mucosal barrier is lost, bacterial translocation
occurs as the luminal bacteria invade the submucosa and enter the systemic circulation via
the portal venous and lymphatic systems.

Reduction of perfusion of the intestinal wall

further compromises the mucosal defences. All these changes have been well documented
in animal models; however, documentation of true bacterial translocation in humans is
lacking. More recent work has shown that lipopolysaccharide and other inflammatory
mediators, but not bacteria, can be recovered from the mesenteric lymphatics. The eventual
drainage of these vasoactive substances into the systemic circulation may lead both to the
systemic manifestations of sepsis and further disruption of the mucosal barrier function.

Due to these alterations in resident microbial flora, the risk of infective complications in
bowel obstruction is increased markedly, especially if bowel resection is required or if an
inadvertent enterotomy is made with intraperitoneal spillage of "obstructed" enteric contents.
With strangulation, there

is

systemic

entry of

bacterial

products,

activation of

immunocompetent cells, release of cytokines, and increased formation of reactive oxygen


intermediates, this leads to systemic inflammatory response syndrome and multiple organ
dysfunction.

Metabolic effects of obstruction

In proximal obstruction dehydration, hypochloremia, hypokalemia, metabolic alkalosis

In distal obstruction third space losses and dehydration

Hypovolemia, hypotension

Haemoconcentration

Oliguria and azotemia

Increased intraabdominal pressure

Restricted ventilation and atelectasis

Impaired venous return

Congestion of the bowel wall and seepage of blood into the lumen (significant if long
segments involved)

Strangulation of the gut

Shock and death

Conclusion
AIO is a common surgical emergency. It is important to understand its natural history and
pathophysiology so that the course of events can be anticipated and the associated adverse events
can be averted by timely appropriate intervention in an effort to decrease the associated high
morbidity and mortality.

77

REFERENCES
1.

Houghton SG, Medina ARDL, Sarr MG. Bowel obstruction. In: Zinner MJ, Ashley SW editors.
th

Maingots abdominal operations.11 ed. Mc Graw Hill; 2007. p.482.


2.

Miedema BW, Johnson JO. Methods for decreasing postoperative gut dysmotility. Lancet Oncol
2003; 4:365372.

3.

Jatoi A, Podratz KC, Gill P, Hartmann LC. Pathophysiology and palliation of inoperable bowel
obstruction in patients with ovarian cancer. J Support Oncol 2004; 2:323337.

4.

El-Amin LC, Levine MS, Rubesin SE, Shah JN, Kochman ML, Laufer I. Ileocecal valve: Spectrum
of normal findings at double-contrast barium enema examination. Radiology. 2003;227:5258.

5.

Sarr MG, Bulkley GB, Zuidema GD. Preoperative recognition of intestinal strangulation
obstruction. Am J Surg 1983;145:176.

6.

Slam

DK,

Calkins

S,

Cason

FD.

LaPlace's

law revisited: Cecal

perforation

as

an

unusual presentation of pancreatic carcinoma. World J Surg Oncol. 2007; 5: 14.


7.

Evers BM. Small intestine. In: Townsend CM, Beauchamp RD, Evers BM, Mattox KL editors.
th

Sabiston textbook of surgery. 18 ed. Gopsons paper Ltd.2008. p.1291.

Index

78

Radiological Evaluation of Intestinal Obstruction in Adults


Anjali Prakash
SMALL BOWEL OBSTRUCTION
The radiological investigations of patients with SBO, the indications for and timing of surgical
intervention have changed over past two decades. The old paradigm of never let the sun set or rise
on an obstructed bowel reflected the clinical and radiological limitations of preoperative recognition of
strangulation. Nowadays imaging has become the primary focus, in the treatment of SBO. Radiology
assumes relevance in assisting the surgeon in addressing the following questions
- Is the small bowel obstructed?
- How severe is the obstruction?
- Where is it located?
- What is the cause?
- Is strangulation present?
1

Various modalities are available to answer these questions and a suggested algorithm is given in Fig
1.

Conventional radiography

This is the preferred initial radiographic examination.

Plain films are diagnostic in 50-60%, equivocal in 20-30% and normal, nonspecific, or
misleading in 10-20%. The radiographs to be done are1. Supine abdomen bladder should be emptied before the film and film should include area
from diaphragm to hernial orifices.
2. Chest radiographs-superior to erect abdomen to detect pneumoperitoneum
79

-chest diseases may mimic SBO


-to serve as baseline
3. Erect abdomen- air fluid levels are seen. Normal appearances- small amount of gas may
be present. Two or more air fluid levels may be seen at D-J flexure and terminal ileum.

It is important to distinguish Large from Small bowel loops:


Large Bowel

SmallBowel

Haustra

present

absent

Valvulae conniventes

absent

present in jejunum

Number of loops

few

many

Distribution of loops

peripheral

central

Radius of curvature of loops

large

small

Diameter of loop

50 mm

30-50mm

Solid faeces

present

Plain radiographic changes may appear after 3-5 hours, if there is complete small bowel obstruction
and will be marked after 12 hrs. With incomplete obstruction, changes on plain radiograph may take
days to appear.

The key radiographic signs that allow distinction between a high grade SBO and a low grade SBO are
the presence of small bowel distention with maximal dilated loops averaging 36mm in diameter and
exceeding 50% of caliber of largest visible colon loop. 2.5 times increase in number of distended
loops in the abdomen compared with normal number. Other significant findings are the presence of
more than two air fluid levels, air fluid levels wider than 2.5cm and levels differing more than 2cm in
height from one another within the same bowel loop.

In dilated bowel loops, which are completely fluid filled, small bubbles of gas may be trapped in rows
between valvulae conniventes on erect film, this is known as string of beads sign. This sign is
virtually diagnostic of small bowel obstruction and indicates peristaltic hyperactivity to overcome
mechanical obstruction. This is also seen sometimes in IBD or adynamic ileus.

X ray categories of SBO

Normal pattern - absence of small bowel gas or small amount of gas within upto four non
distended (less than 2.5cm) loops of small bowel. A normal distribution of gas and stool within a
non distended colon should be visualized.

Abnormal but nonspecific gas pattern- Atleast one loop of borderline or mildly distended small
bowel (2.5-3cm) with three or more air fluid levels on erect film. The colonic gas and faeces
distribution is normal or displays borderline distribution, this pattern is known as non specific

Probable SBO pattern- abnormal gas distribution consisting of multiple gas or fluid filled loops of
dilated small bowel with small/moderate amount of colonic gas.
80

Unequivocal SBO- dilated gas or fluid filled small bowel loops in setting of gasless colon. This
warrants immediate surgery.

In the patients with complete mechanical small bowel obstruction there is no gas in colon. This is a
valuable differentiation between obstruction and adynamic ileus. Small amount of gas may be
present in colon in early stages of SBO. Presence of colonic gas in later stages signifies
putrefaction or iatrogenic cause. Large amount of colonic gas eliminates possibility of SBO.

Serial examination by plain radiography may be required in equivocal cases for analysis of position
and amount of gas.

Causes of small bowel fluid levels-

small bowel obstruction

large bowel obstruction

gastroenteritis

hypokalemia

uremia

saline catharatics.

cleansing enemas

Sonography: This is used when availability of CT is less. It is an operator dependent modality, with
inherent ability in evaluating gas filled structures. At sonography bowel obstruction is considered to
be present when lumen of fluid filled small bowel loop is dilated to more than 3cm. and the length
of segment is more than 10cm, and peristalsis of dilated segment is increased as shown by to and
fro or whirling motion of the bowel contents. This helps to differentiate a mechanical obstruction
from adynamic ileus of peritonitis.

Level of obstruction may be determined by examining the area of transition from dilated to normal
bowel. Causes of SBO like bezoars, intussception, crohns and tumor can be detected by this
method. Obstruction associated with external hernia is ideal for sonographic detection in that the
dilated loop may be traced to a portion of gut in abnormal location.

The Severity of obstruction can be assessed by the presence of free fluid between dilated small
bowel loops, aperistalsis and bowel wall thickening(>3mm) suggests bowel infaction.

Barium and water soluble contrast small bowel radiography: Water soluble contrast (eg
urograffin) gets diluted and results in poor mucosal detail on radiography and is hypertonic. Hence
it is not advisable and has shown to have no therapeutic effect in patient of SBO.

81

Oral barium is better as large amount of fluid in loop proximal to obstruction will dilute contrast and
it will not inspissate and harden. Besides density is better with barium and chances of electrolyte
imbalance are less. Before using barium in small bowel, colonic obstruction has to be excluded.

1. Barium meal follow through


500ml of 42% w/v barium mixture is ingested, fluoroscopic + overhead radiographs at 15-30
minute intervals, continue till ileocaecal valve, when barium has reached caecum, a rectal
tube is inserted and air is insufflated to distend the right colon and barium filled distal small
bowel.
Advantages- patient preference, ease of administration and performance, ability to judge
transit time.
Disadvantages- length of examination, dilution of barium by gastric and intestinal contents,
lack of complete distention of small bowel.

2. Enteroclysis
The intubation and infusion of small bowel by barium, challenges the distensibility of bowel
wall, exaggerating the effects of mild or subclinical obstruction. There is High sensitivity
(100%) and specificity (88%) for SBO and high accuracy in determining the site and cause of
obstruction. It also demonstrates acute angulation in patients with adhesions.
Technique- infusion of 30-40% w/v barium suspension at 60-90 ml/min after duodenal
intubation.
Double contrast enteroclysis infusion of 60-95% w/v barium, followed by infusion of air/methyl
cellulose to distend lumen leaving a thin coating of barium.
Advantages of enteroclysis
-shorter examination time
-better distension
-greater positive and negative for a wide range of SB pathology,
including strictures, adhesions and intrinsic SB disease(eg sprue)

Disadvantages
-more radiologist time
-patient discomfort

Normal Luminal diameter of small bowel on barium examinations


-

atleast < 2.5cms

distended after meal/SBFT- 3.5cm jejunum, 3cm ileum

- enteroclysis
4.5cm upper jejunum
4cm jejunum
3cm ileum
82

3. Capsule endoscopy utilizes a small tablet size camera, that is swallowed by the patient,
recording images of gut till expelled.
Advantages- allows endoluminal views of areas beyond the reach of fibreoptic endoscopes
Disadvantages- requires many hours of patient preparation
- difficult to localise a pathological process that is visualized.

4. CT
Multidetector CT plays a primary role in evaluation of patients with SBO. It is a fast
examination does not require oral contrast, as water serves as a great contrast, allows
assessment of bowel and extramural areas.The sensitivity of CT in detecting SBO ranges
from 94-100%. For incomplete/intermittent obstruction CT combined with enteroclysis is the
best method for evaluating the presence and degree of bowel obstruction.

CT criteria of SBO is the presence of dilated small bowel loops (diameter >2.5cms from
outer wall to outer wall) proximally to normal caliber or collapsed loops distally.The transition
point resembles a beak and is described as BEAK SIGN.

How severe is the obstruction?


In high grade obstruction, there is 50% difference in caliber between the proximal dilated bowel
and the distal collapsed bowel. The small bowel faeces sign is present when intraluminal
particulate material is identified in the dilated small bowel. Its prevalence is low (7-8%) and is more
likely to occur in high grade obstruction. It helps to locate the transition point. The transition point is
determined by identifying a caliber change between dilated proximal and collapsed distal small
bowel loop.

What is the cause of obstruction?


Most intrinsic bowel lesions are at the transition point and manifests as localized bowel wall
thickening. Most extrinsic causes are adjacent to transition point and have associated extraluminal
manifestation.

Is the SBO simple or complicated?


Simple obstruction of the bowel is considered when the bowel is occluded at one or several points
along its course. The proximal part of bowel is distended, depending on severity and duration of
the process.

Closed loop obstruction is diagnosed when a bowel loop of variable length is occluded at two
adjacent points along its course. The CT signs of closed loop obstruction depend on length,
degree of distension and orientation of the closed loop in the abdomen.

83

Characteristic fixed radial distribution of several dilated, usually fluid filled bowel loops with
stretched and prominent mesenteric vessels converging towards point of torsion. The configuration
may be C or U shaped, depending on orientation of loop. At the site of torsion of loop, a fusiform
tapering may be seen beak sign. Due to rotation of loops around a fixed point and volvulus a
whirl sign may be seen.

Strangulation is defined as a closed loop obstruction associated with intestinal ischemia. It


complicates 10% of low grade and 40% of high grade SBO and occurs as a complication of
intussception, torsion, volvulus or other forms of closed loop obstruction. Findings indicative of
strangulation are thickening and increased attenuation of affected bowel wall. Abnormal bowel
wall enhancement absent or poor contrast enhancement, portal or mesenteric venous
gas/pneumatosis intestinalis- representing gangrene.
Unusual mesenteric course- strangulated obstructions are associated torsion or twisting of
bowel and mesenteric vessels, diffuse mesenteric vascular engorgement and haziness of
mesentery is one of the most sensitive signs of strangulation. Bowel wall thickening may be
seen and thickened bowel wall show target sign due to submucosal edema and
hemorrhage.
Serrated beak sign- is highly specific for strangulation. The U or C shaped configuration of
dilated bowel loop with the ends of loop producing beak like narrowing with presence of
mesenteric vascular engorgement.
Ascitis- the presence of large amount of ascitis may point towards strangulation.

Findings of closed loop obstruction and strangulation on X ray

Coffee Bean sign- the strangulated loop may contain gas and arms of the loop separated by
thickened intestinal wall may resemble a large coffee bean.

Pseudotumor sign- the closed loop may fill with fluid and may be visible on a radiograph as a
soft tissue mass or pseudotumor.

Findings on barium examination

Crossing defects obstructing two segments of a loop of bowel secondary to dense adhesions
bands.

Focal fixation of two limbs with intertwining of the involved limbs or twisting of the folds at point of
obstruction suggestive of volvulus.

Abdominal wall herniation with obstruction.

Focal intraperitoneal segregation of a loop of bowel with tight obstruction suggestive of intestinal
herniation.

MR ENTEROCLYSIS
New modality that provide adequate image quality and adequate distension of the small bowel. The
inherent advantage being the potential to detect extraluminal pathologies and to provide detailed
84

information about the wall of small bowel and the entire abdomen. It also does not use ionizing
radiation.

CAUSES OF SBO
Extrinsic
1. Adhesions are the main cause of SBO ranging from 50-80% of all causes. Almost all are
post operative with a minority being secondary to peritonitis.
The diagnosis of SBO due to adhesions is of exclusion because adhesion bands are not seen
at CT, only an abrupt change in the caliber of bowel, without any associated mass lesion,
significant inflammation or bowel wall thickening at the transition point. Adhesions are not
seen CT even if multiplanar reformations are used; unless they are complicated by
inflammation or carcinomatosis in which case they may appear as linear bands of soft tissue.
Among adhesions, adhesive bands and malted adhesions can not be currently distinguished.
Adhesive bands are usually constrictive and prone to high grade obstruction.
Laproscopy is today indicated by some authors, in SBO from adhesive bands, it remains a
contraindication in adhesive SBO from matted adhesion. In a recent report, a closed loop
appearance on CT is the most sensitive sign of presence of adhesive bands. Other signs
such as beak sign and fat notch sign which corresponds to extraluminal compression made
by a band on the bowel at the transition zone, may be helpful in distinguishing the two
causes.

2. Hernias

Diagnosis of internal hernia is almost always radiological, whereas external hernias


is obvious at clinical examination. However USG or CT may be necessary in the following

to diagnose spigelian or obturator hernia in obese patient

inability to obtain good examination due to body habitus

to look for complications

Paradoduodenal hernia- are usually left sided and are believed to occur due to
congenital defect in the descending mesocolon. They have a characteristic appearance of
cluster of dilated small bowel loops, encased in a sac and lying between the pancreatic
body and tail and stomach to the left of ligament of trietz. The herniated loops may
become trapped within this mesenteric sac.

Transmesenteric hernia- when the small bowel herniates through a defect in the
mesentry or omentum, the herniated bowel is compressed against the abdominal wall,
with no overlying omental fat. The herniated bowel tends to appear clustered and lies
inside of colon.

3. Midgut volvulus- malrotation of intestine results from normal embryologic sequence of the
bowel development and fixation is interrupted. The malrotated bowel is prone to torsion,

85

resulting in midgut volvulus. Malrotation results from incomplete rotation (<270 degree of
counterclockwise rotation normally occurring in 5-12wks)

This group of disorders can be divided into following categories1. nonrotation (0 - <90 degrees of counterclockwise rotation occurring before 6wks)
2. reverse rotation (abnormal rotation >90

and <180 degree causing obstruction or

reversal of duodenal /SMA relationships occurring in 6-10wks)


3. malrotation with malfixation ( >180 and <270 degree of counterclockwise occurring
after 10wks)

Malrotation predisposes patients to two problems-

midgut volvulus

SBO

X ray findings
1. partial duodenal obstruction- dilatation of stomach and proximal
duodenum with a small amount of distal gas.
2. gasless abdomen- features of SBO
Barium UGI
1. DJ flexure displaced downward and to the right.
2. abnormal position of jejunum lying to right of spine should alert one to the possibility
of malrotation.
In malrotation with midgut volvulus
o

dilated fluid filled duodenum

proximal SBO

a cockscrew pattern- proximal jejunum spiraling downwards in right or mid


upper duodenum around its mesenteric axis.

o
USG - abnormal location of SMV to the left or posterior to SMA
- abnormal flow whirlpool sign on Doppler shows mesentery and flow within SMV
wrapping around SMA in a clockwise direction.

4. Intussception- uncommon cause of obstruction in adults.


X ray - dilated small bowel
- absence of caecal gas even in prone position
USG - Mass-loop within a loop appearance
-sandwich like appearance.
Barium enema-diagnostic
1. convex intraluminal filling defect-claw sign
2. coiled spring-contrast insinuates between the intussusceptum and intusscepien.
86

CT1. bowel within the bowel configuration


2. with or without mesenteric fat and vessels
3. a leading mass as cause may be identified

Intraluminal causes
1. Gallstone ileus- radiological triad of pneumobilia, ectopic gallstone and SBO.
2. Bezoar SBO due to bezoar is rare, but due to bariatic surgery this has increased. This
prevents adequate digestion of vegetable fibers which become impacted causing obstruction.
At CT, a bezoar appears as an intraluminal mass with an ovoid shape and a mottled gas
pattern.

Intrinsic
Small bowel neoplasms: Primary neoplastic causes of SBO are rare. Intrinsic small bowel
neoplasia constitute less than 2% of GI malignancies. When a small bowel adenocarcinoma
manifest as SBO, it is usually in an advanced state and shows pronounced asymmetric and
irregular mural thickening (>4mm usually >1.5cms) with homogenous or heterogeneous
enhancement, smooth, lobulated or irregular contour.

CT features of inflammatory or ischemic intestinal diseaseare different.they are circumferential,


symmetric thickening of bowel wall <1.5cm, either segmental, diffuse and enhancing
homogenously with i.v. contrast.

Small bowel involvement by metastatic cancer is more common than involvement than primary
neoplasm. It is more frequent in form of peritoneal carcinomatosis, which is suggested when
extensive serosal disease involving the small bowel is seen.

Tuberculosis Enteritis: In India, tuberculosis is a common cause of small bowel obstruction. The
radiographic features of small bowel tuberculosis closely reflect the underlying pathological
changes. The ulcerative form is most common,.the ulcers have stellate or linear shape.stellate
ulcers are characterized by a barium speck with converging mucosal folds. linear ulcers are
perpendicular to the long axis, resulting in spasm and circumferential strictures. Strictures are
usually multiple and short. The hypertrophic form is less common, usually seen in ileocaecal
area.the bowel loops are matted and fixed by adhesion and fibrosis.

Plain X-ray abdomen may show enteroliths with features of obstruction, i.e. dilated bowel loops
with multiple air-fluid levels, evidence of ascitis, perforation or intussusceptions. In addition,
there may be calcified lymph nodes, calcified granulomas and hepatosplenomegaly.

87

In all patients suspected of bowel tuberculosis, barium studies should include the barium meal
follow through/enteroclysis followed by a barium enema, if there is a colonic involvement. The
barium meal evaluates the motility and organic lesions in the terminal ileum and other parts of
small bowel, while the per oral pneumocolon and enema, best evaluate the caecum and
ileocaecal valve. Small bowel enteroclysis scores over cross sectional imaging and
conventional intestinal studies in providing mucosal details and since this investigation requires
adequate distension of intestine, early and incomplete strictures are better detected, as
prestenotic dilatation develops at sites of minimal strictures.The radiographic features of
intestinal tuberculosis have been correlated with the pathological state of disease.

First Stage: In this first stage of superficial invasion of the mucosa, radiological examination
reveals:
a. An accelerated intestinal transit.
b. Disturbances in tone and peristaltic contractions resulting in hyper segmentation of the
barium column, the so-called chicken intestine.
c. Disturbances in secretion, resulting in precipitation, flocculation or dilution of the
barium suspension.
d. Changes in intestinal contours, which are irregular, crenated and interrupted by
spiculae.
e. Changes in the mucosal pattern manifested by softened and thickened folds

Second Stage: The second stage, in addition to above comprise of ulcerations, characterised
by a barium fleck surrounded by either a thickened wall or by converging folds.

Third Stage: The third stage is of sclerosis, hypertrophy and stenosis. In the small intestine
penetrating ulcers cause very short hour glass stenosis, that have smooth, but stiff
contours and in which the mucosal relief has disappeared. Multiple strictures with segmental
dilatation of bowel loops may occur. Other features include fixity of loops, spiculation,
matting and signs of malabsorption).

Mucosal changes that occur in early stages of tuberculous enteritis are not usually
sonographically visible. However, deep ulcerations can be detected and appear as radial
extensions of the echogenic luminal contents into the surrounding thickened wall. With
disease progression, wall thickening and short segment strictures develop in the intestine,
resulting in partial intestinal obstruction and occasionally in intestinal perforations. On
transverse sonograms, areas of narrowing representing strictures appear as segments of
circumferential mural thickening and reduced luminal content. Real time sonography can
assess hyperperistalsis proximal to the obstruction

88

Ileocaecal Tuberculosis: The ileocaecal region is most commonly affected in small bowel TB,
because of physiological stasis, abundant lymphoid tissue, increased rate of absorption in the
region and closer contact of the bacilli with the mucosa of the region.The lesion may be:
i. hyperplastic with long segments of narrowng, rigidity and loss of distensibility, i.e., the
pipe stem colon, which is the commonest,
ii. ulcerative
iii. ulcerohyperplastic and
iv. Carcinoma type with a short annular defect and overhanging edges.

Early involvement of the ileocaecal region is manifest as spasm and hypermotility with edema
of the valve. Thickening of the ileocaecal valve lips and/or wide gaping of the valve, with
narrowing of the terminal ileum (the Fleischner or inverted umbrella sign) are considered
characteristic of tuberculosis. In advanced disease, the characteristic deformity includes
symmetric, annular, napkin ring stenosis and obstruction or shortening, retraction and
pouch formation. The caecum classically becomes conical, shrunken and retracted out of
the iliac fossa due to contraction of the mesocolon. Hepatic flexure may also be pulled
down. There may be loss of the normal ileocaecal angle and the dilated terminal ileum
may appear suspended and hanging from a retracted, shortened caecum (goose neck
deformity) Localised partial stenosis opposite the ileocaecal value with a rounded off
smooth caecum and a dilated terminal ileum resembles a purse string stenosis. The
ileocaecal value becomes fixed, irregular, gaping and incompetent. The terminal ileum
may be fixed and narrowed due to stricture formation. Narrowing of the terminal ileum may
occur due to irritability with rapid emptying through a gaping ileocaecal value with a
shortened, rigid or obliterated caecum Stierlins sign. This represents acute inflammation
superimposed on a chronically involved segment of the ileum, caecum or ascending colon
with a normal configured column of barium on either side. A persistent narrow stream of
barium in the bowel indicates stenosis and is known as the string sign.Both Stierlins sign
and string sign are also noted in Crohns disease and cannot be considered specific for
tuberculosis. Hyperplastic tuberculosis mimics carcinoma and histological diagnosis is
mandatory.

Sonography shows extramucosal changes and can occasionally detect mucosal changes. In
early stages of ileocaecal tuberculosis, a few regional nodes and circumferential thickening
of the wall of the caecum and terminal ileum may be visualised. The bowel wall is
considered thickened when it measures > 5 mm in the small bowel when non-distended,
and > 3 mm when distended. In later stages of disease, the ileocaecal value and adjacent
medial wall of the caecum are predominantly and asymmetrically thickened. These
changes are nonspecific and may be seen in other conditions such as carcinoma, Crohns
disease, lymphoma and amoebiasis. However, in Crohns disease eccentric thickening
may be noted at mesenteric border and a variegated appearance is seen in malignancy.
89

Due to the predilection for TB of the ileocaecal region and the tendency of the ileocaecal
region to be pulled upto a subhepatic position, a pseudo-kidney sign seen in this location
is highly suggestive of a tuberculous pathology. In advanced ileocaecal tuberculosis, gross
wall thickening, adherent loops, large regional nodes and mesenteric thickening may
together form a complex mass of varied echogenicity centered on the ileocaecal
regionThese changes are highly suggestive of tuberculosis in the appropriate clinical
setting. Ultrasound can detect ulcerations, however due to associated spasm, there is low
sensitivity of the same. Lesions in jejunum or proximal ileum can be missed due to
difficulty in scanning the entire length of the intestines, and is also limited by presence of
overlying bowel gas.

CT scans of the ileocaecal region, may show circumferential bowel wall thickening up to 3.0
cm in diameter in terminal ileum and caecum with enlargement of ileocaecal valve and
adjacent mesenteric adenopathyThe bowel wall thickening may be mild and symmetric or
severe and asymmetric with a homogeneous density and areas of slight heterogeneous
appearance. A CT appearance more characteristic of TB is asymmetric thickening of the
ileocaecal valve and medial wall of the caecum with an exophytic extension engulfing the
terminal ileum and massive lymphadenopathy with central low attenuation area. Pericaecal
or mesenteric fat shows either absence or only minimal haziness. CT may also show distal
small bowel obstruction.
CT enteroclysis has a greater sensitivity and specificity than nonhelical CT in patients
suspected of having low grade small bowel obstruction, a feature commonly seen in small
bowel tb.CT enteroclysis allows detection of luminal and extraluminal disease.
Radiological differentiation of early stage ileocaecal tuberculosis from Crohns disease and
lymphoma is usually impossible. CT is capable of identifying changes in bowel wall and
mesentery to provide differentiating factors between advanced intestinal tuberculosis and
Crohns disease. In tuberculosis, bowel wall changes are varied and reflect the various
stages of the disease. These are exophytic soft tissue masses surrounding a constricted
and ulcerated lumen, minimal but asymmetrical bowel wall thickening with spiky or
tethered mucosal outline, minimal symmetrical wall thickening and absence of wall
thickening. Mucosal stratification does not occur. In comparison, Crohns disease has a
uniform pattern of wall thickening, which is concentric or largely symmetrical, ranging from
0.6 to 1.7 cm, few showing mural stratification. Although amebiasis may produce the
typical shrunken caecum seen in TB, associated small bowel involvement is rare. Caecal
malignancy is always limited by the ileocaecal valve

90

The differentiating imaging features of ileocaecal involvement can be summarized as :


TUBERCULOSIS

CROHN'S DISEASE

1.

Asymmetric wall thickening, irregular

Circumferential bowel wall thickening

2.

Fleischner sign on barium studies

Cobblestone appearance on barium

3.

No creeping fat

Creeping fat (abnormal quantity of


mesenteric fat) present

4.

Positive chest film (50%)

Negative chest film

5.

Omental and peritoneal thickening

Normal omentum and peritoneum

6.

Enlarged lymph nodes with lowdensity centers

Enlarged soft-tissue density lymph nodes

Colonic Tuberculosis: The large bowel is involved in 9 per cent of cases without small
bowel involvement. Colonic disease may present as a segmental involvement (long or
short) with spiculation, spasm, rigidity and ulceration. Occasionally, inflammatory polyps,
perforations and fistulae may occur with pericolic abscesses. The differential diagnosis of
extensive colonic tuberculosis include ulcerative colitis, Crohns disease, amoebic colitis,
ischemic and pseudomembranous colitis, as well as malignancy. Anal involvement and
internal fistulae are more common in Crohns disease while free perforation is more
common in TB. The ulceration in TB is circumferential while that in Crohns disease is
along the mesenteric border .

Enterolithiasis
Intestinal calculi may form above any bowel stricture. When the stricture is high in the small
bowel, the enteroliths are usually nonopaque, being composed of choleic acid. In the lower small
bowel, due to a more alkaline medium and a higher concentration of calcium salts, enteroliths
are often opaque. They may be completely opacified or have translucent centres with a ring of
calcification. They vary from being multiple, small stones to a large lamellated calculus and must
be differentiated from renal stones, gallstones, vesical stones and calcified granulomas

LARGE BOWEL OBSTRUCTION


Causes
1. The commonest Cause of large bowel obstruction is carcinoma. 60% situated in Sigmoid
Colon.
2. Diverticular disease
3.

Volvulus of colon

4.

Hernia.
91

Three patterns of large bowel obstruction have been defined.


Type 1A: Ileocaecal valve is competent. Dilated colon with distended thin walled caecum , but no
distension of small bowel is seen.
Type 1B: Progression of 1A results in increasing small bowel distension. Both types can lead to
massive caecal distension, which is then at risk of perforation secondary to ischemia. A
transverse caecal diameter of 9cm is critical above which the danger of perforation.
Type 2: Ileocaecal valve is incompetent. Caecum & ascending colon are not dilated, but
backpressure results in numerous dilated loops of small bowel.

Plain X Ray

The obstructed colon contains large amount of air, identified as by its haustral margin around
periphery of abdomen.

When both small and large bowel dilatation is present, differential diagnosis includes paralytic
ileus. A left lateral radiograph will demonstrate air in rectum in paralytic ileus.

There are many causes of colonic distension without obstruction, including paralytic ileus &
pseudo obstruction. Prior to surgery, a single contrast dilute barium enema /CT should be done to
confirm mechanical obstruction.

Advantage of Double Contrast Barium Enema over Single Contrast BE

Detection of Small polyps

Detection of superficial ulceration.

Advantage of single contrast BE

Patient Comfort

Elderly/arthritic patient

Detection of strictures

Detection of large masses

Evaluation of obstruction

Indication for water soluble contrast enema

Possible perforation

Fistula?

Pre operative emergent study

Therapeutic

How do you distinguish various causes of colonic luminal narrowing?

Benign stricture smooth tapering at both ends.

Malignant stricture- Irregular, abrupt narrowing, apple core, shoulders at one or both ends.

Extrinsic- Intact mucosa, whole lumen is displaced, oblique angles for mass effect.
92

Submucosal intact mucosa, almost right angle interface with luminal surface.

Mucosal- Irregular mucosal surface acute angle interface with luminal surface.

Virtual ColonoscopyCT colonography


It entails cleaning the patients bowel by as colonoscopy preparation, insufflation of room air into
the cleansed colon with a rectal enema catheter and thin section helical CT of the abdomen &
pelvis followed by off line computerized manipulation of the CT data to generate an endoscopic
view of colonic mucosa.

Virtual colonoscopy plays an important role in the diagnosis of distal occlusive carcinoma, which
are defined as lumen that cannot be harvested endoscopically.

It can demonstrate the entire colon in majority of patients and ia accurate in depicting
synchronous colorectal malignancy. Pre operative Barium enema examination in these patients
is technically difficult, is associated with an increased risk of barium inspissation and may
necessitate a delay before surgery to adequately clean the bowel.
By reference to adjacent osseous and soft tissue landmarks an axial CT images and multiplanar
reconstruction, it is possible to predict tumour location more accurately at virtual colonoscopy
than at conventional colonoscopy. This may influence surgical conduct such as location of
incision, level of placement of epidural cathetar, extent of resection and stomal site planning.

Colorectal cancer: Colorectal tumors are the main cause of large bowel obstruction. Most of these
tumors are Adenocarcinoma and cause obstruction by luminal compromise & bowel wall
thickening. Colonic tumours may invade the mesentry and small bowel with concomitant small
bowel

obstruction.

Barium

enema

detects

approx

85%

of

colorectal

cancers.poor

distension,inadequate coating or overlapping loops may impair interpretation.CT is a viable


alternative in frail and elderly patients in whom barium enema is technically difficult.Luminal
narrowing is short (<10 cm), abrupt, irregular and eccentric may resemble apple core.CTis used
for staging. CT also aids in staging the malignancy The entire colon needs to be evaluated for
synchronus lesions.CT can also be used for follow up,every six months for 2-3 years ,then
annually for 5 years. PET-CT can be used for recurrence and surveillance.

Large Bowel Volvulus: Torsion of colon can occur in only those parts which have a long, freely
mobile mesentry. This is commonest in sigmoid colon. Occasionly caecum and ascending colon
may be involved. Compound volvulus involving intertwining of two loops of bowel as ileosigmoid
knot.

Caecal Volvulus: Caecal volvulus can only occur when the caecum & ascending colon are on a
mesentry and this is associated with a degree of malrotation. This accounts for <2% of all cases.
Age Group 30 60 years.
93

Radiological Finding: In about half the patients, the caecum twists and inverts so that the pole of
caecum and appendix occupy left upper quadrant. In other half it twists in an axial plane
without inversion and then the caecum occupies the right half or central half of abdomen.

Distended caecum is seen as large gas filled viscus.

One or two Haustral Markings are identified.

Identification of attached gas filled appendix.

Moderate SBO with left half of colon is collapsed.

Sigmoid Volvulus: This occurs in elderly, mentally retarded and instutionalised patients. The usual
Mechanism is twisting of sigmoid loop around its mesenteric axis. Sigmoid volvulus is usually
chronic, with intermittent acute attacks. The main problem lies in distinguishing a twisted sigmoid
from a distended but nonrotated sigmoid or distended transverse colon looping down into the
pelvis (Pseudovolvulus).
Plain X-Ray
1. An inverted U shaped loop is seen , which is markedly distended & commonly devoid of
haustria /ahaustrial.
2. The ahustial margin can be identified overlapping the lower border of liver shadow (LIVER
OVERLAP SIGN)
3. It may overlie Haustrated dilated desending colon. Left flank Overlap sign and left side of
pelvis. (PELVIS OVERLAP SIGN)
4. The apex of volvulus lies high in abdomen under the left hemidiaphragm with apex at or
above level of D10.
5. Inferiorly, where the two limbs of loop converge, three white lines representing thr two
outer walls and the adjacent inner walls of the twisted loop meet. This is called inferior
convergence. It is usually on the left side of the pelvis at the level of upper sacral segment.
6. Large amount of air is present in sigmoid volvulus and an air fluid ratio of >2:1 is usual.

The left Flank overlap, apex under left hemidiaphragm & inferior convergence sign are highly
specific and sensitive.

Barium Enema
1. A smooth curved tapering of the barium column like a hooked beak is seen at point of
torsion (Bird of prey sign)
2. Mucosal fold show a cork screw pattern at point of twist.
Pseudoobstruction/ Ogilvies Syndrome: This is a clinical condition that presents with large bowel
obstruction without any evidence of mechanical obstruction. The colon may become massively
dilated and if not decompressed, there is a risk of perforation with peritonitis. This is thought to be
due to imbalance in autonomic innervation that leads to a functional large bowel obstruction. When
this condition is acquired, acute or coexisting with other medical condition, it is called Ogilvies
94

syndrome. Radiological diagnosis is of exclusion. There is marked dilatation of entire colon with
faecal loading in the absence of any obstructive lesion.

Adynamic Ileus: This is a common disorder of intestinal motor activity in which fluid & gas do not
progress normally through a nonobstructed small & large bowel. Clinically, patient may have
minimal symptoms to generalized abdominal distension, with a marked decrease in frequency &
intensity of bowel sounds.

The radiographic hallmark of adynamic ileus is retention of large amount of gas & fluid in a
demonstrable point of obstruction. Concomitant distension of the gas filled stomach, an uncommon
occurrence with mechanical small bowel obstruction, is often seen in patients with adynamic ileus
(especially when it is secondary to peritonitis)

Adynamic ileus may be seen in postop cases, peritonitis, secondary to electrolyte imbalance,
metabolic disorder, trauma, acute chest disease.

Localised Ileus: An isolated distended loop of small or large bowel reflecting a localized adynamic
ileus( sentinal loop) is often associated with an adjacent acute inflammatory process eg- localized
segment of jejunum or transverse colon are frequently dilated in pancreatitis.

Pnemoperitonium without peritonitis


1. Post operative
2. Dialysis
3. Laproscopy
4. Silent healed perforation
5. Association with chest condition- pneumonia, emphysema,IPP.

Use of contrast media in suspected perforation: In equivocal cases


1. 100 ml of air injected through NG tube and further film taken after patient lies in left lateral
position for 10 minutes.
2. 50 ml of water soluble contrast like Urograffin given orally, patient placed right side for 5 min
&hen examine under fluoroscopy.
3. CT can be done.

Pneumoperitonium: As little as 1ml of free air can be demonstrated radiographically on erect chest
or left lateral decubitus abdominal films. Patient should be in this position for at least 10 min to
enable air to rise to highest position.On the left side, free air may be difficult to distinguish from
gastric or colonic air. A left lateral radiograph helps by demonstrating gas between liver and
abdominal wall.

95

Sign of pneumoperitonium on supine radiograph:

Right upper quadrant gas- perihepatic, subhepatic.

Riglers sign- visualization of outer & inner wall of bowel

Ligament visualization
Falciform- ligamentum teres
Umbilical inverted V sign- Medial & lateral
Urachus

Triangular air collection

Cupola sign

Football sign

Pseudo Pneumoperitonium -- These mimic free air.

Chilaiditi syndromeInterposition of bowel between liver and diaphragm on the right side
may simulate pneumoperitonium.

Subdiaphragmatic fat

Curvilinear supra diaphragmatic pulmonary collapse

Subphrenic absess

Intramural gas as in pneumotosis intestinals.

REFERENCES
1.

Silva AC, Pimenta M , Guimara es L S. Small bowel obstruction: what to look for. Radiographics
2009; 29: 423-439

2.

th

Gastrointestinal Radiology- a pattern approach 4 edition Eisenburg Ronald Lippincott Williams


& Wilkins 2002

3.

Hwang JY ,Lee JK , Lee JE et al. Value of multidetector CT in decision making regarding surgery
in patients with small Bowel obstruction due to adhesion. Eur Radiol 2009; 1424-4

4.

Delabrouse E, lubrano J, Jehl J, et al. Small bowel obstruction from Adhesive bands and Matted
Adhesion: CT differentiation. AJR 2009; 192: 693-697

5.

Diagnostic Imaging :Abdomen Federle Jeflery, Dresser, Anne, Erase Amirsys First edition.

6.

Qablani A, Panshter D, Dach man MD. Multi detector Row CT of small Bowel distention. Radiol
clin N Am 45(2007) 499-512

7.

Sinha R, Verma R Multidetector row computed tomography in bowel obstruction. Part 2: Large
bowel obstruction Clinical Radiology(2005) 60, 1068-1075

Index

96

Complications of Intestinal Obstruction


Nikhil Talwar
Intestinal obstruction can initiate a complex series of changes altering whole-body fluid and
electrolytes, regional blood flow, and host defence mechanisms. Simple mechanical obstruction can
proceed to vascular compromise, intestinal gangrene and finally to gut perforation.

On the basis of surgical and imaging findings, we can differentiate intestinal obstruction as:

simple;

decompensated;

complicated. (1)

Simple Obstruction
The basic pathophysiological mechanism of simple intestinal obstruction pathophysiology is
distension of the bowel loops located proximally to the obstruction site. The vascular supply of the
intestines is preserved and there is no peritoneal fluid.
The main feature seen in simple intestinal obstruction is distension. (2)

Distension
One of the first effects to be noted in the presence of obstruction is the development of
distension. Distension results from a variety of factors, all of which work to increase it: the
obvious obstruction to further passage of intestinal contents past the point of obstruction, the
presence of swallowed air, the continuing secretion of the bowel above the point of
obstruction, the early diminution and the disappearance of absorption. Air swallowing
accounts for virtually all the air seen in the simply obstructed gut. Nearly three quarters of the
gas in the obstructed gut is nitrogen. Other sources of small intestinal gas are fermentation of
sugars, diffusion from the blood, and production of CO 2 by interaction of gastric acid and
carbonates in pancreatic and biliary secretions. (3)

Despite distending to a large size, obstructed intestine usually develops normal or only slightly
increased intraluminal pressure. This is due to receptive relaxation by the smooth muscle of
the intestinal wall in response to increased intraluminal pressure. Transluminal pressures are
unchanged, maintaining vascular perfusion. (4)

Decompensated Obstruction
If the occlusive status persists, simple obstruction develops into decompensated obstruction. The
increasing intraluminal tension causes a change of parietal microcirculation, which impairs bowel
capability to reabsorb. This happens only when the intraluminal pressure is greater than the
pressure into capillary vessels, causing an alteration of vascular permeability. The bowel loop
progressively becomes decompensated. (1)

97

Fluid and electrolyte losses


Fluid and electrolyte losses play a major role in the course and management of intestinal
obstruction. Fluid losses occur by vomiting and tube suction, and internally by drainage into
the intestinal lumen and the intestinal wall or by transudation into the peritoneal cavity. (5)
Several common patterns of fluid and electrolyte shifts have been described, including:
-

isotonic contraction of the extracellular fluid, leading to haemoconcentration, pre-renal


azotemia, and peripheral vasoconstriction.

metabolic acidosis, especially in strangulation obstruction of more than 24 hours


duration, reflecting increasing anaerobic metabolism in the ischaemic bowel (vide
infra)

deficits of potassium ion with loss of gastrointestinal fluids (possibly aggravated by


increased aldosterone output) (2)

A further electrolyte abnormality- i.e. loss of osmolarity of the extracellular fluid caused by
excessive administration of hypotonic intravenous fluids- is attributable to iatrogenic causes
rather than to the obstructive disease itself. (2)

A plausible explanation for intraluminal fluid sequestration is that intestinal obstruction


initiates an inflammatory cascade by attracting and activating neutrophils. The subsequent
release of toxic oxygen radicals and edema-producing peroxidation products, such as
leukotriene B4 and interleukin-1, exacerbates the plasma extravasation and transudation,
resulting in a net fluid secretion into the obstructed bowel. (6)

The extent and type of fluid and electrolyte loss depends on the level of obstruction and its
duration (Figure 1). An obstruction at the pylorus leads to a loss of almost pure gastric juice,
which results in hypochloremic alkalosis. (2) As the level of obstruction proceeds down the
gastrointestinal tract, the loss of electrolytes becomes less clear, but any point of obstruction
below the ampulla of Vater necessarily will lead to significant loss of alkaline secretions in
addition to those of the acidic stomach contents, and therefore the chemical picture may not
be so precisely defined. Obstruction of the colon does not per se lead to the same kind of
fluid losses. (5)

98

Figure 1. Representative electrolyte derangements in intestinal obstruction.

Natural history of decompensated obstruction


Decompensated bowel may be acute or chronic, and it may resolve or deteriorate:
-

Acute decompensated bowel loop: appears when the obstructive fulcrum suddenly
acts and causes a sharp increase of intraluminal pressure.

Chronic decompensated bowel loop: appears when the occlusion is inveterate.

Regression: if the therapy reduces the tensive effect, the imbalance regresses, with a
progressive reduction of loop diameter, of liquid stasis, and of intraperitoneal fluid.

Deterioration: if the dilatation persists, the occlusion worsens. Repeatedly, the tension
causes a reduction in arterial blood flow with a progressive impoverishment of
intramural perfusion, which contributes to the increasingly thinner appearance of the
walls. Surgery reveals distended and pale loops (Figure 2). (5)

The decompensated bowel repeatedly causes a peritoneal reaction due to involvement of


the visceral serosa. Surgery reveals the presence of more or less turbid peritoneal liquid. (4)

Perforation and peritonitis


In the event of unsuccessful treatment, the natural evolution of the SBO is towards death by
consumption. The parietal ischaemic deficit joins the progressive drop in neuromuscular tone.
The loops become increasingly dilated with very thin walls like Egyptian papyrus without
tone,motility or elasticity. The terminal picture is that of intestinal digestive secretion
impairment. The SBO becomes an adynamic paralytic ileus. (1,2) The inveterate ischaemia
causes trophic mural changes, which predispose to:
progressive erosion fissuration laceration perforation & peritonitis.
99

Perforation of the wall is due to the mechanical effect of loop distension. The phenomena of atrophy
and necrosis are more evident on the antimesenteric border of the loop. (4)

Complicated Obstruction
Complicated obstruction means an occlusive state complicated by vascular changes of the bowel
wall. These complications may present with two different modalities:

vascular changes due to strangulation

vascular changes due to loss of intramural blood circulation

Strangulation obstruction
With strangulation, the vascular supply to a segment of intestine is compromised, either by
extrinsic compression of the mesenteric arcade (from an adhesive band or a hernial orifice) or
secondary to an axial twist of the mesentery (volvulus). Most often, the vascular compromise
involves primarily an obstruction to venous outflow. Less common variations of strangulation
obstruction include local pressure necrosis of a segment of the wall of the intestine by an
obstructing adhesive band; by a hernial orifice, as with Richter's hernia; or from a true closedloop phenomenon whereby the progressive intestinal distention, which is not subject to
proximal decompression (vomiting), produces transmural ischemia.
Strangulation obstruction exerts a much greater insult to the body than does a simple
obstruction (Figure 2). In addition to the pathophysiologic squealae of intestinal obstruction,
the local and systemic consequences of impending or actual tissue death are far reaching.
(1,5)

Figure 2: Natural history of intestinal obstruction


SIMPLE
OBSTRUCTION

CLOSED- LOOP
OBSTRUCTION

PRIMARY
VASCULAR
DISEASE

ABDOMINAL
DISTENSION

Intraluminal
pressure
Distension of
proximal bowel
Impaired
venous return

Rapid intraluminal
pressure increase

Splinted
respirations

Secretion
Absorption

Impaired venous and


arterial circulation

Retrograde
decompression

Bowel wall
edema

Atelectasis,
pneumonia
Intraluminal
fluid loss

Peritoneal
fluid loss

Vomiting,
tube suction

Bowel
Infarction

External
fluid loss

Bacteremia
Endotoxemia

Intraluminal
fluid loss

Hypovolemia

Respiratory
failure
SHOCK

100

Strangulation obstruction can be divided into two pathophysiologic stages:


The first stage is primarily a local phenomenon, with usually few systemic ramifications.
Venous obstruction results initially in vascular engorgement, edema, and local venous
hypertension. Reflex arterial vasospasm follows, with the subsequent onset of relative
tissue anoxia. If the vasospasm is severe enough, capillary integrity is lost, and areas of
intramural hemorrhage occur. Intravascular stasis leads to secondary vascular thrombosis
and further anoxia.

The mucosa is the most sensitive to these changes, and mucosal infarction and slough
follow with subsequent intraluminal hemorrhage. As the mechanic integrity of the mucosa
is lost, luminal bacteria invade the underlying submucosa (bacterial translocation),
eventually overwhelming host defense mechanisms. (7)
At this stage, intestinal viability may be preserved if the offending obstruction is released
and blood flow restored to the intestinal wall. Assuming that the intestinal segment at risk
is short enough, the progression of events up to this point has been primarily a local
occurrence, with few serious systemic sequelae. In contrast, if the segment of intestine
involved is of sufficient length, the loss of fluid, electrolytes, and blood into the wall and
lumen may threaten systemic vascular stability. (4,7)

The second stage ensues due to persistent vascular obstruction and tissue anoxia.
Transmural infarction follows rapidly. There is no longer an impermeable gradient between
the proliferating intraluminal bacteria, their toxins, and the systemic circulation. Various
bacterial substances and other metabolic products related to tissue infarction are released
into the peritoneal cavity, even before intestinal perforation has occurred. (7)
Bacterial translocation

represents

passage of

viable bacteria from

the

gastrointestinal lumen to extraintestinal sites, such as the mesenteric lymph node


complex, liver, spleen, kidney, and blood. Bacterial translocation appears to
contribute to the development of multiple-system organ failure by allowing bacteria
or endotoxin normally contained within the gut to reach the portal and systemic
circulations, where it fuels the septic process. Transudation of bacteria and bacterial
exotoxins occurs across the full thickness of the intestinal wall into the peritoneal
cavity. The highly toxic, reddish brown peritoneal fluid characteristic of strangulation
obstruction contains viable intestinal flora. (5)

Special attention should be given to the mechanisms of ischemia-reperfusion


injury when dealing with the treatment of strangulation obstruction. At operation, the
strangulated segment is either resected if considered nonviable, or, if the circulation
improves and the intestine recovers its normal appearance and function, it can be
replaced in the abdominal cavity, usually with complete recovery. (4) In rare cases,
101

although the strangulated loop appears viable, within a matter of weeks, months, or
even years, a progressive and chronic small bowel obstruction occurs secondary to
fibrous stenosis. This event, referred to as postischemic stenosis, eventually
requires resecting the stenotic bowel segment. (5) Development of this type of
stricture varied from days to years. We now know that the pathophysiology of this
condition is directly related to ischemia-reperfusion injury. (7)

Vascular changes due to loss of intramural blood circulation


Vascular changes in the bowel appear appear only when the intramural venous
circulation significantly slows down. The origin of this event is multifactorial and
unpredictable. The main factors are:
-

the obstructive mechanism, occlusion duration and onset of complex mechanisms

the mesenteric and enteric circulation, already uncertain due to diffuse atherosclerotic
disease

the pathological remains, which alter the abdominal habitat;

the patients age and general status. (1)

Regardless of the cause, in the initial phase, the vascular changes are a reversible phenomenon, with
the possible recovery of intestinal vitality and function. Without a timely resolution, the natural history
of this acute secondary venous ischemia is progression to necrosis, gangrene and perforation
peritonitis. (5)
REFERENCES:
1.

Di Mizio R., DAmario F., Di Mizio V. Computed Tomography Imaging Pathophysiolog. In: Di Mizio R.,
Scaglione M. (eds). Small-Bowel Obstruction Springer-Verlag Italia 2007; 19-26.

2.

Russell J.C., Welch J.P. Pathophysilogy of bowel obstruction. In: Welch J.P. (ed). Bowel obstruction:
Differential diagnosis and clinical management. W.B.Saunders, PA 1990; 28-55.

3.

Miller L.D., Mackie J.A., Rhoads J.E. The pathophysiology and management of intestinal obstruction.
Surg Clin North Am 1962;42:1285-1309

4.

Fondacaro J.D. Intestinal blood flow and motility. In: Shepherd A.P., Granger D.N. (eds). Physiology
of the intestinal circulation. Raven Press, NY 1984; 107-120

5.

Cohn Jr I, Chappuis CW. Bowel Obstruction. In: Taylor MB (ed) Gastrointestinal Emergencies 2

nd

Edition. Lippincott Williams & Wilkins, 1997: 515 -537


6.

Basson MD, Fielding LP, Bilchik AJ, et al. Does vasoactive intestinal petide mediate the
pathophysiology of bowel obstruction? Am J surg 1989; 157(1):109-115

7.

Zeeb I., Pfenninger E., Grunert A. The bowel as an ischaemic organ. Anesthetist 1990; 19(7):343-352.

Index

102

Advances in management of Intestinal Obstruction in adults


Rajdeep Singh
For most surgeons, the management of intestinal obstruction is pretty straightforward operate in
case of acute obstruction, manage conservatively if partial obstruction is suspected. For the most part,
this approach is correct and gives satisfying results. However, managing a patient conservatively is
fraught with risk once strangulation occurs, the mortality rates are very high.

Partial small bowel obstruction


The clinical features of small bowel obstruction are familiar to all general surgeons pain, vomiting
and distension in that order. Obstipation is a late feature, and its absence should not rule out
obstruction. The presence of multiple air fluid levels on erect abdominal x-ray confirms the
diagnosis, and an idea about the level of obstruction can also be made. The absence of external
hernia should be confirmed before deciding on a laparotomy.

The problem arises when a patient is to be labelled as having sub-acute obstruction. For starters,
there is no definition of the term sub-acute obstruction; the accepted term in most studies is
partial obstruction. Generally, if the patient has abdominal distension and constipation (but is
passing flatus) he is labelled as having partial obstruction i.e. gas and some liquid stool can pass
1

the site of obstruction. Moshe has described partial and total obstruction on the basis of x-ray
findings. If air is present in the colon, the obstruction is considered as partial; complete absence of
colonic gas suggests a total obstruction.

Contrast enhanced CT scan


In a case of total small bowel obstruction, no investigation beyond a plain abdominal x-ray in the
supine and erect position is required. A CT scan, however, is useful when the diagnosis is in
doubt, e.g post operative and very obese patients. The typical feature on CT is a transition point
3

between dilated and collapsed bowel. The presence of air in the bowel wall or the portal system is
3

an indicator of bowel ischaemia / strangulation. Although CT remains a good modality for


diagnosis, conventional oral contrast does not delineate mucosal lesions very well. To overcome
this problem, CT enteroclysis has been introduced, which may be done using water only (negative
4

contrast) or dye (positive contrast). The use of negative contrast makes small mural lesions very
4

prominent when iv contrast is given. An added advantage is that it may be done without nasoenteral intubation.

103

CT enteroclysis with negative oral contrast


(from: http://www.auntminnie.com/)

CT enteroclysis with positive oral contrast


(From: http://radiographics.rsna.org)

Oral gastrografin
Conservative management in adhesive obstruction is frequently successful, hence modalities to
predict cases who require early intervention have been devised. One such modality is the use of
oral water soluble contrast. 100 ml of Gastrografin is instilled through the Ryles tube, and a plain
abdominal X-ray taken after 24 hours. The presence of dye in the colon confirms partial
5

obstruction; these cases are likely to respond to conservative management. Although the use of
gastrografin has not reduced the number of cases requiring surgical intervention, the duration of
6

hospital stay in non-operative patients has been reduced. It has been postulated that the
hyperosmolar dye may decrease edema and thus relieve obstruction.

Ascites with obstruction


Another modality to predict need for surgery is the presence of ascites. Free fluid detected
7

radiologically has been shown to correlate with the need for surgical intervention. Of course,
there should be no signs of strangulation in these patients. A high RBC count (>20,000) on
diagnostic paracentesis suggests strangulation, and so the need for surgery. This may not be of
practical use in India, where small bowel obstruction due to tuberculosis is common. In
tuberculosis, there may be associated ascites also.

Diagnostic and therapeutic laparoscopy


Both diagnostic and therapeutic, laparoscopy is most useful in band obstruction. When another
cause is found which cannot be managed laparoscopically, conversion allows treatment in a
single sitting. Bowel distension is a relative contraindication- most cases can be managed
104

laparoscopically. Many surgeons swear by the utility of laparoscopy in obstruction, although


technical expertise is required. Furthermore, it decreases adhesion formation, and since
adhesive obstruction is the leading cause of small bowel obstruction, laparoscopy can drastically
bring down the incidence of recurrent obstruction.

Breath hydrogen testing


Normally hydrogen in the breath increases when a carbohydrate load reaches the colon. It is a
manifestation of anaerobic breakdown of undigested carbohydrates by the colonic bacteria,
usually in the right colon.
In case of small bowel obstruction, the levels of hydrogen are low, as expected. However, partial
relief of obstruction results in a rise of hydrogen levels, which again come down to baseline after
8

some time. On starting a liquid meal, the levels rise again. Thus, measurements of breath
hydrogen levels can indicate when the patient is likely to be relieved.

Capsule enteroscopy
Although this is a promising modality for imaging the small bowel for tumours and sources of
bleeding, it has no utility in obstruction. This is because of high chance of retention of the capsule
proximal to the site of obstruction, necessitating surgery. It may be used once the obstruction is
fully relieved by conservative methods.

Push enteroscopy and intraoperative enteroscopy


Not of much use in obstruction some odd cases may require it to localize the lead point of a
recurrent intussusception.

Postoperative ileus:
Paralytic ileus is defined as functionally impaired transit of intestinal contents because of
decreased peristaltic activity of the gastrointestinal tract, in the absence of mechanical
9

obstruction. Any irritation to the bowel surface can promote ileus: this may be by bowel contents
(as in spillage) or acid (from the stomach or duodenum). Even prolonged exposure to air can lead
to ileus.

Some degree of ileus is considered to be more or less normal after abdominal surgery. In an
uncomplicated case, return of bowel function occurs in a predictable and orderly manner: small
intestinal motility is the first to recover (in 24 hrs), followed by the stomach (24-48 hrs) and lastly
the colon (48-72 hrs).

10

Many surgeons distinguish between early physiologic ileus which resolves

in 2-3 days, and more profound ileus which lasts longer. The former does not require aggressive
intervention, whereas the latter has to be treated.
Some of the factors, apart from poor handling of tissues during surgery, which promote ileus are:

Drugs
o

Opioid use, commonly for postoperative pain


105

anticholinergic drugs,

calcium-channel antagonists

antihistamines,

phenothiazines and tricyclic antidepressants

Metabolic derangements
o

Electrolyte

disturbances

(hypokalemia,

hyponatremia,

hypomagnesemia,

hypermagnesemia, hypocalcemia, or hypercalcemia)

Renal failure

Diabetic ketoacidosis

Hypoparathyroidism

Miscellaneous
o

Intra- or retro-peritoneal inflammation

Neurologic disorders

Critical illnesses

Severe infections (eg pneumonia)

The difficulty lies in ruling out small bowel obstruction (SBO) in the post operative period, which
can occur in upto 1% of patients within 30 days of surgery. SBO requires reoperation, whereas
ileus should be managed conservatively. The presence of colonic gas on plain X-rays usually
1

suggests paralytic ileus. CT scanning with oral contrast will show the dye passing into the colon;
9

transit is delayed in ileus but not absent. On the other hand, postoperative SBO will show a
transition zone between dilated and collapsed bowel, which is pathognomonic. CT is 90% sensitive
and specific.

Treatment
Largely supportive, with correction of electrolytes and control of underlying disease, if any. The use
of nasogastric tubes has been shown to cause more problems than benefit, so are not routinely
used in all cases of ileus. They are reserved for patients who are vomiting or in acute gastric
11

dilatation.

Traditionally, the patient is kept nil per mouth till passage of flatus / stools. This can cause
nutritional depletion, so early feeding is recommended to promote early recovery from ileus by
enteral hormonal stimulation. Sham feeding is an alternative, which is most easily achieved by
asking the patient to chew gum.

12

Results have been variable, but it is an inexpensive method with

no side effects, and worth trying first.

Erythromycin, metoclopropamide and propranolol have been shown to be ineffective in causing


resolution of ileus. Cisapride, a promotility agent, has shown variable results most of the positive
studies used the intravenous route, whereas the negative studies used transrectal route; possibly
9

the effect is dependent on the route of administration. Newer analogues like mosapride and
106

itopride are yet to be evaluated. Since intravenous formulations are not available in India, itopride
may be administered orally. Neostigmine has been tried in paralytic ileus with good results, but is
currently not recommended. Alvimopan is a selective peripheral -receptor blocker, and
antagonises the effects of opiates without affecting their analgesic efficacy. A meta-analysis
showed that alvimopan was significantly more effective in causing early resolution of ileus.

13

Methylnaltrexone is an alternative with similar mode of action.

Prevention
Laparoscopy has been instrumental in reducing the duration of postoperative ileus. This is due to
lesser handling of the gut and no exposure of bowel to air. Other methods include careful handling
of bowel, use of NSAIDs instead of opiates for postoperative pain relief and use of an epidural
9

catheter. Epidural catheters used to provide pain relief should be kept till 72 hrs post-op for
maximal benefit.

Colonic pseudo-obstruction
Initially described in a case of retroperitoneal tumour infiltrating the celiac plexus, the term is now
used to describe any patient with a functional colonic obstruction. It is relatively uncommon; it is
present in 0.05% of cases undergoing cardiac surgery.

14

It is distinct from an ileus in which there

are no muscular contractions, since contractions may be present in colonic pseudo-obstruction but
are not co-ordinated and propulsive.

The exact cause is not known, but is postulated to be because of excessive sympathetic
9

stimulation. This is supported by the fact that surgical division of splanchnic nerves cures pseudoobstruction.

Similarly,

neostigmine

administration

increases

the

acetylcholine

levels

(parasympathomimetic) which opposes sympathetic activity.

88-94% of cases have an underlying pathology. These include postoperative cases (23.1%),
cardiopulmonary disease (17.5%), Non-operative trauma (11.2%), neurologic disease (8%),
9

malignancy (5.4%), intra-abdominal pathology (4.6%) and retroperitoneal pathology (3.5%). The
use of opiates and electrolyte disturbances also contribute to this condition.
Diagnosis is suggested by dilated colon on X-ray, without systemic toxicity clinically.

Differential diagnosis:
1. Colonic obstruction: colicky abdominal pain and obstipation. Although a colon cut off sign
should suggest obstruction, it may be present in pseudo-obstruction also, especially in the
splenic flexure and descending colon.
2. Toxic megacolon: the patient will be much more sick, with loose stools
3. Ischemic colitis: bloody diarrhoea and thumbprinting of the colon on x-ray

107

CT scan with contrast enema is the modality of choice to rule out colonic obstruction. Barium is
preferable; water soluble agents can potentially dehydrate the patient. Of course, barium is contraindicated if perforation is suspected. Colonoscopy is ideal if available in the emergency setting. It
has the advantage of being therapeutic also.

Treatment

Apart from supportive measures like rehydration, nil per mouth and correction of electrolytes,
a rectal tube is passed which may assist in decompressing the sigmoid but is ineffective for
the proximal colon. Conservative therapy may be tried for 2-3 days, provided the caecal
diameter is less than 12 cm (9cm in case of transverse colon).

2mg of rapid iv neostigmine provides a favourable response in 80% of cases. It causes


bradycardia and bronchospasm, so constant monitoring is essential. Cardiac disease,
especially bradycardia, is a relative contraindication.

15

Colonoscopy is the treatment of choice if perforation or ischemia is not suspected. The entire
colon can be decompressed through it and produces clinical improvement, although the
caecal diameter may not decrease on x-rays. A retrospective study showed upto 3.4%
mortality associated with the procedure.

Administration of polyethylene glycol has been shown to decrease recurrence rate after
9

colonoscopic decompression, possibly because of reduced nitric oxide production. Daily


administration is required, and produces mild nausea and abdominal pain.

If there is incipient caecal perforation, surgery is the mainstay of treatment. Even if the patient
is explored suspecting large bowel obstruction and the diagnosis is made during surgery,
decompressing stomas are recommended. An ileostomy will not decompress the colon, so it
is not favoured. If the caecum is thinned out, caecostomy is the best option. A formal matured
caecostomy is better than a tube caecostomy. In case the caecum is gangrenous, the best
option is colectomy with ileo-rectal anastomosis, since the thinned out colon does not hold
sutures well (in case of a right hemicolectomy).

Surgical intervention has a mortality of 6% and morbidity of 30% in pseudo-obstruction, hence


it is reserved for very sick patients of where caecal gangrene is suspected.

Colonic strictures: Strictures in the colon are due to malignancy foremost; this is followed by
tuberculosis in India and Crohns disease in the West. Ischaemic and post operative strictures are
also seen.
The options available for benign strictures of the colon are:

1. Balloon dilatation: done after colonoscopic placement of a balloon catheter. Dilatation is


done under radiologic guidance. Complications include perforation at the site of the
stricture.
2. Colonoscopic incision of the stricture
3. Intra-lesional steroid injection, usually combined with balloon dilatation or incision
4. Colonic stenting
108

5. Surgical resection
6. For Crohns disease, intra-lesional infliximab injections have been reported to be
successful.

16

Palliation of malignant large bowel obstruction: Bowel obstruction can occur in up to 43% of
cases with incurable or unresectable intra-abdominal malignancy. The common sites of origin are
ovarian and colorectal tumours. Metastatic disease from the lung or breast also accounts for some
cases. Since prolonged survival is not expected for these patients, palliative measures are utilized.
These measures may be used in patients with malignant large bowel obstruction while waiting for
surgery. These tide over the emergency and allow the bowel to be prepared for a single stage
resection.
1. Colonic stents: These are commonly used in the west. Two types of self-expanding metallic
stents are available one can be deployed through the colonoscope working channel,
whereas the other requires the delivery system of the stent to be passed alongside the scope.
The former is better since it can be used in proximal colon also.

17

Stent placed in
right colon

It is worthwhile to note that technical success is defined as the proper placement of a stent,
and clinical success is defined as decompression of the obstructed bowel. It does not include
the ability to completely clear the bowel. Hence stents are excellent as a temporizing measure
or for palliation. Technical and clinical success rate is 90%.

17

As with all enteral stents, colonic

stents are designed for permanent placement; they cannot be removed later. If used as a
temporizing measure, the stent is excised alongwith the growth during definitive surgery.
In case of re-obstruction due to tumour ingrowth, a new stent may be placed within the old
one. Chemoradiation can be given alongwith the stent to downstage the disease.
Complications include stent migration, bleeding and perforation.

2. Laser therapy: Nd:YAG laser is commonly used to physically destroy the malignant tissue.
Since it requires multiple sittings (approx 4 in the course of the disease), it is not suited for
acute obstruction or extrinsic compression on colon, since the tumour must be visible on
colonoscopy for it. The laser fibre is passed through the working channel of the colonoscope
and under vision the tumour mass is destroyed.

17

Complications like bleeding, perforation,

pericolic abscess, fistulas and post procedure pain occur in up to 15% cases. Since it is an
expensive modality with high morbidity, it is used less commonly.
109

3. Argon beam coagulation: it is commonly used to control bleeding from oozing surfaces
during colonoscopy. It causes superficial coagulation only. Despite this limitation, there are
reports of argon beam coagulation being used to destroy obstructing tumour.

17

4. Chemotherapy: combined with one of the above mentioned modalities.


5. Anti-tubercular therapy: in case of tubercular strictures. Stenting is not advisable.

Conclusion
The management of acute small bowel obstruction remains the same surgery. Changes have
occurred in the management of partial obstruction, and in the diagnosis thereof. In case of large
bowel obstruction, modalities such as stenting allow the surgery to be done in a planned manner.
Laparoscopy remains the only technical advance in the performance of this surgery.

REFERENCES:
1.

Cappell MS and Batke M. Mechanical Obstruction of the Small Bowel and Colon. Med Clin N Am
2008; 92: 575-97

2.

Moshe Schien In: Scheins Common Sense Emergency Abdominal Surgery. Springer-Verlag,
Heidelberg 2000: 138

3.

Mallo RD, Salem R, Lalani T, et al. Computed tomography diagnosis of ischemia and complete
obstruction in small bowel obstruction: a systematic review. J Gastrointest Surg 2005; 9: 6904.

4.

Maglinte D, Sandrasegaran K, Lappas JC. CT Enteroclysis: Techniques and Applications. Radiol Clin
N Am 2007; 45: 289301

5.

Kumar P, Kaman L, Singh G, Singh R. Therapeutic role of oral water soluble iodinated contrast agent
in postoperative small bowel obstruction. Singapore Med J 2009; 50(4) : 360

6.

Abbas S, Bissett IP, Parry BR. Oral water soluble contrast for the management of adhesive small
bowel obstruction. Cochrane Database Syst Rev. 2007 Jul 18;(3):CD004651

7.

ODaly BJ, Ridgway PF, Keenan N, Sweeney KJ, Brophy DP, Hill ADK, Evoy D, OHiggins NJ,
McDermott EWM. Detected peritoneal fluid in small bowel obstruction is associated with the need for
surgical intervention. Can J Surg, 2009; 52, 201-6

8.

Urita Y, Watanabe T, Maeda T, Sasaki Y, Ishihara S, Hike K, Sanaka M, Nakajima H, Sugimoto M.


Breath Hydrogen Gas Concentration Linked to Intestinal Gas Distribution and Malabsorption in
Patients with Small-bowel Pseudo-obstruction. Biomaker Insights 2009:4 915

9.

Batke M, Cappell MS. Adynamic Ileus and Acute Colonic Pseudo-Obstruction. Med Clin N Am 2008;
92: 649670

10. Condon RE, Cowles VE, Ferraz AA, et al. Human colonic smooth muscle electrical activity during and

after recovery from postoperative ileus. Am J Physiol 1995; 269 :40817


11. Cheatham ML, Chapman WC, Key SP, et al. A meta-analysis of selective versus routine nasogastric

decompression after elective laparotomy. Ann Surg 1995; 221: 46976.


12. Matros E, Rocha F, Zinner M, et al. Does gum chewing ameliorate postoperative ileus? Results of a

prospective, randomized, placebo-controlled trial. J Am Coll Surg 2006; 202 :7738.


13. McNicol E, Boyce DB, Schumann R, Carr D. Efficacy and safety of mu-opioid antagonists in the

treatment of opioid-induced bowel dysfunction: systematic review and meta-analysis of randomized


controlled trials. Pain Med. 2008; 9: 634-59.

110

14. Johnston G, Vitikainen K, Knight R, et al. Changing perspective on gastrointestinal complications in

patients undergoing cardiac surgery. Am J Surg 1992; 163: 5259.


15. Ponec RJ, Saunders MD, Kimmey MB. Neostigmine for the treatment of acute colonic pseudo-

obstruction. New Engl J Med. 1999; 341: 137-41


16. Swaminath A, Lichtiger S. Dilation of Colonic Strictures by Intralesional Injection of Infliximab in

patients with Crohns colitis. Inflamm Bowel Dis 2008; 14: 213-16
17. Adler DG, Merwat SN. Endoscopic Approaches for palliation of luminal gastrointestinal obstruction.

Gastroenterol Clin N Am 2006; 35: 6582

Index

111

Thoracic outlet syndrome


Chintamani
Thoracic outlet syndrome is a broad term that refers to compression of the neurovascular structures in
the area just above the first rib and behind the clavicle. It represents a constellation of symptoms. The
cause, diagnosis, and treatment are controversial. The brachial plexus (95%), subclavian vein (4%),
and subclavian artery (1%) are affected. Most presentations to the emergency department (ED) are
nonemergent and require only symptomatic treatment and referral.

Pathophysiology
The brachial plexus trunks and subclavian vessels are subject to compression or irritation as they
course through 3 narrow passageways from the base of the neck toward the axilla and the proximal
arm. The most important of these passageways is the interscalene triangle, which is also the most
proximal. This triangle is bordered by the anterior scalene muscle anteriorly, the middle scalene
muscle posteriorly, and the medial surface of the first rib inferiorly. This area may be small at rest
and may become even smaller with certain provocative maneuvers. Anomalous structures, such as
fibrous bands, cervical ribs, and anomalous muscles, may constrict this triangle further. Repetitive
trauma to the plexus elements, particularly the lower trunk and C8-T1 spinal nerves, is thought to
play an important role in the pathogenesis of TOS.
The second passageway is the costoclavicular triangle, which is bordered anteriorly by the middle
third of the clavicle, posteromedially by the first rib, and posterolaterally by the upper border of the
scapula.
The last passageway is the subcoracoid space beneath the coracoid process just deep to the
pectoralis minor tendon.

Frequency
Because no objective confirmatory test is available for TOS, there is much disagreement with
regards to its true incidence, with reported figures ranging from 3-80 cases per 1000 people.

Sex
The sex ratio varies depending on the type of TOS (eg, neurologic, venous, arterial). Overall, the
entity is approximately 3 times more common in women than in men.

Neurologic - Female-to-male ratio approximately 3.5:1

Venous - More common in males than in females

Arterial - No sexual predilection

.
Clinical features:

Age: The onset of symptoms usually occurs in persons aged 20-50 years

112

Neurologic symptoms occur in 95% of cases. The lower 2 nerve roots of the brachial plexus, C8
and T1, are most commonly (90%) involved, producing pain and paresthesias in the ulnar nerve
distribution.

The second most common anatomic pattern involves the upper 3 nerve roots of the brachial
plexus, C5, C6, and C7, with symptoms referred to the neck, ear, upper chest, upper back, and
outer arm in the radial nerve distribution.

Neurologic

Pain, particularly in the medial aspect of the arm, forearm, and the ring and small digits

Paresthesias, often nocturnal, awakening the patient with pain or numbness

Loss of dexterity

Cold intolerance

Occipital headache

Weakness

Raynaud phenomenon, hand coldness, and color changes may also be seen, usually due to
an overactive sympathetic nervous system as opposed to ischemia.

Most have a history of neck trauma preceding their symptoms, most commonly from auto
accidents and repetitive stress at work.

Venous - Pain, often in younger men and often preceded by excessive activity in the arms

Swelling of the arm

Cyanosis

Paresthesias in the fingers and hand (may be secondary to swelling as opposed to nerve
compression)

Arterial

Pain

Claudication

Pallor

Coldness

Paresthesias

Often in young adults with a history of vigorous arm activity

Symptoms usually develop spontaneously from arterial emboli.

Examination findings:
In most cases, the physical examination findings are completely normal. Other times, the examination
is difficult because the patient may guard the extremity and exhibit giveaway-type weakness. The
sensory examination is often unreliable.

Provocative tests, such as the Adson, costoclavicular, and hyperabduction maneuvers, are
unreliable. Approximately 92% of asymptomatic patients have variation in the strength of the
radial pulse during positional changes.

113

The elevated arm stress test (EAST) is of debatable use, but it may be the most reliable
screening test. It evaluates all 3 types of thoracic outlet syndrome (TOS).
o

To perform this test, the patient sits with the arms abducted 90 degrees from the thorax
and the elbows flexed 90 degrees. The patient then opens and closes the hands for 3
minutes.

Patients with TOS cannot continue this for 3 minutes because of reproduction of
symptoms. Patients with carpal tunnel syndrome experience dysesthesias in the fingers,
but do not have shoulder or arm pain.

Neurologic
o

A typical patient is a young, thin female with a long neck and dropping shoulders.

A positive EAST result and the presence of a radial pulse are strong indicators of
neurologic involvement of the brachial plexus.

Supraclavicular tenderness may be present.

Usually, no evidence of muscle atrophy is present, although the classic finding is known
as the Gilliatt-Sumner hand, with the most dramatic atrophy in the abductor pollicis brevis,
with lesser involvement of the interossei and hypothenar muscles.

Paresthesias/sensory loss is restricted to the ulnar aspect of the hand and forearm.

Weakness (usually subtle) of affected limb may be noted.

Venous

Edema of the upper extremity

Cyanosis of the upper extremity

Distended superficial veins of the shoulder and chest

Arterial
o

Pallor and pulselessness

Coolness on the affected upper extremity

Lower blood pressure in affected arm of greater than 20 mm Hg (a reliable indicator of


arterial involvement)

Rarely can produce multiple small infarcts on the hand and fingers (embolization)

Etiology of TOS: The 3 major causes of TOS are anatomic, trauma/repetitive activities, and
neurovascular entrapment at the costoclavicular space.

Anatomic
o

Scalene triangle: Anterior scalene muscle frontally, middle scalene muscle posteriorly,
and the upper border of the first rib inferiorly account for most cases of neurologic and
arterial TOS.

Cervical ribs are found in most arterial cases but rarely in venous and neurologic cases.

Congenital fibromuscular bands are noted in as many as 80% of patients with neurologic
TOS.

Transverse process of C7 is elongated.


114

Trauma or repetitive activities


o

Motor vehicle accident hyperextension injury, with subsequent fibrosis and scarring

Effort vein thrombosis (ie, spontaneous thrombosis of the axillary veins following
vigorous arm exertion)

Playing a musical instrument: Musicians can be particularly susceptible owing to their


need to maintain the shoulder in abduction or extension for long periods.

Neurovascular entrapment: This occurs in the costoclavicular space between the first rib and
the head of the clavicle.

Laboratory Studies

With the rare exception of a vascular cause, the vast majority of ED presentations are not
emergent.

Screening tests may be appropriate if indicated and to rule out other causes. Once the
clinical diagnosis is made, most of the imaging studies and other tests should be reserved for
the outpatient setting.

Imaging Studies

Cervical radiography - May demonstrate a skeletal abnormality

Chest radiography
o

Cervical or first rib: This is usually associated with the arterial form of TOS but also can
be a predisposition to developing the neurologic form following neck trauma.

Clavicle deformity

Pulmonary disease

Pancoast tumor

Color flow duplex scanning for suspected vascular thoracic outlet syndrome (TOS)

Arteriography (indications)
o

Evidence of peripheral emboli in the upper extremity

Suspected subclavian stenosis or aneurysm (eg, bruit or abnormal supraclavicular


pulsation)

Blood pressure differential greater than 20 mm Hg

Obliteration of radial pulse during EAST

Venography (indications)
o

Persistent or intermittent edema of the hand or arm

Peripheral unilateral cyanosis

Prominent venous pattern over the arm, shoulder, or chest

Other Tests

The following special studies are generally appropriate in the outpatient setting. They should
be arranged by the primary care physician once the patient has been discharged from the ED.

115

Nerve conduction evaluation via root stimulation and F wave is the best direct approach
to evaluation of neurologic TOS.

Electromyography (EMG) is unreliable and does not provide objective evidence of TOS.

Cervical myelogram, CT scan, or MRI may be appropriate for patients suspected of


having cervical disk disease or spinal cord disease.

MANAGEMENT OF TOS
Emergency Department Care
Most presentations to the ED are nonemergent and require only symptomatic treatment and
referral. Vascular thoracic outlet syndrome (TOS), although much less common than neurologic
TOS, requires more urgent care.

Vascular (arterial and venous)


o

Immediate heparinization

Vascular surgery consultation

Color flow duplex scanning

Angiography or venography

Neurologic - Conservative outpatient physiotherapy

Consultations

Neurologic, orthopedic, or vascular surgery consultation(s) may be indicated depending on


the type of pathologic condition.

Physical medicine and rehabilitation physicians are needed for outpatient workup.

Medication
In patients with evidence of arterial or venous involvement (ischemia or thrombosis), immediate
heparinization is indicated.
Anticoagulants: These agents prevent recurrent or ongoing thromboembolic occlusion of the
vertebrobasilar circulation.

Further Inpatient Care

Vascular
o

Angiography or venography

Color flow duplex scanning

Catheter-directed local infusion of thrombolytic agent

Thrombectomy (for total thrombotic obstruction)

Fogarty catheter embolectomy

Emergent or urgent surgical exploration

Neurologic: Operative therapy is indicated if conservative approach fails.

116

Supraclavicular

decompression

techniques

may

include

anterior

and

middle

scalenectomy, excision of a cervical rib if present and first rib resection.


o

A retrospective survey of 158 workman's compensation patients undergoing surgery for


thoracic outlet syndrome (TOS) showed that 60% were still work-disabled 1 year after
surgery.

Further Outpatient Care

For most patients, conservative treatment is recommended. Stress avoidance, work


simplification, and job site modification are recommended to avoid sustained contraction and
repetitive or overhead work that exacerbate symptoms.

Address myofascial or chronic pain elements through exercise programs, good posture, and
self-management.

Maximize the potential outlet space through a program of stretching and strengthening of the
shoulder-elevating mechanism.
o

Trapezius and rhomboid strengthening (eg, shoulder shrugs and bilateral shoulder
retraction while standing or lying prone)

Shoulder mobilization (eg, hand circles and standing corner pushups)

Postural exercises (eg, cervical and lumbar spine extension)

Inpatient & Outpatient Medications

Coumadin: Anticoagulate for a minimum of 3 months for vascular TOS.

Analgesics are seldom helpful except to assist in the institution of a progressive exercise
program.

Tricyclic antidepressants: A short-monitored course may be helpful if the time course and
symptoms suggest a protracted pain syndrome.

Transfer
Vascular - For definitive diagnosis and treatment if unavailable at current institution

Complications
Neurologic - Chronic pain
Arterial
o Thrombosis
o Thromboembolism
o Acute ischemia
o Poststenotic aneurysm formation
Venous - Thrombosis

Prognosis
Neurologic TOS is generally neither progressive nor likely to resolve spontaneously.
Arterial or venous TOS usually results in a good outcome with adequate treatment.

Index

117

Vascular Grafts
Saket Agarwal
Vascular surgery has shown an explosive growth over the last 45 years. It has been estimated that in
the United States alone, over 350,000 synthetic arterial grafts are implanted each year; the number of
peripheral autogenous vein grafts exceeds 200,000 per year. Many of the advances in vascular
surgery have been made possible by the development of vascular grafts which are used to
reconstruct diseased or injured arteries and veins. As yet the ideal vascular graft has not been found.

The ideal vascular graft should have the following characteristics:


1. It should be strong, capable of lasting the life of the patient, and should not degenerate
chemically or physically with time
2. It should be easily and permanently attachable to the host vessel
3. It should be biocompatible with the host and should not incite an abnormal proliferative
response from the native vessel or the surrounding tissue; and should not damage blood
components
4. It should have a nonthrombogenic luminal surface; remain patent without subsequent
intervention
5. It should resist infection
6. It should not leak blood or serous fluid with restoration of flow
7. It should not occlude when flexed
8. It should be inexpensive and be readily available in appropriate sizes

Historical aspects: (Ref. 1)


In 1906, Carrel and Guthrie first reported successful implantation of venous autografts into the
arterial systems of dogs. This was followed by clinical use of the popliteal vein for arterial
reconstruction after popliteal aneurysm excision by Goyanes in 1906. The first use of a saphenous
vein graft in popliteal artery reconstruction after popliteal aneurysm excision was by Bernheim in
1915. However, the routine clinical use of venous autografts did not begin until the clinical report
by Kunlin in 1949.

Even though the first successful arterial allograft was reported by Hoepfner in 1903, the practice
did not pick up until Gross and associates reported the use of viable arterial allografts in patients in
1948. Early results were encouraging and arterial allografts became widely used, leading to the
establishment of human arterial banks in the late 1940s, freeze-drying being the most popular
method of allograft preservation. In 1952, duBost from Paris replaced an abdominal aortic
aneurysm by an allograft. The clinical use of arterial autografts was introduced by Wylie in 1965.

The development of prosthetic arterial grafts was stimulated by the observation by Voorhees in the
early 1950s that silk threads in the canine vascular system became covered by a glistening
118

endothelium-like cellular coating. Voorhees and associates subsequently described successful


replacement of arteries in animals with a porous textile graft made from the nylon derivative
Vinyon-N. Two years later, the same graft was successfully implanted in humans. The field of
prosthetic vascular grafts has since achieved enormous clinical and laboratory importance.

Uses of Vascular Grafts


Vascular grafts are used in the following settings:
1. To overcome (thru bypass, or resection and replacement) obstructions in aorta or major
arteries as a result of atherosclerosis, thrombosis, embolism, congenital lesions, cicatrix
(strictures), disruption (rupture, laceration), dissection, neoplastic invasion. This includes
coronary bypass grafting.
2. To control/ prevent hemorrhage from aorta or major arteries as a result of trauma or by
aneurysms, by bypass with ligation or resection and replacement.
3. To obtain vascular access for renal dialysis, aortic balloon counterpulsation, extra-corporeal
cardiac/lung support, arteriography.
4. Reinforcement in cardiovascular surgery for cardiac outflow tract augmentation, intra-cardiac
baffles, buttressing of cardiovascular sutures.
5. Extra-anatomic blood conduits/shunts eg. Blalock-Taussig shunts, splanchnic systemic
venous shunts, axillo-femoral and femoro-femoral bypass, and as part of cardiac assist
devices eg. LVAD

Patency is the most important end-point in the evaluation of the clinical performance of any
vascular graft. Primary patency is that achieved without any additional graft-directed
procedures. It reflects the natural history of individual grafts. Secondary patency refers to
grafts that have been maintained patent by one or more additional graft-directed procedures. It
is an indicator of the long-term functional effectiveness of a graft. Assisted primary patency,
refers to secondarily patent grafts that undergo revision prior to actual graft thrombosis. It has
come to be regarded as an indicator of the effectiveness of a clinical follow-up program to
detect failing grafts prior to thrombosis.
Types of Vascular Grafts (Figure 1)

119

Autografts
Autografts can be veins or arteries. Veins are the preferred graft for infrainguinal arterial
reconstruction. The greater saphenous vein, lesser saphenous vein, cephalic and brachial veins,
and superficial femoral and internal jugular veins have been used. The saphenous vein has been
used most frequently for coronary artery bypass grafts and for lower extremity bypass of occluded
superficial femoral, popliteal, and tibial arteries. It has also been used for upper extremity bypass,
and mesenteric and renal artery bypass.

Lower extremity bypasses using autologous saphenous vein may be performed using one of two
techniques. Either the vein may be reversed and sutured end to side or it may be left in-situ and
sutured, with the venous valves destroyed using a valvulotome. With the reversed vein technique,
the main disadvantage is the size discrepancy between the vein and the corresponding arterial
segment. But it is applicable to larger numbers of patients, because many patients do not have an
intact ipsilateral saphenous vein. Both techniques are currently widely employed and generally
produce similar results. The primary patency of reversed femoropopliteal saphenous vein
autografts ranges from 80% to 90% at 1 year, 55% to 86% at 5 years, and 38% to 46% at 10
years. (Ref.2) Reversed saphenous vein grafting to tibial arteries produces patency rates that are
about 10% to 15% lower than those for femoropopliteal grafting at all time intervals. (ref. 2)
Patency is higher when surgery is performed for claudication rather than limb salvage. Continued
cigarette smoking and the use of a small vein (less than 4 mm. after gentle distention) decrease
long-term patency.

As many as 20% to 30% of patients in need of leg bypass do not possess greater saphenous
veins adequate for arterial grafting. (ref. 3), as it may be too small, may have thrombosis or
varicosities or may have been previously removed.

Early postoperative vein graft failure is attributed to technical errors or the presence of an
unrecognized hypercoagulable state. Late failures may follow progression of atherosclerotic
disease above or below the vein graft, or changes in the graft itself (arterialization). This involves
medial and subintimal fibrous hyperplasia, in combination with fibrin deposition on the intimal
surface. (ref. 4) This follows the conversion of normally quiescent myointimal and medial smooth
muscle cells into actively proliferating secretory myofibroblasts. The predominant current theory
regards fibrointimal hyperplasia as a response to endothelial damage occurring during and
following grafting and disruption of the vasa vasorum. Thus importance is placed on gentle vein
harvest techniques and the avoidance of excessive hydrostatic venous distention.

The advantages of autologous veins include easy availability, retention of viability due to an intact
intrinsic blood supply, proportional growth when used in children, their ability to heal in an infected
field, and exhibition of normal flexibility at joints. They display the best long term results for infra-

120

inguinal bypass. Their limitations are that they do deteriorate over time, are available in a limited
number or short length and can have pre-existing disease thus precluding their use.

The arterial grafts include the LIMA, RIMA, radial and gastro-epiploic arteries. They have
numerous advantages, including retention of viability associated with the maintenance of an intact
intrinsic blood supply during grafting, absence of aneurysmal degeneration, resistance to infection,
preservation of normal flexibility at points of joint motion, and possession of growth potential when
used in pediatric patients. The obvious disadvantage is a lack of availability, including inadequate
length of arteries for most potential applications.

The clinical use of arterial autografts is restricted primarily to coronary artery bypass grafting, renal
artery bypass in children, and arterial substitutes in infected surgical fields. Use of the internal iliac
artery is, however, limited in the adult population by its frequent involvement with advanced
atherosclerosis. The external iliac artery may also be used as an arterial autograft, but it requires
prosthetic

replacement

of

the

autograft

donor

site.

Atherosclerotic

arteries

may

be

endarterectomized and used as either bypass conduits or as patch grafts.

Homografts (Allografts)
Arterial homografts were the first widely used arterial substitutes. But results with them and with
venous homografts (ref. 5) have generally been poor, with high incidence of thrombosis,
calcification, aneurysm formation, and rupture.

The only clinically significant homograft in vascular surgery are the umbilical vein homografts.
Prepared from human umbilical cords, they are subjected to glutaraldehyde tanning and multiple
ethanol extractions and are externally reinforced with a polyester mesh tube. Dardik et al have
reported primary patency rates of 70% and 50% at 1 and 5 years at femoropopliteal position
(ref.6,7). These results are comparable with polytetrafluoroethylene (PTFE) grafts. These grafts
exhibit degenerative changes in the elastic layer over time and are prone to the development of
aneurysms. They are technically difficult to implant, and the intima is easily damaged by clamps or
attempts at thrombectomy, and carry the risk of infection.

Xenografts
The commonest used xenografts today are the Contegra (bovine jugular vein conduit) used for
right ventricular outflow reconstruction in congenital heart lesions like tetralogy of Fallot and
truncus arteriosus. They are also used for aortic arch replacement in hypoplastic left heart
syndrome. Bovine carotid arteries fixed in dialdehydes and re-inforced with Dacron mesh are used
as hemodialysis access shunts in some centers. Xenografts carry risk of viral transmission and
aneurysm formation and rupture, because of the accelerated host response they generate.

121

Dacron (PET=polyethylene terephthalate)


Dacron and Teflon are the only textile grafts in clinical use. A textile is basically a network of fibres
called yarns. Dacron is a multifilament polyester yarn, made of 10-20 micron filaments bundled into
yarns. It can be either woven or knitted.
Woven grafts (Figure 2) The threads are interlaced in a simple over and under pattern both in
lenghtwise and circumferential directions. These grafts are less porous, so they are used where
bleeding is a risk and full heparinization is employed. eg. in thoracic aortic aneurysm surgery.
Their disadvantages are that they are stiff, are difficult to handle, have a limited stretch
potential, have a reduced potential for development of a neo-intima by connective tissue in
growth, and display more fraying of cut edges.

Figure 2

Knitted grafts (Figure 3) In a knit structure, the yarns are looped around each other. The yarn
is orientated in a predominantly longitudinal (warp knitted) or circumferential (weft knitted)
direction. Since they are more stable, warp knitted grafts are usually used. Knitted grafts are
softer, more compliant, display lesser fraying and a higher graft healing. They are however,
more porous than woven grafts and so require pre-clotting prior to use.

Figure 3

Textile grafts function most satisfactorily when used for arterial replacement proximal to the
inguinal ligament. Five- and 10-year patencies have been reported as high as 91% and 66%,
respectively, for aortofemoral bypass (Ref. 8,9). Axillofemoral bypass patency has been in the
range of 75% to 77% at 5 years, and femorofemoral bypass patency at 5 years has been 75% to
80% (Ref. 10,11,12). However for infra-inguinal bypass, theire patency results are distinctly inferior
to those of saphenous vein.
122

Expanded PTFE (ePTFE)


PTFE is a fluorocarbon polymer formed into sheets by a paste extrusion process. It is not a textile
but a highly crystalline polymer consisting of solid nodes of PTFE with interconnecting small fibrils.
The intranodal distance is about 40 for grafts in clinical use. PTFE grafts have a highly
electronegative surface charge and are thus hydrophobic and resistant to thrombosis. The grafts
are coated with an outer wrap of PTFE to avoid aneurysm formation. They may be available with
external ring supports to avoid compression and kinking. Wall thickness may be varied, with thinwalled grafts preferred for infrainguinal bypasses. Thick-walled grafts function well as hemodialysis
shunts. Externally supported PTFE axillofemoral grafts provide 5-year patency rates of about 70%.
(Ref. 11)

Poly-urethane grafts have a very smooth non-trombogenic inner surface. However degradation of the
polyurethane polymer leads to weakening and aneurysm formation. Their patency rates have not
been high, (Ref. 13) and they have not been commonly used.

MODIFICATIONS OF PROSTHETIC GRAFTS


1. Velour: (Figure 4) Velour surfaces have loops of yarn extending almost perpendicular to the
fabric surface. Velour surfaces improve the handling characteristics of woven grafts and
provide a scaffold for fibroblast ingrowth, leading to firm graft adherence to surrounding
tissue.

Figure 4

2. Crimping: Crimping imparts greater flexibility and improves radial strength and elongation
potential of the graft. However, it diminishes luminal diameter, increases the thickness of the
graft material, and may also cause deposition of thrombogenic fibrin in the crimped areas.
(Ref. 14)
3. Impregnating with albumin, gelatin, bovine type I collagen: (Ref. 15) This makes grafts
leakproof thus reducing the intra-operative blood loss without increasing the thrombogenicity.
4. Endothelial seeding: This is employed in small caliber grafts to improve their patency. (Ref.
16)
5. Carbon coating (Impra, Carbolo) imparts a negative charge to reduce platelet deposition.
(Ref. 17)

123

6. Trans-luminal grafts: (ref. 18). Usually used in cases of pseudo-aneurysms. Dacron or


PTFE grafts are mounted on expandable metallic stents and placed into the artery using a
coaxial delivery system under fluoroscopic guidance. The graft either self-expands or is
expanded with an angioplasty balloon, to exclude the flow stream from the aneurysm sac.
The grafts are held in place by the outward pressure of the stent itself and/or by hooks that
engage the artery wall. Problems with these grafts include the large size of the delivery
systems currently required to place the grafts, the need for suitable anchoring sites, graft
migration, arterial perforation, possible embolization of the luminal thrombus that is usually
present within aneurysms, perigraft leakage such that the aneurysm is not completely
excluded from the flow stream, and graft kinkage and axial twists.

PROSTHETIC GRAFT HEALING


On exposure to blood flow, the luminal surface of a vascular prosthesis is immediately coated by a
layer of protein, principally fibrinogen. Prosthetic graft healing refers to the development of a living
neointima inside the graft, connected to an external fibrous capsule by means of connective tissue
ingrowth through the graft interstices. Well-healed grafts offer the possibility of decreased
thrombogenicity and increased resistance to infection. In grafts with high flow, the thickness
stabilizes at about 1 mm. and is well tolerated.

COMPLICATIONS OF PROSTHETIC GRAFTING


1. Graft Occlusion. Due to thrombosis or anastomotic neo-intimal hyperplasia which is present
at both proximal and distal anastomoses. Clinically, the distal anastomotic process is more
significant. Both textile and PTFE grafts are affected. Anti-platelet drugs are prescribed to
prevent this complication. Treatment is either medical with heparin or TPA or re-operation
with graft thrombectomy or replacement of the graft.
2. Graft infection Usually caused by Staphylococcus aureus, Staphylococcus epidermidis, and
Escherichia coli. The most common cause of graft infection is contamination at the time of
surgery. Incidence is about 1.5% to 2.5%; it is slightly lower when the graft is completely intraabdominal and higher when a groin anastomosis is present. Aortic graft infections may be
associated with an operative mortality of 10% to 25% and an amputation rate of 15% to 20%.
Almost always, an infected arterial graft must be removed. An extra-anatomic graft is often
necessary (e.g. replacement of an aortic with an axillo-bifemoral graft).
3. Graft failure. Two distinct types of Dacron graft failure have been described. The first
consists of gradual, diffuse graft dilatation, observed with the ultra lightweight knitted Dacron.
The dilatation was caused by expansion of the knit rather than elongation or weakening of
individual fibers. It was occasionally associated with delayed graft rupture or diffuse interstitial
bleeding. Ultra lightweight Dacron has now been abandoned. The second type of graft failure
follows specific defects, such as a dropped stitch in the manufacturing process, or fiber
degeneration. This type of defect usually causes localized holes and leaks, with the potential
for false aneurysm formation.
124

4. Perigraft Seromas. A perigraft seroma is a sterile collection of clear fluid within a


nonsecretory pseudomembrane surrounding a prosthetic vascular graft. It usually occurs in
association with extra-anatomic bypasses, that is, an axillofemoral or femorofemoral graft.
The incidence is around 2%, occurring with both Dacron and PTFE grafts. Treatment has
included observation alone, multiple aspirations, graft removal, injection of perigraft sclerosing
agents. It can present as a lymphocele in the groin.
5. False aneurysms. The incidence of false aneurysm with prosthetic grafting is estimated to be
at least 3%. Both Dacron and PTFE grafts are affected. They can follow degeneration and
fragmentation of the silk sutures, sub-clinical infection, shallow suture placement or arterial
degeneration associated with hypertension. They should be repaired when discovered. The
usual repair consists of a graft-artery re-anastomosis, frequently with the insertion of a short
additional piece of graft material.
6. Erosion into adjacent structures eg. aorto-enteric fistulae. Most aorto-enteric fistulae
present months or years after the initial vascular surgery. The most common site of erosion is
at the proximal anastomosis of an aortic graft into the distal duodenum or duodeno-jejunal
flexure. Any GI bleed in a patient with an intrabdominal vascular graft should raise suspicion
of an aorto-enteric fistula. They often present with a moderate 'herald' bleed prior to an
exsanguinating haemorrhage. CT may show an anastomotic aneurysm but early laparotomy,
removal of the graft, oversew of the aortic stump and extra-anatomical bypass is usually
required.
REFERENCES
1.

Callow, A.D. History of Vascular Graft Development 1986, pp11-15

2.

Taylor, L. M., Jr., Edwards, J. M., and Porter, J. M.: Present status of reversed vein bypass: Long
term results of a modern series. J. Vasc. Surg., 11:193, 1990.

3.

Szilagyi, D. E., Hageman, J. G., Smith, R. F., et al.: Autogenous vein grafting in femoropopliteal
atherosclerosis: The limit of its effectiveness. Surgery, 86:836, 1979.

4.

Sottiurai, V. S., and Arson, R. C.: Ultrastructural studies of arterial grafts. In Bergan, J. J., and
Yao, J. S. T. (Eds.): Evaluation and Treatment of Upper and Lower Extremity Circulatory
Disorders. New York, Grune & Stratton, 1984, p. 371.

5.

Ochsner, J. L., DeCamp, P. T., and Leonard, G. L.: Experience with fresh venous allografts as an
arterial substitute. Ann. Surg., 173:933, 1971.

6.

Dardik, H., Miller, N., Dardik, A., Ibrahim, I. M., Saussman, B., Berry, S. M., Wolodiger, F., Kahn,
M., and Dardik, I.: A decade of experience with the glutaraldehyde-tanned human umbilical cord
vein graft for revascularization of the lower limb. J. Vasc. Surg., 7:336, 1988.

7.

Eickhoff, J. H., Broome, A., Ericsson, B. F., Hansen, H. J. B., Kordt, K. F., Mouritzen, C.,
Kvernebo, K., Norgren, L., Rostad, H., and Trippestad, A.: Four years' results of a prospective,
randomized clinical trial comparing polytetrafluoroethylene and modified human umbilical vein
for below-knee femoropopliteal bypass. J. Vasc. Surg., 6:506, 1987.

8.

Brewster, D. C., and Darling, R. C.: Optimal methods of aortoiliac reconstruction. Surgery,
84:739, 1978.

125

9.

Piotrowski, J. J., Pearce, W. H., Jones, D. N., Whitehill, T., Bell, R., Patt, A., and Rutherford, R. B.:
Aorta bifemoral bypass: The operation of choice for unilateral iliac occlusion? J. Vasc. Surg.,
8:211, 1988.

10. Brief, D. K., Brener, B., and Alpert, J.: Crossover femoro-femoral grafts followed up 5 years or

more: An analysis. Arch. Surg., 110:1294, 1975.


11. Harris, E. J., Jr., Taylor, L. M., Jr., McConnell, D. B., Moneta, G. L., Yeager, R. A., and Porter, J. M.:

Improved modern results of axillobifemoral bypass using externally supported PTFE. J. Vasc.
Surg., 12:416, 1990.
12. Kalman, P. G., Hosang, M., Johnston, K. W., and Walker, D. M.: The current role for

femorofemoral bypass. J. Vasc. Surg., 6:71, 1987.


13. Experimental study of selected small calibre arterial grafts, J. Cardiovasc. Surg. 18, 155 Geeracrt

AJ, Callaghan JC, (1977)


14. Kenney, D. A., Berger, K., Walker, M. W., and Sauvage, L.: Experimental comparison of the

thrombogenicity of fibrin and PTFE flow surfaces. Ann. Surg., 191:355, 1980.
15. Reigel, M. M., Hollier, L. H., Pairolero, P. C., and Hallett, J. W., Jr.: Early experience with a new

collagen-impregnated aortic graft. Am. Surg., 54:134, 1988.


16. Zilla, P., Deutsch, M., Meinhart, J., Puschmann, R., Eberl, T., Minar, E., Dudczak, R., Lugmaier, H.,

Schmidt, P., Noszian, I., and Fischleiu, T.: Clinical in vitro endothelialization of femoropopliteal
bypass grafts: An actuarial follow-up over three years. J. Vasc. Surg., 19:540, 1994.
17. Modified polytetrafluoroethylene: Indium 111-labeled platelet deposition on carbon-lined high

porosity polytetrafluoroethylene grafts, J. Vasc. Surg. 4, 643-649 Tsuchia H, Cameron BL,


Marcus CS, Wilson SE, (1992)
18. Parodi, J. C., Palmaz, J. C., and Barone, H. D.: Transfemoral intraluminal graft implantation for

abdominal aortic aneurysms. Ann. Vasc. Surg., 5:491, 1991.

Index

126

Superior mediastinal syndrome


Ravi Kanan
Superior mediastinal syndrome (or superior vena cava syndrome (SVCS) as it is more commonly
called), conventionally considered an oncological emergency, is the clinical manifestation of
obstruction of the superior vena cava (SVCO), and, can result in a variety of life threatening problems
including dyspnoea and cerebral oedema. William Hunter gave the first pathologic description of SVC
obstruction in a patient with syphilitic aortic aneurysm in 1757. Syphilitic aneurysms and tubercular
mediastinal lymphadenitis used to be common causes of SVCO about fifty years ago.

Today,

malignancy is the most common aetiological factor for SVCS. With increasing use of intravascular
catheters and pacemakers superior vena cava thrombosis caused by these devices is emerging as a
significant cause of SVCS.

Anatomy
The SVC is formed by the union of the right and left innominate veins and is 6 to 8 cm. long. The
terminal 2 cm. of the SVC is within the pericardial sac. It is 1.5 to 2 cm wide. The azygous vein
enters the SVC just above its entry into the pericardial sac. In its location in the superior and
middle mediastinum, the SVC, encircled by chains of lymph nodes that drain all the structures of
the right thoracic cavity and the lower part of the left thorax, is in relation to the sternum, trachea,
right bronchus, aorta and pulmonary artery. Pressures inside the normal SVC are low. It is thin
walled and is easily compressed. It is the major vessel for drainage of venous blood from the head,
neck, upper extremities, and upper thorax.

Typical symptoms and signs may develop quickly or

gradually when this thin-walled vessel is compressed, invaded, or thrombosed by pathology in the
superior mediastinum.

Pathophysiology
The clinical manifestations of SVCO depend on the level of obstruction (supra vs. infra azygous),
on the rapidity with which obstruction occurs and the competence of the valves at the junction of
the internal jugular and subclavian veins. Other critical structures in the mediastinum, such as the
main bronchi, esophagus, and spinal cord, may be involved by the same pathology that lead to
obstruction of the SVC and may confound the presenting symptoms and signs.

Gradual obstruction of the SVC results in the development of an extensive venous collateral
circulation. The azygous venous system is the most important alternative pathway. Other collateral
systems are the internal mammary veins, lateral thoracic veins, para-spinal veins, and esophageal
venous network. The subcutaneous veins are important pathways, and their engorgement in the
neck and thorax is a typical physical finding in SVCS. Despite these collateral pathways, venous
pressure is almost always elevated in the neck and upper limb veins if the SVC is obstructed.
Venous pressures as high as 200 to 500 cm H2O have been recorded

127

Aetiology
Over 85% of SVCO is caused by malignant pathology. About 5% of all lung cancer patients
develop SVCS, accounting for up to 80% of all patients with malignancy presenting with SVCO. A
half of these would be patients with small cell lung cancer and another quarter those with
squamous cell cancer. High grade NHL accounts for about 15% of SVCO. Low grade lymphomas
and Hodgkins disease rarely result in SVCO.

Metastatic disease, commonly from breast or

testicular primaries, sarcomas, and other malignancies, such as gastrointestinal tumors,


transitional cell carcinomas and melanomas, account for the remainder.

Less than 15% of SVCO occurs as a result of benign aetiology. Increasingly, iatrogenic causes
such as long-term central venous catheterization, transvenous pacemakers, balloon-tipped
pulmonary artery catheters and peritoneal venous shunting are reasons for SVC thrombosis.
Data from some general hospitals shows as much as 40% of SVCS to be due to intravenous
devices.

Hyper viscosity states like polycythemia vera, paroxysmal nocturnal haemoglobinuria and
Behsets syndrome can also cause thrombosis of the superior vena cava. Mediastinal fibrosis
resulting from idiopathic fibrosing mediastinitis, histoplasmosis, actinomycosis, tuberculosis and
pyogenic infections, Riedel's thyroiditis, retroperitoneal fibrosis, sclerosing cholangitis, and
Peyronie's disease and radiation therapy to the mediastinum can occasionally cause SVCO.
Aneurysms of the arch of aorta or right subclavian artery and benign tumours like dermoids,
teratoma and thymoma, retrosternal goiter and sarcoidosis have also been cited to cause SVCO.
On occasion, the cause of the SVCO remains idiopathic.

Obstruction of SVC in the pediatric age group is rare. 70% of these are iatrogenic secondary to
cardiovascular surgery for congenital heart disease, ventriculo-atrial shunt for hydrocephalus, and
SVC catheterization for parenteral nutrition. Of the remainder about 2/3rds are caused by
mediastinal tumors. Benign granuloma, and congenital anomalies of the cardiovascular system
and mediastinal fibrosis account for the rest.

Two thirds of the tumors causing SVCS in childhood are lymphomas. The rest are accounted for
by metastases from other paediatric solid tumours including neuroblastoma, and germ cell
tumours. Most children in whom SVCS developed late in the course of their malignancy had
recurrent solid tumors.

Natural history and symptoms


Tumors growing in the mediastinum compress the thin-walled vena cava, leading to its collapse.
Venous thrombosis because of stasis or vascular tumor invasion often appears to be responsible
for acute-onset SVC syndrome. Vena cava obstruction caused by malignancy often progresses
too rapidly to develop sufficient collateral circulation, which might alleviate the syndrome. If the
128

obstruction occurs above the azygous vein, the obstructed SVC could then drain into the azygous
system. The azygous vein, however, is frequently obstructed by malignancy below its origin.

Incompetent internal jugular vein valves, a rare occurrence, cause a dire emergency that is
manifested by the filling of these veins. Patients who present with this finding die within hours or
days of massive cerebral oedema unless treatment is immediately instituted.

Symptoms of SVC syndrome are present for less than 2 weeks before diagnosis in 20% of patients
and for more than 8 weeks in 20%. The most common presenting symptoms are shortness of
breath (50-63% of patients), neck and facial swelling (40-55%), and swelling of trunk and upper
extremities (10-40%). Sensations of choking, fullness in the head, and headache are also frequent
complaints. Chest pain, cough (24%), lacrimation, dysphagia (9%), hallucinations, and convulsions
(5%) are less frequent complaints.

SVC obstruction may occasionally be accompanied by spinal cord compression, usually involving
the lower cervical and upper thoracic vertebrae. The SVC syndrome consistently precedes spinal
cord compression in these cases. The coexistence of these two complications should be seriously
suspected in patients with upper back pain.

The most common physical findings are thoracic vein distention (65%), neck vein distention and
oedema of face (55%), tachypnoea (40%), plethora of the face and cyanosis (15%), oedema of
upper extremities (10%), and paralysis of vocal cords and Horner's syndrome (3%). Veins in the
antecubital fossae are distended and do not collapse when elevated above the level of the heart.
Retinal veins may be dilated on funduscopic examination. Dullness to percussion over the sternum
may be present. Stridor and coma are grave signs.
These symptoms and signs may be aggravated by bending forward, stooping, or lying down.

Diagnosis
The diagnosis is usually based on the clinical findings and the presence of a mediastinal mass
(90%) with or without hilar lymphadenopathy (50%) or a pleural effusion (25%), usually right
sided, on a plain x-ray chest. Only about 16% of patients have normal chest skiagrams.
Contrast enhanced computed tomography can locate the site and degree of SVC occlusion,
presence of venous collaterals and compromise of other structures like the trachea/ bronchus
or the vertebrae and spinal cord which may need urgent treatment. It can be used to guide a
fine needle aspiration and for planning radiation portals. Magnetic resonance imaging scans of
the cervical and upper thoracic vertebrae should be planned in patients with SVC syndrome
and back pain, particularly in the presence of Horner's syndrome or vertebral destruction on
plain films. This is particularly useful in patients with contrast allergy.

129

A digital subtraction superior venacavogram demonstrates the exact site of obstruction and
is the procedure of choice in planning stenting procedures.

The role of FDG-PET (fluorodeoxyglucose-positron emission tomography) scanning remains to


be evaluated in patients with SVCS. It may influence the design of the radiotherapy field in
lymphoma or lung cancer.

SVCS used to be considered to be a potentially life-threatening medical emergency. Radiation


therapy, using initial high-dose fractions, would be commenced even before the histological
diagnosis was established.

Diagnostic procedures, such as bronchoscopy, supraclavicular

lymph node biopsy, mediastinoscopy or thoracotomy were often avoided because they were
considered to be dangerous in a patient with SVCS due to a fear of haemorrhage. However,
the safety of these invasive procedures in patients with SVCS has markedly improved, and the
modern treatment of SVCS has become disease specific from the outset.
Histological/ cytological confirmation of the malignancy and its type is important before
commencing any treatment. There is no data to suggest that untreated SVCO leads on to rapid
death independent of its aetiology.

Identification of the type of malignancy will help tailor

treatment appropriately. Further, when cytotoxic agents are necessary, pre-treatment tissue
diagnosis will help decide the agents to be used (SCLC vs. lymphoma for example). Radiation
therapy or even steroids will make subsequent histology difficult due to nondescript necrosis
and/ or alteration in architecture.
Cytology of sputum (three deep-cough sputum specimens), bronchoscopy biopsy/ brushings/
wash cytology and thoracocentesis of pleural effusions each yield the diagnosis in over twothirds of patients. These are rarely associated with serious complications. Biopsy of palpable
lymph nodes will be rewarding in more than 80% of patients. Biopsy of non-palpable scalene
nodes will help clinch the diagnosis in only 30-40% of cases.

Transbronchial or CT guided

transthoracic needle aspirations are also highly effective and have a sensitivity of about 75%.
There is a small risk of pneumothorax in transthoracic aspirations.
Mediastinoscopy in appropriately selected patients, where the diagnosis could not be
established by less invasive means, has a yield of about 80%. The complication rate is about
5% and includes haemorrhage. Most series report nil mortality.
SCLC and NHL often involve the bone marrow. A biopsy of the bone marrow may provide the
diagnosis and stage, especially in patients with cytopenia or leukoerythroblastic blood smear.
A thoracoscopic biopsy or mini-thoracotomy is indicated if all other procedures have failed.
The traditional opinion that diagnostic procedures carry with them significant hazard, primarily
excessive bleeding, has not been borne out by reviews. A study that looked at 843 invasive
130

and semi-invasive diagnostic procedures found only ten complications, none of them fatal.
Ahmann and others found minimal evidence to suggest that diagnostic procedures such as
demography, thoracotomy, bronchoscopy, mediastinoscopy, and lymph node biopsy carry an
excessive risk in patients with SVCS. In 163 patients treated at Memorial Sloan-Kettering
Cancer Center for anterior mediastinal mass, 44 underwent general anesthesia. No deaths
occurred, and only four patients had prolonged intubation, demonstrating the low risk of modern
anesthesia in thoracic patients.

Management
The goals of treatment of SVCS are to relieve symptoms and to attempt the cure of the primary
malignant process. SCLC, NHL, and germ cell tumors constitute almost one half of the malignant
causes of SVCS. These disorders are potentially curable, even in the presence of SVCS. The
prognosis of patients with SVCS strongly correlates with the prognosis of the underlying disease.

Emergency treatment without establishing the histology and staging is indicated only in the
presence of cerebral dysfunction, decreased cardiac output, or upper airway obstruction.
Standardized and validated criteria to grade the severity of symptoms in the superior vena cava
syndrome and to guide the choice of treatment are lacking. The most commonly referenced
grading systems based on CT scans and venograms are shown is the table below.

Classification of SVC obstruction by computed tomography (CT) and venography.


CT classification
Type IA
Type IB
Type II
Type III
Type IV

Finding
Moderate SVC narrowing without collateral flow
Severe SVC narrowing with retrograde flow in azygous vein
Obstruction above azygous with retrograde flow into thoracic, vertebral, or
other collateral channels
SVC obstruction below azygous with retrograde flow through azygous into
the inferior vena cava (IVC)
SVC obstruction at azygous vein with multiple small peripheral collaterals

From Stanford W, Doty D. The role of venography and surgery in the management of patients with superior vena
cava obstruction. Ann Thorac Surg 1986;41:158.

Venogram classification
Type I
Type 2
Type 3
Type 4

Partial obstruction of the SVC with patency of the azygous vein


Near-complete to complete obstruction of the SVC with antegrade flow in the
azygous vein
Near-complete to complete obstruction of the SVC with retrograde flow in the
azygous vein to the IVC
Complete obstruction of the SVC and azygous vein

From Raptopoulos V. Computed tomography of the superior vena cava. CRC Crit Rev Diagn Imaging
1986;25;373.

131

A scoring system based on the clinical presentation though useful has also not been validated.
Clinical scoring system for SVC obstruction.
Symptom
Arm/head/extremity swelling
Neck or chest vein distension
Cough
Blurred vision
Tinnitus
Headache
Dizziness
Dyspnoea
Plethora
Vocal cord paralysis
Total Up to

Points
1
1
1
1
1
1
1
1
1
1
10 points.

From Nicholson A, Ettles D, Arnold A, et al. Treatment of malignant superior vena cava obstruction: metal stents
or radiation therapy? J Vasc Intervent Radiol 1997;8:781788.

When the therapeutic goal is only palliation of SVCS, or when urgent treatment of the venous
obstruction is required, direct opening of the occlusion should be considered. The newer techniques
of endovascular stenting and angioplasty with possible thrombolysis should provide prompt relief of
symptoms before more specific cancer therapy.
1. Supportive therapy
Non specific general measures may be beneficial in temporarily relieving the symptoms of SVCS.
Bed rest with the head elevated and oxygen administration can reduce the cardiac output and
venous pressure. Diuretic therapy and a reduced-salt diet to reduce edema may have an
immediate palliative effect, but the risk of thrombosis enhanced by dehydration should not be
ignored. While the effects of steroids has not been evaluated, they may improve obstruction by
decreasing a possible inflammatory reaction associated with tumor or with irradiation.

51

Thrombolytic therapy with urokinase, streptokinase, and recombinant tissue-type plasminogen


activator are effective in SVCS induced by indwelling catheters.

2. Radiation therapy
Until the advent of modern chemotherapeutic agents, radiation therapy used to be the definitive
treatment for SVCS often without a pathological diagnosis. The total dose of RT varies between
30 and 50 Gy, depending on the general condition of the patient, severity of the symptoms,
anatomic site, and histological type of underlying malignant tumor. Serial venograms and autopsy
studies suggest that the symptomatic improvement achieved by radiotherapy is not always due to
improvement of flow through the SVC. It is probably also a result of the development of collaterals
after the pressure in the mediastinum is eased.
Improvement in most patients is evident within 3 to 7 days. Complete response is observed in
about 75% of patients with lymphoma and in 25% with lung cancer. Virtually all patients with
lymphoma have at least a partial response, whereas about 15% of patients with lung cancer

132

experience no real benefit from treatment. Following radiation therapy for SVCS, recurrent SVC
syndrome occurs in 15% to 20% of patients with lung cancer but rarely with lymphoma.

3. Chemotherapy
Combination chemotherapy is today the treatment of choice for most patients with malignant
pathology causing SVCS. It may be curative in those with lymphoma, small cell lung cancer or
germ cell tumours. Radiation therapy may be used for consolidation following combination
chemotherapy in these conditions. When chemotherapy is administered, the arm veins should be
avoided. Veins of the lower extremities provide an alternative simple venous access.

4. Endovascular stenting and angioplasty


Percutaneous placement of self-expanding metal endoprostheses gives rapid symptomatic relief in
90% to 100% of patients. When available, stenting is the procedure of choice, especially in the
setting of recurrent SVC obstruction after radiation therapy. Complications are infrequent, but
interventional radiologists experienced in stent placement are not universally available.

Percutaneous transluminal angioplasty using the balloon technique, insertion of expandable wire
stents, or both have been successfully used to open and maintain the patency of SVC obstruction
resulting from malignant and benign causes. Thrombolysis is an integral part of the endovascular
management of SVCS because thrombosis is frequently a critical component of the obstruction
and lysis is necessary to allow the passage of the wire.

The experience with stenting has been growing rapidly with three stents: the Gianturco Z Stent
(Cook Group Inc., Bloomington, Indiana), the WALLSTENT (Boston Scientific, Natick,
Massachusetts), and the PALMAZ stent (Cordis Corp, Miami Lakes, Florida). The WALLSTENT,
the most commonly used device, is a self-expanding metallic stent built of woven stainless steel
wire. Its tight weave deters tumor in-growth. Total occlusion of the SVC is not a contraindication to
stent therapy, and a success rate of 85% in total occlusion situations has been reported. Following
stent placement, almost all patients experience improvement of obstruction and over 90% remain
symptom free till death. However, data on long-term stent patency in patients with SVCS from
benign causes is limited. Complication rates for endovascular therapy have ranged from 0% to
50% and include bleeding, stent migration, stent occlusion, and pulmonary embolus.

Most

complications can be successfully treated with percutaneous methods.

5. Thrombolytic Therapy
Thrombolysis is an important component of comprehensive endovascular therapy. Patients with
SVC thrombosis induced by intravascular catheters and other such devices respond better to
thrombolytic therapy when compared to patients without catheters. The higher yield of thrombolytic
therapy in patients with catheters is probably related to the mechanism of obstruction, the ability to
deliver the agent directly to the thrombus, and earlier recognition of SVCS in patients with
133

malfunctioning catheters leading to prompt thrombolytic therapy. Patients who undergo stenting
for SVCS should receive thrombolytic therapy during and anticoagulants after the procedure.

6. Surgery
The experience with successful direct bypass graft for SVC obstruction is limited. Autologous
grafts of almost the same size as the SVC (including composite spiral grafts constructed from the
patient's saphenous vein), dacron prostheses, expanded polytetrafluoroethylene prostheses and
autologous pericardium have all been used to reconstruct the SVC. The preferred bypass route is
between an innominate or jugular vein on the left side and the right atrial appendage, using an
end-to-end anastomosis.

The most common surgical approach is sternotomy or thoracotomy with extensive resection of the
tumor and reconstruction of the SVC. Case series indicate an operative mortality of approximately
5% and patency rates of 80% to 90%.

However, with malignancy-induced SVCS, surgical

intervention should be considered only after other therapeutic maneuvers with irradiation,
chemotherapy, and stenting have been exhausted. Most patients with SVCS of benign origin have
long survivals without surgical intervention. However, if the process progresses rapidly or if there
is a retrosternal goiter or aortic aneurysm, surgical intervention may relieve the obstruction.

THERAPEUTIC OPTIONS IN SPECIFIC DISEASE STATES


Small Cell Lung Cancer
Chemotherapy alone or in combination with thoracic irradiation therapy is the standard treatment
for SCLC.

Chemotherapy is commonly used as the initial modality to shrink the tumor thus

reducing the field of radiation. Chemotherapy and radiotherapy are comparable when considered
as first line therapy for relief of SVCS due to SCLC. Relief of SVCS occurs within 7 to 10 days of
initiation of therapy. In SCLC patients with recurrent or persistent SVCS after initial chemotherapy,
the obstruction may respond with additional chemotherapy and/ or radiation therapy.

Non Small Cell Lung Cancer


SVCS is a poor prognostic feature in patients with NSCLC.
marginally superior to chemotherapy in relieving SVCS.

Radiation therapy is probably

A short course of hypofractionated

radiation therapy may be superior to conventional fractionation.

Response to radiotherapy is

higher in patients who have received prior chemotherapy.

Non-Hodgkin's Lymphoma
Chemotherapy, radiation therapy or a combination of the two all give equally good results with
nearly 100% of patients achieving complete relief of SVCS within 2 weeks of initiation of treatment.
The presence of dysphagia, hoarseness, or stridor appears to be major adverse prognostic factors
for patients with lymphoma who present with SVCS.

134

With a histological diagnosis of lymphoma, a complete staging work-up before commencing


therapy is advisable. Chemotherapy is the treatment of choice, because it provides local and
systemic therapeutic activity.

Local consolidation with radiation therapy may be beneficial in

patients with large cell lymphoma with mediastinal masses larger than 10 cm.

Nonmalignant Causes (other than intravenous devices)


Patients with nonmalignant causes of SVCS often have symptoms long before they seek medical
advice.

It takes more time to establish the diagnosis, and their survival is markedly longer.

Fibrosing mediastinitis and mediastinal granuloma (commonly histoplasmosis in endemic areas)


are causes reviewed in recent literature. Most patients had an insidious onset of SVCS.

It was

suggested that the good prognosis of patients with benign SVCS caused by fibrosing mediastinitis
does not provide a role for SVC bypass surgery. Surgery may be however advocated for SVCS
caused by benign disorders if the syndrome develops suddenly, progresses, or persists after 6 to
12 months of observation for possible collateral development. In patients whose histoplasmosis
complement fixation titers suggest active disease, ketoconazole treatment may prevent recurrent
SVCS.

Intravenous device-induced obstruction


Catheter-induced thrombosis could result in SVCS. Streptokinase, urokinase, or recombinant
tissue-type plasminogen activator may cause lysis of the thrombus early in its formation. Heparin
and oral anticoagulants may reduce the extent of the thrombus and prevent its progression.
Removal of the catheter, if possible, should be combined with anticoagulation to avoid
embolization. In patients for whom electrodes of a pacemaker must be changed, the broken wire
should be removed to prevent the risk of developing SVCS. Percutaneous transluminal
angioplasty, with or without thrombolytic therapy, and stent insertion have been successfully used
to open catheter-induced SVC obstructions.

Take home points


1. Superior mediastinal or superior vena cava syndrome is the clinical manifestation of
obstruction of blood flow through the SVC.
2. Malignancy (most commonly from the lung) is the commonest cause of SVCS. Intravenous
devices are increasingly being cited as a cause.

Benign pathology causing SVCS is

uncommon
3. Over 70% of SVCS in children is of iatrogenic origin following surgery for congenital
cardiovascular disorders and V-A shunt procedures for hydrocephalus.
4. SVCO/ SVCS commonly causes breathlessness and swelling of the neck, face and upper
extremities. It presents with characteristic features of engorgement of the veins of the neck,
arms and chest wall.
5. Specific treatment of SVCS is best instituted following cytological/ histological diagnosis and
staging. This allows for appropriate selection and sequencing of treatment modalities and
135

drugs. SVCO rarely progresses to rapid death. The only exceptions are when the patient
presents with cerebral dysfunction, decreased cardiac output or airways obstruction.
6. Diagnostic procedures like endoscopy, lymph node biopsy, mediastinoscopy or thoracotomy
do not carry an excessive risk of morbidity or mortality in patients with SVCS.
7. Appropriate chemotherapy and sometimes consolidation with radiation therapy are the choice
of treatment for most malignancies
8. Angioplasty and vascular stents with thrombolytic therapy are used for endovascular device
induced SVCO and for selected patients with malignancy.

It gives prompt and probably

lasting relief from symptoms.


9.

Surgery has a limited role and is reserved for patients who have failed other modes of
treatment. Surgical options may be considered for retrosternal goiters and aortic aneurysms
causing SVCS.

For Further Reading and References


1.

Schechter MM. The superior vena cava syndrome. Am J Med Sci 1954;227:46.

2.

Wilson LD, Detterbeck FC, Yahalom J. Superior vena cava syndrome with malignant causes. N
Engl J Med 2007;356:1862.

3.

Rice TW, Rodriguez RM, Light RW. The superior vena cava syndrome, clinical characteristics
and evolving etiology. Medicine 2006;85:37.

4.

Schindler N, Vogelzang RL. Superior vena cava syndrome. Experience with endovascular stents
and surgical therapy. Surg Clin North Am 1999;79:683.

5.

Schraufnagel DE, Hill R, Leech JA, Pare JAP. Superior vena caval obstruction. Is it an
emergency? Am J Med 1981;70:1169.

6.

Parish JM, Marschke RF, Dines DE, Lee RE. Etiologic considerations in superior vena cava
syndrome. Mayo Clin Proc 1981;56:407.

7.

Chen JC, Bongard F, Klein SR. A contemporary perspective on superior vena cava syndrome.
Am J Surg 1990;97:1005.

8.

Lokich JJ, Goodman R. Superior vena cava syndrome: clinical management. JAMA 1975;231:58.

9.

Sculier JP, Feld R. Superior vena cava obstruction system: recommendation for management.
Cancer Treat Rev 1985;12:209.

10. Bertrand M, Presant CA, Klein L, Scott E. Iatrogenic superior vena cava syndrome. A new entity.
Cancer 1984;54:376.
11. Ingram L, Rivera GK, Shapiro DN. Superior vena cava syndrome associated with childhood
malignancy: analysis of 24 cases. Med Pediatr Oncol 1990;18:476.
12. Ahmann FR. A reassessment of the clinical implications of the superior vena cava syndrome. J
Clin Oncol 1984;2:961.
13. Shimm DS, Lugue GL, Tigsby LC. Evaluating the superior vena cava syndrome. JAMA
1981;245:951.
14. Rowell NP, Gleeson FV. Steroids, radiotherapy, chemotherapy and stents for superior vena caval
obstruction in carcinoma of the bronchus: a systematic review. Clin Oncol (R Coll Radiol)
2002;14:338.
15. Urshel HC Jr, Razzuk MA, Netto GJ, Disiere J, Chung SY. Sclerosing mediastinitis: improved
management with histoplasmosis titer and ketoconazole. Ann Thorac Surg 1990;50:215.

136

16. Kee ST, Kinoshita L, Razavi MK, et al. Superior vena cava syndrome: treatment with catheterdirected thrombolysis and endovascular stent placement. Radiology 1998;206:187.
17. Nicholson AA, Ettles DF, Arnold A, et al. Treatment of malignant superior vena cava obstruction:
metal stents or radiation therapy. J Vasc Interv Radiol 1997;8:781.
18. Rodrigues CI, Njo KH, Karim ABMF. Hypofractionated radiation therapy in the treatment of
superior vena cava syndrome. Lung Cancer 1993;10:221.
19. Scherck JP, Kerstein MD, Stansel HC. The current status of vena caval replacement. Surgery
1974;76:209.
20. Doty JR, Flores JH, Doty DB. Superior vena cava obstruction: bypass using spiral vein graft. Ann
Thorac Surg 1999;67:1111.
21. Avashti RB, Moghissi K. Malignant obstruction of the superior vena cava and its palliation. J
Thorac Cardiovasc Surg 1977;74:244.
22. Magnan PE, Thomas P, Giudicelli R, et al. Surgical reconstruction of the superior vena cava.
Cardiovasc Surg 1994;2:598.
23. Piccione W Jr., Faber LP, Warren WH. Superior vena caval reconstruction using autologous
pericardium. Ann Thorac Surg 1990;50:417.
24. Uberoi R. Quality assurance guidelines for superior vena cava stenting in malignant disease.
Cardiovasc Intervent Radiol 2006;29:319.
25. Nicholson AA, Ettles DF, Arnold A, Greenstone M, Dyet JF. Treatment of malignant superior vena
cava obstruction: metal stents or radiation therapy. J Vasc Interv Radiol 1997;8:781.
26. Joachim Yahalom in Devita, Hellman & Rosenberg's Cancer: Principles & Practice of Oncology,
8th Edition. Editors: DeVita VT; Lawrence TS.; Rosenberg SA. Lippincott Williams & Wilkins. Pp
2428-33.
27. Kent MS, Port JL in Oncology: An Evidence Based Approach. Ed. Chang AE, Ganz PA, Hayes
DF, Kinsella TJ, Pass HI, Schiller JH, Stone RM, Strecher VJ. Springer pp 1291-97.

Index

137

Diabetic Foot
Rajiv Parakh
Background: According to the 2007 estimate by the International Diabetes federation, total number
of diabetic patients in the world were 246 million; India having the largest population, i.e. over 40
million (>25% of this total) Diabetic Foot is a disturbing complication of diabetes that often results
in significant morbidity and motrtality. By a Rule of 15, 15% of people with diabetes develop
ulcers, 15% ulcers develop osteomyelitis and 15% of ulcers result in amputation. Approximately
around 40,000 leg amputations are performed in India every year.

An array of effective interventions are now available to tackle this epidemic in the developing
countries. Establishment of diabetic foot care clinics will be the central focal intervention for this
devastating condition. These clinics could work towards the goal of maximizing limb salvage and
reduction of amputations.

PRINCIPLES OF DIABETIC FOOT ULCER TREATMENT:


I. Management of vascular insufficiency
II. Infection control
III. Pressure management OFFLOADING

The vascular therapeutic option is selected depending upon the degree of peripheral arterial
disease, the prospects of success of re-vascularization, other significant co-morbid conditions and
last but not the least cost affordability of the procedure by the patient. The technique of Subintimal
angioplasty has opened a whole new technology to revascularize the Ischemic diabetic foot.

Diabetic Foot infections must be addressed promptly and effectively as delay increases the risk of
soft tissue loss, bone involvement and poor outcome. Microbiology is useful to identify the
causative pathogens and their antibiotic susceptibilities. A wide range of antibiotics are available,
which provides excellent coverage against the wide spectrum of erobic and aerobic, pathogens.
The severity of infection and the presence of bony involvement largely determine the duration and
eventual out come of the treatment.
Appropriate pressure management Off-loading would involve foot plantar pressure assessment
by the Foot Scan walk-way system. The patient would require appropriate offloading from the
highly susceptible ulcer prone areas; apart from the frank ulcer location, if developed already. The
offloading technique applicable to each patient such as accommodative footwear (shoes)/ insoles/
orthoses (in shoes)/ socks, would vary according to the plantar pressure exerted. The
effectiveness could be assessed by the bipedal in shoe analysis before any further damage
occurs.

138

Conclusion: The prompt management of diabetic foot would help in prevention of 75% of diabetic
foot complications. The multidisciplinary approach would identify feet at risk, spread awareness;
perform early diagnosis and aggressive management of diabetic foot in order to achieve a
reduction in limbs amputations.

Index

139

Vascular Surgery (Endovascular & Conventional) for Peripheral


Vascular Disease
Dr Sanjay Tyagi
Lower-extremity peripheral arterial disease (PAD) is an important manifestation of systemic
atherosclerosis that is associated with marked morbidity and mortality. Although most patients with
PAD are asymptomatic, many have claudication, chronic critical limb ischemia, or acute limb
ischemia.
Depending on the extent of the functional impairment PAD has been classified into Fontaines Stages
and Rutherfords Categories. Critical limb ischemia (CLI) is the term used to designate the condition in
which peripheral artery disease has resulted in resting leg or foot pain or in a breakdown of the skin of
the leg or foot, causing ulcers or tissue loss. If not revascularized, CLI patients are at risk for limb loss
and for potentially fatal complications from the progression of gangrene and the development of
sepsis. The ABI is a simple but reliable tool which correlates well with the severity of lower limb PAD.
Patients with CLI typically have an ABI below 0.4.

The management of CLI requires a multidisciplinary team of experts in different areas of vascular
disease, from atherosclerotic risk factor management to imaging, from intervention to wound care and
physical therapy. In the past decade, the most significant change in the treatment of CLI has been the
increasing tendency to shift from bypass surgery to less invasive endovascular procedures as firstchoice revascularization techniques, with bypass surgery then reserved as backup if appropriate. The
goals of intervention for CLI include the restoration of pulsatile, inline flow to the foot to assist wound
healing, the relief of rest pain, the avoidance of major amputation, preservation of mobility, and
improvement of patient function and quality of life. The evaluating surgeon should be fully aware of all
revascularization options in order to select the most appropriate intervention or combination of
interventions, while taking into consideration the goals of therapy, risk-benefit ratios, patient
comorbidities, and life expectancy.

REVASCULARIZATION PROTOCOLS IN LOWER LIMB PAD


Planning the best revascularisation strategy for a given PAD patient is the most crucial step in the
management of this disease. In 2000, the TransAtlantic Inter-Societal Consensus (TASC)
guidelines contained a classification system for treatment of PAD. The goal of this system was to
indicate the best form of treatment, endovascular (TASC A) or surgical (TASC D), for patients with
lower-extremity arterial occlusive disease based upon highest levels of evidence in published
reports. Those lesions without strongly supportive evidence, but with a greater likelihood of good
response to endovascular (TASC B) or surgery (TASC C), were noted as critical issues requiring
additional assessment. The guidelines have been revised. The following table summarises the
lesions in the aortoiliac and femoropopliteal arterial tree as per the TASC II recommendations.

140

A. Endovascular treatment of choice


Aortoiliac lesions

Femoro-Popliteal lesions

Single < 3-cm stenosis of CIA or EIA


(unilateral/bilateral)

Single < 3-cm stenosis (unilateral/bilateral)

B. Endovascular more often used


Aortoiliac lesions

Femoro-Popliteal lesions

Single 3- to 10-cm stenosis

Single 3- to 5-cm stenosis

Two stenoses < 5 cm in CIA/EIA

Heavily calcified stenoses < 3 cm

Unilateral CIA occlusion

Multiple lesions each < 3 cm (stenoses or


occlusions)
Single or multiple lesions, in the absence of
continuous tibial runoff, to improve inflow for
infrageniculate bypass

C. Endovascular if possible
Aortoiliac lesions

Femoro-Popliteal lesions

Unilateral EIA stenosis or occlusion

Single stenosis or occlusion 5 to 10 cm

Bilateral CIA occlusion

Multiple stenoses or occlusion, each 3 to 5 cm

D. Surgery preferred, endovascular considered on case-by-case basis


Aortoiliac lesions

Femoro-Popliteal lesions

Diffuse/multiple stenoses in any iliac segment


(>10 cm)

Complete occlusion of CFA or SFA or popliteal


and proximal crural
Arteries

Unilateral occlusion of CIA and EIA


Bilateral EIA occlusions
Diffuse disease involving aorta and iliac arteries
Associated aneurysmal surgery requiring surgery
Table I: Modified TASC morphological classification of LL arterial lesions.

With the recent modifications, longer stenoses and short occlusions are considered best treated
with endovascular means. As long as surgical reconstruction options are not lost when performing
percutaneous interventions, endovascular treatment should be the first approach. One must
understand that the reduced morbidity and mortality may come at a cost of diminished durability
and a potential need for reintervention. When used appropriately, an open procedure can follow an
endovascular procedure that has failed; similarly, an endovascular procedure can follow an open
procedure after failure.

Aortoiliac disease
Atherosclerosis affecting the terminal aorta commonly also involves the bifurcation of the
common iliac arteries. These are now preferentially treated with endovascular techniques rather
141

than surgery. The iliac arteries, particularly the external iliac artery, have a high rate of
dissection and elastic recoil and therefore, primary stenting is preferred over provisional
stenting. A meta-analysis of 14 studies performed since 1990 involving either balloon
angioplasty or stenting to treat iliac stenoses revealed higher procedural success with stenting
and a 39% lower risk of long-term failure with stenting compared with balloon angioplasty.

Before endovascular treatment became available, bypass surgery was the primary
revascularization option for patients with diffuse atherosclerotic disease. A Meta analysis of
aortoiliac bypass surgery revealed a 10 year patency of 80-90% but was associated with a 303

day mortality rate of 3.3%. In a study of 505 aortoiliac lesions (88 occlusions and 417
stenoses) among 365 patients with chronic leg ischemia (claudication 62%, rest pain 21%,
ulcer 13%, and gangrene 4%) treated with PTA/stenting the procedural success was 98%. The
30-day mortality rate was 0.5%. Eight years primary patency rate was 74%, primary assisted
patency rate was 81% and secondary patency rate was 84%. Findings confirm that aortoiliac
PTA/stenting is a low-risk revascularization option with long-term outcomes comparable to
surgical bypass.

Figure 1: A. Digital subtraction angiogram showing total occlusion of right common iliac artery and severe
stenosis of left CIA, B. DSA after angioplasty and stenting shows good angiographic result. The patient
reported marked relief of his claudication on clinical follow up.

Endovascular treatment has rapidly replaced open surgery in mild to moderate lesions, defined
as TASC class A and B. There are, however, still controversies whether endovascular
treatment is optimal for more advanced lesions such as severely calcified long segments or
extensive occlusions of the iliac arteries and/or the entire aortic bifurcation, defined as TASC
class C and D. Although, the TASC-II committee still advocate surgical treatment for class C
and D lesions, a recent study of endovascular therapy for aortoiliac occlusions showed good
short term results. Among 173 patients undergoing kissing stenting for aortoiliac obstruction the
primary, assisted primary and secondary patency was: 97%, 99% and 100%, and 83%, 90%
and 95% at 12 and 36 months respectively. There was no significant difference in patency
142

between the TASC groups. Treatment of AIOD with kissing stents was found to be an
acceptable method of restoring circulation in the suprainguinal arteries, with low mortality,
morbidity and with good patency rate irrespective of TASC classification.

Infrainguinal Femoropopliteal disease


Percutaneous transluminal angioplasty (PTA) with or without stenting (PTA/stent) for chronic
lower extremity ischemia has been well established as first-line therapy for aortoiliac occlusive
disease, with a low morbidity and excellent long term patency. Despite similar low complication
rates after infrainguinal PTA/stent, primary patency rates inferior to surgical bypass have fuelled
the argument that this modality should be reserved for patients who are at high surgical risk or
who lack autogenous conduit. The common femoral artery lies over the hip joint and placement
of stents here is suboptimal. Restenosis or stent thrombosis can be associated with acute limbthreatening ischemia as circulation to both the superficial femoral artery (SFA) and the profunda
femoris can be compromised simultaneously. Therefore the disease involving this segment is
best treated by surgical means. Percutaneous treatment of SFA disease however continues to
evolve. Pooled results of SFA PTA indicate 1, 3 and 5-year primary patency rates of 65% to
77%, 48% to 66%, and 42% to 55%, respectively, without delineation of TASC lesion status.

11

Important determinants of successful PTA are lesion location (osteal/proximal/distal),


lesion length, plaque composition (calcification), and morphology (eccentricity) and the
distal run-off. Longer stenoses and occlusions are more likely to have flow-limiting dissection
or suboptimal expansion caused by elastic recoil after angioplasty. Based upon the improved
outcomes in coronary lesions, use of stents in treating difficult SFA lesions was thought to
improve results. Early experiences with stainless-steel stents however did not show any benefit
over angioplasty alone and stenting was relegated to salvage procedure status in the face of
failed angioplasty. Patency with stainless steel, balloon-expanded stents was reported at 54%
to 80% at 1 year, and 28% at 3 years. We need to look upon the possible reasons for these low
patency rates.

The superficial femoral artery (SFA) is a muscular artery, the longest artery in the body which
courses through the thigh in the muscular adductor canal, exiting at a fixed point. The geometry
and elasticity of the SFA are markedly influenced by its proximity to musculature, its continuous
mobility, and its location between two joints. Atherosclerotic lesions in the SFA are longer and
subject to more stretching, twisting, bending and compression in comparison to those in the
coronaries and other vascular beds. The extensive plaque is often intermittently calcified
presenting the risk of further plaque rupture after intervention. These factors have been
implicated in high rates of stent deformation and fractures causing increased restenosis and
vessel occlusions.

12-17

Therefore stent material and design, as well as its physical

characteristics like radial force and flexibility tent to affect the outcomes. Nitinol, an alloy of
nickel and titanium, is more flexible and more able to recover from being crushed than stainless
steel.
143

Studies suggest that nitinol self expanding stents provide the most promising clinical outcomes,
at least in the short-term. A patency rate of 75% to 93% at 1 year and 73% to 76% at 3 years
has been reported with nitinol, self-expanding stents. The results however vary widely
suggesting that differences between nitinol stents based upon one stent design may be
important to clinical outcome. However, most of the data are short-term and few studies provide
results with outcome beyond three years. More recent randomized studies comparing SFA
angioplasty alone with nitinol stenting have shown a reduced incidence of restenosis with
primary stenting. In a recent study of 59 patients (74 lesions), SFA stenting with nitinol stents
(Zilver, Cook, USA) provided a primary patency of 69% at 4.8 years and an assisted-primary
patency of 90% at 5 years. Another retrospective study compared patency rates of above knee
FP surgical bypass using polytetrafluoroethylene (PTFE) graft to PTA/stenting using Smart
stent ( Cordis, Johnson and Johnson, Miami Lakes, Fla) for TASC-II type C & D in 127 patients
and 139 limbs. They found that PTA/S for TASC-II C lesions has a superior midterm patency
than AK-FPB using PTFE, and AK-FPB with PTFE has better primary and assisted-primary
patency than PTA/S for TASC-II type D.

Besides vessel recoil and flow limiting dissections post PTA with uncovered nitinol stents, the
problem of neointimal hyperplasia leading to restenosis still remains. This led to the
consideration of stents covered with material such as expanded PTFE with the theoretic
advantage of elimination of neointimal hyperplasia. A potential problem with this idea is the
occlusion of collateral vessels and the inability to prevent edge restenosis. The Viabahn
endoprosthesis (W.L. Gore & Associates, Flagstaff, Arizona) is an ePTFE self-expanding nitinol
stent graft that has been studied and is approved for use in the SFA. A small, single-center
evaluation of long-term results of ePTFE stent graft in 15 patients found a primary patency of
87% at 2 years. In a registry data of 150 patients, the aSpire self-expanding PTFE covered
stent (Vascular Architects Inc, San Jose, Calif) showed good mid-term results, but a number of
reinterventions were necessary to obtain an optimal secondary patency. The patency was
negatively influenced by the Length of the lesion and clinical symptoms at presentation. A
recent prospective, randomized study comparing covered ePTFE/nitinol self-expanding stentgrafts with prosthetic above-the-knee femoropopliteal bypass randomized 50 limbs each into
two groups. Primary patency at 1 year was approximately 74% for both cohorts, with a mean
follow-up of 18 months. The covered nitinol ePTFE stent graft in the SFA had a 1-year patency
comparable to surgical bypass, with a significantly shorter hospital stay (0.9 versus 3.1 days).

In another effort to address intimal hyperplasia drug-eluting nitinol stents are also being
studied. The only published trial evaluating this potential therapy is a randomized, controlled
trial comparing the sirolimus-eluting SMART stent (Cordis, Miami Lakes, Florida) with the bare
SMART stent for TASC C SFA lesions. At 24 months, the restenosis rates were no different
between the two treatment arms.
144

A number of techniques have recently come up for use in the treatment of lesions affecting the
SFA. These include subintimal angioplasty, extraction atherectomy, laser atherectomy,
cutting balloon atherotomy, and cryotherapy. Devices and specially designed catheters that
aid in the recanalization of CTOs have also been tried. Balloons coated with paclitaxel have
recently been evaluated for simple femoropopliteal disease with encouraging results through 2
years of follow-up.

Infrapopliteal disease
Percutaneous transluminal angioplasty (PTA) of iliac and femoropopliteal lesions is common,
but there is reluctance to treat higher risk infrapopliteal lesions in this manner. This is because
of the small size of tibial vessels and the prevalence of calcified and diffuse atherosclerotic
disease which is associated with a lower rate of procedural success and a higher rate of
restenosis. In an effort to improve acute procedural success and reduce restenosis, bare metal
stents have been used in below-knee lesions. Despite this, in-stent restenosis for patients
treated with either PTA or bare metal stenting continues to be a problem with 3-year primary
patency rates below 25%.

Since the primary goal of treatment is typically prevention of amputation and salvage of a
functioning limb, reported results for infrapopliteal PTA should focus on outcomes and report
limb-salvage rates rather than patency. Drug-eluting stents have markedly reduced restenosis
in the coronary vasculature compared to bare metal stents. However, drug eluting stents are
more expensive and the risk of stent thrombosis mandates longer-term dual antiplatelet
therapy. Though a single centre experience of elective placement of drug-eluting stents in
infrapopliteal lesions in 10 patients suggested feasibility and safety, prospective clinical trials
will be necessary to confirm the benefits and justify the expense of the use of drug-eluting
stents for treating patients with infrapopliteal culprit lesions and chronic limb ischemia.

Figure 2:A. Angiogram of a Popliteal artery bifurcation stenosis. B. Angiogram after kissing balloon angioplasty
shows good angiographic result. Patient had marked relief in limb ischemia on follow-up.

145

SURGICAL REVASCULARIZATION
Given the availability of less invasive percutaneous procedures, the 2005 ACC/AHA guidelines and
the 2007 TASC II consensus document on the management of
PAD recommended initial revascularization with surgery only
when the arterial anatomy is not favorable for a percutaneous
approach eg long segment total occlusion . Rarely, a patient
remains disabled from claudication after attempts at medical
therapy and percutaneous revascularization by angioplasty. In
this setting, surgical revascularization procedures for intermittent
claudication should be limited to patients with disabling
symptoms who can be expected to tolerate the procedure and
live long enough to enjoy the improved quality of life. The same
criteria are used in diabetics even though they are at higher risk
for a worse outcome. Patients who benefit most from elective
surgical revascularization are generally under 70 years of age,
nondiabetic, and have little evidence of disease distal to the
primary lesion. Regardless of whether surgery is performed, all
patients with claudication should undergo evaluation and
treatment of atherosclerotic risk factors (eg, smoking, hypercholesterolemia). Risk factor modification
prevents not only limb loss, but also myocardial infarction. Patients who do not have surgery may also
benefit from other areas of medical management, including supervised exercise and medications.
Preoperative risk assessment Vascular surgery is considered a high-risk surgical procedure. As
a result, preoperative risk stratification should be performed in all patients.
Guideline recommendations The 2005 ACC/AHA guidelines, which were produced in
collaboration with major vascular medicine, vascular surgery societies, made the following
recommendations for surgery in patients with aortoiliac (inflow) disease :

In patients with unilateral disease with acceptable aortic inflow, iliac endarterectomy and
aortoiliac or iliofemoral bypass.

These procedures should be performed in conjunction with femoral-femoral bypass in bilateral


iliac artery occlusive disease if the patient is not a suitable candidate for bilateral aortofemoral
bypass grafting.

Axillofemoral bypass should not be used for the treatment of intermittent claudication except
in very limited settings, such as chronic infra-aortic occlusion associated with severe
symptoms in a patient who is not a candidate for aortobifemoral bypass.

For infrainguinal (outflow) disease :

Bypasses to the popliteal artery above or below the knee should be constructed with an
autogenous vein from the ipsilateral or contralateral leg or arms, if possible.
146

It is reasonable to use a synthetic graft to the popliteal artery below the knee only if no
autogenous vein is available.

The evidence is less well established for femorotibial artery bypasses with autologous vein,
an approach that may be considered in rare instances.

The efficacy of synthetic grafts to the popliteal artery above the knee is not well established
because of reduced patency rates.

Femorotibial bypasses with synthetic grafts should not be performed.

These recommendations in part reflect different rates of long-term graft patency


Graft patency Venous bypass grafts are prone to the development of stenosis, which can reduce
blood flow, precipitate thrombosis, and lead to limb amputation. Vein graft stenosis, which primarily
occurs in the first year, have been noted in 25 to 30 percent of grafts at one year and correction of
such lesions may improve the rates of both graft patency and limb salvage.

The ACC/AHA guidelines noted the following expected patency rates at 5 yrs with different
bypass procedures for inflow (aortoiliac) disease
Aortobifemoral, aortoiliac, or aortofemoral

85 to 90 %

Femorofemoral

70 %

Axillofemoral

50 to 80 % at 3 years

Axillofemoral-femoral

65 %

The patency rates at 5 yrs were generally lower for outflow (infrainguinal) disease:
Femoropopliteal vein graft above or below the knee 65 %
Femoropopliteal synthetic graft

50 % (above knee) and 33 % (below knee)

Femorotibial vein graft

75 to 80 %

25 % at 3 years (these grafts should not be used


for claudication)
Oral anticoagulants may be better than antiplatelet agents for prevention of venous graft occlusion,
Femorotibial synthetic graft

while the reverse may be true for prosthetic grafts.


Duplex ultrasound surveillance Duplex ultrasonography is considered the best method for
detecting graft failure.The criteria for an at-risk graft were a fall in the ABI of 0.1, peak systolic
velocity <45 cm/sec, increase in peak systolic velocity at the site of a stenosis to 150 cm/sec, and
peak systolic velocity ratio across a stenosis >2.0.

CONCLUSION
Over the past decade tremendous advances have been made in the treatment of atherosclerotic
PAD. Historically, patients with symptomatic PAD

were treated medically, with surgical

revascularization reserved as an option for advanced disease. Though surgery had significant
symptomatic improvement it had high morbidity and mortality. The newer percutaneous treatment
options are associated with much lower procedural complications and good long-term outcomes,
147

particularly in large diameter Aortoiliac arteries. The threshold for percutaneous revascularization
needs to be lowered, as greater number of patients with symptomatic PAD can now be benefitted with
lower procedural risks. Surgical revascularization should be reserved long segment total occlusions
and failed endovascular procedures.

REFERENCES
1.

Norgren L, Hiatt WR, Dormandy JA, et al: Inter-society consensus for the management of peripheral
arterial disease (TASC II). J Vasc Surg 2007;45:S5-S67

2.

Tyagi S, Malhotra A, Khalilullah M. Percutaneous transluminal angioplasty for

ischemic arterial

disease of the lower extremities. Indian Heart J. 42:419, 1990.


3.

Bosch JL, Hunink MGM. Meta-analysis of the results of percutaneous transluminal angioplasty and
stent placement for aortoiliac occlusive disease. Radiology 1997;204:8796.

4.

De Vries SO, Hunink MG. Results of aortic bifurcation grafts for aortoiliac occlusive disease: a metaanalysis. J Vasc Surg 1997;26:558569.

5.

Murphy TP, Ariaratnam NS, Carney WI et al. Aortoiliac Insufficiency: Long-term Experience with
Stent Placement for Treatment. Radiology 2004; 231:243249

6.

Bjorses K et al. Kissing stents in the Aortic Bifurcation - a Valid Reconstruction for Aorto-iliac
Occlusive Disease, Eur J Vasc Endovasc Surg (2008), 06:027

7.

Parsons RE, Suggs WD, Lee JJ et al. Percutaneous transluminal angioplasty for the treatment of limb
threatening ischemia: do the results justify an attempt before bypass grafting? J Vasc Surg
1998;28:1066-71.

8.

Norgren L, Hiatt WR, Dormandy JA, et al. Inter-society consensus for the management of peripheral
arterial disease. Int Angiol 2007;26(2):81157.

9.

Cejna M, Turnher S, Illiasch H, et al. PTA versus Palmaz stent in femoropopliteal artery obstructions:
a multicenter prospective randomized study. J Vasc Intervent Radiol 2001;12:23-31.

10. Sabeti S, Schillinger M, Amighi J et al. Primary patency of femoropopliteal arteries treated with
nitinol versus stainless steel self-expanding stents: propensity score-adjusted analysis. Radiology
2004;232:513 -521.
11. Davies MG, Waldman DL, Pearson TA. Comprehensive endovascular therapy for femoropopliteal
arterial atherosclerotic occlusive disease. J Am Coll Surg 2005;201(2):275-296.
12. Scheinert D, Scheinert S, Sax J et al. Prevalence and clinical impact of stent fractures after
femoropopliteal stenting. J Am Coll Cardiol 2005;45(2): 312-315.
13. Schlager O, Dick P, Sabeti S et al. Long-segment SFA stenting the dark sides: in-stent restenosis,
clinical deterioration, and stent fractures. J Endovasc Ther 2005;12:676 -684.
14. Lugmayr HF, Holzer H, Kastner M et al. Treatment of complex arteriosclerotic lesions with nitinol
stents in the superficial femoral and popliteal arteries: a midterm follow-up. Radiology 2002;222:3743.
15. Schillinger M, Sabeti S, Loewe C, et al. Balloon angioplasty versus implantation of nitinol stents in
the superficial femoral artery. N Engl J Med 2006;354:1879-88.
16. Schillinger M, Sabeti S, Dick P, et al. Sustained benefit at 2 years of primary femoropopliteal stenting
compared with balloon angioplasty with optional stenting. Circulation 2007;115:2745-9.
17. M. Ferreira, L. Lanziotti, M. Monteiro et al. Superficial Femoral Artery recanalization with Selfexpanding Nitinol Stents: Long-term Follow-up Results. Eur J Vasc Endovasc Surg 2007;34: 702-708.

148

18. Dosluoglu H, Gregory S, Purandath L et al. Balloon angioplasty/stenting of TransAtlantic InterSociety Consensus-II C lesions of the superficial femoral artery is superior to femoral above knee
popliteal bypass with polytetrafluoroethylene. J Vasc Surg 2008;
19. Saxon RR, Coffman JM, Gooding JM, et al. Long-term results of ePTFE stent-graft versus angioplasty
in the femoropopliteal artery: single center experience from a prospective, randomized trial. J Vasc
Interv Radiol 2003;14(3):30311.
20. Massimo L, Enrico C, Paola De R, et al. Endovascular treatment of long lesions of the superficial
femoral artery: Results from a multicenter registry of a spiral, covered polytetrafluoroethylene stent.
J Vasc Surg 2007;45:32-9.
21. Kedora J, Hohmann S, Garrett W, et al. Randomized comparison of percutaneous Viabahn stent
grafts vs prosthetic femoral-popliteal bypass in the treatment of superficial femoral arterial occlusive
disease. J Vasc Surg 2007;45:1016
22. Duda SH, Bosiers M, Lammer J, et al. Sirolimus-eluting versus bare nitinol stent for obstructive
superficial femoral artery disease: the SIROCCO II trial. J Vasc Interv Radiol 2005; 16(3):3318.
23. Kudo T, Chandra FA, Ahn SS. The effectiveness of percutaneous transluminal angioplasty for the
treatment of critical limb ischemia: A 10-year experience. J Vasc Surg 2005;41:423435.
24. A.G. Grant, C.J. White, T.J. Collins et al. Infrapopliteal Drug-Eluting Stents for Chronic Limb
Ischemia. Catheterization and Cardiovascular Interventions 2008;71:108111
25. Goshima KR, Mills JL, Hughes JD: A new look at outcomes after infrainguinal bypass surgery:
traditional reporting standards systematically underestimate the expenditure of effort required to
attain limb salvage. J Vasc Surg 39:330-335, 2004
26. Norgren L, Hiatt WR, Dormandy JA, et al: Inter-society consensus for the management of peripheral
arterial disease (TASC II). J Vasc Surg 2007;45:S5-S67
27. Bosch JL, Hunink MGM. Meta-analysis of the results of percutaneous transluminal angioplasty and
stent placement for aortoiliac occlusive disease. Radiology 1997;204:8796.
28. De Vries SO, Hunink MG. Results of aortic bifurcation grafts for aortoiliac occlusive disease: a metaanalysis. J Vasc Surg 1997;26:558569.
29. Murphy TP, Ariaratnam NS, Carney WI et al. Aortoiliac Insufficiency: Long-term Experience with
Stent Placement for Treatment. Radiology 2004; 231:243249
30. Bjorses K et al. Kissing stents in the Aortic Bifurcation - a Valid Reconstruction for Aorto-iliac
Occlusive Disease, Eur J Vasc Endovasc Surg (2008),
31. Parsons RE, Suggs WD, Lee JJ et al. Percutaneous transluminal angioplasty for the treatment of
limb threatening ischemia: do the results justify an attempt before bypass grafting? J Vasc Surg
1998;28:1066-71
32. Allaqaband S, Kirvaitis R, Jan F, Bajwa T. Curr Probl Cardiol..Endovascular treatment of peripheral
vascular disease. 2009; 34:359-476
33. Bosiers M, Torsello G, Gissler HM, Ruef J, Mller-Hlsbeck S, Jahnke T, Peeters P, Daenens K,
Lammer J, Schro H, Mathias K, Koppensteiner R, .Nitinol stent implantation in long superficial
femoral artery lesions: 12-month results of the DURABILITY I study. J Endovasc Ther. 2009 ;16 :2619
34. Lyden SP, Smouse HB.J Endovasc Ther. TASC II and the endovascular management of infrainguinal
disease. 2009 16(2 Suppl 2):II5-18.
35. Markose G, Bolia A. J Cardiovasc Surg (Torino). Below the knee angioplasty among diabetic
patients. 2009 ,50:323-9.

149

36. Lumsden AB, Davies MG, Peden EK ,J Endovasc Ther.Medical and endovascular management of
critical limb ischemia. 2009 ;16(2 Suppl 2):II31-62
37. Ganesha B Perera, Sean P Lyden, Current Trends in Lower Extremity Revascularization . Surg Clin of
N Am (2007) 87,1135-1147

Index

150

Recent Advances in the Management of Chronic Arterial


Insufficiency
Pawanindra Lal
i

Overview of Chronic Arterial Insufficiency :


Chronic Arterial Insufficiency of the lower limbs refers to slowly progressive peripheral arterial
occlusive disease wherein the patient suffers from symptoms of limited circulation over a period of
months or years. There is slow deterioration in function along with increase in symptoms and
signs. Due to the slow progression of disease, there is time for the limb to develop alternative
circulation through collateral vessels. Based on the duration of ailment, the following classification
is helpful to distinguish acute ischaemia from chronic ischaemia in the clinical setting. In acute
arterial insufficiency, the presentation is dramatic largely due to the absence of any alternative
collateral circulation. This chapter would mainly focus on various aspects of atherosclerotic chronic
arterial insufficiency of the lower limbs.

Table No 1: Classification of limb ischaemia

Terminology

Definition or comment

Onset:
Acute

Ischaemia <14 days

Acute on chronic

Worsening symptoms and signs (<14


days)
Ischaemia stable for >14 days

Chronic
Severity (acute, acute on
chronic):
Incomplete

Limb not threatened

Complete

Limb threatened

Irreversible

Limb non-viable

The symptoms and signs of chronic arterial insufficiency are


1.

Claudication

2.

Rest Pain

3.

Ulceration

4.

Gangrene

In contrast, the Symptoms and signs of acute limb ischaemia are as shown in Table 2.

151

Table No 2: Symptoms & Signs of Acute Ischaemia


Symptoms or
signs
Pain

Comment

Pallor

Also present in chronic ischaemia

Pulseless

Also present in chronic ischaemia

Perishing cold

Unreliable as ischaemic limb takes on ambient


temperature
Leading to anaesthesia (unable to feel touch on foot or
hand)
Unable to wiggle toes or fingers

Occasionally absent in complete ischaemia

Paraesthesia*
Paralysis*

*Anaesthesia and paralysis are the key to diagnosing complete ischaemia that requires emergency
surgical treatment
AETIOLOGY OF CHRONIC ARTERIAL INSUFFICIENCY OR CHRONIC ISCHAEMIA:
Chronic ischaemia is related to progressive narrowing of the lumen of the artery supplying the limb.
The commonest causes are enumerated below:
1. Atherosclerosis Affecting Large and Medium sized vessels. It is complex chronic inflammatory
process affecting the elastic and muscular arteries and the disease is systemic and segmental in
presentation.
Table No 3: Risk Factors for Atherosclerosis

ii

Hypercholesterolemia - LDL & HDL

Hypertension

Cigarette Smoking Tobacco metabolites on


vascular endothelium 4X higher risk.

Diabetes Mellitus (3-5X)


TABLE 4: Pathophysiological Effects of Smoking

Whole vessel effect

iii

Vasoconstriction
Hypertension

Endothelial effect

Increased endothelial denudation


Increased endothelial cell turnover
Decreased endothelial PGI2 production

Platelets effects

Increased platelet counts


Increased platelet aggregation
Increased

platelet

adhesiveness

production
Lipid effect

Decreased HDL

Coagulation effects

Decreased fibrinolytic activity


Increased blood viscosity
Increased fibrinogen levels
152

Increased TXA2

The atheromatous plaque consists of smooth muscle cells, connective tissue (matrix), lipid and
macrophages. It tends to localise at the sites of bifurcations or bends where turbulence, sheer
stress, flow separation and stasis are known to occur.

2. Buergers Disease (Thromboangiitis obliterans): This is a disease involving medium and small
sized muscular arteries associated with smoking in a relatively young male with predilection for
tibial vessels. Rest pain, gangrene and ulceration are usual presentations with history of migratory
thrombophlebitis.
TABLE 5 - Diagnostic Criteria for Thromboangiitis Obliterans

iv

Age younger than 45 years

Current or recent history of tobacco use

Presence of distal extremity ischemia (claudications, pain at rest, ischemic


ulcers)

Exclusion of autoimmune diseases, hypercoagulable states and diabetes


mellitus

Exclusion of a proximal source of embolization by echocardiography and

3. Takayasus
arteritis is a disease affecting the brachio-cephalic vessels in a young female
arteriography
commonly
referred toarteriographic
as pulse less disease.
Consistent
findings in the clinically involved and noninvolved
limbs
4. Temporal arteritis or giant cell arteritis is a disease affecting the temporal vessels in females
after 50 years of age and presenting with headaches.
5. Raynauds phenomenon (RP) is a manifestation in the upper limbs Primary (also referred to
as Raynauds disease where RP is in the absence of any primary disease and Secondary when
it is associated with occupation/drugs/connective tissue disorders/thoracic outlet syndrome etc.
This is a condition of vasospasm where pallor (vasoconstriction) is followed by cyanosis
(accumulation of deoxygenated blood) and lastly, rubor (return of blood flow leading to reactive
hyperemia).

CLINICAL FEATURES OF CHRONIC ISCHAEMIA


The hall mark clinical presentation of a chronically ischaemic limb is intermittent claudication
progressing gradually to constant rest pain which then leads to colour changes of pregangrene and
ultimately to frank gangrene and ulceration.

Intermittent Claudication :
This is a special character of pain described for arterial disorders. This is a clinical condition where
a cramping, aching or tightness like severe pain appears in the leg affected during exercise,
usually after a fixed level of exercise and is promptly (within two to three minutes) relieved with
16

rest . It Is due to the accumulation of Substance P which fails to get washed away due to poor
blood supply. The site of claudication gives an important clue to the level of blockage. This
153

vascular claudication needs to be differentiated from spinal claudication which is due to


compression of spinal nerves due to spinal stenosis.
Table 6: Difference between Vascular & Spinal Claudication
Vascular Claudication

Spinal Claudication

Never present on standing or start of walking


or on first step

Pain brought on by weight bearing or taking


first step.

Pain is cramping/aching in a muscle group

Pain classically radiated down the back of

supplied by proximal vessels

leg with associated numbness or tingling or

Always brought on by walking and relieved on

altered sensation

rest.

Is brought on by extension of spine and


relieved by flexion, simian stance

Table 7: Presentation according to site of block


Site of Blockage

Clinical Presentation

Aorto-Iliac Disease

Buttock, Thigh & calf claudication. Leriche


Syndrome

Common Femoral Disease

Thigh & Calf Claudication

Superficial Femoral Disease

Calf claudication

Popliteal Artery Disease

Calf claudication

Crural Artery Disease

Calf & Claudication

Table 8 : Boyds classification of intermittent claudication :


Grade I

Pain starts but if the patient continues to walk the metabolites increase the muscle
blood flow and sweep away the P- substance produced by exercise and pain
disappears.

Grade 2

Pain continues but the patient can still walk with effort.

Grade 3

Pain compels the patient to take rest.

Grade 4

Rest pain

Table 9: Factors Affecting Claudication Distance

Excess Weight

Walking Uphill

Walking against Wind

Carrying Shopping/ load

Rest pain: This is said to be the cry of dying nerves. It is a severe pain described as agonizing or
burning felt in the foot at rest, made worse by lying down or elevation of the foot. The pain is felt
first in the most distal part of the leg, in the toes and the instep of the foot. It is due to the
154

ischaemia of the skin and subcutaneous tissues, which are richly supplied by nerves.
Characteristically, the pain is worse at night largely due to absence of gravity effect in the supine
position aiding blood flow to the limb and partly due to lower blood pressure and heart rate while
sleeping leading to decreased blood flow to the limb. The patient might attempt to overcome this
somewhat by using gravity aid and hanging the foot out of the bed or by sleeping in chair. This
attitude leads to pedal oedema and thereby worsening of microvascular perfusion. Paradoxically, a
limb with rest pain may appear bright red due to accumulation of vasodilator metabolites. Rest pain
is completely different from night cramps commonly seen in the elderly.
vi

Critical Limb Ischaemia : It is defined as persistently recurring rest pain requiring regular, analgesia
for more than 2 weeks, or ulceration or gangrene of the foot or toes, with an ankle systolic
pressure of less than 50 mm Hg or a toe systolic pressure of less than 30 mm Hg. This applies to
both diabetic and non- diabetic patients. It is imperative to determine whether the limb is critically
ischemic or not so that appropriate management can be instituted.

Pregangrene: This is an older terminology which refers to the presence of two or more of clinical
findings which are harbingers of imminent gangrene in a critically ischemic limb.

Table 8: PreGangrene

Rest Pain

Oedema

Hyperaesthesia

Colour Changes

Ulceration

TABLE 9 - Fontaine classification of limb ischaemia


Stage 1

No clinical symptoms

Stage 2

Intermittent claudication

Stage 3

Ischaemic rest pain

Stage 4

Ischaemic ulcer, gangrene

Clinical Examination:
Physical examination involves inspection of the extremities for signs of chronic ischaemia like thin,
shiny skin, loss of hair and subcutaneous fat, presence of brittle nails with transverse ridges and
areas of minor ulceration and differentiation from signs of acute arterial occlusion like pallor,
pulselessness, poikilothermia, pain, paraesthesia and paralysis. All the peripheral pulses have to
be palpated with care and recorded. It is important to know the site of palpation of each pulse. It is
important to note temperature difference between two limbs if any, skin changes of ischemia,
muscle wasting, Capillary and Venous Refilling, Buergers Angle, perform Buergers Test, and

155

differentiate an arterial ulcer from a venous ulcer. Similarly, dry gangrene has to be differentiated
from wet gangrene. It is possible for patients with proximal stenosis to have a palpable distal pulse
at rest and it is important to look for their disappearance on exercise. It is also important to perform
a detailed and appropriate neurological assessment to differentiate spinal from vascular
claudication.

INVESTIGATIONS
General:
1. Blood : Routine examination of blood including a hemoglobin percent (low Hb% can decrease
claudication distances and aggravate rest pain), blood sugar examination as diabetics have worse
prognosis, are essential. Erythrocyte sedimentation rate (ESR) is usually raised in Buergers
disease. In patients with high suspicion of underlying connective tissue disorders, specific test like
RA factor, LE cell phenomenon etc. may be carried out. Lipid profile is mandatory in elderly
patients with atherosclerosis.

2. Urine examination for sugar.

3. Plain X-ray of the abdomen will show the presence of arterial calcification and flecks of calcium
may outline an aneurysm.

4. ECG: an abnormality in ECG may influence the decision for surgery, in patients with lower limb
disease.

Tests of global Vascular Status:


5. Hand Held Doppler ultrasound

vii

blood flow detection uses a continuous wave ultrasound

signal, beamed at an artery and the reflected beam is picked up by a receiver. The changes of
frequency in the reflected beam, as compared with the transmitted beam, are due to the
Doppler shift, resulting from passage of beam through moving blood. These frequency
changes are converted to audio signals. This investigation may be used effectively in cases
where a differential diagnosis of atherosclerosis is entertained showing the site of block and
extent of distal run-off. A 8-10 MHz continuous waver Doppler ultrasound probe is used to
assess the posterior tibial (PT), dorsalis pedis (DP) and peroneal arteries. A normal pedal pulse
produces a Doppler signal with 2 or 3 distinct phases with a clear sharp sounding systolic peak.
The reduction in the pitch of this signal and a lack of the phasic components is recongnised as
abnormal finding. In low arterial flow conditions, it becomes difficult to differentiate between
arterial from venous flow. In such a situation, application of compression in the distal part of the
limb would tend to augment in case of a venous signal but will leave the arterial signal
unaffected.

156

6. Ankle Brachial systolic blood pressure index (ABPI)

This measurement gives the quantitative assessment of the global limb arterial perfusion.
Patient lies supine, all measurements are at the level of the heart and only after resting for 1015 minutes. A standard BP cuff of 15-20 cm width is positioned in the ankle just above the
malleoli. A 8-10 MHz Doppler ultrasound probe is used to hear the pedal Doppler signals and
inflated above the systolic pressure for the signals to disappear. The point at which the Doppler
signals first returns on gradually lowering the pressure marks the systolic pressure at the ankle
level. Normally an average of 2 measurement for each of the arteries namely dorsalis pedis and
posterior tibial is used to denote the ankle pressure. Similar procedure is done for brachial
artery. The ratio of the highest recorded systolic pressure at the ankle to the brachial systolic
pressure at the arm forms the ABPI. The ankle brachial index is interpreted in the manner as
given in Table 4. As a thumb rule, patients with ABPI of 0.8 or 0.9 have moderate peripheral
vascular disease, those between 0.5 to 0.8 suffer from intermittent claudication and those with
< 0.5 may suffer from rest pain, ulceration or gangrene.
TABLE 10 Ankle Brachial Pressure Index
ABI

Interpretation

1.1 0.1

Normal

0.6 0.2

Intermittent claudication

0.3 0.1

Ischaemic rest pain

0.1 0.1

Ischaemic ulceration or gangrene

Segmental pressures, i.e. differences in arterial blood pressure between segments of limb can
be detected to give indication of the sites of stenosis, specially as Buergers is said to be a
segmental disease.

7. Toe Pressures Using Photoplethysmograph: These are used when the arterial disease is
suspected between the ankle and the toes. The measurement is done using an occlusion cuff
of 2-3 cm diameter placed around the great toe or 2

nd

rd

or 3

toe and the digital pulse is

recorded by a photoelectric cell placed on the toe. The measurements are recorded on a strip
chart recorder with cuff pressures being recorded simultaneously. Toe pressures are normally
lower than the brachial or the tibial arteries at the ankle due to high resistance created by small
digital arteries. Toe pressures are also indicated as a percentage of the brachial artery
pressure referred to as the Toe Brachial Index (TBI). Normal ratio is 0.8-0.9. Patients with
claudication have TBI of 0.2-0.5 and those with CLI have TBI<0.2

8. Pole Test: This is used to determine the adequacy of lower limb bolld flow in patients with
incompressible vessels or who are unable to tolerate an ankle pressure cuff. It involves
listening to the pedal pulse using the hand held Doppler probe while the patients leg is raised
against a pole. The height at which the Doppler signal disappears is reflected by the markings
157

in mm Hg in a caliberated pole directly. A maximum of 60-70 mm Hg only can be recorded


since the test is limited by the height upto which the patient is able to lift the leg.

9. Transcutaneous Oximtery (TcPO2): It is based on the principle that the partial pressure of the
oxygen which diffuses through to the surface of the skin reflects the oxygen tension of the
underlying tissues. It is time consuming and is best used in the selection of amputation sites
since it correlates well to subsequent stump healing.

10. Walk Test: The basis of this test is that measurement of ABPI before and after a patient has
walked can expose less severe or compensated peripheral vascular disease. The walk can be
standard or graded ( incline) using a tread mill. A reduction in ABPI of >20% indicates
presence of severe arterial disease. In normal limbs, there is a rise or status quo in the ABPI.
As a rough guide, post exercise ABPI of 0.8-0.9 confirms claudication caused by moderate
disease, 0.5-0.7 indicates significant disease and <0.5 denote severe arterial insufficiency.

Tests for Disease Localisation:


6

11. Duplex imaging gives accurate information on the size of artery, the flow rate, turbulence
and the presence of stenosis. The combination of Doppler and color mapping allows easy
recognition of stenotic sites. This has been achieved by the use of pulsed or continuous wave
Doppler and the two- dimensional images produced by the B- scan made either singly or in
combination. Peak systolic velocity at the site of stenosis is compared to that measured
proximally to obtain a peak systolic velocity ratio (PVR) and relates to the degree of stenosis. A
2x increase in PVR at a stenosis corresponds to 50% reduction in diameter on arteriography.
This modality is non invasive and has now become the mainstay of assessment of arterial
insufficiency, and has largely replaced routine use of conventional arteriography. This requires
detailed assessment of each major arterial segment i.e Aorta, Iliacs, Femoropopliteal and
infrapopliteal segments. This investigation has virtually become the first line investigation to
localize the level of block with a great deal of accuracy.

12. Intravascular Ultrasound: Minute ultrasound probes with 10MHz transducers mounted on tips
of small 3-4 F catheters are placed directly in the lumen of the arteries over a guidewire and
produce intravascular ultrasound images which give details of arterial walls, luminal contents
and dimensions. This is not a routine investigation for peripheral arterial disease and as yet is
not cost effective.

13. Arteriography: This is an invasive technique which though has become much safer in the
recent years due to fine 3-4 F catheters, and remains the gold standard to provide a road map
required for vascualt surgeons expecially before surgery is planned. However, alternative
modalities have emerged which seem more attractive and safer largely because they are non
invasive and lack the potential hazards of arteriography like allergies to contrast agents, use of
158

ionizing radiation, and technique related problems like hematoma, arterial spasm, sub-intimal
dissection, infection, pseudoaneurysm, AV fistula and embolisation. Angiography remains still
the preferred investigation before percutaneous transluminal angioplasty or definitive bypass
surgery is performed but is slowly being pushed away by the following non invasive techniques
as they are improving with technology.

14. CT Angiography: The introduction of the helical (spiral) CT scanning and multidetector CT
which uses 2 or 4 helicals to scan the patient, CT imaging has been revolutionized for vascular
imaging wherein a single breathhold time is sufficient to generate the scans from the aortic arch
to the groins with imaging quality as good as conventional angiography. However, it still uses
ionizing radiation and iodinated contrast agents and therefore it has not yet gained usage for
peripheral arterial disease. It is however, the imaging of choice for pre-operatibe assessments
of aneurysms.

15. MR Angiography: Increasing usage of Magentic Resonance Imaging in the last decade and
improvement in technology has seen a shift towards using this modality for assessment of
vascular system. Earlier, Time of Flight MRI and Phase Contrast MRI were used to visualize
moving blood as a white image but the definition and clarity of the vessels was found to be
inferior to angiograms. More recently, Gadolinium Enhanced MRI (Gd-MRI) has significantly
improved this quality of image and made it comparable to conventional angiography. The
disadvantage is the high cost of the contrast material and availability of the MRI technology. As
of now Gd-MRI is being used more often for assessment of peripheral limb ischaemia in
combination with Dupleix Scanning and Conventional catheter angiography has been reserved
where findings of these two investigations are discordant.

TREATMENT OF ATHEROSCLEROTIC CHRONIC ARTERIAL INSUFFICIENCY:


The management of atherosclerotic occlusive peripheral arterial disease is divided into three parts as
follows:
1.

Modification of risk factors and medical management.

2.

Treatment of Intermittent claudication

3.

Treatment critical limb ischemia.

The following flow chart is a useful aid memoire on the management of this condition.

159

FlowChart 1: Treatment Pathway for chronic lower limb ischemia. From: Beard JD, Gaines PA.
Treatment of chronic lower limb ischemia. In: Vascular & Endovascular surgery. Beard JD & Gaines
nd
PA (eds). 2 edition. WB Saunders. London. . 2001:Pp 55-88.
A. Risk Factor modification:
Table 11. Medical Management

Cessation of smoking

Treatment of Hyperlipidemia

Control of Hypertension

Management of Diabetes

Use of anti-oxidants treatment for


homocystinemia

Anti-platelet therapy

B. Treatment of Intermittent Claudication


Intervention is based on several factors which are quality of life issues more than claudication
distance. Also the presence of co-morbid conditions significantly alters intervention.

160

Table 12: Factors affecting intervention in Claudication


Favour of Intervention

Against Intervention

Severe symptoms

Short history

Job affected

Still smoking

No improvement with exercise

Other limiting conditions

Aorto-iliac disease

Femoro-distal disease

Stenosis/short occlusion

Long segment occlusion

programmes
Unilateral Symptoms
Multi-level
disease
a) Exercise
have shown that encouraging
the patients
to walk to near maximum
pain tolerance had beneficial results in more distal disease such a femoral block as compared
to angioplasty. In proximal disease, angioplasty has been found to be superior to exercise
though long term well controlled studies are limited in literature.

b) Use of drugs such as pentoxyfylline, naftidrofuryl, inositol and cinnarizine which have
vasodilator as well as haemorheological properties remains debatable.

c) Endovascular treatment

viii

Percutaneous techniques for treating arterial occlusions

involves the following procedures:

Percutaneous Transluminal Balloon dilatation (Angioplasty) (PTA)

Endovascular Stenting

Endovascular atherectomy

Angioplasty. The mechanism of action of a balloon angioplasty involves fracture and


displacement of plaque along with over stretching of the media and the adventitia. The
initial step involves passage of a guide wire across the narrowed segment or area
followed by proper positioning of the balloon in the segment to be dilated.

Aorto-iliac interventions have the highest long term success with normal distal vessels,
especially for focal stenoses in large high caliber and high flow arteries. The 5 yr patency
rate for PTA of common iliac artery is 70-80 %. Femoro-popliteal interventions have
much lower success unless there is focal disease with good distal run off.

Endovascular Stenting: This involves the use of self expanding metallic stents to keep the
constriction segment open after PTA. Stents are usually preferred for long segment
stenoses in combination with PTA. Studies comparing angioplasty alone versus
angioplasty with stenting have shown higher long term success in the latter group with
similar complication rates. Angioplasty is the first line of treatment for stenosis and
occlusions less than 10 cm in length.

161

Atherectomy: This technique involves the use of a specially designed catheter which can
remove the atherosclerotic plaque from the arterial wall by either shaving, cutting or high
speed rotational ablation. Laser energy has also been used to vaporize and debulk the
plaque where the stenosis is thick before PTA is attempted.

Atherectomy has been used extensively in the last few years for the treatment of CLI
either as a stand alone treatment or in lesions at bifurcations or trifurcations as also in
stent restenoses. However, prospective comparative data is limited.
d) Surgical treatment i) Infra-inguinal bypass: Above knee and below knee femoropopliteal
bypass grafting has been used using saphenous vein and PTFE as the graft material.
Comparative have shown that while saphenous is superior to PTFE in graft patency at 2
years for below knee level, the results are equivocal for above knee level but favour the use
of vein. ii) Supra-inguinal bypass Aorto-bifemoral bypass has >90% patency at 1 year but
higher mortality. Cross femoral or ilio-femoral by pass have similar success rates for
unilateral disease with lower mortality rates. Axillo-bifemoral grafts have a lower patency
rate and are not justifiable for claudication.

Fig 1: Types of Supra-inguinal Bypass surgery. From: Beard JD, Gaines PA. Treatment of chronic
nd
lower limb ischemia. In: Vascular & Endovascular surgery. Beard JD & Gaines PA (eds). 2 edition.
WB Saunders. London. 2001: Pp 55-88.

162

Fig 2: Types of Infra-inguinal Bypass surgery. From: Beard JD, Gaines PA. Treatment of chronic
nd
lower limb ischemia. In: Vascular & Endovascular surgery. Beard JD & Gaines PA (eds). 2 edition..
WB Saunders. London. 2001:Pp 55-88

C. Treatment of Critical Limb Ischemia (CLI):


Most patients with CLI would need intervention unless there are severe co-morbid conditions and has
limited survival.
a) Endovascular Therapy: 50-75% of patients tend to benefit from endovascular intervention and
this should be offered as the first choice. Although, the benefits of angioplasty with or without
stenting are not as prolonged in infra-inguinal disease as compared to supra-inguinal disease, yet
the short term benefits are sufficient to induce healing of the threatened limb. However it is prone
to higher complication rate as compared to claudicants due to risk of embolization and dissection.

The Bypass versus Angioplasty in Severe Ischemia of the Leg (BASIL) trial compared PTA with
surgery in 452 patients with rest pain, ulceration or gangrene of the leg secondary to infra-inguinal
ix

disease . The primary end-point, amputation-freesurvival, was similar for PTA and surgery at 1
year (71% vs 68%, p = NS) and 3 years (52% vs57%, p = NS). Although there was no significant
difference in mortality between the groups at 30 days, surgery was associated with a higher postprocedure morbidity.

BASIL demonstrated that endovascular therapy and surgery were comparable as first-choice
therapy for CLI, but that PTA was less expensive and didnot preclude subsequent treatment with
surgery. Therefore, PTA should be chosen first if a patientis a candidate for either procedure,
x

particularly if the patients life expectancy is less than 2 years .

163

Stents:Despite favorable limb salvage rates, endovascular interventions for the treatment of CLI
10

are associated with modest, 6080%, 1-year primary patency rates . Several stent
technologies have been introduced in an effort to prolong the durability of percutaneous
interventions by minimizing late stent failure from restenosis. Stent types currently being
investigated include: self-expanding stents, covered stents (i.e. stent grafts), Drug Eluting
stents (DES), and bioabsorbable stents.

Cutting

balloon

angioplasty (CBA):

The cutting

balloon

catheter

(Boston

Scientific

Corporation,Natick, MA, USA) is a device in which razor blades (atherotomes) are embedded
on the exterior of the balloon. These atherotomes, whichare arranged longitudinally, score the
plaque surface during balloon expansion (Figure 6). Proponents of the device claim that cutting
balloons are less traumatic to the vessel wall and can limit the extent of dissection following
xi

angioplasty, which has yet to be demonstrated in a convincing manner .


Cryoplasty: The PolarCath (Boston Scientific Corporation) is a device that combines balloon
angioplasty with the delivery of cold thermal energy to the vessel wall. It consists of a
specialized balloon catheter attached to a source of pressurized nitrous oxide (N2O) that is
used to inflate the cryoplasty balloon. As the balloon volume increases, the N2O contained
within it expands, and its temperature falls below freezing. Proponents of the technique theorize
that application of cryoplasty leads to apoptosis and reduced restenosis. However, a recent
study in humans showed no difference for cryoplasty compared with PTA for release of the
xii

growth factors and cytokines that initiate neo-intimal hyperplasia .

Excimer laser-assisted angioplasty (ELA): The proposed mechanism by which the laser
debulks atheromatous plaque is photoablation (i.e. destruction of plaque material by
photochemical energy contained within the UV pulses).38 One advantage of excimer laser over
prior laser technologies is that it causes minimal thermal injury to the surrounding tissue.39
Successful recanalization using excimer laser does not eliminate the need for subsequent
balloon angioplasty because the diameter of even the largest catheter (2.5 mm) is smaller than
the typical diameter of the femoral arteries where it is commonly used. The shallow penetration
depth of the UV pulses limits the speed at which the catheter can be advanced, and therefore
xiii

ELA is a time-consuming endeavor by default . The costs of the catheter, approximately $1500
per device, as well as the price of the laser unit make it a very expensive option. In summary,
ELA is an expensive therapeutic modality that has not been shown to improve outcomes
compared to conventional PTA for the treatment of CLI. Without evidence of superiority
compared to conventional therapies, it cannot be recommended for routine use in CLI.

Atherectomy: Atherectomy is an adjunct, or alternative, to angioplasty for the treatment of


peripheral artery obstruction. The SilverHawk Excision System (Fox Hollow Technologies,
Redwood City, CA, USA) is a directional atherectomy catheter. Plaque is shaved off as the
164

atherectomy blade rotates, and debris is collected inside a nose cone at the tip. At present
there are no randomized data to show that this device is superior to PTA.One disadvantage of
the SilverHawk catheter is its limited ability to treat heavily calcified lesions, which reduces it
usefulness in patients with CLI. Complications of excisional atherectomy include distal
embolization, thrombosis and vessel wall perforation. In one study, the authors concluded that
while immediate results of excisional atherectomy in this cohort were good, the midterm
xiv

restenosis rates were high . Another study concluded that patency rates and limb salvage
rates with excisional atherectomy were similar, but not superior, to other endovascular
xv

modalities .

b) Both supra and infra inguinal bypass surgery is possible in this grup of patients where coexistent morbid conditions are absent. Whereas, PTFE is preferred for the former, autologous
saphenous vein is preferred for the latter. The patency rates for femoro-popliteal bypass are 10%
lower for CLI as compared to claudicants.

c) Drugs: Prostacycline analogues are expensive and when used have shown significant reduction in
death and amputation in short term (6 months).

d) Chemical Sympathectomy is an option in non diabetics which is useful for improving rest pain or
minimal tissue loss. 2 ml of 10% phenol is injected using a translumbar approach under image
intensifier control at L3 level and then L4 level.
e) Pain Relief Morphine sulphate has been used for chronic pain relief.
f) Amputations These are ideal for those with extensive tissue loss, poor case for revascularization
and presence of severe co-morbid conditions along with the above.
TREATMENT OF BUERGERS DISEASE
Up to two- thirds of patients first presenting in vascular clinic with intermittent claudication, can be
treated by conservative methods.
Abstinence from tobacco: The only proven treatment guideline to prevent disease progression and
avoiding an amputation is complete cessation of smoking or other forms of tobacco. Shionoya et
al

xvi

stated that abstinence from tobacco is important cornerstone of treatment of Buergers

disease. Goodman et al

xvii

confirmed that if the patients of Buergers disease cease smoking

completely, their disease, in most cases, may reach a plateau and in some improvement may be
noted. They however pointed out that the beneficial effects from cessation of smoking often cannot
be expected in late stages of disease, hence smoking should be stopped early in disease. Also the
treatment of the disease is useless if smoking is continued. In a series of 120 patients, it was
observed that if there was no gangrene when the patient discontinued smoking, amputation did not
occur in 94% cases whereas 43% of those who continued smoking required one or more
165

amputations

xviii

xix

. Any form of continued usage of tobacco keeps the disease active . Repeated

education and counseling is required for these patients. Raynauds phenomenon or claudication
may continue even after complete discontinuation of tobacco.

Explanation and advice: Many patients are worried by the presence of pain while walking. Once told
about the nature of disease and advice regarding methods to improve their claudication distance
e.g. by walking slowly or by improving underlying systemic disorder like, anemia, congestive
failure, the claudication distance can be increased.

Adjustment of lifestyle: Adjustments to everyday habits of transport can increase mobility within the
claudication distance, e.g use of a bicycle etc.

Exercise & Diet: Taking regular exercise within limits of pain and control of weight in case of obesity.

Care of feet, avoiding socks with holes and amateur chiropody, which can spark off gangrene in the
toes and heels, particularly in diabetic patients.

Heel raise: claudication distance may be improved by raising the heels of shoes by 1 cm. The work of
the calf muscles is reduced thereby.

Analgesics and position: rest pain can be relieved to some extent in some patients by use of
analgesics, elevation of the head end of the bed (Buergers position) and Buergers exercises
(repeated 2 minute elevation and dependency of limb).

Drugs: Despite the clear presence of inflammation in this disorder, anti-inflammatory agents such as
steroids have not been shown to be beneficial. Similarly, strategies of anticoagulation (thinning of
the blood with aspirin or other agents to prevent clots) have not proven effective. Vasodilator drugs
xx

are usually started in these patients but their role is equivocal. Abramson found that vasodilators
increased cutaneous blood supply only and had no role in increasing muscle blood supply. Some
of the drugs used are :
Prostaglandins : Prostacylin or PGI2 (Iloprost) has forty times antiplatelet and vasodilator activity
as compared to PGE1. They are effective in both cutaneous and muscular vessels. Intravenous
infusion of prostacyclin (Iloprost) has been demonstrated in some studies to relieve rest pain for
xxi

up to a month and in some upto 6 months . Low molecular weight dextrans: dextrans of
molecular weight 50000 are used during

acute attack of thromboangitis. They cause

hemodilution, decrease viscosity of blood and improve micro circulation. Intra-arterial infusion is
said to be more effective than intravenous.

166

Intra-arterial Thrombolytic therapy: Selective low dose intrarterial streptokinase (Bolus 10,000
Units followed by 5,000 units per hour) have been used in a very small group of patients with
xxii

alteration of level of amputation or its avoidance in 58% patients .

Praxiline : (niftidrofuryl oxalate) may alter tissue metabolism, increasing the claudication distance
by allowing a greater oxygen debt to be incurred. No proven benefit.
Trental : (oxypentifylline) has some effect on whole blood viscosity by reducing rouleaux
formation. No proven benefit.
Aspirin in dispersible form may be prescribed for its anti-adhesive effect on platelets. No proven
benefit.

Direct Arterial Surgery:

Surgical bypass or revascularization is rarely feasible in patients with

Buergers disease because of occlusion of small and medium sized vessels, presence of
segmental and skip lesions and absence of a distal target vessel for by pass. Shionoya et al

xxiii

undertook arterial reconstruction in 23 of 148 patients of thromboangitis obliterans and performed


22 bypass procedures and 5 thromboendarterectomies. The overall success rates were around
26%. But even this rate has not been duplicated in later studies. Reddy et al

xxiv

found that in south

Indian patients, there was involvement of arteries with little pathology in veins, and therefore
attempted arterialization of veins by creating arterio-venous fistula between the artery proximal to
the site of block and the adjacent vein. A success rate of 72% was reported by them. Saasjima et
al reported a five year primary patency rate of 49% and

secondary patency rate of 62% in 61

xxv

patients after infra-inguinal bypass .

Sympathectomy: Sympathectomy is not beneficial in intermittent claudication, but can relieve rest
pain and ulceration because the effect is mainly on skin and subcutaneous blood vessels. For the
same reason it helps in the healing of superficial ischaemic ulcerations. It might aggravate
claudication by stealing the blood from ichaemic muscles and diverting it to the skin and therefore
is a contraindication for sympathectomy. In vessel wall, sympathectomy is done with following
objective.

To cause vasodilatation by decreasing sympathetic vasomotor tone.

To abolish pain impulses carried by sympathetic fibers.

Nakata et al

xxvi

reported ulcer healing in 58% and relief of rest pain in 64% after lumbar

sympathectomy and concluded that the clinical effects of sympathectomy were because of
increased blood flow to the skin. Methods of conducting sympathectomy are:

1. Surgical sympathectomy

xxvii

Lumbar sympathectomy: Open sympathectomy is done preferably through the extraperitoneal


approach.The sympathetic chain lies on the side of the body of vertebrae, sometimes inside the
psoas muscle sheath. In unilateral surgeries, sympathetic ganglia, L1, L2, L3 and sometimes
167

L4 are removed. In bilateral cases, L1 of one side is preserved ( to avoid retrograde


ejaculation). A transperitoneal approach may also be used, especially in patients where
bilateral lumbar sympathectomy is planned (but used less often in view of its increased
morbidity).The complications of this surgery include paralytic ileus, injury to genitofemoral
nerve, ureteric injury, hemorrhage (because of major vessel injury e.g injury to aorta, inferior
vena cava or avulsion of lumbar veins), and rarely bowel injury. With the advent of minimally
invasive surgery, lumbar sympathectomy is being done laparoscopically through the
retroperitoneal route and has decreased the morbidity of access, to a large extent.

The draw back of lumbar sympathectomy is that it is a temporary procedure and the effect
rarely lasts beyond a period of six months. The reasons for failure include:

Technical- failure to identify the lumbar chain. ( lumbar chain can often be mistaken with
lymphatic chain genitofemoral nerve, psoas sheath, psoas minor etc.).

Cross connections of the chain from the opposite lumbar chain

Regeneration of the cut ends of the chain causing reformation of the chain.

Hypersensitivity of the end organ receptors to the circulating noradrenaline.

Responsiveness of the sympathetic plexus around the vessels.

For upper limb Buergers disease, cervical sympathectomy is done where T1 (lower portion of
stellate ganglion), T2 and T3 are removed. Cervical sympathectomy can be done through:
(a) Supraclavicular route- less morbid but accessibility to the T3 ganglion is slightly difficult.
(b) Axillary route- accessibility to the ganglion is best but requires opening of the thoracic
cavity and increases the morbidity.
(c) Posterior approach- this is the shortest possible route, but the presence of bulky
paravertebral muscles make this a difficult proposition and is rarely used.
(d) Transthoracic laparoscopic sympathectomy is now the standard treatment of choice for the
upper limb disease.
21

2. Chemical sympathectomy :
This is an alternative to surgical sympathectomy but is contraindicated in patients on
anticoagulant therapy. A long 15 cm needle is inserted with local infiltration, first to seek the
side of the vertebral body and secondly to pass alongside it to reach the lumbar sympathetic
nd

rd

th

chain. 5 ml of phenol solution in water is injected beside the bodies of 2 , 3 and 4 vertebrae.
The procedure is done preferably under fluoroscopic or ultrasound guidance and care is taken
to avoid penetrating the aorta or inferior vena cava.

Omental transposition:
Omental transposition to the lower extremity was first described in atherosclerotic occlusive
disease by Casten and Alday

xxviii

. Hoshino et al

xxix

classified omentum according to the number

of arterial branches in the omentum. Type 1 has a single layer of vessels amd is more common
168

than Type 2, which has a double layer. Hoshino et al, have expressed their results in terms of
improvement of five symptoms namely, rest pain, coldness, cyanosis, intermittent claudication
and ulcer healing. They classified their results as excellent (if 4-5 symptoms were relieved71%), good (if 2-3 symptoms were relieved-19%) and fair ( if 1 symptom was relieved-10%).

In India, omental transposition has been done more frequently and with encouraging results,
since there are limited options for limb salvage. The procedure is based on the arterial arcade
formed by the anastomosis of right and left gastroepiploic arteries. For unilateral procedures,
the omental pedicle is based on the right gastroepiploic artery as it is a dominant artery and has
a longer length. For bilateral procedures, both epiploics may be used, though sometimes a
single vessel is used as there is risk of gastric devasularization if both arteries are used. A
subfascial tunnel is made from the inferior end of the laparotomy incision to the inguinal and
further down to the ankle medially. The omentum is lengthened based on the dominant artery in
the pedicle as shown (Fig 3, 4 & 5) and brought down to the distal most portion of the affected
limb through the subcutaneous tunnel. Complications of this procedure include:,gastric
devascularization and necrosis, paralytic ileus, gastric hemorrhage, omental necrosis and
wound infection.

Singh et al, using pedicled omental transposition, reported ulcer healing in 88%, decrease in
rest pain in 72%, increase in claudication distance in 96% and improvement in skin temperature
xxx

in all the 50 patients . Others have reported no significant difference in these parameters
when pedicled grafts were compared with free omental grafts

xxxi

. The effect of omental

transposition is said to be because of its rich vascular supply which directly improves tissue
perfusion and secondly omentum is said to cause neovascularization in the affected limb.

Fig 3 Diagram depicting technique of omental tranfer and lengthening. Numbers 1 represents division of left
gastroepiploc vessel and mobilization of omentum preserving the gastro-epiploic arcade, division of arcade
proximal to rt. Omental vessel (2), ligation of mid omental vessel distally (3) and extended further to gain length
(4). [From: Singh I, Ramteke VK. The role of omental tranfer in buergers disease; New Delhis experience. Aust
N Z J Surg. 1996;66:372-6.]

169

Fig 4 Alternative technique for omental tranfer and lengthening. Number 1 is same as in Fig 1. Number 2
shows division of and right and mid omental vessels and sparing the left omental vessel. [From: Singh I, Ramteke
VK. The role of omental tranfer in buergers disease; New Delhis experience. Aust N Z J Surg. 1996;66:372-6.]

Fig 5 Steps used for bilateral omental transfer. [From:


Singh I, Ramteke VK. The role of omental tranfer in
buergers disease; New Delhis experience. Aust N Z J
Surg. 1996;66:372-6.]

170

REFERENCES:
1.

Beard JD, Gaines PA. Treatment of chronic lower limb ischemia. In: Vascular & Endovascular
surgery. Beard JD & Gaines PA (eds). 2

2.

nd

edition. WB Saunders. London. 2001. Pp 55-88.

Leng GC, Fowkes FGR. Epidemiology and risk factors for peripheral arterial disease. In: Vascular &
Endovascular surgery. Beard JD & Gaines PA (eds). 2

3.

nd

edition. WB Saunders. London. 2001.Pp 1-26.

Simon JC, Lloyd MT, John MP. Non operative treatment of chronic lower limb ischaemia. In: Current
problems in Surgery. Wells SA (ed). Jan 1991. pp 45-46.

4.

Olin JW, Lie JT. Thromboangiitis obliterans (Buergers disease). In : Loscalzo J, Creager MA, Dzau
VJ, eds. Vascular Medicine. 2

nd

ed. Boston:Little,Brown,1996 pp1033-1049.

5.

Boyd AM. The natural course of atherosclerosis of the lower extremities. Angiology 1960;11:10-14.

6.

Tenant WG, Ruckley CV. The critically ischaemic limb. In: Recent advances in surgery (18). Taylor I,
Johnson CD (eds). Churchill Livingston. Edinburgh. 1995;pp 117-139.

7.

London NJM, Cleveland TJ. Assessment of Chronic lower limb ischemia. In: Vascular &
Endovascular surgery. Beard JD & Gaines PA (eds). 2

nd

edition.WB Saunders. London. 2001 Pp 27-

53.
8.

Belkin MJ, Whittemore AD, Donaldson MC, Conte MS, Gravereaux E. Peripheral Arterial Occlusive
disease. In: Sabiston Textbook of surgery. Townsend CM, Beauchamp RD, Evers BM, Mattox KL
th

(eds). 17 edition. Saunders. Philadelphia. 2004. pp1989-2029.


9.

Adam, DJ, Beard, JD, Cleveland, T, et al. Bypass versus angioplasty in severe ischaemia of the leg
(BASIL): multicentre, randomised controlled trial. Lancet 2005; 366:19251934.

10. Kudo, T, Rigberg, DA, Reil, TD, Chandra, FA, Ahn, SS.The influence of the ipsilateral superficial
femoral artery on iliac angioplasty. Ann Vasc Surg 2006; 20: 502511.
11. Rabbi, JF, Kiran, RP, Gersten, G, Dudrick, SJ, Dardik, A.Early results with infrainguinal cutting
balloon angioplasty limits distal dissection. Ann Vasc Surg 2004; 18: 640643.
12. Wildgruber, M, Weiss, W, Berger, H, Eckstein, HH, Wolf, O, Heider, P. Early endothelial and
haematological response to cryoplasty compared to balloon angioplasty of the superficial femoral
artery a pilot study. Br J Radiol 2007.
13. Garnic, JD, Hurwitz, AS. Endovascular excimer laser atherectomy techniques to treat complex
peripheral vascular disease: an orderly process. Tech Vasc Interv Radiol 2005; 8: 150159.
14. Yancey, AE, Minion, DJ, Rodriguez, C, Patterson, DE,Endean, ED. Peripheral atherectomy in
TransAtlantic InterSociety Consensus type C femoropopliteal lesions for limb salvage. J Vasc Surg
2006; 44: 503509.
15. Keeling, WB, Shames, ML, Stone, PA, et al. Plaque excision with the Silverhawk catheter: early
results in patients with claudication or critical limb ischemia. J Vasc Surg 2007; 45: 2531
16. Shionoya S., Ban I., Nakata S., Matsubara J.,Shinjo K., Hirai M. Diagnosis, pathology and treatment of
Buergers disease. Surgery 1974;75:695.
17. Goodman R.M., Elian B., Moses M., Deutsch V. Buergers disease in Israel. Am. J. Path 1959;24:319.
18. Olin JW. Thromboangiitis obliterans (Buergers disease). In: Rutherford RB, ed. Vascular surgery. 5

th

ed.Philadelphia:W.B.Saunders,2000:350-64.
19. Joyce JW, Lie JT. Buergers disease (thromboangiitis obliterans). Rheum Dis Clin North Am.
1990;16:463-70.
20. Abramson D.I. diagnosis and treatment of thromboangitis obliterans. Geriatrics. 1965; 20:28.
21. Fiessinger JN, Schafer M. Trial of Iloprost versus Aspirin treatment for critical limb ischaemia of
thromboangiitis obliterans. Lancet 1990;335:555-557.

171

22. Hussein EA, el Dorri A. Intra-arterial streptokinase as adjuvant therapy for complicated Buergers
disease: early trials. Int Surg 1993;78:54-58.
23. Shionoya S., Ban I., Nakata Y., Matsubaara J., Hirai M., Miyazaki H., Kawai S. Vascular reconstruction
in Buergers disease. Br. J. Surg. 1976; 63:841.
24. Reddy H.T.V., Jacob T.P., Ramamoorthy K. South Indian arteritis and its management with selective
arterialization of vein. Ind. J. Surg. 1980;42:266.
25. Sasajima T, Kubo Y, Inaba M, Goh K, Azuma N. Role of ingrainguinal bypass in Buergers disease:
an eighteen year experience. J Vasc Endovasc Surg 1997;13:186-192.
26. Nakata Y., Suzuki S., Kawai S., Hirai M., Shinjo K., Matsubara J., Ban I., Shionoya S. effects of lumbar
sympathectomy on thromboangitis obliterans. J. Cardiovasc. Surg. 16:1975:415.
27. Murie JA. Arterial disorders. In:Bailey & Loves short practice of surgery. Russell RCG, Williams NS,
rd

Bulstrode CJK (eds).23 ed. London. Arnold. 2000, pp 200-234.


28. Casten DF, Alday ES. Omental transfer for revascularisation of extremities. Surg Gynaecol Obstet
1971;132:301-304.
29. Hoshino S., Hamada O., Iwaya F., Takahira H.,Honda K. Omental transplantation for chronic
occlusive arterial diseases. Int. Surg. 1979;64:21-29
30. Singh I, Ramteke VK. The role of omental tranfer in buergers disease; New Delhis experience. Aust
N Z J Surg. 1996;66:372-376.
31. Talwar S, Jain S,Porwal R, Ladha BL, Prasad P. Free versus pedicled omental grafts for limb salvage
in Buergers disease. Aust N Z J Surg 1998;68:38-40.

Index

172

Critical Limb Ischemia


Arun Gupta
Peripheral arterial disease (PAD)
The prevalence of PAD based on objective testing has been evaluated in several epidemiologic
studies and is in the range of 3% to 10%, increasing to 15% to 20% in persons over 70 years of
age [1]. The most widely used test is the measurement of the ankle-brachial systolic pressure
index (ABI). A resting ABI of 0.90 is caused by hemodynamically significant arterial stenosis and
is most often used as a definition of PAD. In symptomatic individuals, an ABI 0.90 is
approximately 95% sensitive in detecting arteriogram-positive PAD and almost 100% specific in
identifying healthy individuals. Using this criterion, several studies have looked at symptomatic and
asymptomatic PAD patients in the same population. The ratio of the two is independent of age and
is usually in the range of 1:3 to 1:4. [2]

SYMPTOMATIC PERIPHERAL ARTERIAL DISEASE


Intermittent claudication
Intermittent claudication (IC) is defined as a muscle discomfort in the lower limb produced by
exercise and relieved by rest within 10 minutes. Patients may describe muscle fatigue, aching or
cramping on exertion that is relieved by rest. The symptoms are most commonly localized to the
calf, but may also affect the thigh or buttocks. The prevalence of IC would appear to increase from
about 3% in patients aged 40 to 6% in patients aged 60 years. In the relatively younger age
groups, claudication is more common in men but at older ages there is little difference between
men and women. Only about a quarter of patients with IC will ever significantly deteriorate. This
symptomatic stabilization may be due to the development of collaterals, metabolic adaptation of
ischemic muscle, or the patient altering his or her gait. The remaining 25% of patients with IC
deteriorate in terms of clinical stage; this is most frequent during the first year after diagnosis (7%
9%) compared with 2% to 3% per year thereafter. Major amputation is a relatively rare outcome of
claudication, with only 1% to 3.3% of patients with IC needing major amputation over a 5-year
period [3]

Measuring the pressure in the ankle arteries has become a standard part of the initial evaluation of
patients with suspected PAD. A common method of measurement uses a 1012 cm
sphygmomanometer cuff placed just above the ankle and a Doppler instrument used to measure
the systolic pressure of the posterior tibial and dorsalis pedis arteries of each leg.

Patients with claudication who have an isolated iliac stenosis may have no pressure decrease
across the stenosis at rest and, therefore, a normal ABI at rest. However, with exercise the
increase inflow velocity will make such lesions hemodynamically significant. Under these
conditions, exercise will induce a decrease in the ABI that can be detected in the immediate
recovery period and thus establish the diagnosis of PAD. The procedure requires an initial
173

measurement of the ABI at rest. The patient is then asked to walk until claudication pain occurs
following which the ankle pressure is again measured. A decrease in ABI of 15%20% would be
diagnostic of PAD. If a treadmill is not available then exercise may be performed by climbing stairs.

Treatment of Intermittent Claudication


The treatment goals are to relieve symptoms and improve exercise performance. The initial
treatment is focused on structured exercise and drug therapy. Failure to respond to exercise and
drug therapy requires considering limb revascularization.
Exercise
The exercise sessions that are held three times a week, beginning with 30 minutes of training
but then increasing to approximately 1 hour per session. During the exercise session,
treadmill exercise is performed at a speed and grade that will induce claudication within 3
5 minutes. The patient should stop walking when claudication pain is considered moderate.
The patient then rests until claudication has abated, after which the patient should resume
walking until moderate claudication discomfort recurs. This cycle of exercise and rest should
be at least for 35 minutes at the start of the program and increase to 50 minutes as the patient
becomes comfortable with the exercise sessions. In subsequent visits, the speed or grade of
the treadmill is increased if the patient is able to walk for 10 minutes or longer at the lower
workload without reaching moderate claudication pain.
Drug Therapy

Cilostazol is a phosphodiesterase III inhibitor with vasodilator, metabolic and antiplatelet


activity.A meta-analysis of six randomized, controlled trials involving 1751 patients[4]
demonstrated that the net benefit of cilostazol over placebo in the primary endpoint of
peak treadmill performance ranged from 5070 meters depending on the type of treadmill
test performed.

Naftidrofuryl is a 5-hydroxytryptamine type 2 antagonist and may improve muscle


metabolism, and reduce erythrocyte and platelet aggregation. In a meta-analysis of five
studies involving a total of 888 patients with intermittent claudication, naftidrofuryl
increased pain-free walking distance by 26% compared with placebo[5]

Critical limb ischemia (CLI)


The term critical limb ischemia is used for all patients with chronic ischemic rest pain, ulcers or
gangrene attributable to objectively proven arterial occlusive disease. The term CLI should only be
used in the presence of symptoms for more than 2 weeks.

Ischemic rest pain most commonly occurs below an ankle pressure of 50 mmHg or a toe pressure
less than 30 mmHg. Other causes of pain at rest should also be considered in a patient with an
ankle pressure above 50 mmHg [6]. Some ulcers are entirely ischemic in etiology; others may
have other causes like traumatic, venous, or neuropathic causes. In these ulcers healing may not
occur because of the severity of the underlying PAD. Healing requires an inflammatory response
174

and additional perfusion above that required for supporting intact skin and underlying tissues. The
ankle and toe pressure levels needed for healing are, therefore, higher than the pressures found in
ischemic rest pain. For patients with ulcers or gangrene, the presence of CLI is suggested by an
ankle pressure less than 70 mmHg or a toe systolic pressure less than 50 mmHg.

It is important to diagnose CLI because it confers a prognosis of high risk for limb loss and for fatal
and non-fatal vascular events, myocardial infarction and stroke. In general, the prognosis is much
worse than that of patients with intermittent claudication. Observational studies of patients with CLI
who are not candidates for revascularization suggest that a year after the onset of CLI, only about
half the patients will be alive without a major amputation, although some of these may still have
rest pain, gangrene or ulcers. Approximately 25% will have died and 25% will have required a
major amputation.The diagnosis of CLI thus predicts a poor prognosis for life and limb.

The incidence of CLI in most developed countries is stated to be 50-100 per 100 000 every year
[7]. CLI is dominated by pedal pain. In most cases, the pedal pain is intolerably severe; it may
respond to foot dependency, but otherwise responds only to opiates. The pain is caused by
ischemia, areas of tissue loss, ischemic neuropathy or a combination of these; it occurs or
worsens with reduction of perfusion pressure. In most cases, walking capacity is very severely
impaired, with walking often becoming almost impossible. Ischemic rest pain most typically occurs
at night when the limb is no longer in a dependent position but in severe cases can be continuous.
The pain is localized in the distal part of the foot or in the vicinity of an ischemic ulcer or
gangrenous toe. The pain often wakes the patients at night. Partial relief may be obtained by the
dependent position, whereas elevation and cold increase the severity of the pain. Often, patients
sleep with their ischemic leg dangling over the side of the bed, or sitting in an armchair; as a
consequence ankle and foot edema develop. In severe cases, sleep becomes impossible.

Patients with CLI may also present with ischemic ulcers or gangrene. Gangrene usually affects the
digits or, in a bedridden patient, the heel. In severe cases, gangrene may involve the distal parts of
the forefoot. It is usually initiated by a minor local trauma or local pressure like ill fitting shoes.
Gangrenous tissue, if not infected, can form an eschar, shrink and eventually mummify.
Spontaneous amputation may follow.

Treatment of Critical Limb Ischemia


Prevention
Early detection of PAD and aggressive management of cardiovascular risk factors should reduce
the incidence and severity of CLI. Cessation of smoking is associated with a decreased risk of
progression from earlier stages of PAD to CLI. Improper or poorly fitting shoes are a major
contributor to foot ulcerations, especially for people with diabetes. Patients should be educated on
the importance of self-care of the feet, including proper footwear selection.

175

Basic treatment: pain control


The primary goals of the treatment of CLI are to relieve ischemic pain, heal ischemic ulcers,
prevent limb loss, improve quality of life and prolong survival. A primary outcome would be
amputation-free survival. In order to achieve these outcomes, most patients will need a
revascularization procedure. Other components of treatment of patients with CLI are medical
interventions to control pain and infection in the ischemic leg, prevention of progression of the
systemic atherosclerosis and optimization of cardiac and respiratory function. For some CLI
patients with severe co-morbidities or a very limited chance of successful revascularization, a
primary amputation may be the most appropriate treatment.

Pain management is essential in improving function and quality of life. The hallmark of CLI is
ischemic rest pain and painful ulceration. Ideally, relief of pain is achieved by reperfusion of the
extremity. However, while planning the revascularization, adequate pain control must be a goal
of management in all patients. Initial attempts at pain relief should include the use of
paracetamol or nonsteroidal anti-inflammatory medications. Control of pain is usually more
effective if analgesia is given regularly rather than on demand. Placing the affected limb in the
dependent position provides partial relief of ischemic pain in some patients. Therefore, tilting
the bed downward may be a helpful measure in addition to analgesia. Patients with CLI are
often depressed and pain control can be improved by use of antidepressant medications.

Management of ulcers
The management of the patient with CLI and foot ulcers need a multidisciplinary approach.
These patients should be treated according to the following principles.

Local ulcer care and pressure relief


Prior to a revascularization procedure the ulcer can be treated with a non-adherent gauze
and the pressure should be taken away from the site (off-loading). Off-loading can be
achieved by several methods including shoe modifications, orthotics and casting techniques
[8].

Treatment of infection
Local infection tends to run a more severe course and should be treated urgently. Severe
foot infections in diabetic patients are usually polymicrobial with gram positive cocci, gram
negative rods and anaerobic organisms [9]. Once the clinical diagnosis of an infection is
made and cultures of the wound obtained, empiric antibiotic treatment should be initiated
immediately. Broad spectrum antibiotic therapy can be adjusted once the causative microorganisms are determined and results of the culture sensitivity have been obtained. A
growing concern is the rise in the incidence of multidrug-resistant Staphylococcus aureus,
which is up to 30% in some studies. Management of a deep infection usually also includes
drainage and debridement of necrotic tissue.
176

Salvage procedures
Limb salvage after revascularization is defined as preservation of some or all of the foot. An
attempt at a foot salvage should take place after a revascularization procedure has been
performed. A waiting period of at least 3 days has been suggested, this allows for sufficient
time for the restoration of perfusion and for demarcation to occur.

The level of adequate circulation, extent of infection, if any and remaining function of the foot
are factors considered when choosing the level of a foot salvage procedure. Foot salvage
procedures can be divided into two categories. The first category involves amputation of some
part of the foot. The second category of foot salvage involves the debridement of the wounds,
including excision of bone.

Amputation
The incidence of major amputations from large population or nation-wide data varies from 120
to 500/million/year. The ratio of below-knee to above-knee amputations in large surveys is
around 1:1. Only about 60% of below-knee amputations heal by primary intention, 15% heal
after secondary procedures and 15% need to be converted to an above-knee level. About 10%
of the patients die in the peri-operative period [10]

Major amputation in CLI is necessary and indicated when there is overwhelming infection that
threatens the patient's life, when rest pain cannot be controlled, or when extensive necrosis has
destroyed the foot. Primary amputation is defined as amputation of the ischemic lower extremity
without an attempt at revascularization. Revascularization of the lower extremity remains the
treatment of choice for most patients with significant arterial occlusive disease. Secondary
amputation is indicated when the limb continues to deteriorate despite the presence of a patent
reconstruction. Persistent infection despite aggressive vascular reconstruction is the second
most common diagnosis.

Many amputations can be prevented and limbs preserved through a multi-armed, limb-salvage
treatment of ischemic necrosis with antibiotics, revascularization and staged wound closure that
may necessitate the use of microvascular muscle flaps to cover major tissue defects. On the
other hand, amputation may offer an expedient return to a useful quality of life, especially if a
prolonged course of treatment is anticipated with little likelihood of healing.

Drugs
When open or endovascular intervention is not technically possible or has failed,
pharmacological treatment is an option
Prostanoids. Prostanoids prevent platelet and leukocyte activation and protect the vascular
endothelium. These drugs are administered parenterally over several weeks. Side effects
include flushing, headache, and hypotension of a transient nature. Patients on active
177

treatment had a greater chance (55% vs. 35%) to survive and keep both legs during the
follow-up period.[11]. In a recent trial of lipo-ecraprost versus placebo,however, prostanoid
failed to reduce death and amputation during 6 months follow-up[12]
Vasodilators. Direct-acting vasodilators are of no value, as they will primarily increase blood
flow to non-ischemic areas.
Antiplatelet drugs. There is no evidence that these drugs improve outcomes in CLI. However,
as in all patients with PAD, antiplatelet drugs do reduce the risk of systemic vascular events.
Vasoactive drugs. A Cochrane review evaluated eight trials on intravenous naftidrofuryl for
CLI. The drug was not effective in reducing the symptoms of CLI[13]. Pentoxifylline was
evaluated in two placebo controlled studies in patients with CLI, with inconclusive
results[14,15].

Reascularization
Two treatments are currently available; bypass surgery and balloon angioplasty. Those who
favour surgery emphasise good long-term anatomical patency. Proponents of balloon
angioplasty point to the advantage of low procedural morbidity and mortality, reduced costs, the
speed with which the procedure can be undertaken and shortened hospital stay. The BASIL
(bypass versus angioplasty in severe ischemia of the leg) trial which was undertaken to
compare the outcomes of a surgery-first strategy with an angioplasty-first strategy, published
their results in 2005[16]. At the end of the trial 55% of patients were alive without amputation of
the trial leg, 8% were alive with amputation, 8% were dead after amputation and 29% died
without amputation. The two strategies did not differ significantly in amputation-free survival.
REFERENCES
1.

Criqui MH, Fronek A, Barrett-Connor E, Klauber MR, Gabriel S and Goodman D, The prevalence
of peripheral arterial disease in a defined population, Circulation 1985;71: 510551.

2.

Hiatt WR, Hoag S and Hamman RF, Effect of diagnostic criteria on the prevalence of peripheral
arterial disease. The San Luis Valley Diabetes Study, Circulation 1995;91:14721479.

3.

McDermott MM, Criqui MH, Greenland P, Guralnik JM, Liu K and Pearce WH et al., Leg strength
in peripheral arterial disease: associations with disease severity and lower-extremity
performance, J Vasc Surg 2004;39: 523530.

4.

Regensteiner J, Ware JJ, McCarthy W, Zhang P, Forbes W and Heckman J et al., Effect of
cilostazol on treadmill walking, community-based walking ability, and health-related quality of
life in patients with intermittent claudication due to peripheral arterial disease: meta-analysis of
six randomized controlled trials, J Am Geriatr Soc 2002;50:19391946.

5.

Comte LS, Gamand S and Brown TM, Naftidrofuryl in intermittent claudication: a retrospective
analysis, J Cardiovasc Pharmacol 1994;23 :S48S52.

6.

European Working Group on Critical Limb Ischemia. Chronic Leg Ischemia. Circulation
1991;84:1-26.

7.

TASC.Management

of

peripheral

arterial

disease

(PAD).

TransAtlantic

Inter-Society

Consensus(TASC):chronic critical limb ischemia. Eur J Vasc Endovasc Surg 2000;19:S114-243.

178

8.

Nabuurs-Franssen MH, Sleegers R, Huijberts MS, Wijnen W, Sanders AP and Walenkamp G et al.,
Total contact casting of the diabetic foot in daily practice: a prospective follow-up study,
Diabetes Care 2005;28 : 243247.

9.

Frykberg R, An evidence based approach to diabetic foot infections, Am J Surg 2003;186: S44
S54.

10. Tunis SR, Bass EB and Steinberg EP, The use of angioplasty, bypass surgery, and amputation in

the management of peripheral vascular disease, N Engl J Med 1991;325 :556562.


11. UK Severe Limb Ischemia Study Group, Treatment of limb threatening ischemia with intravenous

Iloprost: A randomised double-blind placebo controlled study, Eur J Vasc Surg 1991;5 : 511516.
12. Brass EP, Anthony R, Dormandy J, Hiatt WR, Jiao J and Nakanishi A et al., Parenteral therapy

with lipo-ecraprost, a lipid-based formulation of a PGE1 analog, does not alter six-month
outcomes in patients with critical leg ischemia, J Vasc Surg 2006;43 : 752759.
13. Smith FB, Bradbury AW and Fowkes FG, Intravenous naftidrofuryl for critical limb ischaemia,

Cochrane Database Syst Rev (2000) (2):), p. CD002070.


14. European Study Group, Intravenous pentoxifyllin, Eur J Vasc Endovasc Surg 1995;9 :426436.
15. Norwegian Pentoxifyllin Multicenter Trial Group, Efficacy and clinical tolerance of parenteral

pentoxifyllin, Int Angiol 1996;15 : 7580.


16. Bypass versus angioplasty in severe ischaemia of the leg(BASIL): multicentre, randomised

controlled trial. Lancet 2005;366:1925-34.

Index

179

Lower Limb Amputations and Rehabilitation


Sumit Sural
Incidence
Lower limb amputations are the most common (76% to 80%) of all amputations. Dysvascular
limbs, resulting from either diabetes mellitus or primary peripheral vascular disease, account for
82% of amputations; 97% of dysvascular amputations are in the lower extremities.
Despite advances in revascularization techniques, rates of lower extremity amputations remain
unchanged.

Mortality and Morbidity


The 5-year mortality after amputation of a dysvascular lower limb ranges from 40% to 60%, with
primary vascular disease having a higher morbidity and mortality rate than diabetes mellitus.

Amputation of the contralateral limb is required within 5 years in 30% to 50% of patients who have
amputations of dysvascular lower limbs. Twenty percent of below-knee amputations are converted
to above-knee amputations.

Age of amputation :

Transfemoral amputations occur at a rate of 0.5 per 1000 in diabetic patients younger than 65
years old compared with 4 per 1000 in diabetic patients 75 years old or older.

Morbidity is more frequent after transfemoral amputations than after transtibial amputations,
and patients with transfemoral amputations are much less likely to use a prosthesis
successfully and consistently than are patients with more distal amputations. Younger patients
with traumatic amputations or amputations required for tumor treatment are more successful
with prosthetic use than are patients with amputations of dysvascular limbs.

Level of Amputation:
The level of amputation is always a difficult decision and has a major impact on the patient's
quality of life. There is a good chance of the survival of a below-knee stump if the circulation in the
skin of the proposed flaps appears adequate clinically, and if the blood supply to the muscles is
obviously good at amputation.

If the popliteal pulse is present before operation, below-knee amputation should succeed. The
absence of a popliteal pulse, however, does not exclude below-knee amputation.

There always is a difficult balance between functional considerations (e.g., poor prosthetic use
after transfemoral amputations of dysvascular limbs) and healing consequences (e.g., choosing a
procedure that would not require revision or repeat surgery because of poor healing). Energy
expenditure considerations also are important, particularly with the progressive aging of the lower
180

extremity amputee population. The increased energy consumption of bipedal locomotion for
transtibial amputees ranges from 40% to 50% compared with 90% to 100% in transfemoral
amputees. Many patients seem willing to undergo more than one surgery if it results in their
retaining more limb length, despite potentially higher morbidity. Occasionally, patients with chronic
intractable ankle or foot pain request transtibial amputation.

Selecting the Level of Amputation


Since peripheral vascular disease, with or without diabetes, is the major cause of lower limb
amputations, it is necessary to determine accurately the lowest level at which an amputation would
heal. Previously, this has been assessed best by clinical judgment of tissue vascularity at the time
of surgery. Now, clinical judgment can be augmented by a variety of preoperative testing methods,
the best of which is the transcutaneous measurement of oxygen tension. This technique is
accurate, widely available, easily performed at the bedside, and cost-efficient. The value of this
test can be enhanced by comparing the oxygen tension obtained with and without having the
patient inhale oxygen. An increase in tension after oxygen inhalation is a sign of good local tissue
perfusion. Nutritional status (albumin level of >3 g/dL, lymphocyte count of >1500/mL) also has
been shown to be a predictor for wound healing in amputations. Arteriography is a useful tool for
planning revascularization, but it is not helpful in planning amputation levels. Thermography, for
the determination of the level of amputation for an ischaemic lower limb, tended to overestimate
the degree of ischaemia and to indicate a higher level of amputation than was necessary. with a
new technique: segmental photoplethysmographic skin perfusion pressures, the value of this
noninvasive method will be to enable the surgeon to amputate at a lower level and to diminish
complications and failure of rehabilitation.
No preoperative test is capable of providing an absolute indication of wound healing, however.
Such tests should be correlated with clinical and surgical observations.

Technical considerations :
Meticulous attention to detail and gentle handling of soft tissues are important for creating a wellhealed and highly functional amputation stump. The tissues often are poorly vascularized or
traumatized, and the risk for complications is high.

Skin and Muscle Flaps:


Flaps should be kept thick. Unnecessary dissection should be avoided to prevent further
devascularization of already compromised tissues. Covering the end of the stump with a
sturdy soft-tissue envelope is crucial. Past studies have determined the best type of flaps for
each level of amputation, but atypical flaps are always preferable to amputation at a more
proximal level. With modern total-contact prosthetic sockets, the location of the scar rarely is
important, but the scar should not be adherent to the underlying bone. An adherent scar
makes prosthetic fitting extremely difficult, and this type of scar often breaks down after

181

prolonged prosthetic use. Redundant soft tissues or large dog ears also create problems in
prosthetic fitting and may prevent maximal function of an otherwise well-constructed stump.
Muscles usually are divided at least 5 cm distal to the intended bone resection. They may be
stabilized by myodesis (suturing muscle or tendon to bone) or by myoplasty (suturing muscle
to periosteum or to fascia of opposing musculature). Jaegers et al. showed that transected
muscles atrophy 40% to 60% in 2 years if they are not securely fixed. If possible, myodesis
should be performed to provide a stronger insertion, help maximize strength, and minimize
atrophy. Myodesed muscles continue to counterbalance their antagonists, preventing
contractures and maximizing residual limb function. Myodesis may be contraindicated,
however, in severe ischemia because of the increased risk of wound breakdown.

Tourniquet and Hemostasis: Except in severely ischemic limbs, the use of a tourniquet is highly
desirable and makes the amputation easier. The limb may be exsanguinated by wrapping it
with an Esmarch bandage before the tourniquet is inflated. In amputations for infections or
malignancy, however, expressing blood from the limbs in this manner is inadvisable. In such
instances, inflation of the tourniquet should be preceded by elevation of the limb for 5 minutes.
Major blood vessels should be isolated and individually ligated. Larger vessels should be
doubly ligated. The tourniquet should be deflated before closure, and meticulous hemostasis
should be obtained. A drain should be used in most cases for 48 to 72 hours.

Nerves: A neuroma always forms after a nerve has been divided. A neuroma becomes painful if it
forms in a position where it would be subjected to repeated trauma. Special techniques have
been tried in the hopes of preventing the formation of painful neuromas. These include endloop anastomosis, perineural closure, Silastic capping, sealing the epineurial tube with butylcyanoacrylate, ligation, cauterization, and methods to bury the nerve ends in bone or muscle.
Most surgeons currently agree that nerves should be isolated, gently pulled distally into the
wound, and divided cleanly with a sharp knife so that the cut end retracts well proximal to the
level of bone resection. Strong tension on the nerve should be avoided during this maneuver;
otherwise, the amputation stump may be painful even after the wound has healed. Crushing
also should be avoided. Large nerves, such as the sciatic nerve, often contain relatively large
arteries and should be ligated.

Bone: Excessive periosteal stripping is contraindicated and may result in the formation of ring
sequestra or bony overgrowth. Bony prominences that would not be well padded by soft tissue
always should be resected, and the remaining bone should be rasped to form a smooth
contour. This is especially important in locations such as the anterior aspect of the tibia and
lateral aspect of the femur.

182

TRANSFEMORAL (ABOVE-KNEE) AMPUTATIONS


Amputation levels above the knee can be classified as short transfemoral, medial transfemoral, long
transfemoral, and supracondylar. Amputation through the thigh is second in frequency only to
transtibial amputation. In this procedure, the patient's knee joint is lost, so it is extremely important for
the stump to be as long as possible to provide a strong lever arm for control of the prosthesis. The
conventional, constant friction knee joint used in most above-knee prostheses extends 9 to 10 cm
distal to the end of the prosthetic socket, and the bone must be amputated this far proximal to the
knee to allow room for the joint. When the level of amputation is more distal than this, the knee joint of
the prosthesis is more distal than the knee of the opposite limb, which is cosmetically undesirable and
is especially noticeable when the patient is seated. Amputation stumps in which the level of bone
section is less than 5 cm distal to the lesser trochanter function as and are prosthetically fitted as hip
disarticulations.

In nonischemic limbs, muscle stabilization by myodesis or myoplasty is important when constructing


a strong and sturdy amputation stump. Gottschalk pointed out that in the absence of myodesis of
the adductor magnus, most transfemoral amputations result in at least 70% loss of adduction
power. Most amputations, even at the transfemoral level, are done because of ischemic
problems, and myodesis should not be attempted because a limited vascular supply may be
compromised further. Myoplastic muscle stabilization is desirable in the ischemic limb,
however, to decrease the anterolateral drift of the transected bone end that often occurs.

Post op and Rehabilitation :


Drains usually are removed at 48 hours. The patient is instructed on how to position the stump
properly while in bed, while sitting, and while standing. The stump is elevated by raising the foot of
the bed, which helps manage edema and postoperative pain. The patient is cautioned against
leaving the stump in a dependent position. With transfemoral amputations, the patient is cautioned
against placing a pillow between the thighs or beneath the stump or otherwise keeping the stump
flexed or abducted. These precautions are necessary to help prevent flexion or abduction
contractures.

A major obstacle to rehabilitation after transfemoral amputation is the loss of the knee joint, which
exponentially increases the energy expenditure for locomotion with a prosthesis. This has
consequences for cardiac patients and patients with ischemic contralateral limbs. The patient and
family must be aware of the risks involved with a physically demanding rehabilitation program.
Many transfemoral amputees with vascular disease never use a prothesis consistently. Patients
with bilateral transfemoral amputations frequently elect to use a wheelchair because it is faster,
and oxygen consumption is four to seven times more using bilateral transfemoral prostheses.

183

DISARTICULATION OF THE KNEE


Disarticulation of the knee results in an excellent end-bearing stump. Newer socket designs and
prosthetic knee mechanisms that provide swing phase control have eliminated many of the former
complaints concerning this level of amputation. Although the benefit of its use in children and young
adults has been proved, its use in the elderly and especially in patients with ischemia has been
limited. This is true mainly because the long flaps required instead could allow a more functional,
short transtibial amputation in most instances. These long flaps are subject to necrosis in ischemic
limbs.
The modified Mazet technique of through knee amputation procedure creates shorter flaps to close
the wound and greatly facilitates prosthesis fitting.

The advantages of knee disarticulation are : (1) The large end-bearing surfaces of the distal femur
covered by skin and other soft tissues that are naturally suited for weight bearing are preserved, (2) a
long lever arm controlled by strong muscles is created, and (3) the prosthesis used on the stump is
stable. Knee disarticulation is ideal for nonambulating patients who require amputation because
additional length of the extremity provides adequate sitting support and balance. Knee flexion
contractures and associated distal ulcers common with transtibial amputations also are avoided

TRANSTIBIAL (BELOW-KNEE) AMPUTATIONS


Following the reports of Burgess and others who have performed transtibial amputations successfully
in more than 85% of their patients with peripheral vascular disease, this procedure has become the
most common amputation. The importance of preserving the patient's own knee joint in the successful
rehabilitation of a patient with a lower extremity amputation cannot be overemphasized. Although
many variations in technique exist, basically all procedures may be divided into those for nonischemic
limbs and those for ischemic limbs. These two general techniques vary primarily in the construction of
skin flaps and in muscle stabilization techniques.

In nonischemic limbs, skin flaps of various design and muscle stabilization techniques, such as
tension myodesis and myoplasty, are frequently used. In tension myodesis, transected muscle groups
are sutured to bone under physiological tension; in myoplasty, muscle is sutured to soft tissue, such
as opposing muscle groups or fascia. In most instances, myoplastic closures are performed, but some
authors have advocated the use of the firmer stabilization provided by myodesis in young, active
individuals. In ischemic limbs, tension myodesis is contraindicated because it may compromise further
an already marginal blood supply. Also, a long posterior myocutaneous flap and a short or even
absent anterior flap are recommended for ischemic limbs because anteriorly the blood supply is less
abundant than elsewhere in the leg.

Transtibial amputations can be divided into three levels. The appropriate level must be determined for
each individual patient
184

Nonischemic Limbs: Rehabilitation after transtibial amputations in nonischemic limbs generally is


quite successful, partly because of a younger, healthier population with fewer comorbidities. The
optimal level of amputation in this population traditionally has been chosen to provide a stump
length that allows a controlling lever arm for the prosthesis with sufficient circulation for healing
and soft tissue for protective end weight bearing. The amputation level also is governed by the
cause (e.g., clean end margins for tumor, level of trauma, and congenital abnormalities). A longer
residual limb would have a more normal gait appearance, but stumps extending to the distal third
of the leg have been considered suboptimal because there is less soft tissue available for weight
bearing and less room to accommodate some energy storage systems. The distal third of the leg
also has been considered relatively avascular and slower to heal than more proximal levels.
Contemporary liners and ankle-foot storage systems now allow more options for accommodating a
longer residual limb, but the long-term risk of skin breakdown in older patients with these newer
prosthetic components is unknown. The experience and success of our staff with these transtibial
amputations dictate maintaining certain general guidelines until further research supports a change
in recommendations.

In adults, the ideal bone length for a below-knee amputation stump is 12.5 to 17.5 cm, depending
on body height. A reasonably satisfactory rule of thumb for selecting the level of bone section is to
allow 2.5 cm of bone length for each 30 cm of body height. Usually the most satisfactory level is
about 15 cm distal to the medial tibial articular surface. A stump less than 12.5 cm long is less
efficient. Stumps lacking quadriceps function are not useful. In a short stump of 8.8 cm or less, it
has been recommended that the entire fibula together with some of the muscle bulk be removed
so that the stump may fit more easily into the prosthetic socket. Many prosthetists find, however,
that retention of the fibular head is desirable because the modern total-contact socket can obtain a
better purchase on the short stump. Transecting the hamstring tendons to allow a short stump to
fall deeper into the socket also may be considered. Although the procedure has the disadvantage
of weakening flexion of the knee, this has not been a serious problem, and genu recurvatum has
not been reported.In amputations in non-ischemic limbs equal anterior and posterior flaps are
usually created.

Aftertreatment: Rehabilitation after transtibial amputation in a nonischemic limb is fairly


aggressive, unless the patient is immunocompromised, there are skin graft issues, or there are
concomitant injuries or medical conditions that preclude early initiation of physical therapy. An
immediate postoperative rigid dressing helps control edema, limits knee flexion contracture,
and protects the limb from external trauma. A prosthetist can be helpful with such casting and
can apply a jig that allows attachment and alignment for early pylon use. Weight bearing is
limited initially, with bilateral upper extremity support from parallel bars, a walker, or crutches.

185

The cast can be changed every 5 to 7 days for skin care. Within 3 to 4 weeks, the rigid dressing
can be changed to a removable temporary prosthesis if there are no skin complications. The
patient is shown the proper use of elastic wrapping or a stump shrinker to control edema and
help contour the residual limb when not wearing the prosthesis. The physiatrist and therapist
can assist in monitoring progress through the various transitions of temporary prosthetics to the
permanent design, which may take several months. In recent years, endoskeletal designs have
been more frequently used because modifications are simpler. Formal inpatient rehabilitation is
brief, with most prosthetic training done on an outpatient basis. A program geared toward
returning the patient to his or her previous occupation, hobbies, and educational pursuits can
be structured with the help of a social worker, occupational therapist, and vocational counselor.

Ischemic Limbs: The frequent comorbidities in patients with ischemic limbs demand precautionary
measures and interaction with a vascular surgical team. Because the skin's blood supply is much
better on the posterior and medial aspects of the leg than on the anterior or anterolateral sides,
transtibial amputation techniques for the ischemic limb are characterized by skin flaps that favor
the posterior and medial side of the leg. The long posterior flap technique popularized by Burgess
is most commonly used, but medial and lateral flaps of equal length as described by Persson,
skew flaps, and long medial flaps are being used.
All techniques stress the need for preserving intact the vascular connections between skin and
muscle by avoiding dissection along tissue planes and by constructing myocutaneous flaps. Also,
amputations performed in ischemic limbs are customarily at a higher level (e.g., 10 to 12.5 cm
distal to the joint line) than are amputations in nonischemic limbs. Tension myodesis and
osteomyoplasty are contraindicated in patients with ischemic limbs because the procedures tend
to compromise an already precarious blood supply.

Aftertreatment and Rehabilitation: Rehabilitation in patients with ischemic limbs must proceed
cautiously because of potential skin healing compromise and accompanying medical
conditions. Initial postoperative efforts are centered on skin healing. After transtibial
amputation, a soft dressing can be applied, but a rigid dressing is preferred and can be used
regardless of whether early ambulation is prescribed. If immediate or prompt prosthetic
ambulation is not to be pursued, the stump can be dressed in a simple, well-padded cast that
extends proximally to midthigh and is applied in such a manner as to avoid proximal
constriction of the limb. Good suspension of the cast is essential to prevent it from slipping
distally and impairing stump circulation. This may require compressive contouring of the cast in
the supracondylar area and a waist band, suspension strap, or both. The cast should be
removed in 5 to 7 days, and if wound healing is satisfactory, a new rigid dressing or prosthetic
cast is applied. If immediate or prompt prosthetic ambulation is pursued, a properly constructed
prosthetic cast is best applied by a qualified prosthetist.

186

Success of rehabilitation depends on multiple variables, including cognitive status, premorbid


functional level, condition of the upper extremities and contralateral lower limb, and coexisting
medical and neurological conditions. Patients with ischemic limbs generally are less healthy
than patients with nonischemic limbs; the rehabilitative program generally progresses much
more slowly and more cautiously. Early rehabilitation efforts may be geared toward
independence in a wheelchair, stump care education, skin care techniques to avoid decubitus
ulcers, care of the contralateral intact lower limb, and preprosthetic general conditioning. A soft
dressing is adequate initially for elderly dysvascular patients, whereas immediate postoperative
rigid dressings and earlier weight bearing with a locked knee pylon are appropriate in younger
patients. Immediate postoperative rigid dressings rarely are used in patients with ischemic
limbs because of their vulnerability for wound complications. If a more aggressive approach is
taken toward prosthetic training, more frequent rigid dressing changes are recommended and
possibly the use of clear sockets to allow monitoring of the skin.

Weight bearing on the residual limb usually is delayed until skin healing has progressed.
Patients seem more comfortable if weight bearing is delayed until sutures or staples are
removed. Subsequently, ambulation can be progressed with an unlocked knee and less upper
extremity support. For the definitive prosthesis, a variety of prosthetic knee units are available
that are lighter and accommodate constant or variable gait cadences and provide good stability
during weight bearing. Some patients may require further medical evaluation and clearance
(e.g., chemically induced cardiac stress test or echocardiogram or vascular studies of the
contralateral limb) to evaluate tolerance for prosthetic training. A pain management specialist
may be needed to help treat postoperative phantom limb pain. Many patients receive inpatient
rehabilitation training with subsequent therapy on an outpatient basis or in an extended care
facility or home health setting. Most can become successful prosthetic users.

Rigid Dressing
Since the mid-1970s, there has been a gradual shift from the use of conventional soft dressings
to the use of rigid dressings, especially in centers performing significant numbers of amputations.
The rigid dressing consists of a plaster of Paris cast that is applied to the stump at the conclusion
of surgery. Early weight bearing is not an essential part of the postoperative management
program. If weight bearing ambulation is not planned in the immediate postoperative period, the
rigid dressing may be applied by the surgeon, observing standard cast application precautions,
including appropriate padding of all bony prominences, avoiding proximal constriction of the limb,
and use of dependable cast suspension methods. If weight bearing ambulation in the immediate
postoperative period is anticipated, a true prosthetic cast should be applied, preferably by a
certified prosthetist, with appropriate use of stump socks, contoured felt padding over all bony
prominences, and special suspension techniques. A metal pylon with a prosthetic foot is attached
to the cast and properly aligned for ambulation. Specific details of such prosthetic cast applications
for the major levels of amputation are provided after each discussion of surgical technique. Rigid
187

stump dressings may be employed successfully and beneficially at essentially all levels of
amputation and are applicable to all age groups.

Rigid dressings offer several advantages over soft dressings. Rigid dressings prevent edema at
the surgical site, protect the wound from bed trauma, enhance wound healing and early maturation
of the stump, and decrease postoperative pain, allowing earlier mobilization from bed to chair and
ambulation with support. For transtibial amputations, rigid dressings prevent the formation of knee
flexion contractures. The physiological benefits of upright posture to the respiratory,
cardiovascular, urinary, and gastrointestinal systems are easily recognizable, but the psychological
benefits sometimes are more subtle. In most instances, the hospital stay can be decreased and
the cost of care reduced accordingly. Finally, earlier definitive prosthetic fitting is possible, and a
higher percentage of patients are successfully rehabilitated.

Exercises for the stump are started under the supervision of a physical therapist the day after
surgery or as soon thereafter as tolerated. These should consist of muscle-setting exercises
followed by exercises to mobilize the joints. Patients should be mobilized from bed to chair on the
first postoperative day. Patients with lower extremity amputations should begin physical therapy
within the first several days to begin ambulating using the parallel bars. This is followed shortly by
ambulation with a walker or crutches when patients can control the limb and are comfortable
enough.

The optimal time to begin prosthetic ambulation with protected weight bearing depends on many
factors, including the age, strength, and agility of the patient, and the patient's ability to protect the
amputation stump from injury as a result of excessive weight bearing. The availability of a welltrained team of nurses, therapists, and prosthetists who can carry out a well-integrated prosthetic
treatment program consistently and the desire and willingness of the surgeon to supervise such a
treatment program meticulously are important factors.

The gradual application of functional mechanical stress in the appropriate distribution can enhance
wound healing; however, shearing forces can lead to wound breakdown. Early unprotected weight
bearing can result in sloughing of the skin or delayed wound healing. Any weight bearing before
the stump has healed should be strictly supervised. Advancement of weight bearing status should
be individualized. A young patient with a traumatic amputation above the zone of injury probably
could begin 25-lb partial weight bearing immediately postoperatively. A patient with a traumatic
amputation through the zone of injury or a patient with an amputation performed secondary to
ischemia probably should wait until early wound healing is documented before gradually beginning
partial weight bearing. Weight bearing status should be reevaluated with each subsequent cast
change. If the wound is progressing well, weight bearing can progress in 25-lb increments each
week. Supervision is especially important in patients with peripheral neuropathy who may have
difficulty judging how much weight they are placing on their stumps. Juvenile amputees also
188

require close supervision because they are usually quite comfortable in a temporary prosthesis
and often attempt to walk without support.

Regardless of when prosthetic ambulation is begun, the rigid dressing should be removed and the
wound inspected in 7 to 10 days. Cast loosening, fever, excessive drainage, or systemic
symptoms of wound infection are indications for earlier cast removal. If the wound is healing well, a
new rigid dressing is applied, and ambulation with or without a pylon and prosthetic foot is
continued. The cast should be changed weekly until the wound has healed. After the wound is well
healed, the rigid dressing may be removed for bathing and stump hygiene, and, if desired, an
elastic stump shrinker may be used at night in lieu of the rigid dressing. As stump shrinkage
occurs, continued gentle compression of the stump is maintained by applying an additional stump
sock before donning the plaster socket; this minimizes the need for repeated cast changes. Use of
the rigid dressing is continued until the volume appears unchanged from the previous week. At that
time, the prosthetist may apply the first prosthesis. One or more socket changes frequently are
required over the first 18 months, so many prosthetists prefer to make the initial prosthesis in a
modular fashion.

A lower extremity amputation can be devastating to a patient because it not only challenges his or her
ambulatory capability, but also threatens his or her future independence. The amputation must be
viewed as an opportunity to reestablish or enhance the patient's functional level and facilitate a return
to near-normal locomotion. The amputation should not be viewed as a failed limb salvage or
reconstruction. Meticulous surgical attention must be given to provide an optimal base of support
because the residual limb functions as a sensory-motor end organ with tolerance requirements at
the stump-prosthesis interface to meet the dynamic weight bearing challenges of ambulation.
Developments in the prosthetic field range from early-stage fitting techniques (computer-assisted
stump contour scanning) to the use of advanced prosthetic components (lighter materials, silicone gel
liners, innovative knee units, suspension device alternatives, and ankle-foot accommodative and
energy storage systems).

COMPLICATIONS
Hematoma: Meticulous hemostasis before closure, the use of a drain, and a rigid dressing should
minimize the frequency of hematoma formation. A hematoma can delay wound healing and
serve as a culture medium for bacterial infection. If a hematoma does form, it should be treated
with a compressive dressing. If the hematoma is associated with delayed wound healing with or
without infection, it should be evacuated in the operating room.

Infection: Infection is considerably more common in amputations for peripheral vascular disease,
especially in diabetic patients, than in amputations secondary to trauma or tumor. Any deep
wound infection should be treated with immediate dbridement and irrigation in the operating
room and open wound management. Antibiotics should be tailored according to the results of
189

intraoperative cultures. Delayed closure may be difficult because of edema and retraction of the
flaps. Smith and Burgess described a method whereby the central one third of the wound is
closed, and the remainder of the wound is packed open. This method allows for continued open
wound management, while maintaining adequate flaps for distal bone coverage.

Wound Necrosis: The first step in evaluating significant wound necrosis is to reevaluate the
preoperative selection of the amputation level. If transcutaneous oxygen studies were not
obtained preoperatively, they should be obtained at this point to evaluate wound healing
potential. A serum albumin level and a total lymphocyte count should be obtained. Many
authors have reported significantly more problems with wound healing in patients with serum
albumin levels less than 3.5 g/dL or total lymphocyte counts less than 1500 cells/mL. Nutritional
supplementation has been shown to promote wound healing in this setting. Patients who
smoke tobacco should quit immediately because smoking severely compromises cutaneous
blood flow, lowering tissue oxygen pressure. In a study by Lind et al., the risk of infection and
reamputation was 2.5 times higher in smokers than in nonsmokers.

Necrosis of the skin edges less than 1 cm can be treated conservatively with open wound
management. Some authors recommend continued rehabilitation with weight bearing using a
total-contact prosthesis. Some prefer discontinuing prosthetic use until the wound has healed.
There are several alternatives for management of more severe wound necrosis. The wound
can

be

treated

conservatively

with

local

dbridements

combined

with

nutritional

supplementation. In patients who are better rehabilitation candidates, some authors


recommend total-contact casting with continued progression of weight bearing. These authors
state that weight bearing in a properly fitted total-contact cast stimulates wound healing and
stump maturation. Some prefer to postpone prosthetic use until the wound has healed. Some
have made extensive use of vacuum-assisted closure in this setting.

In cases of severe necrosis with poor coverage of the bone end, wedge resection may be
indicated. As described by Hadden et al., the basic principle of wedge resection is to regard the
end of the amputation stump as a hemisphere. Although local resection increases local tension
on already compromised tissues, resection of a wedge incorporating the full diameter of the
stump would allow for reformation of the hemisphere, while minimizing local pressures. Finally,
hyperbaric oxygen therapy and transcutaneous electrical nerve stimulation have been shown in
some studies to promote wound healing

Contractures: Mild or moderate contractures of the joints of an amputation stump should be


prevented by proper positioning of the stump, gentle passive stretching, and having the patient
engage in exercises to strengthen the muscles controlling the joint. At the knee, increased
ambulation tends to reduce a contracture. In some patients, prosthetic modification may be

190

necessary to adapt to the contracture. Rarely, severe fixed contractures may require treatment
by wedging casts or by surgical release of the contracted structures.

Pain: After the immediate postoperative pain has been resolved, some patients continue to feel
chronic pain as a result of various causes. The first step in management is to diagnose the
cause accurately. Phantom limb pain must be differentiated from residual limb pain, and both
must be distinguished from pain arising from a distant site, such as from a herniated lumbar
disc.

Mechanical low back pain has been shown to be more prevalent in amputees than in the
general population. In a study by Smith et al. of 92 patients with amputations, back pain was
rated more bothersome than phantom limb pain or residual limb pain. In addition to other
accepted treatments for back pain, patients must be instructed on proper prosthetic ambulation
to minimize abnormal stresses on the lumbar spine.

Residual limb pain often is caused by a poorly fitting prosthesis. The stump should be
evaluated for areas of abnormal pressure, especially over bony prominences. Distal stump
edema, often called choking, may result if the end is not completely seated in the prosthesis,
and ulceration or gangrene could result. These problems can be avoided with socket
modifications.

A neuroma always forms after division of a nerve. A painful neuroma occurs when the nerve
end is subjected to pressure or repeated irritation. A painful neuroma usually can be prevented
by gentle traction on the nerve followed by sharp proximal division, allowing the nerve end to
retract deep into the soft tissue. A painful neuroma usually is easily palpable and often has a
positive Tinel sign. Treatment initially consists of socket modification. If this fails to relieve
symptoms, simple neuroma excision or a more proximal neurectomy may be required. Some
authors recommend neuroma excision combined with centrocentral anastomosis of the
proximal stump or a procedure to seal the epineurial sleeve. Rarely, it may be difficult to
distinguish a neuroma from a possible recurrent tumor. Provost et al. have provided some
helpful descriptions of the ultrasound features of a neuroma.

Other possible causes of residual limb pain may be unrelated to the amputation stump, eg
osteoarthritis of the hip or knee. Pain from osteoarthritis of the knee in a patient with a
transtibial amputation, although rare, may be partially relieved by adding a knee joint and thigh
corset to the prosthesis to allow load sharing with the thigh.

Phantom limb sensations are so common after an amputation that they should be considered
normal. Most patients do not find these to be bothersome. The most important part of
management is simply to educate the patient regarding these sensations so that they are not
191

surprised by their presence. Over the first year after amputation, many patients experience a
phenomenon referred to as telescoping, whereby the phantom limb gradually shortens to the
end of the residual limb.

Phantom limb pain is far less common. The exact incidence is difficult to determine because
many authors fail to differentiate between phantom limb pain and phantom limb sensations.
Other authors fail to distinguish between the mere presence of phantom limb pain versus the
presence of severe phantom limb pain, which has a significant effect on the patient.
Subsequently, some reports state that phantom limb pain is present in 80% of amputees. Most
authors would agree that truly bothersome phantom limb pain is much less common and is
probably present in less than 10% of amputees. Although no one specific method of treating
such pain is universally beneficial, some patients may benefit from such diverse measures as
massage, ice, heat, increased prosthetic use, relaxation training, biofeedback, sympathetic
blockade, local nerve blocks, epidural blocks, ultrasound, transcutaneous electrical nerve
stimulation, and placement of a dorsal column stimulator.

Dermatological Problems: Patients should be instructed to wash their stumps with a mild soap at
least once a day. The stump should be thoroughly rinsed and dried before donning the prosthesis.
Likewise, the prosthesis should be kept clean and should be thoroughly dried before donning.

Contact dermatitis is common and may be confused with infection. Skin inflammation is
associated with intense itching and burning when wearing the socket. The most common cause
is failure to rinse detergents from stump socks thoroughly. Other sensitizers include nickel,
chromates used in leathers, skin creams, antioxidants in rubber, topical antibiotics, and topical
anesthetics. Treatment consists of removal of the irritant, soaks, steroid cream, and
compression.

Bacterial folliculitis may occur in areas of hairy, oily skin. The problem may be exacerbated by
shaving and by poor hygiene. Treatment initially consists of improved hygiene and possibly
socket modifications to relieve areas of abnormal pressure. Occasionally, cellulitis develops
that requires antibiotic treatment, or an abscess forms that requires incision and drainage.

Epidermoid cysts may develop at the socket brim. These frequently occur late and are best
treated with socket modification. Excision may be required.

Verrucous hyperplasia refers to a wartlike overgrowth of the skin at the end of the stump. It is
caused by proximal constriction that prevents the stump from fully seating in the prosthesis.
This choking, as previously mentioned, causes distal stump edema followed by thickening of
the skin, fissuring, ulceration, and possibly subsequent infection. Treatment initially is directed
toward treating the infection. The skin should be treated with soaks and salicylic acid to soften
192

the keratin. Socket modification is mandatory because pressure on the distal skin is essential to
treat the problem and to prevent recurrences

HINDFOOT AND ANKLE AMPUTATIONS


Syme amputation: The Syme amputation consists of a bone section at the distal tibia and fibula 0.6
cm proximal to the periphery of the ankle joint and passing through the dome of the ankle centrally.
The tough, durable skin of the heel flap provides normal weight bearing skin. There is apparently
no middle ground for this amputation: when good, it is the most satisfactory functional level in the
lower extremity, but when bad, it is valueless, and the extremity must be amputated at a more
proximal level. The two most common causes of an unsatisfactory Syme stump are posterior
migration of the heel pad and skin slough resulting from overly vigorous trimming of dog ears.
Both can be prevented by attention to surgical technique.

The chief objection to this amputation is cosmetic. The prosthesis used must accommodate the
flair of the distal tibial metaphysis that is covered with heavy plantar skin and is large and bulky.
For this reason, the amputation usually is not recommended for women. The prosthesis used for a
classic Syme amputation consists of a molded plastic socket, with a removable medial window to
allow passage of the bulbous end of the stump through its narrow shank, and a solid-ankle,
cushioned-heel foot prosthesis

Syme amputation for ischemic limbs: In the past, most surgeons did not use the Syme
amputation for ischemic limbs because the failure rate of wound healing was unacceptably
high. More recently, preoperative determination of local tissue perfusion and oxygenation by
such techniques as Doppler ultrasound measurement of segmental blood pressures,
radioactive xenon clearance tests, and transcutaneous oxygen measurements has significantly
increased the success rate of the Syme amputation in these limbs. Wyss et al., Malone et al.,
and Wagner popularized a two-stage technique of the Syme amputation for use in diabetic
patients with an infected or gangrenous foot lesion and have achieved marked success with
this technique in properly selected patients. Several authors have reported, however, that both
stages can be safely combined when infection is not adjacent to the heel pad.

Boyd Amputation: The Boyd amputation also produces an excellent end-bearing stump around the
ankle and eliminates the problem of posterior migration of the heel pad that sometimes occurs
after a Syme amputation. It involves talectomy, forward shift of the calcaneus, and calcaneotibial
arthrodesis. The arthrodesis makes the procedure technically more difficult than the Syme
amputation and produces a more bulbous stump. A satisfactory prosthesis that is cosmetically
acceptable has been designed for use after this amputation.

193

Pirogoff Amputation: The Pirogoff amputation involves arthrodesis between the tibia and part of the
calcaneus; the calcaneus is sectioned vertically, its anterior part is removed, and its remaining
posterior part and the heel flap are rotated forward and upward 90 degrees until the raw surface of
the calcaneus meets the denuded distal end of the tibia. This amputation has no advantage over
that of Boyd and technically is more difficult.
BIBLIOGRAPHY
1.

Canale & Beaty: Campbell's Operative Orthopaedics, 11th ed. 2008,Mosby Elsevier.

2.

K. D. K. Luk, P. S. Yeung and J. C. Y. Leong :Thermography in the determination of amputation


levels in ischaemic limbs. International Orthopaedics. Volume 10, Number 2 / June, 1986.

3.

Van den Broek TA, Dwars BJ, Rauwerda JA, Bakker FC.Photolethysmographic selection of
amputation level in peripheral vascular disease. J Vasc Surg. 1988 Jul;8(1):10-3

4.

G. S. Dowd : Predicting stump healing following amputation for peripheral vascular disease using
the transcutaneous oxygen monitor.Ann R Coll Surg Engl. 1987 January; 69(1): 3135.

5.

H. G. Smith : Amputation above or below the knee for primary peripheral vascular disease. J Bone
& Joint Surgery , Vol 32B, No 3, Aug 1950.

6.

Ernest M. Burgess, and Frederick A. Matsen. Determining Amputation Levels in Peripheral


Vascular Disease J Bone & Joint Surgery , Vol. 63.a, no. 9, December 1981.

Index

194

Recent Advances in Varicose Veins


N S Hadke, Pankaj Kumar Garg
Definition
Varicose veins are defined as superficial veins, which permanently have lost its valvular efficiency,
and as a product of the resultant venous hypertension in the standing position become dilated,
tortuous and thickened.
1

Primary varicose veins (95%) are caused by an increase in venous pressure in the superficial veins
of the leg due to damage to the venous valves between the deep and superficial venous systems.
This increase may be at:
1. the sapheno-femoral junction between the long saphenous vein and the common femoral
vein in the groin
2. the sapheno-popliteal junction between the short saphenous vein and the popliteal vein in
the popliteal fossa
3. other sites (when they are known as perforators).
Secondary varicose veins (5%) occur when the increased venous pressure in the superficial venous
system is due to a disturbance in venous blood flow elsewhere, for example in:
1. pelvic thrombosis
2. extensive thrombosis of the veins in the leg (post phlebitis limb).
3. arterioveonus malformations (congenital or acquired as a result of a fracture).
Secondary varicose veins are invariably associated with venous hypertension in deep venous
system with secondary involvement of superficial venous system.

Anatomy
One of the pitfalls in venous surgery lies in inadequate knowledge of the venous physiology and
anatomy. In contrast to the anatomy of the arteries, the venous anatomy is characterized by
numerous variations, which have a certain impact on the diagnosis and surgery of varicose veins
and chronic venous insufficiency

Some anatomical points of surgical importance:

The lower limb is drained by two sets of veins: superficial and deep. Perforator veins connect
these two systems.

The dorsal metatarsal veins collect blood from the digital veins of the foot and empty into he
dorsal venous arch which continues into the lesser and greater saphenous veins on the
lateral and medial sides of the foot respectively.

The greater and lesser saphenous veins are freely interconnected

195

At the saphenopopliteal junction (SPJ), short saphenous vein commonly gives off an upward
extension, called the Giacomini vein, which may run deep and parallel to the profunda femoris
vein, or superficially, curving round to join the lesser saphenous vein via its posteromedial
branch in the upper thigh.

The fibular branch of the LSV posterior arch vein (Leonardo"s vein) has connections with the
posterior fibular vein via Cocketts perforating veins. Neglected insufficiency in the posterior
arch vein is quite often the cause of recurrence or even venous ulcer in the lower leg.

The superficial venous system of the lower limb is arranged as described in current textbooks
3,4

in 50 % or less of patients . There is marked variation in the anatomy of the superficial


venous system involving the origin, course, size, duplication and depth of truncal and tributary
veins (TV), the number and topography of perforating veins, the valvular distribution and the
arrangement of communicating veins.

From a surgical point of view, the most important variations occur at the venous junctions, the
saphenofemoral junction (SFJ) in the groin and the saphenopopliteal junction (SPJ) in the
popliteal fossa. The anatomical arrangement of the individual tributaries at the SFJ, namely
the superficial epigastric, iliac circumflex and external pudendal veins as well as the lateral or
medial accessory saphenous veins can be very different from one leg to another.

The anatomy of the SSV is even more complicated, because not only the tributaries may
vary, but also the location of the saphenopopliteal junction. In only 50 to 70 % of the cases is
the saphenopopliteal junction located in the popliteal fossa, whereas in about 10 % it is found
below it. In the remaining 30% to 40 %, the SSV terminates clearly above the popliteal fossa,
with or without connection with the popliteal vein.

The anatomic relationships between the LSV and the saphenous nerve and the SSV and the
sural nerve should also have an effect on the selection of the surgical technique in the
treatment of the insufficient superficial veins. A cadaver study reveald an intimate relationship
between the LSV and the saphenous nerve in the lower leg and the results indicated that the
risk of nerve damage can be reduced by making the distal incision prior to extraction of the
7

LSV immediately below the knee. The sural nerve descends anterolaterally to the SSV and
gives off two lateral cutaneous calcaneal branches. This should be known when performing
the surgical stripping of the SSV to avoid sural nerve damage.

There are numerous perforating veins present on both sides of the leg and the thigh which
connect the superficial to the deep venous system, either directly to the main axial veins
(direct perforators) or indirectly to muscular tributaries or soleal venous sinuses (indirect
perforators). In the mid and distal calf the most important direct medial perforators do not
196

originate directly from the great saphenous vein (GSV). The most significant calf perforators,
termed the Cockett perforators, connect the posterior arch vein to the paired posterior tibial
veins. The next group of clinically relevant perforating veins is the paratibial perforators, which
connect the GSV and its tributaries to the posterior tibial and popliteal veins. There are three
additional direct perforating veins that connect the GSV to the popliteal and femoral veins.
Boyds perforator, just distal to the knee, connects the GSV to the popliteal vein. Dodds and
Hunterian perforators are located in the thigh and connect the GSV to the proximal popliteal
or the femoral veins. In the distal calf, the small saphenous vein is connected by direct
perforators to the peroneal veins (Bassis perforators). The indirect perforators connect
tributaries of the small saphenous vein to either the muscular venous sinuses of the
gastrocnemius or soleus veins before entering the deep axial system. Position of these
perforators is highly variable from person to person.

This is important to be stressed that incompetence in few perforators in the initial part of
disease will ultimately lead to incompetence in rest of the perforators. So perforator surgery
has to be radical in nature and isolated perforator ligation will lead to nothing but recurrence.

There are perforators present in foot also which become important channels of venous
drainage in deep venous incompetence grade III and IV if superficial vein surgery is taken.

Epidemiology
Venous disease, including varicose veins and chronic venous insufficiency (CVI), is one of the
most commonly reported chronic medical conditions and a substantial source of morbidity in world.
Yet, little epidemiologic research has been conducted in the in the world including India. . Much of
what we know about the prevalence and determinants of chronic venous disease is the result of
studies conducted primarily in European populations. Estimates as to the prevalence of varicose
veins vary widely, from 2% to 56% in men and from 1% to 73% in women. There has been only
one study till today which has thrown light on the prevalence of varicose veins in India. Malhotra in
his paper published in 1972 reported a prevalence of 6.8% and 25.1% in north and south India
respectively. This epidemiological study was conducted in Indian rail road workers. The variation in
prevalence may be explained in part by numerous factors unrelated to actual differences in
population frequency. Study methodology, namely, variation in disease criteria, use of diagnostic
imaging, and population composition with respect to age, race, gender, and geographic location
accounts for some of the discrepancy in population estimates.

Venous Hemodynamics and Pathophysiology


The Muscle Pump: Venous return against gravity is primarily dependent upon muscle pumps located
within the foot and calf. Muscular contraction (systole) within facial compartments directs venous
blood from sinusoidal intramuscular veins into the deep stem veins and thence up the leg and
thigh towards right atrium. Reverse flow (reflux) in deep venous system during muscle relaxation
197

(diastole) is prevented by the closure of valves. Superficial veins collect blood from the superficial
tissues, and during diastole this blood enters the deep system via the perforating veins along a
pressure gradient. During systole, blood is prevented from re-entering the superficial system
through the closure of the perforating veins.

Ambulatory Venous Pressure: When standing motionless, with venous valves in the neutral
position, the pressure in the veins of the foot gradually increases until it equals the hydrostatic
pressure developed by the column of blood stretching between the foot and the heart; in a person
of average height, perhaps 90 mmHg. With active movement, the muscle pumps and valves come
into play and the venous column is divided into several smaller columns, each at a lower pressure.
As a result, the pressure in the foot veins falls in health to less than 25 mmHg upon walking - the
ambulatory venous pressure (AVP). Patients with muscle pump and/or venous valve failure, and/or
venous outflow obstruction, demonstrate a raised AVP. Such sustained venous hypertension is the
main factor contributing to the development of skin changes.

Venous Recirculation: In patients with varicose veins there is often a recirculation of venous blood
within the leg. During calf relaxation, abnormally large volumes of blood enter the muscle pump
from the superficial varices (increased preload). The muscle pump expels blood from the leg only
for it to re-enter the leg by refluxing down superficial varices (akin to aortic regurgitation). This
blood then re-enters the muscle pump through perforating veins in the lower calf and so on.

By far the most powerful force propelling venous return flow is the musculovenous pumping
mechanism, which can handle large volumes rapidly and generate a force well in excess of that
8

required for venous return against gravity. When the limb is in the dependent position, a normal set
of valves in the deep and superficial veins will prevent reflux of blood against the normal direction of
venous flow.
Failure of competence in the venous valves at saphenofemoral and saphenopopliteal junction will
lead to retrograde flow down the limb when the patient stands up or after exercise movement has
resulted in slack veins in the lower part of the leg. In the superficial veins, this is the basis of the
most common venous disorder simple varicose veins.

Venous insufficiency is a condition of inadequate venous return and hypertension when the patient is
in an upright position. An increase in venous pressure results in a corresponding increase in
capillary pressure and characteristic changes in the skin and subcutaneous tissue. Capillary
transudation with protein molecules leads to deposition of fibrin, which forms a barrier to nutritional
9

exchange between the capillaries and the surrounding tissue. Leukocytes are trapped in the
capillaries causing further damage to the endothelium and the vessel walls and slowing down
microvascular circulation.

10

Extravasated hemosiderin gives the characteristic brown skin

pigmentation. The outflow of fluid and corpuscles from the capillaries into the interstitial tissue
9

initiates some of the mechanisms leading to symptoms of CVI. Swelling, venous eczema and
198

dermatitis, lipodermatosclerosis, pigmentation and finally venous ulcer take many months, or even
years, to develop. Sensory neuropathy is another feature of severe chronic venous insufficiency,
and its distribution is coincident with trophic changes.

11

Classification of Chronic Venous Disease


An international Ad Hoc Committee of the American Venous Forum produced a consensus
document for the classification and grading of chronic venous disease, the CEAP classification,
which was formally endorsed by the American Venous Forum and by the Joint Council of the
Society for Vascular Surgery and the North American-International Society for Cardiovascular
Surgery (Table 1), limbs with chronic venous disease are classified according to clinical signs (C),
cause (E), anatomic distribution (A), and pathophysiologic condition (P).

12

If the physician accepts

that the anatomic and physiologic complexities of the venous system of the lower extremities are
observable through physiologic and imaging techniques, correlations between disease states and
treatment alternatives can be developed through the organized approach imposed by the CEAP
system.

13

In the daily practice, the clinical classification is the most important and practical one

(Table 2). During this study an American Venous Forum committee on venous outcomes
assessment developed a venous severity scoring system based on the best usable elements of
the CEAP system

14

The use of the Venous Clinical Severity Score (VCSS), the Venous Segmental Disease Score
(VSDS) and the Venous Disability Score (VDS) was found to be easy and useful both in research
and in the daily practice, when planning the treatment of primary varicose veins. These new
scoring methods are meant to complement the current CEAP system.

14

In the VCSS nine clinical

characteristics of CVD are graded from 0 to 3 with specific criteria to avoid overlap or arbitrary
scoring. Zero to three points are added for differences in background conservative therapy
(compression and elevation) to produce a 30-point maximum flat scale (Table 3). VSDS combines
the anatomic and pathophysiologic components of CEAP. Major venous segments are graded
according to to the presence of reflux and/or obstruction. It is entirely based on venous imaging,
primarily duplex scan findings. This scoring scheme weights 11 venous segments for their relative
importance when involved with reflux and/or obstruction, with a maximum score of 10. VDS is
simply a modification of the existing CEAP disability score (Table 4).

Table 1. Classification of chronic lower extremity venous disease (Porter & Moneta 1995)
Mark

Definition

C
E

Clinical signs (grade0-6), supplemented by (s) for symptomatic and (a) for
asymptomatic presentation
Etiologic Classification (Congenital, Primary, Secondary)

Anatomic Distribution (Superficial, Deep, or Perforator, alone or in combination)

Pathophysiologic Dysfunction (Reflux or Obstruction, alone or in combination)

199

Table 2. CEAP Clinical classification of chronic lower extremity venous disease (Porter &
Moneta 1995).
Class
Clinical signs
0

No visible or palpable signs of venous disease

Teleangiectases, reticular veins, malleolar flare

Varicose veins

Edema without skin changes


Skin changes ascribed to venous disease (pigmentation, venous eczema,

lipodermatosclerosis)

Skin changes (as defined above) in conjunction with healed ulceration

Skin changes (as defined above) in conjunction with active ulceration

Surgical management is indicated with CEAP class 4 and above. CEAP class 3 and below
requires management only on cosmetic ground.
Table 3. Venous Clinical Severity Score (VCSS)
Attribute

Absent = 0

Mild = 1

Moderate = 2

Severe = 3

Pain

None

Occasional

Daily

Limit activities

Varicose veins

None

Few, scattered

Multiple (LSV)

Extensive (LSV,
SSV)

Venous edema

None

Evening, ankle

Afternoon, leg

Morning, leg

Pigmentation

None

Limited area

Wider (above 1/3)

Inflammation

None

Cellulitis

Wide (lower
1/3)
Cellulitis

Induration

None

Focal (<5 cm)

< lower 1/3

Entire lower 1/3

Number of AC

Duration of AC

None

< 3 months

3 months 1
year

> 1 year

Size of AC

None

< 2cm dia

2-6 cm dia

> 6 cm diameter

Cellulitis

Intermittent
Most days
Continually
use
LSV, long saphenous vein; SSV, short saphenous vein; AC, active ulceration; lower 1/3,
lower 1/3 of the leg.
Comp therapy

Not used

Table 4. Venous Disability score (VDS)


Score

Definition

Asymptomatic

Symptomatic, but able to carry out usual activities* with-out compressive therapy

Able to carry out usual activities* only with compression and/or limb elevation

Unable to carry out usual activities* even with compression and/or limb elevation

*Usual activities = patients activities before the onset of disability due to venous disease.

200

CLINICAL FEATURES
Symptoms:
Unsightliness:
o Many patients with varicose veins complain of the unsightliness produced by tortuous dilated
veins in their lower limbs.
o Massive varicosities in men often cause few symptoms while minor varicosities in women
may be the source of major concern.
Aches and pains:
o Diffuse dull ache felt throughout the leg, which gets worse as the day passes and is
exacerbated by prolonged standing.
o Relief of the discomfort by wearing a elastic stocking provides good circumstantial evidence
that the pain is of venous origin.
o History of bursting pain during exercise (venous claudication) may indicate venous outflow
obstruction.
Ankle edema:
o Not a common or prominent feature of varicose veins.
o Usually mild and only become noticeable at the end of the day.
o Other causes of edema, such as deep vein obstruction or lymphatic obstruction, must be
excluded if there is marked edema and the patient complains of swelling of the lower leg as
well as ankle.
Superficial thrombophlebitis
Hemorrhage
Eczema, pigmentation, lipodermatosclerosis and ulceration

Physical Signs of Varicose Veins:


Inspection: The legs should be examined with the patient standing on a low stool or platform, suitably
undressed to expose the whole of both lower limbs from the groins to the toes.
Palpation and percussion: Some varicose veins are more easily felt than seen. The upper end of
dilated long saphenous veins can often be felt along its course in the thigh even when it cannot be
seen. A dilated short saphenous veins is invariably easier to feel than to see because it lies
beneath the layer of fascia covering the fascia.

After palpating the terminal segments of the long and short saphenous veins, the hand should be
gently passed over the inner side of the thigh and leg and up the posterior surface of the calf to
detect other sites of venous dilatation that might not have been detected by inspection. Any
difference in the temperature of the two limbs should also be recorded.
The cough impulse test (Morrisseys test): A visible or palpable venous expansion that occurs
on coughing indicates the absence of competent valves between the right atrium and the vein
201

under examination. When this sign is detected in the groin over a large saphena varix, it
indicates long saphenous incompetence and may be accompanied by a palpable thrill,
indicating turbulent retrograde flow.

The tourniquet test (the Brodie-trendelenburg test): This simple bedside was designed to
assess the direction of blood flow and the source of refilling of the superficial veins. The patient
must be laid flat on the couch and the limb is elevated to at least 45 to empty all the
subcutaneous veins. When the veins have been emptied, a narrow rubber tourniquet is applied
around the thigh as close to the groin as possible. It must be applied tightly to prevent all
superficial vein reflux. Saphenofemoral incompetence is indicated if the varices below the
tourniquet remain collapsed for between 15 and 30 seconds after the patient stands up, and
rapidly refill when the tourniquet is removed.

Multiple tourniquet test: Three tourniquets are tied after emptying the leg veins. First tourniquet
is tied just below the sapheno-femoral junction, second tourniquet is tied just above knee and
third tourniquet is tied just below knee. This helps in dividing greater saphenous vein in multiple
segments. Perforator incompetence in a particular segment will lead to increase in size in veins
in that particular segment. This can be made more prominent by releasing tourniquet from
below upwards.
Perthes test / Perthes maneuver: The Perthes maneuver is a traditional technique intended to
distinguish antegrade flow from retrograde flow in superficial varices. Antegrade flow in a
variceal system indicates that the system is a bypass pathway around deep venous
obstruction. This is critically important because if deep veins are not patent, superficial varices
are an important pathway for venous return and must not be sclerosed or surgically removed.
To perform the Perthes maneuver, the affected lower extremity is wrapped with elastic
bandage. With the elastic bandage on, the patient is instructed to move around exercise.
Increase in the size of varices indicates incompetence of deep venous system. Severe crampy
pain is complained of if there is deep venous obstruction
Modified Perthes test: A modification of Perthes' test in which a tourniquet is applied round the
upper part of the thigh after observing the veins. The patient is asked to walk quickly with the
touniquet in place. If the size of varicose veins decrease, the deep veins are patent and
competent. If they increase in size, the deep veins are incompetent. Severe crampy pain is
complained of if there is deep venous obstruction

INVESTIGATIONS
Doppler examination: Confirmation of saphenofemoral or saphenopopliteal reflux using a simple
hand-held 8 MHz Doppler (HHD), also known as continuous wave (CW) Doppler is increasingly
replacing the use of tourniquet tests in the clinic. The examination begins with the patient standing.
202

The probe is placed over the SFJ, which is found by insonating the femoral artery and moving
medially. Squeezing the calf will result in a prograde signal. In the presence of SFJ incompetence,
release of calf compression will result in a retrograde signal (greater than 0.50 seconds) that is
abolished by long saphenous vein (LSV) compression. The directional Doppler ultrasound flow
detector may also be used to detect sapheno popliteal reflux down the short saphenous vein, and
it has been used to determine the exact site of the sapheno-popliteal junction which may vary
15

considerably in position . Short saphenous incompetence is confirmed if retrograde flow after calf
squeezing is abolished by digital or tourniquet compression which occludes the upper end of the
short saphenous vein.

Duplex ultrasonography: Duplex ultrasound is capable of imaging the superficial and deep veins of
the leg and the communication between these two systems and is now accepted as the best
16

method of investigating cases of saphenous reflux and perforating vein incompetence . It has also
been suggested that before deciding upon treatment, all patients with varicose veins should have a
full Duplex examination. This represents a considerable advance over the simple hand-held
Doppler flow detector because it is often very difficult to know exactly from which vessel the
reflected ultrasound is coming. This is not only very valuable in the groin and popliteal fossa,
where the deep and superficial systems meet, but especially helpful in the calf where duplex
ultrasound can be used to assess incompetence of the perforating veins and localize their position.
Duplex ultrasound has a good specificity but needs further assessment against a reliable gold
standard. Ascending phlebography is now no longer used to assess the size and incompetence of
calf communicating veins because, although its specificity is good, its sensitivity is poor. It is
unusual for phlebography to fail to detect any incompetent perforators but duplex ultrasound has
now largely replaced it because it is easier to obtain.

Perforator mapping is a time consuming test and is done on the day before surgery because the
sites of incompetent perforators are marked on the skin of the patient with a non erasable marker.
The patient stands in an upright non-weight-bearing position for the affected extremity. Perforator
vein incompetence (PVI) is defined as outward flow of more than 0.3 second (or 0.5 second by
some) or longer than antegrade flow during the relaxation phase after release of manual
compression. Although duplex scanning misses smaller perforator veins, it has 100% specificity
and the highest sensitivity of all diagnostic tests to predict the sites of incompetent perforating
17

veins .
Table 2. Diagnostic tests to predict the sites of incompetent perforating veins
TEST
SENSITIVITY (%)
SPECIFICITY (%)
18
Physical examination
60
0
18
Hand-held Doppler
62
4
18
Ascending phlebography
60
50
17
Duplex scanning
79
100

203

Ascending Phlebography: Until recently, ascending phlebography has been the method of choice to
demonstrate patency and define the anatomy of veins. A second role has been to detect
incompetent perforating veins. It is still used as the gold standard to establish the accuracy of
new investigations that determine the presence or absence of disease or its anatomic extent.
However, the development of several noninvasive tests, particularly duplex scanning, now makes
it unnecessary in most cases. Its current application is limited to cases in which duplex scanning is
unavailable, inadequate, or equivocal. Although phlebography has been deemed the gold standard
in the detection of the presence, site, and anatomic extent of chronic venous obstruction, it cannot
provide a quantitative functional assessment of its severity or the adequacy of collateral veins.

Descending Phlebography: The aim of descending phlebography is to demonstrate reflux in either


the superficial or deep veins and to determine the points of leakage from the pelvis to the lower
limbs and from deep to superficial veins. It is also used to provide information on the anatomic
localization and morphology of the venous valves, assess the extent of reflux, and delineate the
venous anatomy in complex cases. Descending phlebography is performed by puncturing femoral
vein and injecting contrast medium to assess retrograde venous flow. The lower limit of contrast
medium reflux is observed fluoroscopically and images taken of this. It can also assess
saphenofemoral incompetence. Any reflux into this vessel is abnormal. Five grades of reflux (0 to
4) have been described as follows:
Grade 0, indicates no reflux below the confluence of the superficial femoral and profunda
femoris veins;
Grade 1 reflux down to the first valve below the site of injection
Grade 2 - reflux down to the upper third of the thigh
Grade 3 reflux down to, but not below the knee joint
Grade 4 reflux below the knee joint

Pathological reflux through the popliteal vein has been shown to be associated with symptoms, but
the association is not clear-cut. The disadvantages of descending phlebography are that it is
invasive and costly and has potential complications. The development of duplex scanning that can
be used to detect the presence and anatomic extent of reflux has resulted in a decrease in the
number of descending phlebograms. The latter are now performed mainly when deep venous
reconstruction is being considered or before redo surgery for varicose veins when duplex scanning
is not conclusive.

Varicography: Varicography involves the direct injection of contrast medium through a butterfly
cannula into the superficial vein under investigation. It has a particularly valuable clinical role in the
elucidation of the anatomic connections of recurrent or residual varicose veins as a road map to
guide the surgeon. On the operating table, it facilitates the use of minimal incisions and precise
surgery. It is also used to define abnormal drainage patterns in patients with venous
malformations.
204

Varicograms show the superficial connections, the perforating veins, the tortuosity, the dilatation
and the extent if the varicose veins but they do not give any information about valve function or
venous reflux which must be assessed separately by duplex scanning or descending
phlebography.

Magnetic resonance venography: Magnetic resonance venography is safe, does not involve
ionizing radiation as does phlebography and is not operator dependent like duplex ultrasound. At
present Magnetic resonance venography is in its infancy but its role will undoubtedly increase in
future. The efficacy of Magnetic resonance venography in deep vein thrombosis have been
assessed against duplex ultrasound, contrast phlebography or both using a variety of MR
techniques and it has been shown that in many cases MR can be as effective as or , on occasion,
19

superior to these other imaging studies . But, it is expensive and not available at all places.

TREATMENT
Compression therapy: Graduated compression hosiery is often the first line of treatment in the
management of varicose veins. Graduated compression leads to multiple effects on the venous
system in the leg, including decrease in edema, increase in venous velocity, decrease in venous
volume and decrease in venous return. This form of therapy is relatively inexpensive, essentially
risk free, and can be effective in improving symptoms related to superficial venous reflux in and
varicose veins. Compression therapy is main modality of treatment in post phlebitic limb and grade
III and IV deep venous reflux. Compression therapy may relieve symptoms, conceal veins and
prevent deterioration of the skin changes associated with venous hypertension. However,
stockings may be uncomfortable (especially in hot weather) and their beneficial effect lasts only as
long as they are worn. Compression must be strong (20-30 mmHg at the ankle), graduated
(maximal at the ankle reducing to 75% at the calf and 50% at the thigh) and, replaced regularly
(every 6 months). Some authorities believe that stockings reduce recurrent varicose veins after
surgery for uncomplicated varicose veins.

Surgical treatment of varicose veins:


Indications for Treatment:

When recognizable changes appear in the skin of the lower leg, i.e. presence of ankle flare,
lipodermatosclerosis or venous ulcer.

If there are problems with hemorrhage or recurrent superficial thrombophlebitis.

If the patient wishes to be treated for symptomatic or cosmetic reasons.

Those who are medically unfit because of presence of varicose veins.

Objectives of Treatment:
1. Ablation of the hydrostatic forces of axial reflux i.e. disconnection of saphenofemoral and
saphenopopliteal junction and stripping of greater and lesser vein.
205

2. Removal the hydrodynamic forces of perforator vein reflux

Options available for surgical treatment of varicose veins are as follows:

Ablation of saphenous vein reflux: greater or smaller

Incompetent perforators interruptions

Elimination of residual varicosities

Ablation of Saphenous Vein Reflux: Greater or Smaller


A.

Saphenofemoral

Junction

Ligation:

Saphenofemoral junction

ligation alone,

sometimes referred to as a Trendelenburgs procedure, is associated with a high rate of


recurrence of varices. Recent research has shown that it is necessary to remove the
saphenous vein to ensure that as much venous reflux as possible is eliminated.
A few sound principles:
1. In a patient of normal build the SFJ lies directly beneath the groin crease; in the
obese it lies above. An incision made below the crease is likely to be too low.
2. Do not divide any vein until the SFJ has been unequivocally identified.
3. Beware of the superficial external pudendal artery that usually passes between GSV
and CFV but passes superficial to the GSV in 5% of cases.
4. Follow and divide all tributaries (Superficial circumflex iliac, superficial inferior
epigastric, superficial external pudendal) beyond secondary branch points. Failure to
do so leaves a network of superficial veins connecting the veins of the thigh with
those of the perineum, the lower abdominal wall and the iliac region. These crossgroin connections are a frequent cause of recurrence.
5. Ligate the GSV deep to all tributaries flush with the CFV.
6. Divide the deep external pudendal vein as it comes off the CFV
7. Retract the lower margin of the wound to identify and ligate the posteromedial thigh
branch that often joints the GSV high in the thigh. Failure to do so increases the risk
of haematoma formation after stripping above the bandage, as well as medial thigh
recurrence. A high anterolateral branch should be dealt with similarly.

B. Stripping: Several randomized trials have clearly shown that routinely stripping the LSV
reduces the risk of recurrence developing through the Hunterian perforating veins and to
remove a vein in the thigh which is difficult to treat later by sclerotherapy

21

Stripping

markedly reduces the risk of recurrence by:


1. Disconnecting the thigh perforators and saphenous tributaries
2. Preventing

any

neovascularisation

arising

from

the

saphenous

stump

reconnecting with the GSV.

Perhaps the most common problem with conventional stripping of the GSV has been that
of saphenous nerve damage. Stripping the vein either to or from the ankle has long been
206

recognized as carrying a significant risk of this unpleasant complication. Cox et al

22

reported a 37% incidence of objective sensory impairment in the distribution of the nerve
3 months postoperatively, although not all patients were subjectively impaired by it.
23

Holme et al

carried out a study to determine whether or not stripping the LSV to the

ankle carried a higher risk of nerve damage than stripping to the knee.

17

They found that

39% of patients undergoing stripping to the ankle showed evidence of damage to the
saphenous nerve, compared to only 7% in those stripped to the knee, a difference that
was highly significant statistically.

It is interesting to speculate on the mechanism of saphenous nerve damage when the


vein has been stripped only as far as the knee. Trauma within the femoral triangle is one
possibility. Inadvertent passage of the stripper out of the LSV and through the fascia lata
is another. For this reason, and because the main GSV below this level is rarely
varicose, many now recommend stripping to the knee. The GSV should be stripped to
approximately one hands breadth below the knee. At this level the below knee perforator
(Boyd) would have been crossed but the saphenous nerve would not yet have joined the
vein. Also, important perforating veins below the knee are a part of the posterior arch
circulation and not the great saphenous vein.

Alternatives to stripping: New venous surgical techniques have been developed in an


effort to reduce the number and size of lower-extremity incisions and hematomas, to
eliminate postoperative discoloration, and to reduce the recuperation time.
Radio frequency (RF) ablation: The intervention employs radiofrequency (RF)
energy mediated heating of the vein wall to destroy the intima and denature
collagen in the media with resulting fibrous occlusion of the vein.

24

the

Closure system (VNUS Medical Technologies Inc., San Jose, CA) consists
of a bipolar heat generator and collapsible catheter electrodes suitable for use
in veins ranging from 2 to 12 mm in diameter. The procedure is usually
performed under conscious sedation and local anesthesia in an outpatient
setting. The catheter is preferably introduced into the saphenous vein at the
knee percutneously under ultrasound (US) guidance or through a small
incision and direct exposure of the vein. The position of the catheter at the
saphenofemoral junction is confirmed by US. Local tumescent anesthetic is
instilled in the subcutaneous tissues superficial to the vein under US
guidance. The vein wall temperature is allowed to equilibrate at 85Cafter
turning on the circuit and graduated withdrawal of the catheter is performed at
a rate of 3 cm/min. The heating is controlled by monitoring temperature and
impedance of the vein wall via a feedback system. Veins up to 12 mm in
diameter are treated.

207

The mechanics of the surgical procedure are relatively straight forward with a
few caveats. The treated vein should be relatively straight, free of severe
tortuosity or thrombus and without aneurysm. Contraindications include a post
phlebitic vein that cannot be accessed, a mega saphenous vein (>12 mm),
and significant dilation of the proximal saphenous vein with an aneurysmal
SFJ.

Endovenous laser therapy: Endovenous laser therapy (EVLT) is similar to RF


ablation, but laser energy is used for ablation of the saphenous vein.

25

The

procedure is faster and easier to perform than RF ablation and there is no


size limitation of the saphenous vein that can be treated. Both the 810-nm
and the 940-nm diode lasers are effective in inducing thrombotic vessel
occlusion. Laser-induced indirect local heat injury of the inner vein wall by
steam

bubbles

originating from

boiling

blood

is

proposed

as

the

pathophysiological mechanism of action of EVLT. This causes collagen


contraction and endothelial damage. The result is thickening of the vein wall
and contraction or thrombosis of the lumen.

The use of diode laser energy to ablate the saphenous vein is a method that
obviates the need for general anaesthesia and is associated with less pain
than traditional surgical stripping of the great saphenous vein. This procedure
can be performed in an office based setting using local anaesthesia following
preoperative assessment with duplex ultrasound.

Foam Sclerotherapy: An increasing number of authors have recently reported


successful injection of incompetent GSV with 3% polidocanol in the form of
foam.

26

The foam is generated by mixing liquid and air in a standardized

procedure of forward and backward movements within a close double-syringe


system. The GSV is punctured directly under US guidance, and the foam
injected. Results are verified by serial post treatment duplex examinations

C. Saphenopopliteal Ligation: Some surgeons advocate routine stripping of the short


saphenous vein should be disconnected and never stripped. The short saphenous vein
operation should be carried out first, if a long saphenous vein operation is to be
performed under the same anaesthetic.

Failure to mark the SPJ preoperatively will lead to a misplaced incision in a significant
number of cases that will necessitate further blind incisions or abandonment of the
procedure. Clinical examination and hand held Doppler are not reliable. Insist on a
duplex ultrasound.
208

D. Ligation of the Lower Leg Perforating Veins: Surgery for these veins is usually
required in patients with lipodermatosclerosis or ulceration. The presence of incompetent
perforators in patients with advanced CVI (clinical classes 4 to 6) is an indication for
surgical treatment in a fit patient. Whereas open perforator ligation is done only in those
with healed ulceration, a clean, granulating open ulcer is not a contraindication for
subfascial endoscopic perforator vein surgery (SEPS).
Subfascial ligation of the medial communicating veins (Lintons operation): In view
of considerable wound complications associated with Lintons radical operation of
subfascial ligation, which included long medial, anterolateral, and posterolateral calf
incisions, it was soon abandoned and he advocated only a long medial incision from
the ankle to the knee to interrupt all medial and posterior perforating veins

53

A long

vertical incision is made through the skin and subcutaneous fat down to the deep
fascia, approximately 1 cm behind the subcutaneous posterior border of the tibia. Any
subcutaneous veins that are divided are ligated. The deep fascia is incised in the
same line as the skin incision and is held open gently with a self-retaining retractor.
As the subfascial space is opened, leashes of communicating vessels can be seen
passing from the posterior tibial vessels between the muscles to the undersurface of
the deep fascia. These vessels are isolated, divided and ligated. When all the
communicating veins have been ligated, the deep fascia and skin are carefully
approximately.

The disadvantage of Linton procedure is that the lateral perforating veins can not be
taken care by this procedure.
Extrafascial ligation of perforators (Cocketts procedure): This operation is not
commonly employed today. The aim of surgery is to clear all the extrafascial enlarged
veins and to divide perforating veins. However, the perforating veins may be difficult
to accurately locate in this plane and the dissection tends to be traumatic because of
adherence of subcutaneous fat and connective tissue to the fascia due venous ulcer
and lipodermatosclerosis and associated with a higher incidence of skin necrosis.

Posterior approach (Robs procedure): This is done if the perforators on the lateral
side are also to be ligated. The incision is a posterior subfascial one and the
perforators on both the sides are ligated and divided. This procedure offers advantage
in the fact that the incision is away from the areas of ulceration and thus results in
good healing.

209

Subfascial endoscopic perforator surgery (SEPS): The major drawback of open


procedure was a high incidence of wound complications. Edwards in 1976 designed a
device called the phlebotome to ablate the incompetent perforators from sites remote
from the diseased skin. The phlebotome is inserted through a medial incision just
distal to the knee, deep to the fascia, and advanced to the level of the medial
malleolus. Resistance is felt as perforators are engaged and subsequently disrupted
with the leading edge. Hauer

28

introduced the endoscopic technique for division of

perforating veins in 1985. His work was soon followed by other investigators in
Europe, who used different types of endoscopes or mediastinoscopes to perform the
surgery with direct vision through a single incision made in the proximal calf.
The use of laparoscopic instruments was described by ODonnell, who infused saline
beneath the fascia to facilitate the visualization and dissection of the subfascial plane.
29

In Australia, Conrad began using carbon dioxide insufflation in 1993 and published a
report on his first seven patients in 1994. This technique, the two port technique,
employs one port for the camera and a separate port for instrumentation, thereby
making it easier to work in the limited subfascial space. All perforators encountered
are divided either with the harmonic scalpel or electrocautery or sharply between
clips. The surgeons apply metal clips to the perforating vein before the transection or
simply use electrocautery to cauterize the veins. However, the use of metal clip in a
potentially infected wound with chronic unhealthy skin and ulcer may not be desirable.
The repeated movement in and out of the operative field to reload metal clips can be
time consuming when multiple perforators are found. On the other hand, the
application of electrocautery in the limited subfascial space may cause inadvertent
damage to the surrounding soft tissue by the electrical currents. The production of
smoke during dissection by electrocautery may obscure the operative field, and
intermittent evacuation of smoke is needed. The ultrasonic scalpel uses precise
ultrasonic vibration to coagulate and transect the vessels in a smoke-free
environment.

30,31

It has been widely used in different areas, both in laparoscopic and

open surgery. The scalpel vibrates at a rate of 55000times/sec. This mechanical


action results in protein denaturation and the formation of coagulum, which seals off
blood vessels. The same action causes vaporization of cells resulting tissue
fragmentation. This dual action makes dissection quicker resulting in decreased
operating time.

Complications
1. Major venous damage: Deep veins can be damaged during varicose veins surgery
through attempts to control bleeding and misidentification of anatomy. Complete
division of the common femoral vein is estimated to occur once in every 10,000
varicose veins operations.
2. Arterial damage.
210

3. Nerve damage. Popliteal dissection, stripping and distal avulsions may result in
damage to the divisions of the sciatic nerve (usually the common peroneal nerve),
saphenous and sural nerve.
4. Haematoma. This is the commonest cause of discomfort after varicose veins and
can be minimized by operating the patient in the head-down position, careful
hemostasis, and evacuation of all clots from the stripper tunnel and use of a
tourniquet.
5. Venous thromboembolism.
6. Necrosis of the wound edges: this is the most common and troublesome
complication of both the subfascial and extrafascial operations. It appears to occur
more frequently after the extrafascial operation

E. Elimination of Residual Varicosities


Sclerotherapy: The aim of injection sclerotherapy is to place a small volume of
sclerosant in the lumen of a vein empty of blood, and then appose the walls of that
vein with appropriate compression. The vein fibroses and gets closed without the
formation of clot. The sclerosant must remain localized within the segment of vein to
be treated. The vein must be kept empty of blood both during and after the injection.
Patients should be mobilized immediately afterwards and be encouraged to walk on a
daily basis. This measure allows symptoms and signs of allergic reactions to appear
and be treated. The comfort of elastic compression can be evaluated, and the deep
venous circulation is stimulated and any sclerosant that has entered from the
superficial injection is flushed. Immobility is a relative contraindication to
sclerotherapy.

Indications of sclerotherapy:
1. Telangiectasia
2. Reticular varicosities and reticular veins
3. Isolated varicosities
4. Below knee varicosities
5. Recurrent varicosities

Contraindications:
1. Presence of arterial occlusive disease
2. Patient immobility
3. Hypersensitivity to the drug
4. Acute thrombophlebitis
5. Huge varicosities with large communications to deep veins

211

Technique:
1. The patient is examined standing and varices are marked with an indelible
pen.
2. A number of 2ml syringes fitted with 26 gauge needles are filled with 0.5 ml of
sclerosant. Maximum volume that can be given during one treatment is
around 10 ml of sclerosant.
3. The skin is cleaned and venepunctures are made at 5 cm intervals along the
course of each vein.
4. The patient lies down, veins are transfixed and the needle is slowly
withdrawn. As soon as the blood appears in the vein, the vein is emptied and
the sclerosant is injected into the empty vein.
5. Cotton wool balls are placed and fixed with micropore tape.
6. When all injections have been completed, crepe bandages are applied and
the patient is encouraged to walk.
7. Compression bandages are worn for 3 weeks. After this period the legs are
carefully inspected and untreated varices or failed injection sites are reinjected.

Complications: The complications of injection sclerotherapy include:


1. Anaphylaxis.
2. Allergic reactions. Typically symptoms include urticaria, peri-orbital and oral
swelling, bronchospasm and migraine.
3. Ulceration. Ulceration follows extravascular injection. Commonly it is due to
arterial occlusion caused by sclerosant reaching a terminal arteriole. Another
cause is reactive vasospasm because of a large volume of injection.
Treatment is

symptomatic. Unless the ulcer is obviously infected (rare)

antibiotics have no role.


4. Arterial injection. This is a serious complication that is accompanied by
severe pain distal to the injection site. The most vulnerable artery appears to
be the posterior tibial artery at the ankle. Treatment includes analgesia,
cooling of the foot, and infusion of heparin and dextran.
5. Pigmentation. Pigmentation is due to the deposition of haemosiderin, often
following superficial thrombophlebitis. Most commonly seen in those treated
with sodium tetradecyl sulphate and hypertonic saline and least common with
polidocanol.
6. Superficial thrombophlebitis. This occurs when clot remains in the lumen of
the sclerosed vein and is largely due to inadequate compression. Localised
haematoma is particularly painful and may be eased by aspiration with a
needle or scalpel under local anaesthesia.

212

7. Deep venous thrombosis. The risk is reduced by careful patient selection and
by advising patients to walk immediately after injection treatment and
thereafter on a regular basis each day.
8. Nerve damage. Can occur due to approximate injection and/or pressure from
bandaging.
9. Telangiectatic matting: or neoangiogenesis is the new appearance of red
telangiectasias in a site of prior sclerotherapy. It is believed to be a complex
process in which new vessels grow in response to endothelial growth factors
or platelet-derived growth factors. Prevention is best achieved through use of
dilute solutions and in small volume.
REFERENCES:
1.

Matthew Metcalfe Daryll Baker. Varicose veins. SURGERY 22:12; 321-323

2.

Gza Mozes, Stephen W. Carmichael and Peter Gloviczki. Surgical anatomy of the Veins of the
Lower Limb. Perspect Vasc Surg Endovasc Ther 2000; 12; 107-116.

3.

Shah DM, Chang BB, Leopold PW, Corson JD, Leather RP & Karmody AM (1986) The anatomy of
the greater saphenous venous system. J Vasc Surg 3(2): 273-283.

4.

Kupinski AM, Evans SM, Khan AM, Zorn TJ, Darling RC 3rd, Chang BB, Leather RP & Shah DM
(1993) Ultrasonic characterization of the saphenous vein. Cardiovasc Surg 1(5): 513-517.

5.

Blomquist HE (1968) The surgical anatomy of the sapheno-femoral junction. Ann Chir Gynaecol
Fenn 57(3): 325-328.

6.

De Maeseneer MG, De Hert SG, Van Schils PE, Vanmaele RG & Eyskens EJ (1993) Preoperative
colour-coded duplex examination of the saphenopopliteal junction in recurrent varicosity of the
short saphenous vein. Cardiovasc Surg 1(6): 680-683.

7.

Holme JB, Holme K & Sorensen LS (1988) The anatomic relationship between the long
saphenous vein and the saphenous nerve. Relevance for radical varicose vein surgery. Acta Chir
Scand 154(11-12): 631-633.

8.

Scurr JH & Tibbs DJ (1997) Varicose veins and venous disorders. In: Tibbs DJ (ed) Varicose
veins, Venous disorders, and lymphatic problems in the lower limbs. Oxford University Press,
Oxford,p 3-20.

9.

Allegra C & Carlizza A (2000) Oedema in chronic venous insufficiency: Pathophysiology and
investication. Phlebology 15: 122-125.

10. Dormandy J & Thomas P (1989) The role of leucocytes in chronic venous insufficiency and
venous leg ulceration. Phlebology 4: 113.
11. Padberg Jr FT, Maniker AH, Carmel G, Pappas PJ, Silva MB & Hobson RW (1999) Sensory
impairment: A feature of chronic venous insufficiency. J Vasc Surg 30(5): 836-843.
12. Porter JM & Moneta GL (1995) Reporting standards in venous disease: an update. International
Consensus Committee on Chronic Venous Disease. J Vasc Surg 21(4): 635-645.
13. Kistner RL, Eklof B & Masuda EM (1996) Diagnosis of chronic venous disease of the lower
extremities: the CEAP classification. Mayo Clin Proc 71(4): 338-345.
14. Rutherford RB, Padberg FT, Comerota AJ, Kistner RL, Meissner MH & Moneta GL (2000) Venous
severity scoring: An adjunct to venous outcome assessment. J Vasc Surg 31(6): 1307-1312.
15. Roberts AK, Hoare MC, Royale JP. The detection of saphenopopliteal incompetence using
Doppler ultrasound and operative venography. J Cardiovasc Surg 26, 1985; 400-401
213

16. Coleridge-Smith PD, Scurr JH. Duplex scanning for venous disease. Curr Pract Surg 1995; 7:182188
17. Pierik EG, Toonder IM, van Urk H, Wittens CH. Validation of duplex ultrasonography in detecting
competent and incompetent perforating veins in patients with venous ulceration of the lower leg.
J Vasc Surg 1997; 26:49-52.
18. ODonnell TF Jr, Burnand KG, Clemenson G, et al. Doppler examination vs clinical and
phlebographic detection of the location of incompetent perforating veins: A prospective study.
Arch Surg 1977; 112:31-35.
19. Carpenter JP, Holland GA, Baum RA, Riley CA. Magnetic resonance venography for the
detection of deep venous thrombosis: comparison with contrast venography and duplex
ultrasonography. Radiology 1994; 191:880.
20. Goldman MP. Sclerotherapy of superficial venules and telangiectasias of the lower extremities.
Dermatol Clin 1987; 5:369.
21. Dwerryhouse S, Davies B, Harradine K, et al. Stripping the long saphenous vein reduces the rate
of reoperation for recurrent varicose veins: five-year results of a randomized trial. J Vasc Surg
1999; 29: 589.
22. Cox SJ, Wellwood JM, Martin A: Saphenous nerve injury caused by stripping the long
saphenous vein. Br Med J 1:415-417, 1974
23. Holme JB, Skajaa K, Holme K: Incidence of lesions of the saphenous nerve after partial or
complete stripping of the long saphenous vein. Acta Chir Scand 156:145-148, 1990
24. Merchant RF, DePalma RG, Kabnick LS: Endovascular obliteration of saphenous reflux: A
multicenter study. J Vasc Surg 2002;35:1190-1196.
25. Proebstle TM, Lehr HA, Kargl A, et al: Endovenous treatment of the greater saphenous vein with
a 940-nm diode laser: Thrombotic occlusion after endoluminal thermal damage by lasergenerated steam bubbles. J Vasc Surg 2002;35:729-736,
26. Hamel-Desnos C, Desnos P, Wollmann JC, et al: Evaluation of the efficacy of polidocanol in the
form of foam compared with liquid form in sclerotherapy of the greater saphenous vein: Initial
results. Dermatol Surg 2003;29:1170-1175.
27. Linton RR. The post-thrombotic ulceration of the lower extremity: Its etiology and surgical
treatment. Ann Surg 1953; 138:415-432.
28. Hauer G. [Endoscopic subfascial discussion of perforating veins preliminary report]. [German].
Vasa. 1985; 14:59-61.
29. Conrad P. Endoscopic exploration of the subfascial space of the lower leg with perforator vein
interruption using laparoscopic equipment: a preliminary report. Phlebology 1994;9:154-157.
30. Kumar A, Agarwal PN, Garg PK. Evaluation of subfascial endoscopic perforator vein surgery
(SEPS) using harmonic scalpel in varicose veins. Int J Surg. 2009 Apr 22. [Epub ahead of print]
10.1016/j.ijsu.2009.04.005
31. Lee DWH, Chan ACW, Lam YH, et al. Subfascial endoscopic perforator vein surgery (SEPS)
using the ultrasonic scalpel. Surg Endosc 2001; 15:1491-1493..

Index

214

Deep Vein Thrombosis


K M Rai
Deep vein thrombosis (DVT) is a common problem in clinical practice. It impacts the surgeon in
several ways. It is an important cause of sudden, unexpected death in post-operative patient, due to
pulmonary embolism (PE). It is a rare, yet preventable cause of gangrene that may result in limb loss.
It is also a source of considerable morbidity, often leading to post-phlebitic limb or venous ulceration.
A large majority of DVT can be prevented by appropriate measures. DVT is detectable in 25-35% of
postoperative patients if prophylaxis is not employed; the incidence may be as high as 59% in
patients undergoing hip surgery. DVT has also been reported in 20-30% of patients after myocardial
infarction or stroke. PE causes 50,000 deaths in USA annually, though there is some evidence that
the incidence of PE has declined in recent years. Unfortunately, a large number of clinicians in this
country feel that DVT is not a major issue in Indian patients, and are reluctant to use
thromboprophylaxis in surgical patients. The fact is that DVT is a major problem in this country, but
largely remains undiagnosed and unreported.

Approach to Management
A logical approach is obviously desirable in patients suspected to be suffering from DVT. The
important issues to be addressed in management of DVT are listed below.

Does the patient suffer from DVT?


What confirmatory tests are in order?
What is the etiology?
What is the best initial management?
Is hospitalization required?
What is the role of thrombolytic therapy?
When is surgery indicated?
What should be the duration of anticoagulation?
Can DVT be prevented?
Does the patient suffer from thrombophilia?
How should pulmonary embolism (PE) be managed?

Does the patient suffer from DVT?


The diagnosis of DVT can be difficult. A large majority of patients are asymptomatic. A high index of
suspicion is necessary. Clinical features in a hospitalized patient include:
Symptoms
Pain / swelling in the leg /calf
Low-grade pyrexia
Unexplained tachycardia

215

Signs
Edema leg / calf / thigh
Homans sign (calf tenderness on forced ankle dorsiflexion)
Moses Sign (calf tenderness on direct pressure)
Pratts sign (tenderness on squeezing the calf from the sides)
Raised local temperature
Dilated superficial veins
Phlegmasia alba dolens (painful white leg)
Phlegmasia cerulea dolens (painful blue leg)
Features of overt PE: chest pain, breathlessness, hemoptysis, collapse

Differential Diagnosis: DVT needs to be differentiated from the following clinical conditions:
calf muscle tear / hematoma, compartment syndrome, ruptured Bakers cyst, local cellulites,
myositis, superficial thrombophlebitis, ruptured plantaris tendon, acute arterial occlusion, and
rarely acute osteomyelitis or a rapidly growing bone tumor (e.g. Ewings sarcoma).

What confirmatory tests are in order?


Since the diagnosis of DVT is notoriously inaccurate, confirmation is mandatory. A host of tests are
available; judicious selection from the following is advisable. The single most important diagnostic
test is Color Doppler (Duplex Ultrasound scan), repeated after 48 hours if necessary.
Plasma D-Dimer Assay. This is a useful screening test. D-Dimer ia a fibrin degradation
product, and is elevated in DVT. However the elevation is non-specific, and is seen in many
conditions including post-operative states and acutely ill patient. The usefulness of the
investigation lies in excluding DVT; a normal D-Dimer value has 98% specificity in excluding
DVT.

Hand held Doppler. Portable, hand-held Doppler is reasonably accurate (70-80%) in


diagnosing DVT of major veins. Absence of flow signal over the femoral vein, loss of
phasicity (absence of change in audible signal on deep inspiration), and failure of
augmentation of signal on the squeezing the calf is diagnostic.

Duplex Ultrasonography. This non-invasive test has recently become the standard test for
diagnosing DVT. The ability of high resolution machines to actually visualize the deep veins,
their flow, and the location and nature of thrombus makes this an ideal modality for
diagnosing DVT. Doppler compression ultrasound (CUS) is quick and simple, and relies on
non-compression of a major vein by the ultrasound probe. Formal Duplex Ultrasonograpghy
involves studying the flow characteristics in the major veins of the extremity. Both tests are
operator dependent however sonography skills can be acquired fairly easily, even by
technicians.

216

Impedance plethysmogarphy (IPG). The test has an overall accuracy rate of about 80%.
While DVT involving major veins is detected reasonably accurately, DVT of smaller (e.g.
calf) veins is easy to miss.

Radionuclide scans employing Iodine 125 labelled fibrinogen or Indium 111 tagged platelets
have been used extensively in the past for non-invasive diagnosis of DVT with reasonable
accuracy. The advent of Duplex scanning have rendered them less important.
Venography. This was the gold-standard in diagnosis of DVT for years. The availability of
large number of reliable non-invasive tests, have led to its decreasing use in recent years. It
may still be required in the following settings: when the clinical suspicion of DVT is high, but
it is not confirmed by non-invasive tests, in ilio-femoral / pelvic / IVC thrombosis when
results of Duplex scan are inconclusive, and prior to iliofemoral thrombectomy or placement
of IVC filters.

Magnetic Resomnance Venography. This non-invasive test is replacing conventional


venography. Problems with resolution of smaller veins remain, but are rapidly being
overcome with newer generation machines.

Ventilation-Perfusion scan (V/Q scan). This used to be the standard test for diagnosing PE.
With the advent of CT Pulmonary Ahgiography it is fast becoming obsolete.

CT Pulmonary Angiography. This is rapidly replacing V/Q san for diagnosis of PE.

X Ray Chest, and ECG are sometimes diagnostic in massive PE. These are discussed at the
end of this chapter.

What is the etiology of DVT?


Virchows triad still holds true after centuries: venous thrombosis occurs due to one of the three
basic factors: (i) changes in the vessel wall, (ii) diminished rate of blood flow, and (iii) increased
coagulability of blood. These are often present in the surgical patient. Changes in vessel wall take
place following placement of large catheters in central veins, and following previous DVT;
decreased blood flow is present in post-operative patient, myocardial infarction or debilitating
disorders; and increased coagulability of blood is seen following major trauma or surgery, in
malignancy, in infections, in thrombophilia, and in myeloproliferative disorders. The list of
predisposing factors is mentioned in Table 1.

217

Table 1. Predisposing factors for DVT


Age > 40 years
Major surgery / Trauma
Varicose veins
Past history of DVT/PE
Malignancy
Pregnancy / puerperium
Oral contraceptives
Sepsis
Nephrotic syndrome

Obesity
Immobility (bed rest> 4 days)
Recent myocardial infarction
Heart failure
Stroke
Polycythemia / thrombocythemia
Connective tissue disorders
Thrombophilia
Inflammatory bowel disease

What is the best initial management?


Heparinization followed by oral anticoagulation is the cornerstone of management of DVT. The
treatment aims at (i) prevention of death (from fatal PE), (ii) preventing recurrent thromboembolism,
and (iii) preventing chronic venous insufficiency (post-phlebitic syndrome). It should be understood
that anticoagulants do not dissolve the already formed clot (bodys natural fibrinolytic system takes
care of that); they only prevent extension of thrombus and decrease the chances of PE. Other
supportive measures include bed rest (controversial), elevation of leg, compression stockings (or
crepe bandage).

Heparin (Unfractionated heparin, UFH). This unique pentasaccharide binds to antithrombin III
(AT III) and potentiates the latters inhibition of thrombin and activated factor Xa. It also acts as
a catalyst in inactivation of thrombin by plasma cofactor II, an action independent of AT III.
Other minor effects include release of tissue factor pathway inhibitor; suppression of platelet
function; increase in vascular permeability; and binding to WBCs, endothelial cells and several
plasma proteins. A loading dose of 1-2 mg/kg (5,000 -10,000 units for 50 kg adult) is
administered, followed by a continuous infusion of 1,000-2000 units / hour. Repeated assay of
APTT (activated partial thromboplastin time) or PTTK (plasma partial thromboplastin time with
kaolin) should be done, and the test (patient) value kept 1.5-2 times the control value.
Alternatively ACT (activated clotting time) may be used to adjusting the dose of heparin.
Monitoring heparin therapy is mandatory as it has been reported that inadequate heparinization
is worse than no heparinization. Baseline and biweekly platelet counts should be done for
timely detection of heparin induced thrombocytopenia (HIT).

Low molecular weight heparin (LWMH). These are low molecular weight derivatives of heparin,
made by nitric acid, alkali or enzymatic depolymerization. They differ from heparin in several
ways. The bioavailability is more (>90% as compared to about 20% of heparin) after
subcutaneous injection. The plasma half-life is longer, with a predictable, linear clearing so they
can be given once or twice a day. They have a more predictable therapeutic response, so no
monitoring is required (patients can thus be treated on outpatient basis, thereby reducing
hospitalization costs). They have little very effect on platelet function and vascular permeability
218

and therefore lower bleeding reactions than heparin. They also inactivate platelet bound factor
X a. A large number of LWMH are available commercially (e.g. enoxaparin, daltaparin,
naldroparin, etc.). They differ chemically and pharmacokinetically, and the dosing schedule
recommended by manufacturer should be followed. There are no trials to prove the efficacy of
one LWMH over the other in surgical patients. There are several clinical trials to suggest that
they are as (or more) effective as heparin in the initial management of DVT. A recent trial has
shown that unmonitored LWMH therapy was as safe and effective as OAC in long-term (3-6
month) management of DVT. The incidence of subsequent valvular incompetence was also
lower in the LWMH group. The incidence of side effects (bleeding, osteoporosis and
thrombocytopenia) was also much lower with LWMH. Common agents include Enoxaparin
(Clexane), Daltaparin, Tinzaparin, and Nandroparin.

Oral anticoagulants. Two groups of oral anticoagulants (OAC) are in clinical use: (i) the coumarin
derivatives e.g. warfarin (Warf 5mg, Warf 1mg, 2mg, and 5 mg tablets), or nicoumalone
(Acitrom 1, 2 and 4 mg tablets) and (ii) the indanedione derivatives e.g. phenindione (Dindevan
50 mg). The coumarin derivatives are more commonly used, as the incidence of side effects is
much lower with them. These drugs inhibit Vitamin K dependent coagulation factors (factor II,
VIII, IX and X). OAC also inhibit some of the naturally occurring anticoagulants (Protein C and
S), which may temporarily induce a paradoxical hypercoagulable state. It is therefore
recommended that warfarin therapy should be overlapped with heparin for 4-5 days. Their peak
effect occurs only after 36-48 hours. Monitoring is preferably by INR (international normalized
ratio), which should be kept between 2.0 and 3.5. If facilities for INR estimation are not
available, therapy should be controlled by prothrombin time (PT) estmation: the test (patient)
value should be elevated to 2 2 1/2 times the control value. There is considerable difference
in dose-response relationship of OAC amongst individuals, and therapy should be closely
monitored (once a week after adequate anticoagulation). A number of drug-interaction take
place with other drugs, and patients should be warned to check with their physician before
starting any new drug. The antidote for bleeding due to OAC is Vitamin K (dose 5-10 mg sc,
repeated if required) till INR or PT normalizes. In case bleeding is severe, fresh frozen plasma
may be required. Coumarin-induced skin necrosis is a rare but serious complication.

Newer agents. New anticoagulants that are under evaluation in clinical trials include: 1) Activated
protein C and soluble thrombomodulin; 2) Inhibitors of the factor VIIa/tissue factor pathway; 3)
Factor Xa inhibitors, both indirect and direct; and (4) Direct thrombin inhibitors. Of these, the
latter two seem most promising. Fondaparinux (Arixtra), a synthetic pentasaccharide,
selectively inhibits Factor Xa. Recent multicentric RCTs have shown that it is as effective as
LWMH in the mgt of DVT, with fewer side effects. Once a day dose is also an advantage of this
parenteral agent.

219

At present, the greatest clinical need is for an oral anticoagulant to replace warfarin for longterm prevention and treatment of patients with venous and arterial thrombosis. Ximelagatran,
an oral direct thrombin inhibitor, was the first of a series of promising new agents that might
have fulfill this need. Unfortunately, liver toxicity has led to its withdrawal from the market.
Dabigatran, a similar agent is under intensive study, and is likely to be approved for clinical use
soon. These agewnts can be used with an oral fixed dose without the need for coagulation
monitoring or dose adjustment. Hence, they offers significant potential to facilitate the
management of anticoagulation in or out of hospital.

Is hospitalization required?
There are several published studies to suggest that results after ambulant, domiciliary treatment of
DVT are as good as after hospitalization. If the patient is admitted for some other indication, the
period may be utilized for optimization of anticoagulant therapy. Other (relative) indications for
hospitalization include DVT involving extensive segments of vein causing a massively swollen leg,
proximal (ilio-femoral) DVT, presence of a free-floating thrombus on color Doppler, suspected PE,
and lack of a responsible adult at home.

What is the role of thrombolytic therapy?


The results of thrombolytic therapy are better (i) by direct (intraluminal instillation) rather than a
systemic approach, (ii) in iliofemoral thrombosis (IFT) rather than femoro-popliteal thrombosis (FPT),
(iii) in acute DVT (<10 days duration) rather than sub-acute or chronic DVT, and (iv) in first episode
of DVT compared to recurrent DVT. Systemic thrombolytic therapy has largely been abandoned in
favour of catheter-directed thrombolysis in DVT. Though thrombolytic therapy achieves superior clot
lysis rates as compared to anticoagulants, this advantage is offset by the higher risk of major
bleeding complications. It is therefore indicated mostly in DVT of the ilio-femoral segment, since the
chances of post-phlebitic sequelae are high in this subgroup of patients. The reason is that 95% of
thrombosed calf veins recanalize, as do 50-60% of femoral veins, but less than 20% of thrombosed
iliofemoral veins recanalize completely. Iliofemoral obstruction, even partial, can cause damage to
valves of distal veins, causing post-phlebitic sequelae.
In IFT, the catheter is introduced via the jugular vein and negotiated in the thrombus whereas in FPT
a sheath is placed in the political vein under Doppler guidance, and the catheter negotiated into the
thrombus. Urokinase infusion is started at the rate of 1,50,000-2,00,000 units/hr. Heparin is also
infused concomitantly via the sheath. The therapy is monitored by periodic venograms (12 hourly).
Any residual narrowing of iliac veins is treated by intravascular stenting. The results of thrombolysis
are comparable to surgical thromboembolectomy, with considerably less morbidity. However it is
labour intensive, and mandates repeated monitoring. The procedure is especially useful if operative
risk is prohibitive. Since the therapy takes about 48 hrs, it is contraindicated in phlegmasia cerulea
dolens (DVT with impending venous gangrene). Oral anticoagulation should be continued after
successful thrombolysis.

220

When is surgery indicated?


The role of surgery in DVT is limited to venous thrombectomy or caval interruption procedures. The
indications for performing these procedures are becoming increasingly rare.

Venous Thrombectomy. The frequency of this operation, once popular, has decreased
considerably with the use of anticoagulants and thrombolytic therapy. The classic indication of
this operation is massive iliofemoral thrombosis, especially that causing phlegmasia cerulea
dolens (painful blue leg), more so if it is associated with compartment syndrome or impending
venous gangrene. It may also been done in a patient of phlegmasia alba dolens or iliofemoral
thrombosis if contraindications to thrombolytic therapy exist. A venography of the opposite
iliofemoral segment is required in addition to the usual diagnostic tests to exclude an IVC
thrombus. The operation is performed under general anaesthesia with PEEP (positive end
expiratory pressure), to prevent PE. The femoral vein is exposed in groin, and thrombus
extracted from iliac veins using a special venous Fogarty thrombectomy catheter. Distal
thrombectomy is accomplished by squeezing the calf and thigh to expel the thrombus. The
adequacy of proximal thrombectomy should be checked by completion venography. An arteriovenous fistula may be created in groin to maintain the patency of iliac vein; this is disconnected
after a few weeks. IVC thrombectomy is performed via a right subcostal incision, exposing the
IVC by medial visceral rotation. Post-operative anticoagulation should be continued after these
procedures.

Caval interruption procedures. With the availability of IVC filters (see later) caval interruption
procedures like IVC ligation or plication are rarely required.

What should be the duration of anticoagulation therapy?


The duration of anticoagulant therapy in the first episode of DVT should be 6 months. For recurrent
DVT longer anticoagulation is recommended, as is for thrombophilia.

Can DVT be prevented?


The answer is a BIG YES. ACCP 2008 Guidelines deal with detail regarding this issue. Prevention of
DVT can be achieved by general or specific measures. General methods include maintaining
adequate hydration, avoiding hemoconcentration, meticulous surgical technique, postoperative
physiotherapy and early ambulation.

Without specific thromboprophylaxis measures, the incidence of fatal PE after surgical operations
ranges from 0.8% in general surgical operations to about 70% after hip replacement surgery. PE is
one of the leading causes of mortality after hip replacement, accounting for about 35% of postoperative deaths in this condition. Prophylaxis is recommended in moderate and high-risk surgical
patents Table 2. Heparin and low molecular weight heparins (LWMH) are the most commonly used
drugs. The incidence of major haemorrhagic complications is low, whereas minor complications like
221

wound haematomas are not uncommon. Caution should be exercised in giving spinal or epidural
anaesthesia in patients on DVT prophylaxis, as there is a small but significant incidence of
intraspinal hematomas, which occasionally prove fatal. The various strategies available are listed in
Table 3. The more commonly employed techniques are discussed below.

Low-dose Heparin. 5000 IU heparin, started 2 hours prior to surgery, and continued 8 or 12 hourly
for a few days, is the most studied and utilized regimen. Several studies have conclusively proved
its benefit, with reduction in fatal PE to less than 0.1%.

LWMHs. These synthetic preparations are at least as effective as heparin in preventing DVT and
PE. The complication rate is also lower than heparin. They should ideally be started the night
prior to surgery.

Hirudin. This leech extract has been shown to be as effective as heparin in prevention of DVT
following hip replacement in two trials.

Oral anticoagulants. Low dose warfarin (1-2 mg/day), elevating the prothrombin time (PT) by about
3-4 seconds is probably as effective as heparin. Repeated monitoring required for this form of
therapy remains a drawback.

Intermittent pneumatic compression. These devices enhance blood flow in the deep veins thereby
reducing venous stasis; they are also said to increase blood fibrinolytic activity. However they
may not reduce the incidence of pelvic vein thrombosis seen in hip replacement surgery. They
are a valuable alternative in surgical patients who are at a high risk of bleeding, or where even
minor bleeding is unacceptable (e.g. neurosurgical operations).

Graduated compression stockings (TED stockings). The mode of action of these devices is not
clear; they probably act by increasing velocity of blood flow in veins. They do decrease the
incidence of DVT, but it is not clear whether the risk of PE is reduced or not.

Table 2. Risk of DVT in surgical patient.


Low risk

Moderate risk

High risk

Age< 40 yrs

Age > 40 years

History of old DVT/PE

Minor surg of < 30 min

Surgery lasting > 30 min

Major orthopedic surgery

No other risk factor

Abdominal / pelvic surgery,


especially for malignancy

222

Table 3. Prophylaxis against DVT


Pharmacological methods

Mechanical methods

Low-dose heparin

Motorized foot mover

Low-dose LWMH

Static elastic compression

Dextran

Electric calf muscle stimulation

Heparin analogues

Intermittent calf muscle compression

Platelet function inhibitors

Vena cava interruption / IVC filters

Hirudin

Does the patient suffer from thrombophilia?


Thrombophilia is a group of disorders in which there is an increased propensity for venous
thrombosis due to lack of naturally occurring anticoagulants in the blood. Protein C or S deficiency,
Antithrombin III deficiency, antiphospholipid syndrome or Factor V (Leiden) gene defect may
predispose to a thrombophilic state. Other conditions include lupus anticoagulant, activated protein C
resistance, PNH (paroxysmal nocturnal haemoglobinuria) antibody, hyper homocystinemia, and
dysfibriniogenemias. These primary hypercoagulable states account for 40-50% of all DVT in
Caucasians. Screening for thrombophilia is indicated in following circumstances: (i) if a young patient
(<40 yr) presents with DVT without any predisposing cause, (ii) patients with a positive family history
for DVT, (iii) recurrent episodes of DVT or PE, (iv) if both DVT and superficial thrombophlebitis are
simultaneously present, (v) if heparin resistance is noted in the patient, and (vi) in women with
repeated abortions, when no other cause is detectable. An important point to remember is the timing
of the test for thrombophilia. If the test is performed during the acute phase of DVT, a false positive
test is likely because coagulation factors are consumed in the thrombotic process, and trhe serum
concentration may therefore be low. For this reason, anticoagulant therapy should be continued for
3-6 months. The test should be performed after discontinuation of therapy for two weeks. If
thrombophilia is detected, anticoagulation should be continued lifelong. However it may be
worthwhile repeating these tests from a different laboratory before this course of action is pursued.

How should pulmonary embolism (PE) be managed?


Pulmonary embolism is a dangerous condition. The manifestations are protean, ranging from a total
lack of signs or symptoms, to a collapsed, cyanosed, acutely ill patient. It has been estimated that
there are 6,30,000 episodes of pulmonary thromboembolism (PE) every year in USA, and about
50,000 deaths are attributed annually to it. Inadequate treatment of DVT is associated with a 20-50%
risk of PE. It is interesting to note that about 50% of patients with PE do not show any clinical
evidence of DVT. This description is limited to acute PE, which is encountered in surgical practiced
and sometimes requires surgical intervention; chronic PE is not addressed.

Etiology 95% of PE follows DVT in leg. The source of embolus in the remaining 5% is from right
ventricle, pelvic, renal or hepatic veins. Embolisms of foreign bodies (e.g. bullets) or septic
material are clinical curiosities.
223

Clinical Features Depend on the size of the emboli. A high index of suspicion is required for
diagnosing this condition. A large majority of patients may be completely asymptomatic.
Amongst the symptomatic patients, the following symptoms may be noted.
Symptoms The common symptoms, in decreasing order of frequency are,
Dyspnoea
Pleuritic chest pain
Cough
Hemoptysis
Signs Are usually non-specific. These include
Tachypnoea (Respiratory rate > 20/min)
Localized crepitations (rales)
Loud P2 (second heart sound)
Tachycardia
Fever
Evidence of DVT

Features of massive pulmonary embolism These include syncope, disorientation or altered


sensorium, central chest pain, central cyanosis, raised JVP, and acute cor pulmonale. About
11% of patients with features of acute massive PE die within one hour. Of those who
survive, a diagnosis is not made in 30%.

Investigations Routine investigations include ECG, chest X ray, and arterial blood gas (ABG)
analysis. Specific investigations include a ventilation/perfusion scan, angiography or spiral CT
scan. Duplex scanning of leg veins is added to confirm the source of thromboembolism.

Chest X Ray The initial chest radiograph is rarely diagnostic, and often normal. Several
abnormalities may be noted. These include
Elevation of one dome of diaphragm
Parenchymal infiltrates/infarction
Oligemia of affected lungfield (Westermarks sign)
Pleural effusion
ECG is useful to exclude other causes of chest pain, notably myocardial infarction. It may
show the following
Sinus tachycardia
T wave inversion (Leads V1-V4)and non-specific ST changes
Right bundle branch block
S1Q3T3 pattern with right axis deviation and RBBB (right bundle branch block) is
diagnostic, but found in less than 20% of cases.

224

ABG (arterial blood-gas analysis) may show low PaO2, with a normal or low PaCO2 and
acidosis. However a normal PaO2 does not exclude PE.
Ventilation/Perfusion lung scan (V/Q scan) This is the mainstay of diagnosis in patients who
are not acutely ill. The specificity is about 86%. The perfusion scan is performed using
albumin labeled with technetium 99m, whereas the ventilation scan is done using xenon
133 or 127, or lately using with technetium 99m aerosols. Ventilationperfusion mismatch
(normal perfusion but no ventilation) is classically seen in a localized area of the lung.
Traditionally the perfusion scan is performed first, and if a perfusion defect is noted, the
ventilation scan is done. Failure of a segment of lung to show perfusion in the presence of
adequate ventilation is diagnostic of PE. These tests are often reported as high-,
intermediate-, or low-probability positive scans.

Pulmonary angiography is the most specific and accurate investigation in the diagnosis of PE.
It has a low mortality (less than 0.5%) and morbidity; this has become even lower with
DSA. It is usually done in two settings: when the diagnosis is in doubt, or when massive
PE is suspected where a decision regarding surgical embolectomy or thrombolysis has to
be made urgently. In the latter instance, the catheter can be left in place for thrombolytic
therapy. The classical abnormality seen is intraluminal filling defects or an abrupt cutoff of a
major artery (>2.5 mm in diameter).

Spiral (Helical) CT scan. Contrast-enhances spiral CT is replacing V/Q scan for diagnosis of
PE in stable cases. It is said to be more reliable than the V/Q scan. As mentioned above,
angiography remains the investigation of choice in massive PE.

Treatment General supportive measures include oxygen therapy by mask or nasal prongs, pain
relief by intravenous morphine (3-5 mg), correction of acidosis, fluid therapy (maintaining a
CVP of about 12 mm Hg), and ionotropic support with dobutamine (2.5 10
microgram/Kg/min) or isoprenaline (0.5-10 microgram/min), if indicated.
Heparin. Heparin remains the drug of choice for PE causing no or minimal haemodynamic
disturbances. A loading dose of 150-200 mg/kg is given, followed by continuous infusion,
maintaining the APTT to 1.5-2.5 times the normal. Heparin is changed to oral
anticoagulants after a few days, and these should be continued for at least six months. An
INR (international normalized ratio) of 2-3.5 should be maintained.

Thrombolytic therapy. Thrombolytic therapy is an attractive alternative, especially in submassive and massive PE. It may also be used in patients of PE who do not respond
adequately to heparin therapy. It is also useful in patients with underlying cardio-pulmonary
disease, who have a prohibitive surgical risk (of dying from surgical embolectomy). Tissue
plasminogen activator is probably better with fewer side effects and a better clot lysis rate
(82% as against 48% by urokinase infusion). These agents can be given either by
225

intravenous or by intrapulmonary route (via angiography catheter); the latter is usually


preferred.

Pulmonary Embolectomy This was first described by Trendelenberg in 1908; he exposed the
th

pulmonary artery via the 4 interspace. This approach is still being practiced, especially in
centers where facilities for cardiopulmonary bypass are not available, even though the
mortality approaches 50%. An alternative (and better) surgical approach to pulmonary
artery is by median sternotomy with cardiopulmonary bypass. Some form of pulmonary
embolectomy (surgical, catheter aspiration) is indicated in massive PE. In a patient with
sudden collapse and no right-sided cardiac output, emergency open surgical embolectomy
can be life saving.

Catheter Embolectomy An embolectomy catheter with a suction-cup at its tip is introduced via
the jugular vein or femoral vein, and negotiated into the pulmonary artery. The thrombus is
sucked into the catheter and pulled back to the phlebotomy incision, maintaining he suction
on the cup. It is then delivered out of the phlebotomy incision. Several passages of the
catheter are usually required for an adequate enbolectomy. Significant reduction in
pulmonary artery obstruction can usually be achieved. This proposition of minimally
invasive surgery under local anaesthesia in critically ill patients is obviously attractive.

Inferior Vena Cava Filters These are an alternative to IVC (inferior vena cava) ligation or
plication in patients with repeated PE. The indications for placement of IVC filters are
mentioned in Table 4. The initial filter described by Mobinuddeen had a propensity to
migrate. Greenfield described his stainless steel filter, which became very popular; a
titanium filter was subsequently introduced. Several commercial devices are currently
available. These filters, preloaded in catheters are introduced via a jugular or femoral vein
approach, and placed in the IVC below the renal veins. IVC filters are not without their own
peculiar problems (e.g. migration, peri-filter thrombosis), and their placement should be
undertaken in trained centers. Recent developments include filters which can be retrieved
at a later date.

Table 4. Indications for IVC Filter placement in Pulmonary Embolism


Absolute Indications

Relative indications

Anticoagulation (AC) contraindicated

Large (>5 cm) free-floating iliac thrombus

Recurrent PE despite anticoagulation

Propagating thrombus despite AC

Bleeding forcing discontinuation of AC

Chronic PE with cor pulmonale

After pulmonary embolectomy

High-risk patient *

Failure of IVC interruption

Septic PE

* A high risk patient is one with significant COPD (chronic obstructive pulmonary disease) with > 50%
decrease of pulmonary bed who would not be able to tolerate even minor PE from DVT.
226

Conclusion
DVT is common in clinical practice. Awareness regarding the condition is lacking in the country, even
amongst physicians. Prophylaxis against DVT should be given where indicated, because this decreases
the incidence of pulmonary embolism. DVT should be treated appropriately and aggressively. Low
molecular weight heparins have made the treatment of DVT simple, because this does not entail any
laboratory monitoring.

Index

227

Venous Ulcers
AK Kakar, Pankaj Garg
Chronic venous disease, including chronic venous insufficiency and chronic venous ulceration, is a
common and important medical problem that causes significant morbidity. Venous ulcers are
expensive to treat and adversely impact patients quality of life.

1,2

Studies have shown that an

estimated 5% to 8% of the world population suffers from venous disease and approximately 1%
develops venous ulcers.

2,3

Venous disease with venous ulceration is a chronic disease entity requiring

long-term care. Non-healing ulcers can be complicated by cellulitis that may require hospitalization.
Venous ulcer recurrences are common with rates ranging from 54% to 78%.

Venous ulcers occur more commonly in the elderly, the peak prevalence occurring between ages 60
5

and 80 years ; however, most first ulcers occur before the age of 60 years, affecting work
5,6

productivity. Venous ulcers have slight female predominance, with a variable female-to-male ratio
7

ranging from 1.5:1 to 10:1. Advancing age, sex, phlebitis, trauma to the legs, congestive heart failure,
family history of leg ulcers, obesity, occupation involving prolonged standing, and number of
pregnancies are risk factors that have been described with chronic venous insufficiency and,
subsequently, with venous ulcers.

8,9

PATHOPHYSIOLOGY
The venous system of the lower extremity comprises 3 components: the superficial veins, perforator
veins, and the deep veins. The deep veins lay within the muscles of the lower extremity, whereas the
superficial veins lie above the fascia overlying these muscles. The perforator or communicating veins
connects the superficial and deep vein systems. The superficial veins are low-pressure systems,
whereas the deep veins are high-pressure systems. All 3 venous systems have 1-way valves, which
only open toward the deep venous system and, under normal conditions, prevent reflux of blood.
During ambulation, as the calf muscle pump contracts, the deep veins are compressed, thus
propelling blood proximally toward the heart. With the brief rise in pressure, the valves of the 3 venous
systems close preventing retrograde flow of blood.

6,10

As the calf muscle relaxes, the deep veins

empty, allowing a drop in pressure. The venous valves open, allowing blood to flow from the
superficial veins through the communicating veins to the deep venous system.
venous insufficiency, this series of events does not occur.

11

In patients with

11

Venous hypertension, a sustained elevation of ambulatory venous pressure, is the hallmark of venous
disease and may be caused by an abnormal calf muscle pump. An abnormal calf muscle pump may,
at times, be due to incompetent veins or valves of the lower extremities, muscular dysfunction, limited
12

mobility, or any combination of the three.

Vein incompetence may be acquired or congenital and

often is due to valvular dysfunction or their absence, leading to venous reflux.

13

In approximately two-

thirds of patients with CVU, damage involves both superficial and deep venous systems. Contraction
of the calf muscles, specifically the gastrocnemius and the soleus muscles, serves as a pump to
228

empty the intramuscular deep veins and decrease the volume of venous blood present in the lower
extremities.

14

The pressure of the column of blood in the deep veins must be less than the pressure

exerted by the calf muscles in order to force blood against gravity and back to the heart for reoxygenation and distribution through the arterial system. Thus, muscular weakness may allow venous
blood to pool in the extremities.

15

Anatomically, the plantar venous plexus of the foot has a wider

vessel diameter than does the outflow tract of the posterior tibial deep veins, thus aiding the cephalad
flow of venous blood. Compression of the plantar plexus is assisted by ambulation, increasing the
performance of and decreasing the strain on the calf muscle pump. Venous ulcers may occur in
selected bedridden patients who lack the benefit of the calf muscle pump and the plantar plexus that
facilitate the ascension of blood back to the heart.

For people who experience short periods of recumbency, this lack of mobility is no problem. In fact,
lying down relieves the increased pressure caused by standing. Erect, ambulatory patients who lack
proper compensation of the venous system will suffer from venous pooling near the ankle. Increased
venous pressure with concomitant reduced differential between the arteriolar and venular side of the
capillary bed may trap leukocytes in the post-capillary venules.

16

These leukocytes may activate and

release proteolytic enzymes, which leads to the formation of free radicals that ultimately may cause
tissue damage.

16,17

Activated leukocytes also can release cytokines such as tumor necrosis factor

(TNF), interleukin 1 (IL-1), and various leukotrienes. In addition to leukocyte activation, margination of
white cells leads to oxygen deprivation of nearby tissues

18

and may result in ischemia. The

marginated white cells can act as a diffusion barrier to oxygen and nutrients necessary for tissue
survival.

Concomitantly, venous blood pooling leads to dilatation and subsequent venous tortuosity,
accompanied by a decrease in the number of capillaries, an increase in capillary intraluminal
pressure,and stretching of the interendothelial pore due to increased pressure. Pore widening causes
an increase in capillary permeability and edema formation. Additionally, macromolecules such as
fibrinogen and alpha-macroglobulin leak into the dermis through the dilated capillary pores.

18

Alpha-

macroglobulin may bind growth factors (GF) such as TNF and transforming growth factor beta
(TGFb), which are needed for wound repair.

19

Trapping these growth factors may make them

unavailable for tissue repair.


Fibrinogen leaking into the dermis leads to the formation and deposition of a fibrin cuff around
dermal blood vessels.

18

Systemic abnormalities in fibrinolysis, seen in patients with venous disease,

contribute to the pericapillary fibrin cuff, which also may act as an additional diffusion barrier to
18

oxygen and nutrients.

Recently, it also has been proposed that arterio-venous (AV) shunting may play a role in the
pathogenesis of venous ulcers.

20

This theory is supported by the presence of elevated oxygen content

of venous blood, premature venous filling, increased blood flow in the skin of the legs on angiography,

229

and decreased capillary density in leg skin in patients with venous insufficiency possibly
representing hypoperfusion of the nutritive capillaries.

CLASSIFICATION
Clinical severity of chronic venous insufficiency (CVI) was divided into four classes in 1988 by the Ad
Hoc Committee for Reporting Standards of the Society of Vascular Surgery and the North American
Chapter of the International Cardiovascular Society

21

Class 0 is asymptomatic, with no signs or

symptoms of disease. Class 1 is mild disease, presenting with limited swelling and local dilatation of
subcutaneous veins. Class 2 is moderate disease characterized by hyperpigmentation, moderate
edema, and subcutaneous fibrosis. Class 3 is severe disease, in which patients have chronic leg pain,
ulcers or pre-ulcerative changes, dermatitic changes, and severe edema. With increasing severity, the
deep venous system becomes progressively more involved. In one study, 90.3% of patients with class
1 disease have solely superficial reflux, while conversely, 60% of patients with class 3 disease have
deep venous reflux.

22

Additionally, valve closure times of the superficial veins were significantly

shorter in class 0 than the other classes, indicating superficial reflux increases with worsening clinical
changes. The number of incompetent perforator veins (veins that connect the superficial to the deep
system) is also highest in class 3. Rarely are patients with isolated deep or perforating vein
incompetence encountered. These changes may be measured by a variety of methods, including
photoplethysmography, air plethysmography, and duplex ultrasonography.

In 1996, the classification of venous ulcers was redefined based on clinical manifestations (C),
etiologic factors (E), anatomic distribution of involvement (A), and underlying pathophysiologic
findings (P).

23

This new CEAP classification system provides additional information to compare limbs

accurately.

CLINICAL ASSESSMENT OF LEG ULCER


History
The patients history provides important information necessary for the differentiation of the types of
ulcers that develop in the lower extremity. In addition to the standard history, we use five focused
questions to provide the essential information for further defining the etiology of ulcer formation.

When Did the Ulcer First Appear?


Duration of the ulcer should be accurately documented to provide a framework for chronicity of
the process. The time framework should identify the treatment modalities that have been
applied and their effect on ulcer healing. This perspective allows the clinician to have a more
realistic management strategy for long-standing versus acute ulcerations.

How Quickly Did It Develop?


Venous ulcers have a rapid onset. Patients complain of focal aching or burning followed shortly
by an ulceration of the skin. Arterial ulcers alternatively begin with pain and gradually progress
230

to ulceration. Ulcers that are caused by tumors are of gradual onset. The time course of the
ulcer is based on the history and clinical manifestations at the time of evaluation. This can be
used by the clinician in the differential diagnosis and plans for management.

Did Anything Initiate the Ulcer Formation?


The focus in this part of the history is to identify factors that may have precipitated ulcer
formation, such as trauma, infection, recent thrombophlebitis, tight garments, ill-fitting shoes,
and behavior that induces ulcers. These precipitating factors should be avoided in the future.

What Symptoms Are Associated with the Ulcer?


Arterial ulcers are secondary to atherosclerotic disease, vasculitis, or hypertensive ischemia.
These ulcers are usually painful. Frequently patients achieve some degree dependent position.
Venous ulcers are the end result of a moderate to severely dysfunctional venous valvular
system. These ulcers are far less painful and commonly improve with elevation and a decrease
in the peripheral edema associated with this process.

Past Medical History


Frequently the past medical history provides clues to the etiology of lower extremity ulcer
formation. A history of anemia, rheumatoid arthritis, and collagen vascular disease can be the
underlying cause of the development of lower extremity ulcerations. Previous deep vein
thrombosis may result in the postphlebitic syndrome which can lead to tissue breakdown.
Claudication and pain at rest are symptoms of arterial insufficiency which may lead to ulcer
formation. Concomitant medications that the patient is using could also contribute to tissue
breakdown. All of these factors are important in the assessment of the patient with lower
extremity ulceration.

Physical Examination
A complete physical examination must always be performed. In addition, we recommend that
attention be directed toward the involved extremitys circumference, edema, induration, color,
temperature, and pulses, as well as the location, size, and appearance of the ulcer.

Extremity Circumference
The initial step in the assessment of lower extremity ulcers is to measure the leg circumference
bilaterally at points 15 cm above and 15 and 30 cm below the medial tibia1 plateau. This
provides a baseline from which the efficacy of therapeutic intervention such as compression
bandages, gradient elastic stockings, and pneumatic compression can be followed. In addition,
possible etiologies for the underlying cause of ulceration may be discerned, such as extremity
enlargement from previous deep vein thrombosis, lymphedema, or injury.

231

Edema and Induration


The extremity must be evaluated for the presence of edema and/or induration. Edema is
described as pitting or nonpitting in quality. The length of the leg to which it extends should be
measured. Edema has multiple causes but whether it is present bilaterally or unilaterally may
focus the search for an etiology toward systemic versus local causes. Induration is a more
severe form of edema in which the underlying tissue and skin become firm and orange peel-like
in appearance. This change signifies high pressure and impaired drainage of the venous
system.

Color and Temperature


Color and temperature are indicators of blood flow to the lower extremities. In both venous and
arterial diseases the lower extremities can be violaceous in color. The differentiating point
would be capillary refill, which is delayed with arterial disease. Dependent rubor is present only
in arterial insufficiency and is secondary to reactive hyperemia from impaired arterial circulation.
The temperature of the skin is usually normal or warm with venous disease as opposed to cool
with arterial insufficiency.
Pulses
The pulses of the lower extremity (femoral, popliteal, posterior tibial, and dorsalis pedis) must
be palpated. Pulsed are graded from 0 to 3. The abdomen is examined for any enlargement of
the aorta as well as for the presence of bruits. In addition, we include auscultation of the
femoral arteries in this portion of the examination.

Ulcer Location, Size, and Appearance


Accurate documentation of the ulcer location on the lower extremity is important in the
development of a differential diagnosis of its cause. Arterial ulcers occur frequently at the point
most distal from the area of occlusion. They can be on the toes, dorsum of the foot, or lateral
aspect of the lower extremity. Hypertensive ulcers are located primarily on the lateral malleolus.
Venous ulcers are situated over the medial malleolus because this area is drained by the
greater saphenous vein, but they have also been present over the posterior, anterior, or lateral
aspect of the ankle.

DIFFERENTIAL DIAGNOSIS OF LEG ULCER


The differential diagnosis of leg ulcer etiologies is endless. In this section the focus is on the more
commonly encountered diseases (Table 1). Each area has been chosen because of its frequency and
is reviewed with respect to its manifestations.

Table. 1 Differential Diagnosis of Leg Ulcers


1.

Vascular
Arterial
Venous
Lymphatic
232

2.

3.

4.

5.

Vasculitis
Allergic vasculitis
Periarteritis nodosa
Rheumatoid arthritis
Lupus erythematosus
Hypertension
Hematologic
Sickle cell anemia
Thalassemia
Polycythemia Vera
Metabolic disorders
Diabetes mellitus
Pyoderma gangrenosum
Tumors
Squamous cell carcinoma
Myocosis fungoides
Miscellaneous
Drugs
Factitial

Arterial Ulcers
Arterial occlusive disease secondary to atherosclerosis (atherosclerosis obliterans) is a frequent
cause of lower extremity ischemic ulcerations. These are located on the distal end of the digits,
around the nail base, or over bony prominences of the lower extremities. The ulcers are initially
small and shallow but progressively increase in size. The ulcer base is frequently covered by
necrotic debris and exudate. Little granulation tissue is present. The ulcers appear as punched-out
lesions. Ulceration and gangrene are common manifestations of thromboangiitis obliterans
(Buergers disease) in young men and women younger than 40 who are smokers.3 The lower
extremities are most frequently involved with ulceration along the margins of the nails. The correct
age, location, and smoking history are essential to make the diagnosis. In long-standing or severe
hypertension the arterial walls may become thickened, with a reduction in luminal diameter and
damage to the tissues at the capillary level. This condition, although infrequent, commonly affects
women in their fifth and sixth decades. These ulcers originate on the lateral surface of the ankle or
higher. They have a cyanotic appearance with very little granulation tissue or drainage. Often
these ulcers cause severe pain out of proportion to their size.

Venous Ulcers
Venous ulcers are probably the most common type of lower extremity ulceration. Chronic venous
insufficiency secondary to varicose veins, postphlebitic injury, and congenital arteriovenous
malformations are the etiologies for the development of this problem. The ulcers are commonly
located over the distal medial aspect of the extremity over the medial malleolus. The ulcer may
occur spontaneously or secondary to trauma. The base of these ulcers has extensive granulation
tissue with serosanguineous drainage present. These ulcers may or may not be painful.
Sometimes stasis dermatitis accompanies venous ulceration. This is located around the periphery

233

of the ulcer and frequently can resemble macerated tissue. In addition brown pigmentation
secondary to hemosiderin deposition can also be present surrounding the ulcer.

Vasculitis Ulcers
Ulcer formation secondary to vasculitis falls in a broad category of diseases including polyarteritis
nodosa, hypersensitivity angiitis, Wegeners granulomatosis, allergic granulomatosis, and
necrotizing vasculitis6 The important points in making the diagnosis are the history of the
presenting illness, laboratory testing, and a biopsy specimen of the appropriate organ system to
document the presence of vasculitis and help differentiate its cause. These ulcers appear primarily
on the lower extremities from the midcalf to the dorsum of the foot. The lesions also have a
punched-out appearance with necrotic central tissue. They can be unilateral or bilateral and are
frequently painful.

Hematologic Ulcers

Sickle Cell Anemia: Ulceration occurs in approximately 75% of patients with sickle cell
anemia. The pathophysiology of this process involves a lowered oxygen tension and pH in
areas of stasis in the distal portions of the lower extremities. The ulcers have sharply defined
borders with good granulation tissue at the base. The shape is usually round or oval and may
or may not be painful. Sickle cell ulcers are very refractory to healing as long as the patients
hemoglobin remains below 10 g/dL.

Thalassemia Minor: The presence of ulceration with thalassemia minor is infrequent. 6


Ulcers occur predominantly in patients with moderate disease and hemoglobin levels less
than 9 g/dL. The mechanism for tissue damage is probably inadequate tissue oxygenation
due to a reduced amount of hemoglobin A. The ulcers appear similar to those of patients with
sickle cell anemia.

Polycythemia Vera: Ulcer formation in this group of patients most likely has a dual origin.
Either the increased viscosity of the blood results in venous thrombosis, valvular
incompetence, and venous ulceration, or local hypoxia occurs at the capillary level and
9

causes tissue damage. Physical examination identifies the most likely etiology for the
process. The ulcers have the same clinical characteristics as venous ulcerations.

Metabolic Leg Ulcers

Diabetes Mellitus: The etiology for ulcer formation in the lower extremities of patients with
diabetes mellitus is multifactorial. These patients may have small vessel disease of the
peripheral arterial circulation, resulting in impaired dermal oxygenation leading to ulceration.
lo Sensory neuropathy is another diabetic complication that may cause ulcers to form at sites
of repeated trauma such as the toes, heels, and metatarsal heads on the plantar surface of
the foot. Finally, diabetics are prone to developing skin infections which could be the nidus for
ulcer formation or exacerbate existing lesions. The leg ulcers from arterial disease secondary
to diabetes mellitus have the same locations and symptoms as those in patients with
234

atherosclerosis obliterans. The neuropathic ulcers in diabetics are often surrounded by a thick
callous with a gray-colored base which contains very little granulation tissue. Frequently the
severity of the sensory neuropathy makes these ulcers painless. If these types of ulcers
develop purulent drainage, underlying osteomyelitis must be considered. There are a number
of rare causes of ulcers in the lower extremities of diabetics, including necrobiosis lipoidica
diabeticorum, diabetic dermopathy, and bullae diabeticorum.1

Pyoderma Gangrenosum: Pyoderma gangrenosum presents as an acute necrotizing ulcer


predominantly on the lower extremities. Pyoderma gangrenosum frequently produces an
irregular ulcer with a raised, inflammatory border and a boggy, necrotic base. This skin lesion
begins as a deep-seated, painful nodule or as a superficial hemorrhagic pustule, either de
novo or after minimal trauma. The lesion breaks down and ulcerates, discharging a purulent
and hemorrhagic exudate. The ulcer is extremely painful. A biopsy of the lesion is not always
diagnostic for pyoderma gangrenosum but may exclude other diseases. This lesion was once
pathognomonic for ulcerative colitis but has been observed in regional enteritis, gastric ulcers,
diabetes, mellitus, empyema, and many other disorders.

Tumors Causing Ulcers

Squamous Cell Carcinoma: Squamous cell carcinoma occurs most frequently on


sunexposed areas of the face, neck, and hands. This type of cancer should be suspected
when ulceration presents on the lower extremities at sites of old scars, burns, and previous
radiation. The ulcers are shallow with a wide, elevated, indurated border and never heal.
When a chronic leg ulcer of any etiology has been present for a long period and is not
healing, squamous cell carcinoma should be considered.

Mycosis Fungoides: The most common type of lymphoma affecting the skin is cutanous Tcell lymphoma or mycosis fungoides. There are three stages of presentation: patch, plaque,
and tumor. During the tumor stage of the disease is ulceration may occur secondary to
necrosis of the tumor. The ulcers are variable in size and have a necrotic center with a rolled
border.

Miscellaneous Causes of Leg Ulcers

Medications: Bromide and iodide compounds can produce skin lesions Evaluation of the
patient with an ulcer of the lower extremities resembling erythema nodosum. These
compounds were tremity can be approached by noninvasive methods. In more commonly
used years ago in sedatives and expectorants and as part of other medications. The skin
ulcers usually occur on the anterior surface of the tibia and are extremely painful.

Radiation: Ionizing radiation to the lower extremities in doses above 10 Gy may cause an
acute dermatitis which can ulcerate 6 to 8 weeks following the acute reaction. These ulcers
235

are extremely painful and are characterized by a punched out appearance, very little
granulation tissue, and slow healing. As mentioned previously, squamous cell carcinoma
could develop at the site of previous radiation scarring and manifest as a nonhealing ulcer.

Decubitus Ulcers: Decubitus ulcers are seen frequently in patients who are bedridden
secondary to neurologic causes or general debilitation. The lesions occur from prolonged
pressure to a small surface area, on the lower extremity primarily the malleoli and heels.

Rheumatoid Arthritis: Lower extremity ulceration occurs in rheumatoid arthritis by two path
physiologic mechanisms. First, a necrotizing vasculitis may occur in rheumatoid arthritis,
resulting in ulcerations that are extremely painful as described under Vasculitis U1cers.
Second, rheumatoid nodules may undergo necrosis and ulcerate. This form is less common
than vasculitis in producing ulcers of the lower extremities in patients with this disease.

DIAGNOSTIC STUDIES
The clinical diagnosis may be supported by further diagnostic testing as indicated, specially if other
diagnoses are being considered in the differential.
Vascular Studies
The initial evaluation of a venous leg ulcer should rule out concurrent arterial disease. Using a
standard sphygmomanometer, the clinician can determine an ankle to brachial pressure index
(ABPI). If the patient has an ABPI between 0.5 and 0.8, it indicates that there may be concurrent
arterial and venous disease. If the ABPI is less than 0.5, the ulcer is more likely to be arterial in
25

origin.

Color duplex ultrasound often is the initial technique of choice for patient evaluation because it is
widely available and easy to use. With this technique, a clinician can delineate the patients
vascular architecture and determine the presence or absence of venous reflux. It is important
that the clinician assesses the greater and lesser saphenous veins, the perforating veins, the
femoral vein, the popliteal vein, as well as the deep veins of the calf. For a venous evaluation,
the patient is examined in the standing position because previous techniques examining the
patient in the supine position have been shown to be less accurate. Compression of the calf by
manual pressure on the bulk of the muscle produces a systolic flow of blood in the anterograde
direction. After the diastolic release of the calf muscle, a patient with valvular incompetence will
demonstrate retrograde flow in the vein being evaluated.

25

Despite the widespread use of this

technique, considerable skill is necessary for a thorough evaluation of the deep veins.
Functional testing such as plethysmography can be a complementary method alongside
ultrasound for the evaluate of calf muscle dysfunction

26,27

by observing the changing volumes of

the lower legs before and after exercise. In a well functioning system of venous return, the
volume of the calf should decrease during exercise and increase with rest. The change in the
volume is graphed and analyzed against normal values. By applying pressure with a tourniquet,
236

one can limit the flow through the superficial vessels therefore testing the deep venous system
in isolation.

Radiological Studies
Computed tomography of the venous system may be used and requires less contrast dye than
venography (discussed below). Magnetic resonance imaging is becoming more popular for
imaging the soft tissue surrounding the vessels, and magnetic resonance venography can show
occluded vessels and alteration of flow. In end-stage CVI, the patient will oftendisplay
subcutaneous fibrosis and infiltration of the extrafascial spaces.

28

Invasive Techniques
The gold standard for defining the patients venous anatomy and demonstrating reflux is
venography. In ascending venography, the patient is upright while a tourniquet is applied above or
below the knee. Contrast dye is introduced, and if the dye is seen distal to the tourniquet, the
patient is assumed to have venous reflux. In descending venography, the patient placed in the
supine position and the contrast is injected into the common femoral vein. The patient is then tilted
downward, and the level to which the contrast dye leaks is observed. A leak below the level of the
knee considered significant for reflux.

A recent comparison between various invasive and noninvasive techniques were performed by
Mantonis group. They found continuous wave Doppler and ambulatory strain gauge
plethysmography of little value in the workup of patients with deep venous insufficiency.
Descending paleography was technically possible in less than one third of patients. They
suggested colour duplex doppler ultrasound should be used as a first line diagnostic tool, with
ascending phlebography used only when the triple ultrasound is inconclusive.

29

Biopsy
Biopsy is rarely warranted in the case of classic venous disease. If there is any doubt as to the
diagnosis, or if the physician is concerned about the presence of another diagnosis such as
infection or malignancy, a skin biopsy with preservative-free saline can performed, with half sent in
formalin to pathology and the other half for culture.

Tissue Culture
Although tissue culture has been hailed as the gold standard in the assessment of wound
infection, recent studies have shown a culture swab to be equivalent in the initial evaluation of
bacterial wound infection.

30

However, if there is a concern for antimicrobial resistance or the ulcer

is refractory to treatment, a deep tissue biopsy has been shown to be more sensitive for resistant
organisms

31

In these cases, bacterial, fungal and atypical mycobacterial organisms should be

ruled out.

237

THERAPY
General Principles
The core principles for management of venous ulcerations are (1) clean wound base and (2)
compression.
The Clean Ulcer
The aim of wound care is to provide an optimum environment for healing. A clean ulcer with
healthy-appearing bee fyred granulation tissue at its base is considered the best environment.

Dbridment: It generally is agreed that ulcers should be dbrided of any dead tissue. Numerous
reasons for performing dbridement have been proposed. Necrotic material on an ulcer bed may
enhance bacterial colonization, leading to infection. Necrotic material may stimulate inflammation
leading to destruction of surrounding healthy tissue. It may also act as a physical barrier to
reepithelialization. There is a variety of methods of dbridment, including surgical, mechanical,
autolytic, and enzymatic.

Treating Infection: When clear evidence of an infection is present, such as a cellulitis


surrounding the wound, empiric therapy should be initiated. The use of oral antibiotics for
asymptomatic infection is controversial. Wounds are almost always colonized with bacteria, even
when a patient is on antibiotics. In a study of 656 chronic wounds of various etiologies, almost all
ulcers (95.1%) were colonized with at least one bacterial species despite more than one quarter
being treated with antibiotics.

32

Oral antibiotics may not penetrate in sufficient concentration in a

wound to be effective. It has been recently considered that bio-films (colonies of bacteria
surrounded by a polysaccharide capsule) may act as a barrier to the diffusion of antibiotics into
the wound. Ongoing studies are examining the possibility of disrupting this barrier with enzymatic
therapy or other agents.

33

In the meantime, physical removal of these biofilms may be achievable

using methods of debridement already outlined. Biofilms are likely barriers to healing in a wound
and may physically block the action of topical therapies. Use of specific topical antibiotics also is
very controversial. Although considered ineffective in improving wound healing in the past couple
of decades,

33

there has been a recent surge of interest in the use of topical antimicrobials in

literature and anecdotal common usage. Slow-release iodine and silver have been added into
numerous wound care dressings, and reports have begun to validate their use. Silver sulfadiazine
1% cream has been shown to be superior to placebo in reducing the size of ulcers that were not
thought to be infected. It is thought that silver sulfadiazine may permit keratinocyte replication and
have an anti-inflammatory affect.
antibacterial properties.

35

34

Additionally, low concentrations of silver ions exhibit

Because of the increased risk of contact allergy in patients with venous

insufficiency, it generally is recommended to avoid specific topical antibiotics, particularly


Bacitracin and Neosporin because they are common sensitizers.

36

Wound Care: Topical Agents: A plethora of topical preparations are now on the market under
the rubric of wound care materials. The choice of agents can be bewildering. One of the most
important principals of wound care, one that is often misunderstood by patients and practitioners
238

alike, is the recognition that a moist environment will best promote wound healing.

37,38

Before

these publications in the 1960s, it had been considered that a dry environment was optimal for
wound healing. There are many classifications of wound dressings, including that outlined in the
next sections. Different classes are now being combined so that new dressings can be a
synergistic combination of an alginate with an antimicrobial and hydrogel, silver with alginate, or
collagen with a hydrocolloid. Different wound dressings are appropriate for different ulcerations
and even different phases of healing of ulcerations. For example, for dry wounds, hydrogels,
hydrocolloids and impregnated gauze work well, and for exudative wounds it is best to use
alginates, foams, or dry gauze.

Compression: Compression is undoubtedly one of the most important factors in the healing of
venous ulcers.

39

Compression not only supplements the pumping action of the calf muscle but

also increases tissue pressure to reverse the gradient between the capillaries and the
intravascular space, allowing for the reabsorption of tissue edema.

40

It is important to rule out

concomitant arterial disease before initiating compression therapy, or risk compromising the
patients arterial supply and tissue anoxia. Several values for the ABPI have been used as a cutoff, ranging from 0.7 to 0.9.

41

Below these values, it is recommended to avoid compression.

To heal venous ulcers, compression therapy should be performed in two consecutive treatment
phases. The first treatment phase is the decompression phase, which should take place at the
time of an active leg ulcer. The goal of this phase is to reduce edema and promote wound
healing. For the decompression phase, three types of compression may be utilized: (1) inelastic
compression bandages, (2) multi-layered elastic bandages, and (3) mechanical compression
42

using intermittent pneumatic compression boots .

Inelastic compression bandages provide limited pressure at rest, but high pressure with activity.
The prototype of the inelastic bandage is the Unna boot, a moist, zinc oxide-impregnated paste
bandage that hardens to an inelastic form. Unna boots require frequent reapplication because
they do not accommodate for changes in leg volume as edema subsides, and they have limited
absorptive capacity for highly exudative wounds. Modified, less rigid Unna boots have similar
properties as the traditional Unna boot and are referred to as inelastic short-stretch bandages.
The multi-layered elastic bandage system is comprised of a cotton or wool layer for absorption of
exudate, one or two elastic wraps, and a self-adherent wrap that maintains the bandage in place.
Multi-layered elastic bandages exert continuous pressure (40-45 mm Hg at the ankle) at rest and
with activity. They require less frequent reapplication than inelastic bandages because they have
the ability to conform to the lower extremity better and have superior absorptive capacity for
highly exudative wounds. The disadvantage to multi-layered inelastic compression bandages is
that they require a certain degree of expertise for adequate application. Mechanical compression
is reserved for patients who are unable to ambulate and for those who fail to respond to standard
compression therapy.
239

For the second phase or maintenance phase, which occurs after wound healing, elastic
graduated compression stockings are used to control venous HTN and prevent ulcer recurrence.

Skin Grafts and Flaps: Skin grafts and flaps have been used for the management of chronic
ulcerations. They should only be applied to a clean, uninfected ulceration with an adequate
vascular supply. It has been suggested that the benefit of skin grafts are the transplanted cells,
which can secrete growth factors and other products that might enhance healing. Full-thickness or
split-thickness grafts can be used. Allogeneic (cultured) keratinocytes also may be used but can
be expensive. There is increasing interest in tissue-engineered skin. Graft skin (Apligraf) is a
bilayered skin equivalent that includes dermal and epidermal components and is manufactured by
harvesting neonatal foreskins and extracting both keratinocytes and fibroblasts that are then
cultured separately to create the epidermal and dermal components.Graftskin has been approved
by the Food and Drug Administration (FDA) for use in diabetic neuropathic ulcerations and
venous ulcerations. Dermagraft is comprised of human fibroblasts on a bioabsorbable scaffold;
studies indicate that this product also may be useful for venous ulcerations.

Surgical Intervention/Procedures: One study of venous ulcers showed that no more than 15%
of patients had isolated deep venous reflux, whereas in 53% of patients there was superficial
reflux only.

43

Patients with reflux on in the superficial and perforating veins may be more

amenable to treatment, and may actually have a clinical cure after surgery, no longer requiring
the use of compression stockings.

In the well-selected patient with CVI, vascular surgery or sclerotherapy can treat insufficiency in
the superficial and perforator veins. This can speed up healing time and improve long-term
44

prognosis. By eliminating or repairing venous incompetence , one can reduce the risk of
recurrent venous ulceration, but it is important to use vascular imaging to distinguish this problem
from that of postthrombotic syndrome. Such conditions are treated much differently. Subfascial
endoscopic perforator vein surgery has been described for treatment of venous ulceration with
proven incompetent perforators.

45

Prevention of Recurrence: The cornerstone of prevention of recurrence of venous ulcerations is


compression

46

Interestingly, although this is the conventional view, there are no trials that have

compared compression with no compression for the prevention of recurrence. A Cochrane review
cited circumstantial evidence for the benefit of compression as a whole, and referred to
evidence that high compression is superior to moderate compression for the prevention of
recurrence. Patient education is important in the prevention of recurrence as well.

240

46

Oral Agents for the Treatment of Venous Ulcers


Pentoxifylline is a xanthine derivative that is thought to help treat occlusive disease by
decreasing blood viscosity with approval by the FDA for the treatment of claudication.

48

In a

systemic review of clinical trials, it has been found to be helpful in treating venous ulcers and
has been recommended as an adjunctive treatment in treatment regimens.

49

Although some

argue that it may only provide marginal benefit, it has an excellent risk profile with adverse
effects similar to placebo (rare gastrointestinal upset).

49

Zinc was popularized as a topical treatment for leg ulcers during the past century, and one study
found it helpful for arterial and venous ulcers.

50

Although it may have a mild antimicrobial

effect, there is no evidence that zinc can improve wound healing.

50

It is argued that although

Unna boots (made with zinc paste) are used in the treatment of venous ulcers, they may be
effective because of a compressive effect and not because of the composition of the
plaster.

51

A metaanalysis did not find sufficient evidence that oral zinc sulfate could improve

the healing of venous ulcers.

52

Diuretic treatment of peripheral edema caused by CVI is a temporizing measure that does not
address the true physiologic problem.

53

In the treatment of venous ulcers, however, they

may occasionally be found useful to acutely decrease the volume of leg edema and allow for
better wound care and compression to begin.

Oral micronized purified flavonoid fraction modulates leukocyte adhesion and prevents
endothelial damage, and there is evidence that it promotes venous leg ulcer healing.

54

Adjunctive Management/Advanced Techniques/Investigational Techniques


Several supplemental techniques have been tried or are under investigation. The topical
application of Simulium vittatum erythema protein extracted from black flies may locally increase
blood flow to aid in wound healing

55

Topical autologous platelets have no significant adjuvant

effect on healing of chronic venous leg ulcers

56,57

Platelet derived growth factors, however, have


58

become commonplace in wound care centers, and have been shown to be helpful in diabetic ,
neuropathic,

59

and decubitus

60

ulcers. In the laboratory, they show promise for the promotion of

wound healing in venous ulcers,

61

and a clinical trial is now underway.

62

Overall, clinical trials

using growth factors to accelerate wound healing have been disappointing. Recombinant PDGF63

BB (becaplermin) has been approved by the FDA for use in diabetic foot ulcers. , and a
recombinant GCSF product (Filgrastim) is proven to be effective as a subcutaneous injection for
the treatment of infected diabetic foot ulcers.

64

Cymetra, a collagen filler often used in cosmetic


65

applications, was found to be helpful in healing sinus tracts , and was recently tried for chronic
ulcers, including pyoderma gangrenosum. At this time, none of these treatments have been
comprehensively studied for the treatment of venous ulcers.

241

REFERENCES
1.

Phillips T, Stanton B, Provan A, Lew R. A study of the impact of leg ulcers on quality of life: financial,
social and psychological implications. J Am Acad Dermatol 1994;31:49 - 53.

2.

Ruckley C. Socioeconomic impact of chronic venous insufficiency and leg ulcers. Angiology
1997;46:67 - 9.

3.

Vanhoutte P, Corcaud S, De Montrion C. The demographics of venous disease of the lower limbs.
Angiology 1997;48:557- 8.

4.

Bergqvist D, Lindholm C, Nelzen O. Chronic leg ulcers: the impact of venous disease. J Vasc Surg
1999;29:752- 5.

5.

Callam M, Ruckley C, Harper D, Dale J. Chronic ulceration of the leg: extent of the problem and
provision of care. Br J Med 1985;290:1855- 6.

6.

Valencia IC, Falabella A, Kirsner R, Eaglstein W. Chronic venous insufficiency and venous leg
ulceration. J Am Acad Dermatol 2001;44:401 - 2.

7.

Callam MJ. Epidemiology of varicose veins. Br J Surg 1994;81:167- 73.

8.

Abbade L, Lastoria S. Venous ulcer; epidemiology, physiopathology, diagnosis and treatment. Int J
Dermatol 2005;44:449- 56.

9.

Scott TE, Lamarte WW, Gorin DR, et al. Risk factors for chronic venous insufficiency: a dual case
control study. J Vasc Surg 1995;24:703 - 10.

10. Browse NL, Burnand KG, Irvine AT, Wilson NM. Physiology and functional anatomy. Diseases of
veins. New York7 Oxford University Press; 1999. p. 49- 65.
11. Falanga V. Venous ulceration. J Dermatol Surg Oncol 1993;19:764- 71.
12. Dinner MI, Peters CR. Surgical management of the ulcers on the lower limbs. J Dermatol Surg Oncol.
1978;4:696699.
13. Welch HJ, Young CM, Semegran AB, et al. Duplex assessment of venous reflux and chronic venous
insufficiency: the significance of deep venous reflux. J Vasc Surg. 1996;24:755762.
14. White JV, Katz ML, Cisek P, Kreithen J. Venous outflow of the leg: anatomy and physiologic
mechanism of the plantar venous plexus. J Vasc Surg. 1996;24:819824.
15. Norgren L. Chronic venous insufficiency a well known disorder with many question marks.
Angiology. 1997;48:2326.
16. Chaetle TR, Scott HJ, Scurr JH, Coleridge Smith PD. White cells, skin blood flow and venous ulcers.
Br J Dermatol. 1991;125:288290.
17. Coleridge Smith PD, Scurr JH, Dormandy JA. Causes of venous ulceration: a new hypothesis. Br
Med J. 1988;296:16931727.
18. Browse NL, Burnand KG. The cause of venous ulceration. Lancet. 1982;ii:243254.
19. Falanga V, Eaglstein WH. The trap hypothesis of venous ulceration. Lancet. 1993;341:10061008.
20. Malanin K. About the pathophysiology of venous leg ulceration. JAAD. 2002;47:157158.
21. Malanin K. About the pathophysiology of venous leg ulceration. JAAD. 2002;47:157158.
22. Labropoulos N, Delis K, Nicolaides AN, et al. The role of the distribution and anatomic extent of
reflux in the development of signs and symptoms in chronic venous insufficiency. J Vasc Surg.
1996;23:504510.
23. Subcommittee

on

Reporting

Standards.

Classification

of

CVI.

1994.

Available

at:

www.phlebology.com.
24. Moffatt CJ, Franks PJ, Doherty DC, et al: Prevalence of leg ulceration in a London population. Qjm.
2004;97:431-437.
25. Labropoulos N, Leon LJ: Duplex evaluation of venous insufficiency. Semin Vasc Surg 2005;18:5-9.
242

26. Weingarten MS, Czeredarczuk M, Scovell S, et al: A correlation of air plethysmography and colorflow-assisted duplex scanning in the quantification of chronic venous insufficiency. J Vasc Surg
1996;24:750-754.
27. Bays RA, Healy DA, Atnip RG, et al: Validation of air plethysmography, photoplethysmography, and
duplex ultrasonography in the evaluation of severe venous stasis. J Vasc Surg 1994;20:721-727.
28. Gmelin E, Rosenthal M, Schmeller W, et al: Computertomographie und Kernspintomographie des
Unterschenkels bei chronischer Veneninsuffizienz. Rofo: Fortschritte auf dem Gebiete der
Rontgenstrahlen und der Nuklearmedizin. 1989;151:50-6.
29. Mantoni M, Larsen L, Lund JO, et al: Evaluation of chronic venous disease in the lower limbs:
comparison of five diagnostic methods. Br J Radiol 2002;75:578-83.
30. Neil JA, Munro CL: A comparison of two culturing methods for chronic wounds. Ostomy Wound
Manage. 1997;43:20-2.
31. Pellizzer G, Strazzabosco M, Presi S, et al: Deep tissue biopsy vs.superficial swab culture monitoring
in the microbiological assessment of limb-threatening diabetic foot infection. Diabetes Med
2001;18:822-7.
32. Tammelin A, Lindholm C, Hambraeus A: Chronic ulcers and antibiotic treatment. J Wound Care
1998;7:435-7
33. Leaper DJ: Prophylactic and therapeutic role of antibiotics in wound care. Am J Surg. 1994;167:15S19S ; discussion 19S20S
34. Bishop JB, Phillips LG, Mustoe TA, et al: A prospective randomized evaluator-blinded trial of two
potential wound healing agents for the treatment of venous stasis ulcers. J Vasc Surg 1992;16:251-7.
35. Silver S: Bacterial silver resistance: molecular biology and uses and misuses of silver compounds.
FEMS Microbiol Rev 2003;27:341-53.
36. Marks JG, Belsito DV, DeLeo VA, et al: North American Contact Dermatitis Group patch test results
for the detection of delayed-type hypersensitivity to topical allergens. J AmAcad Dermatol
1998;38:911-8.
37. Winter G: Formation of the scab and the rate of epithelization of superficial wounds in the skin of the
domestic pig. Nature 1962;193:293-4.
38. Hinman C, Maibach H: Effect of air exposure and occlusion on experimental human skin wounds.
Nature 1963;200:377-8.
39. Partsch H: Compression therapy of the legs. A review. J Dermatol Surg Oncol 1991;17:799-805.
40. Bradley L: Venous haemodynamics and the effects of compression stockings. Br J Community Nurs
2001;6:165-75.
41. Cullum N, Nelson EA, Fletcher AW, et al: Compression for venous leg ulcers. Cochrane Database of
Systematic reviews 2005
42. Smith PC, Sarin S, Hasty J, et al: Sequential gradient pneumatic compression enhances venous ulcer
healing: a randomized trial. Surgery 1990;108:871-5.
43. Darke SG, Penfold C: Venous ulceration and saphenous ligation. Eur J Vasc Surg 1992;6:4-9.
44. Masuda EM, Kistner RL: Long-term results of venous valve reconstruction: a four- to twenty-oneyear follow-up. J Vasc Surg 1994;19:391- 403.
45. Whiteley MS, Smith JJ, Galland RB: Subfascial endoscopic perforator vein surgery (SEPS): current
practice among British surgeons. Ann R Coll Surg Engl 1998;80:104-7.
46. Lorimer KR, Harrison MB, Graham ID, et al: Venous leg ulcer care: how evidence-based is nursing
practice? J Wound Ostomy Continence Nurs 2003;30:132-42.
47. Nelson EA, Bell-Syer SE, Cullum NA: Compression for preventing recurrence of venous ulcers.
243

Cochrane Database of Systematic Reviews 2000:CD002303


48. Margolis DJ: Pentoxifylline in the treatment of venous leg ulcers. Arch Dermatol 2000;136:1142-3.
49. Jull AB, Waters J, Arroll B: Pentoxifylline for treating venous leg ulcers. [see comment][update of
Cochrane Database Syst Rev. 2000;(2): CD001733; PMID: 10796661]. Cochrane Database of
Systematic Reviews2002:CD001733
50. Brandrup F, Menne T, Agren MS, et al: A randomized trial of two occlusive dressings in the treatment
of leg ulcers. Acta Derm Venereol 1990;70:231-5.
51. Margolis DJ, Berlin JA, Strom BL: Which venous leg ulcers will heal with limb compression
bandages? Am J Med 2000;109:15-9.
52. 104. Wilkinson EA, Hawke CI: Does oral zinc aid the healing of chronic leg ulcers? A systematic
literature review [see comment]. Arch Dermatol 1998;134:1556-60.
53. Felix W: Medikamentose Therapie bei venosen Durchblutungsstorungen des Beines. Hautarzt
1979;30:198-201.
54. Coleridge Smith PD: From skin disorders to venous leg ulcers: path physiology and efficacy of
Daflon 500 mg in ulcer healing [see comment]. Angiology 54:S45-S50, 2003 (suppl 1)
55. Cupp MS, Ribeiro JM, Champagne DE, et al: Analyses of cDNA and recombinant protein for a potent
vasoactive protein in saliva of a blood-feeding black fly, Simulium vittatum. J Exp Biol
1998;201:1553-61.
56. Senet P, Bon FX, Benbunan M, et al: Randomized trial and local biological effect of autologous
platelets used as adjuvant therapy for chronic venous leg ulcers [see comment]. J Vasc Surg
2003;38:1342-48.
57. Weed B, Davis M, Felty C, et al: Autologous platelet lysate product versus placebo in patients with
chronic leg ulcerations: a pilot study using a randomized, double-blind, crossover trial. Wounds
2004;16:273-82..
58. Smiell JM, Wieman TJ, Steed DL, et al: Efficacy and safety of becaplermin (recombinant human
platelet-derived growth factor-BB) in patients with nonhealing, lower extremity diabetic ulcers: a
combined analysis of four randomized studies. Wound Repair Regen 1999;7:335-46.
59. Wieman TJ, Smiell JM, Su Y: Efficacy and safety of a topical gel formulation of recombinant human
platelet-derived growth factor-BB (becaplermin) in patients with chronic neuropathic diabetic ulcers.
A phase III randomized placebo-controlled double-blind study. Diabetes Care 1998;21:822-27.
60. Mustoe TA, Cutler NR, Allman RM, et al: A phase II study to evaluate recombinant platelet-derived
growth factor-BB in the treatment of stage 3 and 4 pressure ulcers. Arch Surg 1994;129:213-19.
61. Vasquez R, Marien BJ, Gram C, et al: Proliferative capacity of venous ulcer wound fibroblasts in the
presence of platelet-derived growth factor. Vasc Endovasc Surg 2004;38:355-60.
62. Margolis DJ, Cromblehome T, Herlyn M, et al: Clinical protocol. Phase I trial to evaluate the safety of
H5.020CMV:PDGF-b and limb compression bandage for the treatment of venous leg ulcer: trial A:
Hum Gene Ther 2004;15:1003-19.
63. Gough A, Clapperton M, Rolando N, et al: Randomised placebo controlled trial of granulocyte-colony
stimulating factor in diabetic foot infection. Lancet 1997;350:855-9.
64. Banta MN, Eaglstein WH, Kirsner RS: Healing of refractory sinus tracts by dermal matrix injection
with Cymetra. Dermatol Surg 2003;29: 863-6.

65. Kranke P, Bennett M, Roeckl-Wiedmann I, et al: Hyperbaric oxygen therapy for chronic wounds.
Cochrane Database of Systematic Reviews 2004:CD004123

Index
244

Evaluation of the lower extremity veins


Rashmi Dixit
The venous system of the lower extremities is divided into superficial and deep systems. The deep
veins which are dominant run alongside their corresponding arteries. The superficial veins are located
in the superficial fascia and consist of greater and lesser saphenous veins and their tributaries.
Numerous perforators connect these two systems.

Deep Venous Thrombosis


Lower extremity deep venous thrombosis (DVT) is an important clinical problem as pulmonary
embolism can occur as a complication of DVT. The clinical diagnosis of DVT is known to be
imprecise.
Sonography and CDFI have revolutionized the diagnosis of deep venous thrombosis (DVT). The test
is extremity accurate, easy to perform, relatively inexpensive and completely safe. It has essentially
replaced contrast venography in diagnosing symptomatic patients.
Sonography: With optimal grey scale settings, the normal vein lumen is echo free with the exception
of valve cusps. Normal valve leaflets are thin and slightly echogenic and may not be seen during
routine examination. Damaged valves appear thickened and may not respond normally to valsalva
maneuver. Grey scale images also document intraluminal thrombus and compressibility. Normally
with application of moderate pressure, patent veins collapse and anterior and posterior walls
appose . Inability to completely obliterate the vein lumen with compression is the major sonographic criterion for diagnosis of venous thrombosis. As the echogenicity of the thrombus is
variable direct visualization of echoes within the venous lumen is less reliable. However direct
compressibility is difficult to evaluate in the pelvis, adductor canal and calf veins.

Doppler: Colour Doppler facilitates vessel identification and confirmation of patency of venous
segments unable to be compressed directly. There are several flow characteristics that are
present in patent venous system which may be absent or altered with significant proximal venous
obstruction. These characteristics include spontaneous flow, cardiac and respiratory phasicity, the
valsalva response and augmentation. Absence of flow in a venous segment by colour or pulsed
Doppler are findings highly suggestive of thrombus. Several studies have reported high sensitivities and specificities for diagnosis of DVT but the accuracy of this technique is not as
extensively documented as is venous compressibility and in most institutions the two are used
together.

Respiratory phasicity results from the normal flow velocity changes that occur in response to
variation in intrathoracic pressure. The presence of cardiac and respiratory phasicity in a vein
suggests patency of the venous system between the thorax and site of insonation. When DVT is
present, the venous segment distal to the thrombosis shows absence of respiratory phasicity.
However respiratory phasicity may not be depressed in patients who are shallow breathers, who
245

have spinal cord injuries and when the thrombosis is partial. Respiratory phasicity may be made
more prominent by asking the patient to take a deep breath which results in cessation of flow.
Evaluation of phasicity should be perormed at both groins to facilitate comparison.

Augmentation entails mechanically propelling venous blood from distal portion of an extremity to
the point of insonation by squeezing the calf. This results in a rush of blood which is detected by
Doppler upstream, and is said to indicate absence of significant obstruction between the site of
augmentation and insonation.

Isolated calf vein thrombi are difficult to detect by CDFI and routine imaging of calf veins is not
performed at many centers. While evaluating for lower limb DVT proximal portion of great
saphenous should also be evaluated as thrombosis within this can extend into the deep system.

The sensitivity and specificity of sonography and Doppler in the diagnosis of symptomatic DVT is
95 per cent and 98 per cent respectively but lower in asymptomatic cases. Causes of misdiagnosis
include - underlying chronic venous disease, Isolated calf/iliac vein disease, venous duplication,
small focal thrombi.

Acute vs Chronic DVT: The distinction between acute and chronic residua of venous thrombi is of
great clinical importance as chronic thrombi are epithelialized and unlikely to embolise.
However sonographic distinction between acute and chronic DVT may be difficult to make and
venography is the technique of choice.

Since CDFI is a simple, accurate, non invasive diagnostic test for upper and lower extremity DVT,
other cross sectional modalities are rarely indicated for diagnosing DVT.

CT Venography: CT venography may be performed after helical computed tomographic pulmonary


angiography for pulmonary embolism. In this setting evaluation can be made for both pulmonary
embolism and lower extremity DVT without the need for additional contrast medium. Venous
imaging may be performed after a delay of 2 to 3 min. CTV is specific but less sensitive and has a
lower positive predictive value than ultrasound.

However CTV may prove to be useful in assessing the proximal extent of thrombus into the iliac
veins or IVC in patients where these are difficult to evaluate by Doppler. Findings in acute DVT
include filling defects and venous dilatation. In chronic DVT, web like or thread like filling defects
that are, peripherally located or calcified may be seen. The most common pitfall in interpretation of
CT venograms is an apparent intraluminal filling defect caused by flow related inhomogeneous
enhancement and sub optimal opacification can result in false negative study.

246

MR Venography: This plays a limited role compared with ultrasound and contrast venography. MR
venography may be performed using a non contrast TOF MRA. However the complex flow
patterns with slow flow cause problems for both TOF MRA and PC MRA.

CE-MRA may be performed by an indirect technique (i.e. following MR angiography) or by a direct


technique using diluted gadolinium injection from pedal veins/antecubital vein. The direct
technique results in superior contrast to noise values within the vein resulting in better image
quality and a more detailed depiction of the venous system. Like CT venography MR venography
may provide information regarding proximal extent of a thrombus and can be accompanied
byapulmonary angiography.

Venography: Although contrast venography is considered the gold standard in the diagnosis of acute
and chronic DVT, it is not always dependable. Sensitivity and specificity is reported to be 89 per
cent and 97 per cent respectively. Interobserver variability is 10 per cent to 15 per cent. The
procedure is uncomfortable for the patient and has a small but definite risk of significant
complications. For these reasons venography should be reserved for patients with equivocal or
technically inadequate sonogram.

A fresh clot produces intraluminal, worm- like filling defect. Several projections of the calf veins
may be required to accurately detect thrombi in this location. Abrupt occlusion of a vein can reflect
acute on chronic thrombosis. Non filling of deep veins, preferential filling of superficial veins and
opacification of collateral veins may occur with acute or chronic DVT. Inflow defects or underfilling
with contrast may mimic a thrombus.

Chronic Venous Disease


Venous incompetence is a common problem. Symptoms are normally chronic and may present as
pain, leg swelling, skin changes, obvious varicose veins and skin ulceration. The two major chronic
venous disorders of the legs are chronic venous insufficiency (CVI) and primary varicose veins. CVI
can occur due to a defect in valve function or damage from prior episode of DVT.

Primary varicose veins are the result of valve incompetence in the superficial veins with normal deep
calf vein valves. In this common condition absent valves or abnormal valve function in the common
femoral, superficial femoral or upper saphenous vein allows reflux of blood into the lower leg veins.
Elevated venous pressure results in superficial varicosities without other symptoms of CVI.

Imaging: Imaging is central to the management of patients with chronic lower extremity venous
disease. The most important determinants are patency of the deep system, valvular incompetence in
superficial, deep and perforating veins, the extent of reflux and exact site of incompetent veins.

247

Sonography: Colour Doppler sonography is the standard tool for studying patients with CVI and
varicose veins when invasive therapy is being considered. It can also identify venous reflux in the
superficial and deep systems. If the deep venous system is normal, varicose veins is considered to
be a primary problem. Sonography can also identify residual deep vein occlusion or partial
recanalization.

Reflux is defined as the retrograde flow of blood in veins of the lower extremity caused by absent
or incompetent valves. Assessment of incompetence is performed by applying distal compression
and observing the direction of flow. In the normal situation flow will not reverse following release of
compression. If flow reversal for longer than 0.5 sec is observed then the venous system is
incompetent. This must be performed with the patient standing and weight supported on the
contralateral limb. Refluxing and non refluxing segments may be seen in the same vein.
Assessment of reflux should be made in the superficial and deep venous system.

The more proximal veins may also be assessed following a Valsalva maneuver. In the normal
condition there should be complete retardation of flow without flow reversal, should reversal be
observed this is again evidence of venous incompetence.

Perforating Veins: Incompetent perforating veins can also be identified by duplex sonography. One
looks for veins coursing between the deep and superficial veins and then during manual
compression and release one looks for bidirectional flow. Compression can be applied proximal
or distal to the duplex interrogation site. In one study all perforators >4 mm were incompetent,
irrespective of whether flow reversal was seen or not 34 and those less than 3 mm were
competent. Sonography can also be used to mark out the incompetent perforators (Fig. 27.18),
however it may miss some incompetent perforators detected by venography.

Doppler can also be used to evaluate patients postoperatively. In patients with varicose veins and
reflux, superficial femoral venous reflux could be abolished by greater saphenous stripping. If the
deep venous reflux persists after surgery the prognosis for cure of symptoms may be guarded.

Venography: Ascending or descending venography is needed only when the results of duplex
sonography are inconclusive, the study is technically inadequate or the anatomy is complex.
The appearance of chronic DVT can vary from recanalised veins with narrow, irregular, web
filled lumens with distorted valves and incompetent perforators to non- opacification of deep
veins with preferential filling of superficial veins and collateral channels. Descending
venography, though considered the gold standard is not without limitations. False positive
results may occur due to seepage of high density radiographic contrast through a competent
valve, also presence of a competent valve upstream does not allow evaluation of the valves
located downstream.

248

In patients with primary varicose veins, descending venography, ascending venography or


varicography may show filling of varicosities that communicate with valve less, dilated
perforating veins.

Venous Mapping: CDFI can be used for venous mapping for vein harvesting for autologous
grafts. A superficial vein typically needs to be larger than 2 mm in diameter but not varicose to be
suitable graft material.

BIBLIOGRAPHY
1.

Diana Gaitini Multimodality Imaging of the Peripheral Venous System Int J

Biomed Imaging. 2007;

2007: 54616.
2.

Valji K (Eds) Pelvic and Lower extremity veins. In Vascular and Interventional Radiology, WB
Saunders ,374-393 1999.

3.

Garg K, Mao J: Deep venous thrombosis; spectrum of findings and pitfalls in interpretation on CT
venography. AJR 177: 319-23, 2001.

4.

Peterson DP, Kazerooni EA, Wakefield TW, et al: Computed tomographic venography is specific but
not sensitive for diagnosis of acute lower extremity deep venous thrombosis in patients with
suspected pulmonary embolic. Journal of Vascular Surgery 34(5): 798-803, 2001.

5.

Prince MR, Grist JM, Debatin JF (Eds): 3D Contrast MR venography in 3D contrast MR angiography
(2nd ed) Springer 163-72, 1993.

6.

Zwicbel WJ, Colour duplex imaging and Doppler spectrum analysis: Principles, capabilities and
limitations. Semin in Ultrasound, CT and MR 11(2): 84-96, 1990.

7.

Phillips GWL, Chang LS: The value of ultrasound in the assessment of incompetent perforating
veins. Australas Radiol 40: 15, 1996.

Index

249

Carcinoma Gall Bladder


Ravi Kant, Bina Ravi
Natural history: Carcinoma Gall Bladder (CA GB) has overall 5- year survival of 5%, and median
survival of < 6 months. Chemotherapy has very little role to play and only potential cure is by
adequate Surgery.

Incidence: The highest incidence of Carcinoma Gall Bladder is in Indian women & in Chile in Latin
America.

Table 2.1 Incidence of Carcinoma Gall Bladder in the World


Country

Per 100,000 population

Indian women

21.5

Chile

15.5

Pakistani women

13.8

Native American in Mexico

9.8-14.5

Latin America

3.7-15.5

Eastern Europe-Czech, Poland, Slovakia, Yugoslavia

High

Saudi Arabia

High

USA

1.2

Table 2.2 Incidence of CA GB


Women>Men

2-6:1

Hispanic>Nonhispanic

2:1

Nonwhite>white

Least in whites

American Indians, Alaskans natives, Asian pacific


islanders
North India>South India

Highest
Least in South Indians

Etiology: Epidemiological studies point to many factors. The commonest associated factor is
gallstones (70-90%), yet of all the gallstones patients, only less than 4% develop Carcinoma Gall
Bladder. Risk factor of a Polyp becoming malignant is (a) less than three in number, (b) larger
than 1cm and (c) in an elderly person. Multiple polyps -smaller than 1 cm are unlikely to become
malignant.

250

Table 3.1 Risk factors for development of Carcinoma Gall Bladder


3.1

Cholelithiasis

3.2

Polyps

3.3
3.5

Higher concentration
oxidation products
Porcelain Gall Bladder

3.4
3.6

Higher concentration of secondary bile


acids
Cholecystenteric fistula

3.7

Anomalous Pancreatobiliary junction

3.8

Chronic infection with Typhoid bacillus

3.9

Sclerosing Cholangitis

3.10

Inflammatory Bowel disease

3.11-1

Chemicals like- Methyldopa

3.11-2

Oral contraceptives

3.11-3

Contaminated Mustard oil

3.11-4

Occupation in rubber industry

3.11-5

Fertilizers in Indo-Gangetic land mass

of

free

radical

Cholelithiasis & Gall Bladder cancer- a mini debate:


Points in favor:

Gall stones result in Gall bladder inflammation by (a) direct mechanical, (b) altering gall
bladder function, (c) incomplete emptying resulting in stasis and dilation.

Gall

stones

Gall

bladder

inflammation

Epithelial

dysplasia

Metaplasia

Adenocarcinoma.

Larger the stone, the greater the above impact. Possible reason greater duration and intensity
of epithelial irritation.

Gall bladder cancer has higher incidence of Gall stones than any other cancer, including any
biliary cancer.

RR of 4.95(95% CI, 3.3-7.4); 2.2(95%CI, 1.2-4.2) among the Cohort studies

R of 7.1 (95% CI, 4.5-11.2); in Case Control studies.

Gall Bladder Cancer patients as compared to Gall stones patients Symptomatic as well as
Asymptomatic have (a) more stones (>11), (b) larger stones (p= 0.001), and (c) higher
average number, weight, & volume of gall stones.

Points against:

out of all gall stone patients, only less than 4%, and in some series less than 15 patients have
gall bladder cancer.

1. Applied Anatomy :

No serosa between Gall bladder and Liver. Only a narrow Lamina propria & a single muscular
layer. Thin wall of Gall bladder. Once across the muscular layers, cancer can spread by
lymphatics and hematogenous- venous route.

Rokitansky Aschoff sinus

Cystic plate: fibrous lining between gall bladder and liver (& no serosa).

Segment IVb & V of Liver: In close approximation of Gall bladder. Hence Surgical removal
for cure.

251

Lymphatic drainage: Gall Bladder N1= Cystic & PericholedochalN2 Posterosuperior


PancreatoduodenalSuperior Mesenteric, / RetroportalCeliac,

M1= Interaortocval

(Shirai 1992)

2. Pathology:

Gross: Infiltrative, nodular, nodular-infiltrative combined, papillary, Papillary-infiltrative


combined. Papillary and nodular have better prognosis.

Microscopic: Adenocarcinoma: Well & poorly differentiated, Papillary, Intestinal type, Signet
ring, Clear cell, Colloid. Papillary & metaplastic type have better prognosis

Spread of disease: Direct, Lymphatic, Hematogenous, Transperitoneal. Direct invasion of


Liver (a) invasion of hilum along the Glissons sheath, (b) short direct communicating veins
that drain directly into segment IVb of liver, and veins accompanying extra-hepatic ducts
into the liver.

3. Clinical Picture: Presence of palpable mass, weight loss, jaundice, suggest advanced stage.

Table 6.1 Symptoms & Signs from Five Large Reviews (from De VIta)
S/s (%)

North 98

Chao 91

Perpetuo 78

Glenn 59

Burdette 57

Abdominal pain

62

54

97

86

82

Jaundice

13

46

44

23

50

Weight loss

28

77

35

47

Anemia

NR

NR

th

4. Staging : Most accepted is TNM/ AJCC 6 edition classification


th

Stage

Modified Nevin

Japanese

TNM/ AJCC 6 ed

In situ carcinoma

Confined to GB

T1, N0, M0
T1a= Lamina propria invasion
T1b= Muscular invasion
T2= invasion of perimuscular connective
tissue Transmural invasion =T2, N0, M0
T3, N0, M0
Local invasion of single organ= T3, N0,
M0
T3= perforating serosa or invading any
single organ
LN Mets: T1-T3, N1, M0
Locally advanced T4, any N, M0
T4= invading portal vein, hepatic artery, or
multiple extra-hepatic organs (locally
unresectable)
Distant mets; Ant T, Any N, M1

capsule

II

Mucosal or muscular

N1LN , Minimal

invasion

Liver or bile duct


invasion

III

Transmural direct liver

N2LN , Marked

invasion

Liver or bile duct


invasion

IV

Lymph node +

Distant mets

Distant mets

252

5. Investigations5.1 USG: Discontinuous mucosa, echogenic mucosa, mass (but not benign vs. malignant),
sumucosal echolucency, Doppler blood flow assessment, newer contrast enhanced
ultrasound techniques, apart from gall stones, liver involvement & ascites. Useful for portal
vein or hepatic artery involvement by color Doppler technique. Not accurate for CBD
involvement, lymph node involvement & peritoneal involvement.

5.2 CT scan & MRI: Essential prior to definitive surgery. Mass, organ involvement, assessment
of regional lymph node= >1cm size, & ring like heterogeneous enhancement (80% accuracy);
CT is poor for peritoneal involvement which are best seen by laparoscopy. Protrusion of
Caudate lobe with lymph node involvement is diagnostic and specific.

Table 8.21 Excellent accuracy of CT scan for staging of CA GB


Stage

Sensitivity %

Specificity %

T1 vs. T2

80

98.8

T2 vs. T3

92

96

T3 vs. T4

100

100

5.3 MRI: MR cholangiography especially when jaundice is present (confusion with Mirizzis,
MR/CT angiography. MR is 70-100% accurate for liver, and 60-70% accurate for lymph node
involvement.

5.4 PET:

results

in

Superior

imaging,

diagnosis

and

staging.

False

positive

in

Xanthogranulomatous cholecystitis. Sensitivity 75% & specificity 88%. Important to detect


incurable stage.

5.5 Tumor markers: CA 19-9 (high sensitivity 75% and high specificity =75%) & CEA
(Carcinoembryonic antigen) (high specificity 90% and low sensitivity= 50%)

5.6 Molecular markers: Presence of p53, K-ras, p21, DCC gene, Chromosome 9p abnormality,
over expression of c-erbb2 gene, decreased expression of nm23 gene, up regulation of Cyclin
D1, p16,and under expression of suppressors like retinoblastoma gene under expression,
p27, MSH2.

5.7 FNAC: Not recommended in curative stage. (Seedlings rupture).


unresectable.

Mandatory if Tumor is

Other cancers, where prior to surgery FNAC is NOT recommended are

Pancreas, Ovarian, Testis, Curable Hepatocellular carcinoma apart from curable Gall
bladder carcinoma.

253

6. Treatment:
Stage:
TNM
/ AJCC 6
Edition
Ia

Rx

1b

Cholecystectomy + Liver & Lymph node resection +


Negative cystic duct margin is mandatory even if it means resection of bile duct.

II

For T2 & T3

Simple Cholecystectomy

Complete resection of tumor en bloc with segment IVb & V of Liver +


If inflow structures involved than Extended Right hepatectomy +
Negative cystic duct margin is mandatory even if it means resection of bile duct +
Lymph node resection of hepato-duodenal ligament +

III

Abandon surgery if celiac or retro-pancreatic or peritoneal or other distant


metastases found
Unresectable

IV

Unresectable

6.1 Polyp: Suspicious polyps are sessile, solitary, >1cm in size, significant blood flow on color
Doppler. Recommendations: less than three in number- cholecystectomy. More than three in
number- observation as pseudo tumors are more likely. Polyps are 15 year younger and
carcinoma in situ is 5 years younger to clinical gall bladder cancer.

6.2 Porcelain: It means presence of calcification in wall of gall bladder. Associated with high risk
of gall bladder cancer (previously 10-50% but now 5-10%). Cholecystectomy recommended. If
calcification is stippled, higher risk of development of gall bladder cancer.

6.3 Staging

Laparoscopy:

avoids

unnecessary

laparotomy

by

visualizing

peritoneal

involvement. Decreases unnecessary laparotomy by 18%- MSKCC and shortens hospital


stay. Up to 48% may be spared laparotomy (Weber 2002).

6.4 Lymph node resection: All lymph nodes in hepato-duodenal ligament, sometimes
necessitating resection of supra-duodenal CBD.

7. Prognosis: Good if Papillary type on gross well differentiated on Microscopic, and early stage.
Otherwise, overall 5-year survival is 5%.
SUGGESTED READINGS:
1.

Angelica MD & Jarnagin. Tumors of Gallbladder in Cancer by De Vita 8

th

Edition, Year 2009. Page

764-781.
2.

Reddy, SK & Clary, BM. Surgical Management of Gall Bladder Cancer. In Bennet JJ Editor of Biliary
Tract Cancer. Surgical Oncology Clinics of North America. April 2009, Vol 18: No 2, 305-322.

Index

254

Hepatocellular Carcinoma
Durgatosh Pandey, Karthikeyan Senniappan, Naveen Sharma
Introduction
Hepatocellular carcinoma (HCC) is the sixth most common cancer worldwide and the third
commonest cause of mortality due to cancer. The prognosis, in general, is grave due to late stage at
presentation and the coexisting background liver disease with long term survival rates of 3-5%. The
distribution is skewed towards males with male to female ratio of 4:1.

Etiology

1-3

Cirrhosis of liver
1. Hepatitis B virus
2. Hepatitis C virus
3. Alcohol
4. Autoimmune chronic active hepatitis
5. Cryptogenic
6. Non alcoholic fatty liver disease (NAFLD)

Metabolic liver disease


1. Hemochromatosis
2. Wilsons disease
3. Alfa 1 antitrypsin deficiency
4. Glycogen storage diseases

Chemical carcinogens
1. Aflatoxin B1 (by aspergillus flavus mould)
2. Thorotrast
3. Anabolic steroids
4. Cigarette smoking
5. N-nitrosoamines, Pyrrolizidine alkaloids etc

Pathology
Macroscopic types:
Pushing type: well encapsulated, grows by pushing away the neighbouring structures like
blood vessels; good resectability
Infiltrating type: poorly demarcated, invades into nearby blood vessels; risk of positive
resection margins
Hanging type: growth attached to liver by a small fibrovascular stalk; easily resectable.

Microscopic picture:
HCCs range from well-differentiated lesions that reproduce hepatocytes arranged in cords,
trabeculae or glandular patterns, to poorly differentiated lesions, often composed of large
multinucleate anaplastic tumor giant cells. In the better differentiated variants, globules of bile may
255

be found within the cytoplasm of cells and in pseudocanaliculi between cells. Acidophilic hyaline
inclusions within the cytoplasm may be present, resembling Mallory bodies. About 50-70% of
tumours stain positive for alfa fetoprotein and 50-90% for polyclonal CEA

Other variants of HCC include fibrolamellar, clear cell, giant cell, sarcomatoid, mixed hepatocholangiocellular, oncocytic, sclerosing types

Clinical features
A detailed history should be elicited especially pertaining to viral hepatitis, chronic liver disease, blood
transfusions, intravenous drug abuse, and family and occupational history.
Symptoms and signs: Abdominal pain is the commonest symptom. The patient typically has weight
loss, anorexia, generalised weakness and malaise. Hepatomegaly or a liver mass may be
palpable. Bruits may be present due to the highly vascular nature of the tumour.

Depending on the extent of the background liver disease, the patient may have jaundice, ascites,
splenomegaly and signs of liver failure viz. caput medusa, spider angiomas, gynecomastia,
testicular atrophy, muscle wasting, Dupuytrens contracture, flapping tremors, parotid swelling,
palmar erythema and menstrual irregularities in females.

Paraneoplastic syndromes associated with hepatocellular carcinoma are hypoglycaemia,


erythrocytosis, hypercalcemia, hypercholesterolemia, dysfibrinogenemia, carcinoid syndrome,
increased thyroid binding globulin and porphyria cutanea tarda.

Diagnosis:
1. Clinical: Any patient with chronic liver disease patient with sudden or gradual onset of above
described symptoms and signs should be investigated for HCC.
4

2. Ultrasonogram is a good screening modality but its accuracy to detect primary liver tumors,
particularly in cirrhotic background is limited.
3. Triple phase helical CT is the current investigation of choice.

Rapid enhancement during

arterial phase of contrast and washout in the later venous phase is typical of HCC. It is a good
investigation to assess the local extent of tumour, adjacent liver status, number of lesions,
major blood vessel involvement, extrahepatic spread (portal nodes, peritoneal metastasis and
ascites). CT scan also identifies details such as central scarring in fibrolamellar tumors.

CT scan can also be utilized for calculating the total liver volume (TLV), tumor volume, and for
the calculation of future liver remnant (FLR). Thus CT volumetry is valuable to determine
whether a patient will have enough remnant liver to be able to tolerate a major liver resection.
However, in a cirrhotic liver, CT volumetry has its limitations as it cannot account for the
degree of functional normalcy of the remnant liver. In such cases, a standardized FLR is
calculated using the following formula:

256

Standardized TLV = -794.41+1267.28 x BSA (body surface area in sq.m)


Standardized FLR= measured FLR/ std. TLV

To prevent post operative hepatic failure and its complications standard FLR should be at
least 20% of TLV in normal liver patients and at least 40% of TLV in cirrhotic patients.

7,8

MRI is not superior to CT in the detection of the tumor nodules, in determination of


resectability and safety of surgery. MRI has its greatest value in differentiating hemangiomas
from primary liver tumors in doubtful cases.

4. Serum tumor markers: AFP (alfa-fetoprotein)

9,10

: Serum AFP more than 200 ng/ml is highly

suggestive of HCC. However, false positivity is common in benign liver diseases such as
cirrhosis, massive liver necrosis, chronic hepatitis, and other situations like normal pregnancy,
fetal distress or death, fetal neural tube defects such as anencephaly and spina bifida and
gonadal germ cell tumors. Serum AFP is elevated in only 50-70% of cases.
PIVKA-2 is des-gamma carboxy prothrombin protein induced by vit.K abnormality. It is
increased in 80% of HCC patients with false positivity seen in patients with vit.K deficiency.

11

5. The American Association for the Study of Liver Diseases (AASLD) has developed criteria for
diagnosis of HCC:

12

Hepatic mass > 2 cm within a cirrhotic liver

Serum AFP >200 ng/ml

Radiological appearance of HCC (arterial vascularisation with washout on one study


or arterial vascularisation on two separate dynamic studies)

In general, biopsy is not essential. If lesion is between 1 and 2 cms, image guided
biopsy is suggested. If lesion is <1 cm, follow up is suggested every few months.

Liver functional status determination


As HCC is etiologically intimately related with liver cirrhosis, it is very important to determine the
functional status of the background liver in order to select the modality of treatment for cirrhotic
patients.
Child-Pugh Classification
POINTS
FACTOR

Bilirubin (mg/dL)

<2

2-3

>3

Albumin (g/dL)

>3.5

2.8-3.5

<2.8

PT (increased in seconds)

1-3

4-6

>6

Ascites

None

Slight

Moderate

Encephalopathy

None

Minimal

Advanced

257

Grade A, 5-6 points; grade B, 7-9 points; grade C, 10-15 points.

In general, the patients with Child A cirrhosis can safely undergo major liver resection. Child C
cirrhotics cannot tolerate liver resection and are candidates for transplantation. Child B cirrhotics
should be judged carefully regarding their suitability for resection or transplantation.

Indocyanin green clearance test: This is based on the capacity of the liver to clear the infused
indocyanin green dye from circulation. Hepatic retention is measured at 15 mins. When retention
rate is <10%, the patient is likely to tolerate major liver resection. If the retention at 15 min is more
than 30%, the risk of liver failure is high after any resection.

13

Staging
A number of staging systems are followed and the important ones are enlisted here:
American Joint Commission on Cancer (AJCC) Staging

14

Primary tumor (T)


TX

Primary tumor cannot be assessed

T0

No evidence of primary tumor

T1

Solitary tumor without vascular invasion

T2

Solitary tumor with vascular invasion, or Multiple tumors no more than 5 cm

T3

Multiple tumors more than 5 cm or Tumor involving a major branch of the portal or
hepatic vein(s)

T4

Tumor(s) with direct invasion of adjacent organs other than the gallbladder or with
perforation of visceral peritoneum

Regional lymph node (N)


NX

Regional lymph nodes cannot be assessed

N0

No regional lymph node metastasis

N1

Regional lymph node metastasis

Distant metastasis (M)


MX

Distant metastasis cannot be assessed

M0

No distant metastasis

M1

Distant metastasis

Stage grouping
I

T1

N0

M0

II

T2

N0

M0

IIIA

T3

N0

M0

IIIB

T4

N0

M0

IIIC

Any T

N1

M0

IV

Any T

Any N

M1

258

Cancer of the Liver Italian Program (CLIP) Staging System: It is the most validated staging system.
Variables

15

Points
0

Single

Multiple

<50%

<50%

>50%

Child-Pugh score

AFP (ng/ml)

<400

>400

Portal vein thrombosis

No

Yes

Morphology and hepatic replacement

Score = sum of points for four variables.


Score ranges from 0 to 6; scores of 4 to 6 are generally considered advanced disease, whereas
scores of 0 to 3 have a potential for long-term survival.
Okuda Staging System

16

Parameter

Value

Points

Tumor size

>50%

<50%

Present

Absent

>3

<3

>3

<3

Ascites

Serum albumin (g/dl)

Serum bilirubin (mg/dl)

Stage 1:

0 points

Stage 2:

1-2 points

Stage 3:

3-4 points

Treatment Recommendations
The treatment of HCC depends on two main factors: tumor stage and the functional status of the
background liver.
Stage I and II HCC
Several options exist for the management of early stage HCC: surgical resection, local tumor
ablation using radiofrequency or ethanol, or liver transplantation. Resection or transplantation
offers the best option for cure. Non-cirrhotics and Child A patients should be considered for
partial hepatectomy. Child C patients are best treated with liver transplantation provided the
availability of a suitable donor. Child B patients may be treated with either liver resection or
transplantation depending on the severity of the background liver decompensation.
In patients who are not candidates for liver resection and are on waiting list for liver
transplantation, local ablative strategies like radiofrequency ablation or percutaneous ethanol
injection can be employed to buy time for transplantation. These local ablative methods may also
be used with varied results for patients who are not candidates for either resection or
transplantation.
259

Stage III HCC


In patients without cirrhosis or in Child A patients, surgical resection (usually major hepatectomy)
may be feasible and provides the best chance for cure. Preoperative portal vein occlusion may
be done to induce compensatory hypertrophy of the contralateral lobe of the liver in order to
make the liver resection safer.

17

Novel approaches may also be tried viz. neoadjuvant

embolisation to decrease the size of primary tumour to allow less extensive surgery, and the
delay in time will allow extrahepatic disease to manifest in high risk patients thereby avoiding
unnecessary surgery. These candidates are generally not considered suitable for transplant due
to very high recurrence rate, though there have been encouraging reports of transplantation for
even multifocal and large HCC.
Stage IV HCC
The prognosis is extremely poor. No surgical treatment is recommended and these patients are
treated with best supportive care or palliative chemotherapy. Before labelling the patient to have
intrahepatic metastatic disease, the possibility of multicentric HCC should be considered,
especially in cirrhotics.

Liver Resection
A detailed knowledge of the segmental anatomy is essential for any surgeon who contemplates a
liver resection for HCC. Briefly, the liver can be divided into two lobes, each having its own portal
venous and hepatic arterial supply and biliary drainage. The right lobe has four segments:
segments 5,6,7,8 and the left lobe has three segments: segments 2,3,4. Segment 1 or the caudate
lobe is wedged between the portal vein and the inferior vena cava and is considered to be
separate from the right or the left lobes. There are three major hepatic veins. The middle hepatic
vein serves as a demarcation between the right and the left lobes and drains the adjoining
segments of the either lobe (segments 4,5,8). The right and left hepatic veins drain the
corresponding lobes.

A consensus on the uniform terminology for various types of liver resection was reached in the
IHPBA conference 2000 at Brisbane

18

and is reproduced below (figure 1).

Surface tumours may be treated with non-anatomic wedge resection with at least 1 cm margin of
normal liver tissue all around the tumor. For deep tumours and large tumours, anatomic liver
resection should be performed. Intraoperative ultrasound aids in planning the surgical approach by
delineating the major vessels, and also detecting other multicentric tumors.

19,20

It may also aid in

performing radiofrequency ablation of the additional tumors, when considered appropriate. The
mortality rates of major hepatectomy are less than 5% in experienced centers.

21

Large liver tumors more than 10 cm in size were previously considered unresectable. However,
experience with liver resection has enhanced the safety of this surgery and even such large
tumors can be aggressively treated with major hepatectomy.
260

22

The multicentric lesions (if present)

in such setting can be treated with radiofrequency ablation or transarterial chemoembolization


while the dominant large tumor is resected.

Liver transplantation
Liver transplantation is an attractive option for HCC in cirrhotic patients as it has the potential to
cure both the aspects of the disease (the tumor as well as the liver cirrhosis). Milan criteria

23

was

evolved to select patients who would have excellent outcome after transplantation to justify the
allocation of already scarce cadaveric organ. This criteria was proposed by Mazzaferro and
colleagues and included a solitary tumor less than 5 cm in size, or three or fewer tumors with none
more than 3 cm in size. Further modification of these criteria was proposed by the University of
California, San Francisco (UCSF criteria)

24

according to which patients with more extensive HCC

can be transplanted with good post-transplant outcome. With the advent of living donor liver
transplantation (LDLT), the indications of liver transplantation have been further expanded.

25

Concerns about donor autonomy and safety must be addressed while considering LDLT for HCC.

Local ablative procedures


Radiofrequency ablation (RFA) is the most widely used therapy worldwide. It uses thermal heat to
ablate the tumours (AC of 400-500kHZ).

26,27

An 18 G probe is inserted into the tumour either

percutaneously under USG guidance or under laparoscopic vision or by a laparotomy and needle
electrodes are used to pass alternating current. The heat thus generated kills the tumour cells. The
maximum size of tumours suitable for satisfactory ablation is 5 cms and one ablation takes 20
mins. Larger tumors have also been ablated using multiple punctures. The major risk is in tumours
close to main portal pedicles where bile duct injury and obstruction can occur. The effect is limited
in tumours near major vessels which may not be ablated properly due to the heat sink effect of
blood flow through the vessels.

28

Local recurrence rate following RFA is 5-20%. It can be repeated

if needed and is used for non-surgical patients with small tumours and as a bridge for surgical
candidates who await liver transplantation.

Percutaneous Ethanol injection (PEI) is chemical ablation directly destroying the cancer cells by
ethanol. The maximum size of tumours ablated is 3 cms and usually requires multiple injections.
The recurrence rate is 15% and there is a risk of intraperitoneal bleeding from highly vascular
tumours. Acetic acid can also be used instead of ethanol. This modality is used for nonsurgical
candidates with small tumours and to bridge the time gap for HCC patients awaiting liver
transplantation

Transarterial approaches
Transarterial chemo-embolisation (TACE): Agents like cisplatin, doxorubicin are used together with
embolising agents like starch microspheres, lipiodol and gelatin.

29,30

Superselective delivery of

chemotherapeutic drug through hepatic artery branch leads to a high concentration of the drug
within the tumor, especially when combined by embolization. It has been most widely used as a
261

palliative procedure for unresectable HCC. TACE is the initial treatment of choice in ruptured HCC
to stop bleeding. It can also be used as a neoadjuvant approach to make a large tumor smaller
and suitable for resection as well as a bridge before transplantation. TACE as an adjuvant
treatment following surgery has been found to improve survival. Occasionally, it causes complete
necrosis of small tumors. Side effects include high grade fever, abdominal pain, anorexia, ascites,
transient elevation of liver enzymes and cholecystitis due to cystic artery spasm. However no
definite dosages for the drugs have been devised so far and studies define the tumour stage and
burden in relation to the responses observed.

Transarterial radiotherapy: Agents used are yttrium-90 in glassmicrospheres or iodine-131 in lipiodol.


These too require hepatic arterial delivery by an interventional radiologist. The tagged isotopes
deposit in the tumour due to affinity of the carrier molecule and emit beta rays that destroy the
tumour cells. There appears to be reasonable survival benefit
problem.

32

31

but radiation hepatitis remains a

Major toxicities are liver toxicity, pneumonitis, and GI bleeding and hence should be

used with caution in patients with poor liver function.

REFERENCES
1.

Beasley RP, Hwang LY, Lin CC, et al. Hepatocellular carcinoma and hepatitis B virus. A
prospective study of 22 707 men in Taiwan. Lancet 1981;2:1129

2.

Rehermann B, Nascimbeni M. Immunology of hepatitis B virus and hepatitis C virus infection.


Nat Rev Immunol 2005;5:215

3.

Seitz HK, Stickel F. Risk factors and mechanisms of hepatocarcinogenesis with special
emphasis on alcohol and oxidative stress. Biol Chem 2006;387:349

4.

Tanaka H, Nouso K, Kobashi H, et al. Surveillance of hepatocellular carcinoma in patients with


hepatitis C virus infection may improve patient survival. Liver Int 2006;26:543

5.

Murakami T, Kim T, Kawata S, et al. Evaluation of optimal timing of arterial phase imaging for the
detection of hypervascular hepatocellular carcinoma by using triple arterial phase imaging with
multidetector-row helical computed tomography. Invest Radiol 2003;38:497.

6.

Vauthey JN, Abdalla EK, Doherty DA, et al. Body surface area and body weight predict total liver
volume in western adults. Liver Transpl 2002;8:233.

7.

Kubota K, Makuuchi M, Kusaka K, et al. Measurement of liver volume and hepatic functional
reserve as a guide to decision-making in resectional surgery for hepatic tumors. Hepatology
1997;26:1176.

8.

Shirabe K, Shimada M, Gion T, et al. Postoperative liver failure after major hepatic resection for
hepatocellular carcinoma in the modern era with special reference to remanant liver volume. J
Am Coll Surg 1999;188:304.

9.

McIntire KR, Vogel CL, Primack A, et al. Effect of surgical and chemotherapeutic treatment on
alpha-fetoprotein levels in patients with hepatocellular carcinoma. Cancer 1976;37:677

10. Buamah PK, Cornell C, James OF et al. Serial serum AFP heterogeneity changes in patients with
hepatocellular carcinoma during chemotherapy. Cancer Chemother Pharmacol 1986;17:182.
11. Sakon M, Monden M, Gotoh M, et al. The effects of vitamin K on the generation of des-gammacarboxy prothrombin (PIVKA-II) in patients with hepatocellular carcinoma. Am J Gastroenterol
1991;86:339.
262

12. Bruix J, Sherman M. Management of hepatocellular carcinoma. Hepatology 2005;42:1208.


13. Miyagawa S, Makuuchi M, Kawasaki S, et al. Criteria for safe hepatic resection. Am J Surg
1995;169:589.
14. American Joint Committee o Cancer. AJCC staging Manual. 6

th

Ed. New York: Springer-Verlag,

2002.
15. Cancer of the Liver Italian Program (CLIP) Investigators. Prospective validation of the CLIP
score: a new prognostic system for patients with cirrhosis and hepatocellular carcinoma.
Hepatology 2000;31:840.
16. Okuda K, Ohtsuki T, Obata H, et al. Natural history of hepatocellular carcinoma and prognosis in
relation treatment. Study of 850 patients. Cancer 1985;56:918.
17. Palavecino M, Chun YS, Madoff DC, et al. Major hepatic resection for hepatocellular carcinoma
with or without portal vein embolization: perioperative outcome and survival. Surgery
2009;145:399.
18. Terminology Committee of the International Hepato-Pancreato-Biliary Association. IHPBA
Brisbane terminology of liver anatomy and resection. HPB 2000;2:333.
19. Torzilli G, Makuuchi M. Intraoperative ultrasonography in liver cancer. Surg Oncol Clin N Am
2003;12:91.
20. Shukla PJ, Pandey D, Rao PP, et al. Impact of intraoperative ultrasonography in liver
surgery.Indian J Gastroenterol 2005;24:62.
21. Wei AC, Tung-Ping PR, Fan ST, et al. Risk factors for perioperative morbidity and mortality after
extended hepatectomy for hepatocellular carcinoma. Br J Surg 2003;90:33.
22. Pandey D, Lee KH, Wai CT, et al. Long term outcome and prognostic factors for large
hepatocellular carcinoma (10 cm or more) after surgical resection. Ann Surg Oncol 2007;14:2817.
23. Mazzaferro V, Regalia E, Doci R, et al. Liver transplantation for treatment of small hepatocellular
carcinomas in patients with cirrhosis. N Engl J Med 1996;334:693.
24. Yao FY, Ferrell L, Bass NM, et al. Liver transplantation for hepatocellular carcinoma: expansion
of tumor size does not adversely impact survival. Hepatology 2001;33:1394.
25. Pandey D, Wai CT, Lee KH, Tan KC. Living donor liver transplantation for hepatocellular
carcinoma: a single institution experience. Indian J Gastroenterol 2008;27:148.
26. Livraghi T, Meloni F. Treatment of hepatocellular carcinoma by percutaneous interventional
methods. Hepatogastroenterology 2002;49:62.
27. Bleicher RJ, Allegra DP, Nora DT, et al. Radiofrequency ablation in 447 complex unresectable
liver tumors: lessons learned. Ann Surg Oncol 2003;10:52
28. Lu DS, Raman SS, Limanond P, et al. Influence of large peritumoral vessels on outcome of
radiofrequency ablation of liver tumors. J Vasc Interv Radiol 2003;14:1267.
29. Lo CM, Ngan H, Tso WK, et al. Randomized controlled trial of transarterial lipiodol
chemoembolization for unresectable hepatocellular carcinoma. Hepatology 2002;35:1164.
30. Llovet JM, Real MI, Montana X, et al. Arterial embolization or chemoembolization versus
symptomatic treatment in patients with unresectable hepatocellular carcinoma: a randomized
controlled trial. Lancet 2002;359:1734.
31. Carr B. Hepatic arterial 90-Yttrium glass microspheres (Therasphere) for unresectable
hepatocellular carcinoma: interim safety and survival data on 65 patients. Liver Transpl
2004;10:S107.

32. Park HC, Seong J, Han KH, et al. Dose-response relationship in local radiotherapy for
hepatocellular carcinoma. Int J Radiat Oncol Biol Phys 2002;54:150.
263

264

265

266

Index

267

Biliary Stricture
PK Mishra, R Rajesh
Introduction
Biliary strictures can be benign or malignant. Malignant strictures arise due to cholangiocarcinoma or
carcinoma at the neck of gall bladder. These need to be dealt with separately. We would mainly deal
here, with benign biliary stricture in a patient with previous cholecystectomy which is the commonest
setting of this problem. Benign strictures due to congenital biliary atresia and strictures occurring after
liver transplantation are in a special category and beyond the scope of this discussion.

Causes of Benign Biliary Stricture

A. Congenital Biliary Atresia.


B. Bile Duct Injury
I.

Postoperative
a.
b.
c.
d.
e.
f.

Cholecystectomy or Choledochotomy
Biliary enteric anastomosis
Liver resection
Pancreatic surgery
Gastric operations
Liver transplantation

II.

Blunt or penetrating trauma

III.

Endoscopic or percutaneous biliary procedures

C. Inflammatory
I.

Cholelithiasis or choledocholithiasis

II.

Chronic pancreatitis

III.

Recurrent pyogenic cholangitis

IV.

Liver or sub hepatic abscess

V.

Parasitic infections

VI.

Chronic duodenal ulceration

D. Primary Sclerosing Cholangitis


E. Radiation injury
F. Papillary stenosis

Post Cholecystectomy Bile duct injury


Incidence: Bile duct injuries are reported in 0.2 to 0.3 % of open
Error! Bookmark not defined., Error! Bookmark not defined.

2, 3

and 0.4 to 1.3% of laparoscopic

cholecystectomy in larger studies. Actual incidence may

be higher.

Mechanism of injuries: Cholecystectomy, whether open or laparoscopic, should not be taken


casually. Higher injuries in laparoscopic cholecystectomies may be due to the learning curve and
inherent problems of laparoscopic approach as some of these may be inflicted by even
experienced laparoscopic surgeons. Mostly, it is due to wrong interpretation of the biliary
268

anatomy.

An important aspect in the prevention is to remember that there is no normal biliary

anatomy. Tenting of the CBD with excessive traction, injudicious use of cautery, improper clip
application and operating in field obscured by hemorrhage have been considered some of the
important mechanisms of injury. Excessive dissection of CBD may disrupt its blood supply and
lead to late stricture. Operating in patients with inflammation or choledocho-duodenal fistula or
Mirizzis syndrome is also potentially hazardous. Classical laparoscopic injury consists of removal
of a portion of CBD with or without clipping of the proximal hepatic duct.

Classification: Bismuths classification is the most accepted classification of biliary injuries.


Bismuth Classification of Bile duct stricture
I.
Hepatic duct stump more than 2 cm.
II.
Hepatic duct stump less than 2 cm.
III.
Hilar stricture with confluence intact.
IV.
Hilar stricture with destroyed confluence and separated right and left ducts
V.
Aberrant right sectoral duct injury with or without bile duct injury

This classification is simple and useful for prognostication. Strasberg classified bile duct injuries
7

from A to E. A is a minor leak still in continuity with CBD such as from cystic duct stump or injury
to duct of Luschka. Type B is ligation of right aberrant sectoral duct. Type C is transection of right
aberrant sectoral duct without occlusion reflecting the leak of bile. Type D is a lateral injury to bile
duct. Type E is bile duct stricture classified as per Bismuth from E1 to E5. Although widely used,
both these classification do not factor in the vascular injury, presence of sepsis or cholangitis,
pattern of presentation, time since injury or presence of portal hypertension. Several other
classifications have been proposed like Hannover, Siewert, Neuhaus and Stewart Way. Each
has its draw backs and is not used extensively like Strasberg Bismuth system.

269

Presentation
Some of these injuries may be obvious intraoperatively. Experienced help should be sought in
dealing with these. Some of these repairs may present later with biliary strictures. Patients with bile
duct leaks present early with signs of sepsis or general illness. If the drain is in place, bile leak is
obvious. Patients with complete cut off also present early with progressive jaundice. Fourth
category of patients is those which have partial injuries which gradually present over next few
months. These also include patients with leak which have stopped with constriction of the bile duct.
About 70% of injuries have presented by 6 months

Error! Bookmark not defined.

. Some of these may have

recurrent cholangitis, fever, pruritus or unexplained malaise and weakness. During examination,
tender hepatomegaly may be seen in those having longstanding obstruction, cholangitis or
abscess. Presence of splenomegaly should alert the surgeon for portal hypertension. This may
arise due to concomitant vascular injury, secondary biliary cirrhosis or coexistent liver disease.
Icterus and signs of pruritus are seen usually present.

Pathological consequences
Fibrosis: The high concentration of bile salts in the biliary canaliculi incite a inflammatory process
resulting in fibrogenesis which is the deposition of collagen and other extracellular matrix proteins
8

around the biliary canaliculi in portal tracts resulting in fibrosis and scarring. Though prolonged
biliary obstruction cause secondary biliary cirrhosis, it rarely results in typical features of cirrhosis.
In advanced cases there is marked fibrosis with well preserved lobular structure. Though it takes
several years to manifest these pathological features, it can occur within 2 years of development of
stricture. After biliary decompression, these pathological changes are potentially reversible and the
liver function gradually normalizes. If patient develops clinical features of liver failure like spider
angiomata or encephalopathy, preexisting liver parenchymal disease should be ruled as it is rare
for benign biliary obstruction to manifest these features.

Atrophy: In view of prolonged asymmetric involvement of biliary ducts and associated vascular injury,
there usually develops a lobar atrophy with compensatory hypertrophy of the remaining liver
resulting in rotational deformity and anatomical changes in the hilar area which influence the
operative approach for these patients. Usually in long standing benign biliary strictures, there is
atrophy of right lobe with gross hypertrophy of left lobe

Portal hypertension: Patients with biliary stricture can develop portal hypertension secondary to portal
fibrosis, portal vein injury and/or underlying liver parenchymal disease. As these patients with
portal hypertension have a hospital mortality of 25- 40%, documentation with liver biopsy is must
for both management and medico legal purpose. Recently it has been found that these patients
without portal injury usually have latent portal hypertension (mild to moderate)without much clinical
features of portal hypertension which normalizes after decompression.

270

Investigations
Biochemical parameters: Liver function tests usually shows evidence of cholestasis with fluctuating
level of serum bilirubin level. When elevated, serum bilirubin usually below 10 mg/dL, unless
secondary biliary cirrhosis has developed, or there is complete cut off. Serum alkaline
phosphatase is usually elevated. Serum aminotransferase levels can be normal or minimally
elevated except during episodes of cholangitis. If advanced liver disease exists, hepatic synthetic
function can be impaired, with lowered serum albumin and a prolongation of prothrombin time.

Radiologic Examination: Detailed pre operative evaluation of the type and extent of bile duct injury
with stricture with adequate control of the factors that can worsen the surgical outcome (like
sepsis, cholangitis, bilioma) optimizes the chances for favorable outcome.

Abdominal ultrasound and computed tomography (CT) play an important initial role in the
evaluation of patients with benign postoperative biliary strictures.

Ultrasonography abdomen as an initial, non invasive study can assess for dilated intrahepatic
radicals, bilioma which requires percutaneous drainage, approximate level of biliary obstruction
and stricture. Along with Duplex imaging it can be used to assess the vascular injury which
occurs in about 12-32% of the patients.

10

This evaluation is very important in terms of

successful outcome of the surgical biliary reconstruction, as biliary injury along with vascular
injury has less favourable outcome . Though it guides us initially for the further line of
management, Ultrasonogram abdomen is limited in assessing the extent and type of biliary
stricture.

Contract enhanced CT abdomen is probably best initial study to evaluate a case of Bile duct
injury. Properly done CT helps in assessing any intra abdominal collection, definite level of bile
duct stricture, dilated intrahepatic radicals with cholangitic abscess and also vascular injury
with liver atrophy-hypertrophy complex. But CT is also limited in evaluation of the type and
extent of biliary stricture.

The gold standard for evaluation of patients with bile duct strictures is cholangiography.
Percutaneous transhepatic cholangiography (PTC) is usually more valuable than
endoscopic retrograde cholangiography (ERC). PTC is more useful in that it defines the
anatomy of the proximal biliary tree that is to be used in the surgical reconstruction.
Furthermore, PTC can be followed by placement of percutaneous transhepatic catheters, which
can be useful in decompressing the biliary system either to treat or prevent cholangitis or to
control an ongoing bile leak. These catheters can also be of assistance in surgical
reconstruction and provide access to the biliary tree for non operative dilation. ERC is often less
useful than PTC because the discontinuity of the extra hepatic bile duct usually prevents
271

adequate filling of the proximal biliary tree. But for patients with lateral injury with bile leak,
ERCP is both diagnostic and therapeutic in identifying the leak and biliary stenting at the same
time which may avoid surgical intervention.

The development of magnetic resonance cholangiopancreatography has provided a


noninvasive technique that provides excellent delineation of the biliary anatomy.

11

The quality

of these images has led us to advocate this technique as the initial step in the evaluation of
patients with suspected bile duct injuries and may eliminate the need for a diagnostic ERC/PTC
in many patients.

In patients suspected of having early postoperative bile duct injury, a radionucleotide biliary
scan (HIDA) can confirm bile leakage. It can be useful in assessing patients with underlying
liver disease to document liver dysfunction or obstruction to clearance and their relative
contribution.

In patients with postoperative external bile fistula, injection of water-soluble contrast media through
the drainage tract (Fistulogram) can often define the site of leakage and the anatomy of the
biliary tree. This is a simple and easily available tool which gives valuable information.

Distinction between benign and malignant stricture


Though it is very difficult to clearly distinguish the nature of stricture pre operatively, certain features
can guide us in their differentiation.
Benign

Malignant

Age

Usually young

Elderly

Duration of symptom

Variable

Short duration

Cholangitis

usual

Unusual, if no intervention

Depth of jaundice

Variable

>15 mg%

Weight loss/ anorexia

rare

common

Imaging of stricture

Long stricture with regular


margins and sectoral
involvement

Short stricture, irregular


margins, thick walled, more
dilated proximal ducts with bile
duct hyperenhancement in
portal venous phase.

Management
Theoretically, these patients can be managed by endoscopic, radiological percutaneous and surgical
therapy. However, endoscopic and radiological methods are suitable for definite management in very
few cases. Endoscopic stenting may be helpful in managing bile leaks in partial injuries of CBD,
sectoral ducts or cystic duct stump leaks. Some partial injuries have been treated by progressively
increasing the stents to achieve complete dilatation. Similarly, radiologic percutaneous techniques are

272

useful in some cases especially for post operative dilatation or for drainage in patients with sepsis. By
and large these patients are young and surgery is the treatment of choice.
Preoperative management
Aim of the preoperative management is to precisely define the injury, determine any complications
like atrophy-hypertrophy, portal hypertension, or secondary biliary cirrhosis. Associated renal
complications, cholangitis, coagulopathy and sepsis should be taken care of. Essentially the
surgery should be done in optimum condition without any hurry 6-8 weeks after the injury.

12

Associated medical risk factors should be also optimized. In the immediate preoperative period
coagulopathy should be corrected with vitamin K, sepsis controlled and fluid and electrolytes
corrected. Adequate blood and fresh frozen plasma should be arranged. Type IV injuries may
require hepatotomy and are generally more difficult. Similarly, patient with portal hypertension and
secondary biliary cirrhosis may have difficult operative course. At the time of consent these
information should be discussed with relatives.

Operative Procedure
Restoration of bile flow is achieved by a bilio-enteric anastomosis. Rarely, when the stricture is in
pancreatic or immediate supraduodenal CBD, a choledochoduodenostomy can be constructed.
Most often the reconstruction is by a Roux loop with hepaticojejunostomy. Requirements of a good
bilioenteric anastomosis are:
1. Adequate stoma size (>2cm)
2. Good vascular supply
3. Tension free anastomosis
4. Should drain all segments of the liver
5. Mucosa to mucosa anastomosis.

Access to proximal ducts is relatively easy in Bismuth type I and II strictures. In Type III and IV
strictures the hilar plate lowering technique described by Blumgart is used. In this Hepp-Couinaud
technique the left duct is approached by incising the Glissons capsule at the base of Quadrate
lobe. This lowers the left bile duct and by further dissection, gradually the area of confluence and
the extra hepatic right duct. This allows space for mucosa to mucosa side to side anastomosis
between the jejunal Roux loop and the healthy bile duct above the stricture. If extra length of left
duct is required the dissection can be taken into the ligamentum Teres. Type IV strictures may
rarely require hepatotomy or part excision of quadrate lobe to approach the right duct.

Isolated Sectoral duct Injury. These are difficult to manage especially if accompanied by bile leak
as the ducts are small and difficult to approach. Asymptomatic remote injuries should be left
alone. Symptomatic injuries with recurrent cholangitis should be treated with repair or resection
of the segment depending on the atrophy.

13

Recent asymptomatic injuries should be treated

with repair to prevent atrophy and complications.

273

Error! Bookmark not defined.

Use of stent for bilioenteric anastomosis is controversial. Some use it routinely in all cases.

14

Advantage being post operative decompression, access for imaging and intervention. We use it
only in cases of difficult or unsatisfactory anastomosis or in small ducts. How long should these
stents be kept is also variable and can be from couple of weeks to a year. When it is
anticipated that patient may again have stricture or in cases of second or more interventions
after Hepaticojejunostomy, an access loop is made.

15

The distal limb of the roux loop, beyond

the HJ, is left long and brought out subcutaneously or subperitoneally. This allows for easy
access for radiologic interventions.

Results: Previous series reported 5-8% mortality. This has been reduced substantially with wider
experience in specialized centres and many large series have reported no mortality. Still patients
may succumb while awaiting definitive management with sepsis and complications. Overall 8090% good results are reported. Poor prognostic factors are 1. Surgeons inexperience. 2.
Presence of sepsis and cholangitis 3. Previous attempts at repair 4. Small duct size 5. Long delay
in repair 6. Liver cirrhosis and portal hypertension.

Non operative Approaches: These include endoscopic and the radiologic percutaneous balloon
dilatation and stenting. These can only be used for partial injuries and the results are not better
than the surgical management.

16

However in post operative strictures, in patients in whom surgery

is contraindicated and as part of multimodality approach these are extremely useful.

Biliary stricture with Portal Hypertension: This is a difficult group of patient with high rate of
complication and mortality.

17

If serious bleed is encountered than a splenorenal shunt should be

done before definitive repair.

Liver Transplantation: Very rarely, transplant may be required for long standing biliary stricture with
secondary biliary cirrhosis with portal hypertension although even there it should not be the first
line approach.

18

Biliary Stricture after Other Operations


These may arise after Gastric and hepatic resection, portacaval shunts, Liver transplantation, and
CBD explorations. Bilioenteric anastomosis may also become strictured after reconstruction.

Post Inflammatory Bile Duct Stricture


Recurrent cholecystitis in some cases may lead to ongoing inflammation and stricture of the bile
ducts. Gall stones may erode into the CBD in Mirizzis syndrome. Recurrent pyogenic cholangitis may
lead to intrahepatic stones and strictures. Chronic pancreatitis causes a smooth, long stricture at the
lower end. If the liver function tests are normal it need not be treated even if severe stenosis is seen
on

imaging

except

if

the

patient

is

being

274

operated

for

chronic

pancreatitis

itself.

Choledochoduodenostomy is simpler but recurrent inflammation and fibrosis may necessitate


Hepaticojejunostomy.

Post Traumatic Biliary Stricture


Both blunt and penetrating injuries may lead to biliary stricture. Hemorrhage and associated injuries
take precedence in management. Bile flow is diverted and a later definitive repair is done. Biliary
fistulas after hepatic injury, which do not close after prolonged conservative treatment, can be
anastomosed to roux loop. Bilio-enteric anastomosis is done for ductal injuries. Endoscopic or
percutaneous approaches can also be used.
References
1.

Jarnagin WR, Blumgart LH . Biliary Stricture and Fistula. In Blumgart LH ed in Surgery of the Liver
Biliary Tract and Pancreas. 2007, Saunders, Philadelphia.

2.

Roslyn JJ, et al Open Cholecystectomy :A contemporary analysis of 42,474 cases.Ann Surg 218; 12937.

3.

Strasberg SM, Hertl M, Soper NJ. An analysis of the problem of biliary injury during laparoscopic
cholecystectomy. J Am Coll Surg Am 1995:180: 101-125.

4.

Way LW, Stewart L, Gantert W, et al. Causes and prevention of laparoscopic bile duct injuries:
analysis of 252 cases from a human factors and cognitive psychology perspective. Ann Surg
2003;237(4):4609.

5.

Branum G, Schmitt C, Baillie J, et al. Management of major biliary complications after laparoscopic
cholecystectomy. Ann Surg 1993;217(5):53240

6.

Bismuth H. Postoperative stricture of the bile duct. In Blumgart LH ed : The biliary tract:Clinical
Surgery International. Churchill Livingstone. Edinburgh. 209-18.

7.

Strasberg SM, Hertl M, Soper NJ. An analysis of the problem of biliary injury during laparoscopic
cholecystectomy. J Am Coll Surg 1995;180(1):10125.

8.

Friedman SL et al.Molecular mechanisms of hepatic fibrosis and principles of therapy. J


Gastroenterol. 1997 Jun;32(3):424-30.

9.

Ibrarullah M, Sikora SS, Agarwal DK, Kapoor VK, Kaushik SP, 'Latent' portal hypertension in benign
biliary obstruction.HPB Surg. 1996;9(3):149-52. .

10. Mathisen O, Soreide O, Bergan A. Laparoscopic cholecystectomy: bile duct and vascular injuries:
management and outcome. Scand J Gastroenterol 2002;37(4):47681
11. Ragozzino A, De Ritis R, Mosca A, et al. Value of MR cholangiography in patients with iatrogenic bile
duct injury after cholecystectomy. AJR Am J Roentgenol 2004;183(6): 156772.
12. Lillemoe KD. Current management of bile duct injury. Br J Surg 2008;95(4):4035.
13. Lillemoe KD, Petrofski JA, Choti MA, Venbrux AC, Cameron JL. Isolated right segmental hepatic duct
injury: a diagnostic and therapeutic challenge J Gastrointest Surg. 2000 Mar-Apr;4(2):168-77.
14. Lillemoe KD, Melton GB, Cameron JL, et al. Postoperative bile duct strictures: management and
outcome in the 1990s. Ann Surg 2000;232(3):43041.
15. Al-Ghnaniem R, Benjamin IS. Long-term outcome of hepaticojejunostomy with routine access loop
formation following iatrogenic bile duct injury. Br J Surg 2002;89(9):111824.
16. Lillemoe KD, Martin SA, Cameron JL, et al. Major bile duct injuries during laparoscopic
cholecystectomy. Follow-up after combined surgical and radiologic management. Ann Surg
1997;225(5):45968
275

17. Chapman WC, Halevy A, Blumgart LH, et al. Postcholecystectomy bile duct strictures. Management
and outcome in 130 patients. Arch Surg 1995;130(6):597602

18. Nordin A, Halme L, Makisalo H, et al. Management and outcome of major bile duct injuries after
laparoscopic cholecystectomy: from therapeutic endoscopy to liver transplantation. Liver Transpl
2002;8(11):103643.

Index

276

Choledochal Cyst
Vijay Arora
Introduction
Cystic dilatation of the common bile duct (CBD), also known as choledochal cyst, is a fairly
uncommon anomaly of the biliary tract. Although it was first described by Vater and Ezler in 1723,
Douglas published the first complete clinical description of the anomaly in a patient in 1853. He
speculated about the congenital nature of this anomaly.

In 1959, Alonso-Lej et al published an extensive review of 94 cases in the literature and added two
cases of their own. They classified choledochal cysts into 3 types. In 1977, Todani et al further
classified this anomaly into 5 types. Subsequent subtypes based on cholangiographic findings
have been described.

Frequency
Population prevalence estimates of choledochal cysts range from approximately 1 case in 13,000
people to 1 case in 2 million people. Cystic diseases of the bile duct are more common in Japan
and Asia

Choledochal cysts can occur in persons of any age. Two thirds of the cysts are diagnosed before
the patient is aged 10 years. Approximately 20% of cysts are diagnosed in much older patients. In
rare cases, choledochal cysts have been detected at prenatal ultrasonography as early as 15
weeks' gestation

PATHOPHYSIOLOGY
Pathogenesis
The exact cause of choledochal cyst remains obscure. Approximately 20% are diagnosed in
adults, including elderly patients. Several theories have been postulated, as follows:

Weakness of the wall of the bile duct

Obstruction of the distal choledochus

Combination of obstruction and weakness

Reflux of pancreatic enzymes into the CBD secondary to an anomaly of the pancreaticobiliary
junction

Babbitt and colleagues in 1969 found many with an anomaly of the pancreaticobiliary junction. In
these patients, a small distal CBD entered the pancreatic duct at 2-3.5 cm from the ampulla of
Vater, whereas the normal common channel is 5 mm or less. This may represent failure of normal
separation of these two ducts during embryologic development. This proximal junction precludes
the proper functioning of the sphincter of Oddi. The pressure in the pancreatic duct (30-50 cm
H2O) exceeds the pressure in the CBD (25-30 cm H2 O) favoring reflux of pancreatic secretions

277

into the CBD. They also noted a high amylase content in the fluid from the cysts. The reflux of
pancreatic juice could lead to weakness and dissolution of the wall of the CBD.

Experimental support for this concept was reported in 1974 by Kato and associates who
anastomosed the main pancreatic duct to the gallbladder in dogs. Within 9 days after the
anastomosis, all the tested animals had varying degrees of dilatation of the CBD, with edematous
changes of the CBD wall. They concluded that proteolytic enzymes were responsible for the
damage.

In 1984, Todani et al conducted an analysis of endoscopic retrograde cholangiopancreatograms


and other cholangiograms and confirmed this long common-channel anomaly.

All of these theories are applicable to choledochal cyst type I, III, and IV anomalies, but they cannot
be used to explain type II and V choledochal cysts in which the CBD is normal. Perhaps genetic
factors play a role. Despite this, the two most accepted theories are still reflux of pancreatic enzymes
into the CBD secondary to an anomalous pancreaticobiliary junction and obstruction of the distal
CBD.

Pathologic features
Grossly, the size of a type I choledochal cyst widely varies. The cysts contain a few hundred milliliters
of bilious fluid that is rich in pancreatic enzymes. The cyst wall thickness also varies, ranging
from very thin to a few millimeters in thickness.
Sludge and stones are sometimes present within the cyst. The bile duct distal to the cyst is usually
stenotic. The liver may have variable degrees of fibrosis or established cirrhosis with portal
hypertension. Histologic studies of the wall of choledochal cysts show dense fibrous connective
tissue with inflammation and ulceration of the mucosa and submucosal layers. The

278

inflammation is significantly less in younger patients than in older children in whom chronic
inflammatory changes abound
Carcinoma arising in a choledochal cyst wall or remaining biliary tree after complete cyst excision is
well recognized. Malignancy is believed to be the result of chronic inflammation and metaplasia.
The typical malignancy is adenosquamous carcinoma or occasional cases of small cell
carcinoma.

Prenatal diagnosis
With the use of prenatal ultrasonography, an increasing number of choledochal cysts have been
reported in the fetus. Incomplete gastric obstruction by a large cyst is one of the typical clinical
manifestations in newborns and young infants. The earliest reported choledochal cyst was detected in
a fetus at 15 weeks' gestation, which may correspond to the timing of the formation of pancreatic
enzymes.
The prenatal demonstration of a cystic structure inferior to the liver strongly suggests the diagnosis.
Fetal development should be carefully monitored with serial ultrasonography after such a discovery.
Most centers prefer to excise the cyst shortly after birth. A waiting period of a few weeks is necessary
to stabilize the baby and allow for proper preoperative evaluation. Surgical excision in the neonatal
period has been shown to be technically feasible and well tolerated by the patient.

Clinical presentation
Two distinct clinical groups of patients are recognized with regard to age at presentation. The first
group is the infantile group consisting of babies younger than 1 year, with or without obvious
hepatomegaly, with obstructive jaundice and acholic stools. This clinical picture is indistinguishable
from that of biliary atresia in the absence of a palpable mass in the right side of the abdomen.
However, the cystic mass can usually be detected either at clinical examination or on
ultrasonography; this finding suggests a diagnosis of choledochal cyst.

Other symptoms, such as vomiting, fever, and abdominal pain with hyperamylasemia are extremely
infrequent. In infants with a prenatal diagnosis of choledochal cyst, jaundice often does not manifest
until 1-3 weeks after birth.

In contrast, infants older than 1 year, with the so-called adult form of choledochal cyst, generally
have one or more components of the classic triad: pain, jaundice, and a palpable mass. The entire
triad is present in fewer than 30% of patients. Jaundice is intermittent and often associated with vague
abdominal pain. The pain has been described as being similar to that of cholangitis or recurrent mild
pancreatitis. Undiagnosed choledochal cysts can lead to choledocholithiasis, cirrhosis with portal
hypertension, cyst rupture, or biliary carcinomas

Differential Diagnoses
Pseudocyst, Pancreatic
279

Other Problems to Be Considered

Hepatic cyst

Cholangiocarcinoma

Choledocholithiasis

Cholangitis

Gallbladder duplication

Anatomy
Regarding the anatomic classification of choledochal cyst, in 1977, Todani et al modified the classic
Alonso-Lej classification by adding two new types (types IV and V). Others have subsequently added
further subtypes. The types are as follows:
Type I

Cystic or fusiform dilatation of the common bile duct (CBD); most frequent type (90-95% of
the cases).

Type II

Diverticulum of the CBD, with normal size CBD

Type III Choledochocele, a cystic dilatation of the distal intramural portion of the CBD, typically
protruding into the second portion of the duodenum
Type IV Cystic or fusiform dilatation of the CBD associated with cystic, fusiform, or saccular
dilatation of intrahepatic bile ducts, also termed form fruste
Type V Cystic, fusiform, or saccular dilatation of the intrahepatic bile ducts associated with a normal
CBD; may be associated with hepatic fibrosis (referred to as Caroli disease)

Laboratory studies
Laboratory studies that may be useful for the diagnosis and preoperative evaluation of a patient with a
choledochal cyst include direct bilirubin, alkaline phosphatase, serum aspartate aminotransferase
(AST), serum alanine aminotransferase (ALT), gamma-glutamyl transferase (GGT), and coagulation
profiles. A CBC count should also be obtained to exclude any associated or underlying anemia prior
to surgery.

280

Imaging Studies
Imaging studies are the cornerstone of diagnosis of choledochal cysts. They serve not only to confirm
the diagnosis but also to outline the anatomy of the anomaly in preparation for surgical intervention.

Ultrasonography is the best initial study. In neonates, it may be the only test needed.
Ultrasonography can demonstrate changes in the bile ducts as well as in the liver.

Endoscopic retrograde cholangiopancreatography (ERCP) remains the criterion standard


diagnostic study. In expert hands, ERCP can be performed with a high rate of success, even in
small infants. When successful, ERCP clearly shows the anatomy of the pancreaticobiliary
junction. With forceful injection of contrast even small choledochoceles can be imaged,
presumably by distension of the cyst wall.

Magnetic resonance cholangiopancreatography (MRCP) has largely supplanted ERCP as the


diagnostic test of choice for choledochal cysts because it offers high resolution detailed images of
relevant anatomy, is noninvasive, and does not suffer from complications such as postprocedure
pancreatitis. MRCP detects most choledochal cysts with sensitivities from 90-100% and
specificities from 73-100%, with the exception of small choledochoceles and minor ductal
anomalies. MRCP has been shown to be effective in neonates, children, adults, and fetuses.

CT scanning may also be useful to delineate the cyst and its relationship to surrounding structures. In
older patients, especially adults, CT scanning combined with cholangiography may be useful.
Upper GI imaging and cholangiography with oral or intravenous contrast enhancement are of
limited value in the setting of hyperbilirubinemia and are generally outdated. Scintigraphy
with technitium-99m diisopropyl iminodiacetic acid (DISIDA) may show complete obstruction
of the distal bile duct without any drainage to the intestine

Medical Care
The treatment of choice for choledochal cysts is complete excision. Appropriate antibiotic therapy and
supportive care should be given to patients presenting with cholangitis. Patients who present at a late
stage, after the development of advanced cirrhosis and portal hypertension, may not be good
candidates for surgery because of the prohibitive morbidity and mortality rates associated with these
comorbid conditions.
a) No medical therapy specifically targets the etiology of choledochal cysts, nor is any drug or
any type of nonsurgical modality curative.
b) Patients who present with cholangitis should be treated with broad-spectrum antibiotic
therapy directed against common biliary pathogens, such as Escherichia coli and Klebsiella
species, in addition to other supportive measures, such as volume resuscitation.
c) Again, it must be emphasized that these means are supportive and that surgery is the only
currently available definitive therapy.
281

Surgical Care
The treatment of choice for choledochal cysts is complete excision of the cyst with construction of
a biliary-enteric anastomosis to restore continuity with the gastrointestinal tract. According to Jordan
and associates, both partial resection of the cyst and internal drainage procedures expose patients
to increased risks of cholangitis, pancreatitis, and cholangiocarcinoma.

The positive results of proper surgical treatment were reinforced by Visser and colleagues. These
investigators reported a series of 39 adult patients with choledochal cysts. Cholangiocarcinomas or
gallbladder cancers were noted in 8 patients (21%) at the initial operation performed by the authors.
Seven of these patients had previously undergone a partial cyst excision, drainage procedure, or
expectant management. No cancer was noted during the follow-up care of the patients who
underwent complete cyst excision.

Shimotakahara

and

coworkers

compared

Roux-en-Y

hepaticojejunostomy

to

hepaticoduodenostomy for biliary reconstruction following choledochal cyst excision. The authors
concluded that hepaticojejunostomy was a better choice because of an unacceptably high rate of
duodenogastric bile reflux (33.3%) in the hepaticoduodenostomy group.
Lee and associates reported 3 cases of laparoscopic choledochal cyst excision and Roux-en-Y
reconstruction in children. One was converted to open operation owing to involvement of the
confluence of the lobar hepatic ducts. All children have done well postoperatively.

Jang and coauthors described their experience with laparoscopic surgical management of
choledochal cysts in a series of 12 adult patients (mean age=37.3 y). Complete cyst excision and
reconstruction via Roux-en-Y hepaticojejunostomy was accomplished in all patients using
laparoscopic techniques. No mortalities and no anastomotic complications occurred. Mean operative
time was 228 minutes. Patients were discharged from the hospital after an average stay of 5.8 days.

Reports of robotically-assisted laparoscopic resection of choledochal cysts are beginning to


appear. Woo and colleagues reported such a case in the management of a 5-year-old child with a
type I choledochal cyst. The cyst was excised successfully. The total robotic operative time was 390
minutes, and the time for the entire procedure was 440 minutes. No complications occurred. The
patient was reported well after 6 months of follow-up.

Lee and colleagues reviewed their experience with choledochal cyst excision in 198 children to
determine the benefit of operating early in the neonatal period. They found a lower complication rate
and less hepatic fibrosis in neonates who underwent excision of a choledochal cyst within the first 30
days of life.

Woon and colleagues emphasized the importance of treating cyst-associated complications, such as
pancreatitis and sepsis, before attempting to define cyst anatomy with ERCP or MRCP. This aids in
282

delineating the extent of involvement of the biliary tree and the exact type of choledochal cyst.
Furthermore, they reiterated the importance of complete cyst excision and reconstruction with Rouxen-Y hepaticojejunostomy.

The surgical management for each choledochal cyst type is described below.
Type I

The treatment of choice is complete excision of the involved portion of the


extrahepatic bile duct. A Roux-en-Y hepaticojejunostomy is performed to restore
biliary-enteric continuity.

Type II

The dilated diverticulum comprising a type II choledochal cyst is excised in its


entirety. The resultant defect in the common bile duct is closed over a T-tube.

Type III

Choledochocele. The choice of therapy depends upon the size the cyst.
Choledochoceles measuring 3 cm or less can be treated effectively with
endoscopic sphincterotomy. Lesions larger than 3 cm typically produce some
degree of duodenal obstruction. These lesions are excised surgically through a
transduodenal approach. If the pancreatic duct enters the choledochocele, it may
have to be reimplanted into the duodenum following excision of the cyst.

Type IV

The

dilated

extrahepatic

duct

is

completely

excised

and

Roux-en-Y

hepaticojejunostomy is performed to restore continuity. Intrahepatic ductal disease


does not require dedicated therapy unless hepatolithiasis, intrahepatic ductal
strictures, and hepatic abscesses are present. In such instances, the affected
segment or lobe of the liver is resected.
Type V

(Caroli disease): Disease limited to one hepatic lobe is amenable to treatment by


hepatic lobectomy. When this occurs, the left lobe usually is affected. Hepatic
functional reserve should be examined carefully in all patients before committing to
such therapy. Patients with bilobar disease who begin to manifest signs of liver
failure, biliary cirrhosis, or portal hypertension may be candidates for liver
transplantation.

Lilly technique: Occasionally, the cyst adheres densely to the portal vein secondary to long-standing
inflammatory reaction. In this situation, a complete, full-thickness excision of the
cyst may not be possible. In the Lilly technique, the serosal surface of the duct is
left adhering to the portal vein, while the mucosa of the cyst wall is obliterated by
curettage

or

cautery.

Theoretically,

this

removes

the

risk

of

malignant

transformation in that segment of the duct. Useful in repeat surgery.

Intraoperative cholangiography obtained via puncture of the cyst or via the gallbladder is always
obtained. It outlines the exact anatomy of the choledochal cyst and its relationship with the pancreas.
Cholecystectomy is routinely performed at the same time.

Biliary reconstruction can be performed with a Roux-en-Y hepaticojejunostomy as high as possible,


near the hilum of the liver. Some authors, including Raffensperger and Shamberger, have interposed
283

a reversed segment of jejunum to prevent reflux. This idea has not been universally accepted. No
stents are routinely necessary.

Surgical Therapy
Treatment of choledochal cysts is surgical, except in type V multiple intrahepatic cysts, which can
benefit from medical management for variable periods of time. In the past, operative aspiration
and external drainage were used extensively because most patients were quite sick, and a
simple quick procedure was convenient. These external drainage procedures of the biliary tree
were unsuccessful because of numerous complications, including repeated cholangitis and
biliary fistulae. Mortality rates were high. Today, in the setting of acute severe disease,
percutaneous cholecystostomy drainage can be performed prior to the definitive procedure.
This is safe and generally well tolerated; however, it is not necessary in most patients.

Internal drainage, either with cystoduodenostomy or cystojejunostomy with Roux-en-Y biliary


reconstruction, was used in the past. These procedures left the cyst behind, and the free reflux
of pancreatic enzymes into the cyst via the anomalous pancreaticobiliary junction resulted in a
high incidence of calculi, recurrent cholangitis, anastomotic strictures, and carcinoma
arising from the cyst. Of patients treated with either cystoduodenostomy or cystojejunostomy,
65% remained symptomatic, and 40% required repeat surgery at a later date. Recurrent
cholangitis and chronic inflammation in the remaining cyst eventually produces metaplasia that
leads to malignant transformation.

Contraindications
The treatment of choledochal cyst is typically complete surgical excision at the time of
presentation, with the exception of type V (multiple intrahepatic cysts) which may benefit from
conservative therapy including percutaneous drainage and medical management.
Complications
Complications after surgery have been mainly observed with types I, IV, and V choledochal
cysts. They are much less common in excisional procedures. The overall morbidity rate is less
than 10%. Mortality and repeat surgery rates are low after excision, compared with those
associated with internal drainage operations.

Postsurgical Complications Include The Following:


Cholangitis - 2.3% incidence of cholangitis after cyst excision. 88% of patients who
previously underwent cystoenterostomy had cholangitis.

Biliary stone formation - 25% rate of choledocholithiasis and a 33% rate of hepatolithiasis
after cystoenterostomy. Stones can be observed in the intrapancreatic bile duct. Usually,
cholangitis and stone formation are observed in the same patient. These complications are
thought to result from many factors, including the following:
284

a) Stricture of the anastomosis


b) Residual debris in the intrahepatic bile duct
c) Dilated intrahepatic ducts, especially in type IV and type V choledochal cysts

Anastomotic stricture
a) Apart from technical errors, anastomotic strictures may be a progressive
phenomenon after surgery.
b) Hata et al found a 4.1% rate of anastomotic strictures. The diameter of an adequate
anastomosis is usually reduced by 20-30% after a few weeks.
c) Such a reduction in the anastomotic diameter may result from excessive
devascularization of the duct during dissection. A wide anastomosis as far as the
hepatic hilum may prevent anastomotic stricture. Residual debris in the intrahepatic
bile ducts: Residual debris is commonly observed in older patients. Debris left within
the intrahepatic duct or pancreatic duct during cyst excision may be responsible for
postexcisional stone formation and pancreatitis.

Intrahepatic bile duct dilatation: Dilatation usually regresses after cyst excision and
hepaticojejunostomy in young patients. In older patients and adults, this dilatation tends
to persist. Dilatation and residual debris may cause cholangitis and stone formation.
Some authors recommend endoscopic examination of the duct during surgery to clean
out all the debris.

Malignancy
a) The risk of carcinoma in the retained cyst approaches 50% in patients treated with
cystoenterostomy and is approximately 20 times greater than in the general population.
b) Total cyst excision had been promising in eliminating the risk of cancer
development. However, sporadic cases of carcinoma in the intrahepatic ducts and distal
common duct after complete cyst excision have been reported.
c) Yamataka et al have recommended excision of the intrapancreatic terminal
choledochus.
d) With regard to intrahepatic ducts, adequate bile drainage may prevent malignant
transformation.

Further Outpatient Care


Patients need lifelong follow-up because of the increased risk of cholangiocarcinoma, even after
complete excision of the cyst.
Prognosis
The prognosis after excision of a choledochal cyst is usually excellent.

Index

285

Causes, Presentation and Surgical Management of Obstructive


Jaundice
Rajneesh K Singh, JR Reddy, P Sihag

Introduction
Jaundice or icterus is a generic term used for yellow discoloration of the skin, mucous membrane or
sclera caused by a heterogeneous group of disorders. It is useful to divide the causes of obstructive
jaundice into two categories, cholestasis from parenchymal liver disease mechanical obstruction from
a block of the intrahepatic or extra hepatic biliary tract.

Surgical jaundice or Obstructive jaundice occurs due to the intra or extra hepatic obstruction to the
biliary flow. It can present as a problem in diagnosis and management because there is a group of
jaundiced patients in whom it is very difficult to distinguish between organic / structural obstruction
and a medical cause of jaundice particularly intra hepatic cholestasis.

Table 1 - Causes of Biliary Tract Obstruction


Type I. Complete Obstruction
Carcinoma head of pancreas
Common bile duct ligation (for e.g. during cholecystectomy)
Gall bladder carcinoma
Cholangiocarcinoma
Parenchymal liver tumours ( primary or secondary) (rare cause)
Type II. Intermittent Obstruction
Choledocholithiasis
Periampullary tumours
Duodenal diverticula
Choledochal cyst
Polycystic liver disease
Biliary parasites
Hemobilia
Type III. Chronic Incomplete Obstruction
Strictures of the common bile duct
Congenital
Traumatic ( Iatrogenic)
Sclerosing cholangitis
Post radiotherapy
Stenosis of biliary-enteric anastomosis
Chronic pancreatitis
Cystic fibrosis
Sphincter of Oddi stenosis
Type IV. Segmental Obstruction
Traumatic
Intrahepatic stones
Sclerosing cholangitis
Cholangiocarcinoma

286

Pathophysiology of Obstructive Jaundice


Biliary obstruction produces local effects on the bile ducts that lead to derangements of hepatic
function and ultimately to widespread systemic effects. Patients who are jaundiced are at increased
risk of developing hepatic dysfunction, renal failure, cardiovascular impairments, nutritional
deficiencies, bleeding problems, infections, and wound complications and of dying after surgery.
Hepatobiliary Factors
i.

With biliary obstruction, the bile canaliculi become dilated, and the microvilli become distorted
and swollen. In patients with long standing obstruction, intra hepatic bile (ductules)
proliferation occurs with increase in the length and tortuosity of the canaliculi. In the setting
of partial or complete biliary obstruction as biliary pressure increases ( upto 30 cm HO)(1) ,
the tight junction between hepatocytes and bile duct cells are disrupted , resulting in an
increase in bile duct and canalicular permeability, this results in an inflammatory response
followed by increased fibrogenesis with deposition of type I collagen in the portal triads (2).

ii.

Impairment of macrovascular and microvascular perfusion of the liver has been reported in
patients with obstructive jaundice. This alteration of hepatic perfusion may explain the
increase risk of hepatocellular dysfunction when performing liver resections in patients with
obstructive jaundice (3).

iii.

When biliary pressure increases to greater than 20 cm HO, hepatic bile secretion is
diminished, as a result excretory products of the hepatocytes reflux directly into the vascular
system leading to systemic toxicity. In addition hepatic metabolic and synthetic functions are
also depressed.

iv.

Kupffer cells demonstrate decreased endocytosis, phagocytosis, clearance of bacteria and


endotoxin

Cardiovascular Factors
Following hemodynamic and cardiac disturbances have been reported in experimental animals
with obstructive jaundice (4) - decreased cardiac contractility; reduced left ventricular pressures;
impaired response to - agonistic drugs; decreased peripheral vascular resistance. The
combination of depressed cardiac function and decreased total peripheral resistance most likely
makes jaundiced patients more susceptible to the development of post operative shock than nonjaundiced patients.

Renal Factors
Important factors that may play a role in the development of renal failure in obstructive jaundice
include (5) - depressed cardiac function; hypovolemia; endotoxemia.

Coagulation Factors
Disturbances of blood coagulation also commonly present in jaundice patients. The most
frequently observed clotting defect is prolongation of the prothrombin time due to low levels of
vitamin K dependent factors. This problem results from impaired Vitamin K absorption from the
287

gut, secondary to lack of intestinal bile. This coagulopathy is usually reversible by parenteral
administration of Vitamin K.

Immune System Factors


Jaundiced patients have numerous defects in cellular immunity that make them more prone to
infection. Absence of bile from the intestinal tract also plays a role in the infectious complications
seen in patients with obstructive jaundice, due to the increased bacterial translocation from the gut
in the setting of bile duct obstruction (6).

Acute cholangitis is a bacterial infection of the biliary ductal system. Clinical cholangitis results
from the combination of two factors: significant bacterial concentrations in the bile and biliary
obstruction. The most common organisms recovered from bile in patients with cholangitis include
Escherichia coli, Klebsiella pneumoniae, enterococci and Bacteroides fragilis. The fever and the
chills associated with cholangitis are the result of systemic bacteremia caused by cholangiovenous and cholangio-lymphatic reflux that occurs when the intra-biliary pressure rise beyond
20cm of H2O.
Wound Healing Factors
Delayed wound healing and a high incidence of wound dehiscence and incisional hernia have
been observed in patients undergoing surgery to relieve obstructive jaundice (7).

Clinical Presentation
Three main symptoms that are seen in patients with obstructive jaundice are: jaundice, pain and
fever. In addition to the above patients can give history of biliary colic, passing clay coloured
stools, generalised pruritis, vomiting, hemetemesis, malena, and anorexia and weight loss.

Classically, pain is a discriminating feature in jaundiced patients. Patients with biliary tract
obstruction resulting from the tumour usually have painless jaundice, whereas patients with an
acute attack of pain or a long history of intermittent episodes of jaundice accompanied by pain
usually have gall stone disease, but up to 60-70 % of patients with gall bladder carcinoma and
carcinoma head of pancreas present with epigastric, right upper quadrant or back pain. In the
event of cholangitis, intermittent jaundice is accompanied by rigors and fever (Charcots triad),and
in severe cases is also associated with mental obtundation and shock (Reynolds pentad).

Jaundice unaccompanied by pain, and especially if the gall bladder is palpable, almost always
indicates malignancy. Courvoisiers law proposes that in the absence of a palpable gallbladder a
malignant cause of bile duct block is unlikely. There may be several exceptions to this. A double
impaction of stone in the bile duct and neck of gallbladder may give rise to a palpable gallbladder
without malignant obstruction. In malignant disease gallbladder may not be palpable because of
prior cholecystectomy, enlarged liver overhanging the gallbladder, stent placed in bile duct, a low
288

insertion of cystic duct below the level of block in the bile duct, biliary hilar malignancies such as
cholangiocarcinoma or carcinoma neck of the gallbladder, etc.

Itching can be an initial feature of biliary obstruction, but in prolonged cholestasis itching can occur
in association with partial biliary obstruction. Classically, itching precedes jaundice in
cholangiocarcinoma. However this is not always so. Some patients with periampullary carcinoma
can present with jaundice and history of fluctuation in the intensity of jaundice following an episode
of upper GI bleed (malena), this is attributed to intermittent sloughing of the tumour leading to an
incomplete obstruction of the bile duct.

INVESTIGATIONS
Liver Function Tests
Alkaline phosphatase (ALP): Elevation of alkaline phosphatase in hepato-biliary disease is due to
increased synthesis by the biliary ductular endothelium, perhaps stimulated by bile acids and it
usually precedes the onset of symptoms and jaundice. Slight or moderate increase in alkaline
phosphatase (one or two times normal) occurs in parenchymal liver disease. However, a marked
rise in alkaline phosphatase (ten times normal or more) occurs consistently in intra or
extrahepatic biliary obstruction. Simultaneous determination of gamma-glutamyl transpeptidase
and or serum bile acids confirms that the rise in ALP is due to obstructive jaundice. The most
sensitive indicator of extrahepatic biliary obstruction, regardless of the etiology or location, is
serum ALP(8). The level of ALP is not an indicator of function and has no prognostic significance.
ALP can even be elevated in patients with parenchymal liver disease like Primary Sclerosing
Cholangitis. It is also useful for follow up in patients who have had surgery to relieve biliary tract
obstruction, and is also elevated when there is segmental or partial obstruction of the biliary tree,
this is especially useful, as the bilirubin is often normal in these patients.

Gamma-glutamyltranspeptidase (GGT): GGT increases markedly ( upto 40-fold) in mechanical bile


duct obstruction; it has been proposed that SGPT / GGT ratio is better able to differentiate
between obstructive jaundice and hepatitis than alkaline phosphatase or any of the enzymes
taken alone.

Coagulation Profile: The liver is the main site of synthesis of most of the coagulation factors,
abnormalities of which can be determined by measuring the prothrombin time (PT) which
measures the rate of prothrombin conversion to thrombin in the presence of thromboplastin,
calcium and requires the integrity of most of the vitamin K dependent clotting factors (factors
II,VII,IX,X).Vitamin K is a fat soluble vitamin, absorption of which requires presence of bile salts
in the intestine, which is absent in patients with obstructive jaundice. So, PT is prolonged in
patients with obstructive jaundice but parenteral administration of Vitamin K should reverse the
abnormal coagulation. If vitamin K administration does not improve the prothrombin time in

289

patients with obstructive jaundice a concomitant hepatocellular disease should be suspected. In


this case the administration of fresh frozen plasma would correct the prothrombin time.

Tumour Markers
Carbohydrate antigen (CA 19-9): The CA 19-9 antigen is a sialated oligosaccharide formed on the
circulating mucin in cancer patients. It is most widely used serum marker in pancreatic cancer. It
has a reported sensitivity and specificity of about 8090%, and is suggestive, rather than
confirmatory, of the diagnosis of pancreatic cancer. It is normally also present within the cells of
the biliary tract and can be elevated in acute or chronic biliary diseases. In particular, the levels
may be elevated during episodes of cholangitis and also in a jaundiced liver due to decreased
metabolism. CA 19-9 is neither sensitive nor specific for pancreatic cancer because 15 % of
patients do not secrete CA 19-9 owing to their Lewis antigen status. But in patients with Gall
bladder cancer CA 19-9 is a more sensitive marker with sensitivities and specificities of
approximately 75% at a level greater than 20 U/ml.

Imaging
Ultrasonography (USG): It is the most useful non-invasive initial investigation for distinguishing
medical from surgical cause of jaundice and to differentiate extrahepatic from intrahepatic biliary
obstruction. USG is initial screening investigation in patients with suspected obstructive jaundice.
It confirms the presence of biliary block and provides information about the site and nature of
block. USG is more sensitive in detecting gall stones (95%) and intrahepatic obstruction, but less
sensitive for detecting common bile duct (CBD) stones (50%) and pathology and lesions of the
pancreas (9). USG evidence of CBD dilatation of more than 7 mm has been described as the
best predictor of choledocholithiasis (10). In one study when dilated CBD with stones was found
by USG in combination with cholangitis and elevated AST and bilirubin, the likelihood of having
stones in the CBD was 99%. It is reliably able to differentiate malignant from non malignant
causes of SOJ. USG accurately predicts the level of biliary obstruction in majority of the cases
(92%), but it is less accurate in suggesting the cause (71%) (11). This is the first essential step in
the algorithm of management, and determines the further approach and course that the patient
has to follow.

Duplex Ultrasonography: This is an investigation that may be useful in determining vascular


involvement in patients with hilar cholangiocarcinoma and matches CT angiography in providing
information about biliary ductal, periductal and vascular involvement (13).

Contrast enhanced Computed Tomography (CECT): CT scan has limited value in diagnosing CBD
stones (sensitivity of 76-90%) (12), But is more specific in detecting the level of obstruction and
cause of obstruction than USG. It is better in evaluating operability, pre operative staging and CT
Angiography gives better assessment of invasion or compression of vessels. The workhorse in
the work-up of patients suspected of a pancreatic or a periampullary neoplasm is a multi-detector
290

spiral CT and is probably the single most useful diagnostic and staging modality as it provides
complete and accurate information of the lesion and its adjacent vascular structures like portal
vein, SMA, SMV, splenic vein and celiac axis and also about involvement of periampullary lymph
nodes and retroperitoneal structures. CT scanning should also be performed on all patients
suspected of having gall bladder cancer. Findings of gall bladder cancer include a mass
protruding into the lumen of the gall bladder or completely replacing the gall bladder and focal or
diffuse thickening of the gall bladder wall. CT scanning also offers information about presence or
absence of distant metastasis, regional LN involvement and local invasion of liver and porta
hepatis.

The CT criteria used to define a potentially resectable pancreatic cancer are

The absence of extra-pancreatic disease

Preservation of fat plane between tumour and the SM-PV (superior mesenteric and
portal vein)

Absence of tumour involving or encasing the SMA, celiac or hepatic arteries

Positive predictive value of CT to determine disease as unresectable approaches 100%

Spiral CT (Helical) Scan improves biliary tract imaging by producing several overlapping
images in a shorter time than traditional CT scan. CT cholangiography and helical CT technique
gives optimal results in biliary tract obstruction and can differentiate between neoplastic and
non neoplastic causes of jaundice. With the advent of 3D CT cholangiography, it has been
shown that similar information can be obtained as MRCP and PTC (percutanoeus transhepatic
cholangiography) for patients with carcinoma gall bladder with obstructive jaundice (15). CT
angiography has replaced the need for conventional angiography to assess the arterial and
portal venous involvement in patients with malignant SOJ.

Once CT scan has been done the following possibilities emerge:


1. Low bile duct obstruction
2. Hilar bile duct obstruction
3. Obstruction level indeterminate / Inadequate

291

Figure CT scan showing double duct sign of periampullary carcinoma (CBD dilated upto the lower end with
main pancreatic duct dilatation).

Figure CT scan showing advanced gallbladder carcinoma with obstruction of the bile ducts at the hilum

Magnetic Resonance Cholangiopancreaticography (MRCP): MRCP takes advantage of the fact


that bile has high signal intensity on T2 weighted images, whereas the surrounding structures do
not enhance and can be suppressed during image analysis. Common bile duct stones are seen
as low intensity signal defects surrounded by high intensity bile. Stones as small as 2mm can be
detected even in the absence of biliary dilatation (12). Recent studies with state of art techniques
have sensitivities of 90-100% and specificities of 92-100% in the diagnosis of choledocholithiasis
(12). MRCP is very useful for diagnosis of benign conditions so the biliary tract causing SOJ, like
Choledochal cyst (type and extent) and benign biliary strictures (type, associated aberrant biliary
292

anatomy and atrophy hypertrophy complex). In hilar cholangiocarcinoma MRCP is the principal
imaging radiographic technique and provides an accurate assessment of biliary ductal anatomy
and the type and extent of biliary block. MRCP combined with MR angiography in hilar
cholangiocarcinoma provides important staging information assessment of the surrounding
vascular structures and thereby helping in further treatment planning. MRCP also has a high
sensitivity and specificity for diagnosing etiology of obstruction. MRCP also combines favorably
with ERCP in differentiating benign from malignant strictures (14).

Figure MRCP showing multiple CBD stones

Figure- MRCP showing Bismuth type 4 post-cholecystectomy benign biliary stricture

Endoscopic Ultrasonography (EUS): EUS is being increasingly used for patients with low bile duct
obstruction particularly due to periampullary carcinoma. The advantages include better local
staging, possibility of a tissue diagnosis using guided FNA, and increased accuracy for
diagnosing nodal disease. The disadvantages include expense, and operator dependence. EUS
has been shown to have a diagnostic accuracy of 95% for bile duct stones (16). Compared with
ERCP, EUS is semi-invasive with almost no procedure related complications and negligible
293

failure rate. EUS offers higher resolution than MRCP and is therefore better able to detect small
stones

Hepatobiliary Scintigraphy- Hepatobiliary Iminodiacetic Acid (HIDA Scan): It is a powerful non


invasive tool to detect bile leak and iatrogenic biliary obstruction. When there is a clinical
suspicion of bile duct injury after surgery, HIDA scanning should be one of the first tests
considered. The degree of leak can be assessed, and this can help triaging of patients with bile
leak to conservative or operative repair. After biliary drainage has been achieved, a follow up
scan can assist in assessing the efficacy of biliary drainage and also triaging patients who
require further intervention.

Endoscopic Retrograde Cholangiopancreaticography ( ERCP): ERCP, a technique used to


evaluate and treat biliary and pancreatic disorders has been in vogue for the last five decades,
but with the advent and easy availability of MRCP use of ERCP as diagnostic investigation for
the pancreato-biliary disorders has decreased significantly. Although it is still used occasionally in
the diagnosis of periampullary or ampullary malignancies by obtaining tissue biopsy and brush
cytology. As therapeutic procedure ERCP is widely used in the following conditions

Removal of CBD stones

Pre surgical biliary decompression in patients with cholangitis

Endoscopic palliation of obstructive jaundice in unresectable periampullary carcinoma

Percutaneous Transhepatic Cholangiography-PTC (Direct Cholangiography): Percutaneous


Transhepatic Cholangiography is a widely available imaging technique for the detection of ductal
calculi especially intra hepatic ductal calculi because of generally better ductal filling. In patients
with post cholecystectomy benign bile duct strictures who require percutaneous biliary drainage,
PTC provides a better delineation of the type of stricture and intrahepatic biliary anatomy than
MRCP but the disadvantage is that it cannot image any excluded ductal system. Direct
cholangiography is an important investigation for diagnosis and preoperative evaluation of
cholangiocarcinoma, in general PTC affords a better image of hilar cholangiocarcinoma than
does ERCP.

Positron Emission Tomography:

Positron

Emission

Tomography

is

being

used

more

frequently in Carcinoma Gall Bladder and Hilar Cholangiocarcinoma to identify patients with
distant metastasis that would contraindicate surgical resection. Analysis of data from MSKCC
about use of PET in cholangiocarcinoma showed that 24% of the 62 newly diagnosed patients
had their management changed as a result of detection of occult metastasis (38). FDG-PET has
been used to detect gallbladder cancer in patients with suspicious or indeterminate conventional
imaging, and it appears to have a sensitivity and specificity of approximately 80%. Standard PET
imaging is limited by low resolution and only partial anatomic information. These limitations often
restrict its use in the staging of gallbladder cancer since it is often unable to detect low volume
294

disease (peritoneal carcinomatosis) or give detailed information on the site and resectability of
lymph node disease. The combination of the biologic/functional information of PET images with
the anatomic information of CT images into integrated PET/CT has the ability to overcome many
of these limitations.(39)

Staging Laparoscopy: Role of staging in patients with malignant surgical obstructive jaundice is
controversial, whereas certain routinely use staging laparoscopy prior to contemplating surgical
resection, the rest use it on a more selective basis.
Various studies have shown conclusively that laparoscopy identies the majority of patients with
unresectable hilar cholangiocarcinoma or gallbladder carcinoma, thereby reducing both the
incidence of unnecessary laparotomy and the length of stay. The yield of laparoscopy is lower for
hilar cholangiocarcinoma but can be improved by targeting patients at higher risk of occult
unresectable disease. All patients with potentially resectable primary gallbladder cancer and
patients with T2/T3 hilar cholangiocarcinoma should undergo staging laparoscopy before surgical
exploration (41, 42, 43).

Usefulness of staging laparoscopy in periampullary cancers is debatable as the yield is


significantly low as compared to Hilar cholangiocarcinoma and carcinoma gall bladder, besides
with newer generation of CT scanners, the incidence of missed hepatic and peritoneal
metastasis is less than 20%.

Preoperative Preparation of patient with Obstructive Jaundice: Involves attention to and


correction of the following factors:

Correction of anemia by pre operative packed cell transfusion

Replenishment of depleted liver glycogen reserve due to hepatocellular dysfunction by oral or


intravenous administration of dextrose

Correction of fluid and electrolyte deficits

Prothrombin time may be prolonged due to Vitamin K deficiency as result of obstructive


jaundice, the same may be corrected by parenteral administration of Vitamin K for 3-5 days
before surgery

Fresh frozen plasma may be needed to correct coagulation derangements in cases of severe
hepatocellular dysfunction

Patients with obstructive jaundice are more prone for renal failure in the postoperative period
so adequate hydration should be maintained in the peri-operative period

Broad spectrum prophylactic antibiotics with gram negative cover based on previous culture
sensitivity reports

Patient may require preoperative biliary drainage (PBD) either by ERC and stenting or
percutaneous biliary drainage in the setting of cholangitis, severe malnutrition, grossly
elevated bilirubin (>20-25 mg%). Routine PBD in absence of the above indications not
recommended as it significantly increases post operative morbidity
295

SURGICAL MANAGEMENT
Choledocholithiasis
1. Open CBD exploration: First surgical exploration of the CBD was done in 1890 by Ludwig
Courvoisier. Although commonly used in the management of common bile duct stones in the
era of open cholecystectomy, open bile duct exploration is used infrequently in the present
age of minimally invasive surgery. If ERCP has failed or is not possible, if the surgeon does
not have the experience and necessary tools to perform laparoscopic duct exploration, or if
laparoscopic efforts have failed, then open exploration becomes necessary. A small- caliber
duct (< 6 mm in diameter) is a relative contraindication to choledochotomy.

Intra operative cholangiography (IOC) - Approximately 10-15% of patients undergoing


laparoscopic cholecystectomy harbor common bile duct stones, the need for routine
IOC is a matter of much debate (17). Of the 4% of patients with silent CBD stones at
laparoscopic cholecystectomy, only 15% go onto to develop symptoms from retained
stones. Hence a large number of IOCs would have to be at cholecystectomy in order to
detect one common bile duct stone that would go on to cause symptoms in patients
without

preoperative

evidence

of

CBD

stones,

hence

routine

IOC

during

cholecystectomy is not recommended. Although IOC does not appear to prevent CBD
injury, it allows for earlier detection of such injuries and thus more successful initial
repair (18).

Intra operative Ultrasonography (IOUS) - evaluation of the biliary tree with IOUS
appears to be as effective as IOC in identifying CBD stones without the additional risk
of radiation exposure

2. Laparoscopic CBD exploration ( LCBDE): With increasing experience in laparoscopic


techniques and the demand for single procedure minimally invasive duct clearance,
laparoscopic CBD exploration has gained widespread acceptance, and success rates for duct
clearance are between 80-90%, comparable with open method of CBD exploration (18).
Access to the biliary system after obtaining a cholangiogram can be transcystic (LTCBDE) or
transductal using a choledochotomy.

296

LTCBDE vs. Lap Choledochotomy (19)


Variables
Skill
Stones
Number
Size
Location

LTCBDE
Endoscopy

Lap Choledochotomy
Lap suturing

<8
<9mm
Distal to cystic duct

Any number
Any size
Entire duct

CBD diameter
Drain
Contraindication

Any
Optional
Friable cystic duct
Intrahepatic stones
Multiple, large stones
No T-tube
Shorter hospital stay

>6mm
Suggested
Small- diameter CBD

Equipment intensive
New Skill required

Lap suturing
T-Tube

Advantages
Disadvantages

Quick
T-tube for postoperative access

Techniques for Treatment of Choledocholithiasis (20)

Method

Success Rate (%)


70-95%

Length of Stay
(days)
1-2

Return to
work (days)
7-10

Transcystic duct
extraction
Laparoscopic CBDE
Open CBDE
ERC/ ES

85-100
90-100
85-95

4-7
5-10
2-3

14-30
20-42
7-14

Single Stage Vs. Two stage treatment of Choledocholithiasis


Preliminary findings of multi-center prospective randomized trial comparing two-stage vs single-stage
management (EAES ductal stone study- Group Apreoperative ERC with ESE followed by LC during
the same hospital admission. (ii) Group Bsingle stage laparoscopic management consisting of LC
and laparoscopic stone extraction either by the trans-cystic duct route or by direct supraduodenal
common duct exploration) indicate equivalent success rates and patient morbidity between the two
management options but a shorter hospital stay (cost benefit) with the single stage laparoscopic
treatment. Trans-cystic duct extraction is a more benign procedure than laparoscopic supraduodenal
CBD exploration and is accompanied by a significantly shorter hospital stay. Evidence from three
trials involving over 400 patients found no difference in primary treatment success (88% for both
arms), morbidity or mortality (24-26).

While the above results seem to suggest that in fit patients, single stage laparoscopic treatment is the
better option than two staged procedure (ERCP followed by laparoscopic cholecystectomy), the
choice of the treatment would clearly depend on the available expertise, resources and the past
experience of the surgical unit..(44)

297

Surgical Drainage Procedures


Surgical biliary drainage procedures must be considered in the following situations (21)

Multiple stones

Incomplete removal of all stones

Impacted , irremovable distal bile duct stones

Markedly dilated common bile duct

Distal bile duct obstruction from tumour or stricture

Reoccurrence after previous bile duct exploration

Methods of surgical drainage include


Transduodenal sphincteroplasty
Choledochoduodenostomy
Choledochojejunostomy

Transduodenal sphincteroplasty: Transduodenal sphincteroplasty is useful in the management


of Choledocholithiasis when there is stone impaction at the ampulla of Vater, papillary
stenosis, multiple stones particularly in the presence of a non dilated bile duct.

Choledochoduodenostomy (CDD): Choledochoduodenostomy is indicated in patients with


recurrent stones requiring repeated interventions, impacted or giant stones, biliary sludge and
ampullary stenosis. The funnel syndrome in which a distal bile duct stenosis exists in the
presence of CBD stones is one of the most classical indications for CDD. A common bile duct
diameter of at least 1.2 cm is important in assessing the feasibility of CDD because this allows
a wide enough stoma to ensure good biliary drainage and avert stenosis and future
cholangitis. Sump syndrome is caused by food and debris accumulating between the stoma
and the papilla of Vater. Stomal patency is felt to be the most important factor for preventing
both cholangitis and sump syndrome. Long term studies reveal that 70-80% of patients are
asymptomatic 5 years after surgery (22).

Choledochojejunostomy (CDJ): An alternative to CDD is CDJ which can be done with either a
loop of jejunum or using a Roux-en-Y configuration. It is usually required when duodenum is
not available i.e. scarred duodenum, prior gestrectomy. The Roux-en-Y usually is brought
retrocolic using a 60cm afferent limb to protect against intestinal reflux and secondary
cholangitis. A comparison of CDD and CJ was evaluated by a French group. The authors
concluded that CDD is preferable given the similar outcomes because it is easier and faster to
perform than CJ and allows for easy endoscopic interventions if needed in the future. (23)

Post Cholecystectomy bile duct strictures


In general operative treatment of bile duct injuries need not be rushed, the exceptions being treatment
of bile duct injuries recognized at the time of initial cholecystectomy or rarely emergency treatment of
suppurative cholangitis or biliary peritonitis. For most patients, there is ample time to treat coexisting
298

conditions and to perform full investigation, both of which increase the likelihood of successful
outcome.

Cholangitis is a frequent occurrence in bile duct strictures especially after ductal intubation
(percutaneous or endoscopic). Administration of intra venous antibiotics is important as a preliminary
to surgical treatment, and the results of bile cultures obtained at the time of PTC, should be used to
direct therapy. Patients with severe cholangitis and sepsis are unlikely to respond to antibiotics alone
and should be submitted to percutaneous drainage prior to surgery. Jaundice without cholangitis is
not an indication for biliary intubation.

Early Repair: Early repair, more so in the presence of sepsis, is fraught with dangers. Schol et al.
(27) in a nationwide survey of 49 Bile duct injuries (BDIs) in the Netherlands observed that early
repair was associated with higher incidences of leak, stricture formation, and death.

We do not recommend early repair and have performed early (within 4 weeks) repair in only 11 out
of 362 patients in whom we have performed HJ for BDI between 1989 and 2005 (unpublished
data). Early repair may be done in a patient with a ligated/ clipped duct after LC when there is no
bile leak, no cholangitis, andgood proximal dilatation.(28)

Elective repair: Tension-free, mucosa-to-mucosa HJ performed in a single layer, using interrupted


fine absorbable sutures between unscarred proximal bile ducts (right and left hepatic) and a 60cm-long Roux loop of jejunum is the procedure of choice for BBS. The hilar plate needs to be
lowered and the extra hepatic part of the left hepatic duct exposed.

Factors associated with stricture recurrence or poor outcome after operative reconstruction

Proximal stricture ( Bismuth type 3 and 4)

Multiple prior attempts at repair

Portal hypertension

Hepatic parenchymal disease ( cirrhosis or hepatic fibrosis)

End to end biliary anastomosis

Surgeon inexperience

Intra hepatic or multiple strictures

External or internal biliary fistula

Intra abdominal abscess or bile collection

Surgical results
It appears that excellent long- term results can be achieved in roughly 80-90% of patients who
undergo repair of bile duct strictures. Without a doubt, the length of follow-up is important, because
although 80% of recurrences present within 5 years of repair, 5% of the recurrent strictures present
more than 12 years after repair.
299

Periampullary Carcinoma: Resectional surgery for pancreatic and periampullary carcinoma is


pancreaticoduodenectomy, which can be either a classic Whipple procedure or its modification a
pylorus preserving pancreaticoduodenectomy. In a classic Whipple procedure, a 30-40% distal
gastrectomy is performed by dividing the right gastric and right gastroepiploic arteries. For a
pylorus preserving pancreaticoduodenectomy , the proximal portion of the gastrointestinal tract is
divided 2-3 cm beyond the pylorus.

Standard Pancreaticoduodenectomy (PD) vs. Pylorus Preserving Pancreaticoduodenectomy


(PPPD)
Traverso and Longmire (1978) hypothesized that preservation of the of the stomach and the pyloric
function would improve gastrointestinal function and reduce morbidities associated with a
gastroenterostomy. A RCT (33) demonstrated no difference in long term survival, quality of life and
postoperative weight gain between PD and PPPD.

In the light of the available evidence PPPD should be designated as standard procedure for
pancreatic and periampullary neoplasm because no study till date has shown any advantage to the
removal of the stomach and the proximal duodenum. Classical PD should be performed only when
there is evidence of gastric or proximal duodenal invasion or bulky growth and grossly abnormal
peripyloric nodes.

Role of Pre Op Biliary Drainage (PBD)


Two Meta- analyses (34, 35) on this subject have concluded that there was no difference in
overall death rate between patients who had PBD and patients who had surgery without PBD.
Instead, the overall complication rate was significantly adversely affected by PBD. The length of
hospital stay was also prolonged. The role of PBD in patients with biliary obstruction undergoing
pancreatic resection for periampullary carcinoma is controversial at best. But what can be
concluded from the available literature is that PBD as a routine practice is not warranted. We
would refer a patient for PBD if there were cholangitis, grossly elevated bilirubin > 20-25 mg%
and severe malnutrition that would preclude a safe resection.

PJ vs. PG
A prospective RCT comparing pancreaticojejunostomy vs. pancreaticogastrotomy as a mode of
reconstruction following pancreaticoduodenectomy showed no difference in the leak or fistula
rate between the two types of anastomoses (37).
Postoperative Complications

Pancreatic Fistula (2-24%)

Intra-abdominal abscess (1-12%)

Post pancreatectomy hemorrhage (1-10%)


300

Delayed Gastric emptying (10-15%)

Palliative Therapy
Three mains symptoms requiring palliation are obstructive jaundice, gastric outlet obstruction and
pain.
Palliation can be achieved by the following means
Operative therapy
Non Operative therapy

Operative Palliation
Operative palliation is most beneficial in patients without widespread metastatic disease and with
a life expectancy of more than several months
Operative palliation of Obstructive Jaundice: The most effective operative procedure to palliate
jaundice is choledochojejunostomy / hepaticojejunostomy. Other less effective methods are
cholecystojejunostomy and simple drainage through a T-Tube inserted above the site of
obstruction.In patients who are expected to survive longer than 6 months , a

prophylactic

gastrojejunostomy can be added to the palliative procedure ( Triple Bypass) as upto 30% of
patients of carcinoma head of pancreas can go on to develop gastric outlet obstruction.

Non Operative palliation: Patients found to have distant metastases, unresectable bulky local
disease, or disseminated intra-abdominal tumors and patients with debilitating disease in whom
anesthesia and surgery are unsafe are appropriate candidates for nonoperative therapy. With the
advent of self expanding metallic stents these are the most used palliative treatment for
obstructive jaundice in these patients.l. Nonoperative palliation is reliable for obstructive jaundice
but not for duodenal obstruction. Therefore, patients with symptomatic duodenal obstruction
should be managed operatively with gastrojejunostomy whenever possible. (36)

Gall Bladder Carcinoma


The standard template on which all operations for gall bladder cancer are based is the extended
cholecystectomy. This consists of cholecystectomy with enbloc resection of segments IV B and V or
2cm wedge of adjacent liver parenchyma and lymphadenectomy of the cystic, pericholedochal,
periportal and posterior pancreaticoduodenal lymphnodes residing in the hepatoduodenal ligament,
as well as the ? local interaortocaval lymphnodes. Our favored procedure is extended
cholecystectomy (EC) which includes a 2 cm nonanatomical wedge of liver in the GB bed and the
lymph nodes in hepato-duodenal ligament, behind the duodenum and head of pancreas and along the
hepatic artery to the right of celiac axis. CBD excision is not performed as a routine but in selected
cases only, e.g., GB neck mass or direct inltration of the CBD. Patients with obstructive jaundice due
to CBD inltration are not considered for resection (30)

Analysis of the MSKCC experience demonstrated that only 25% of patients presenting with gall
bladder cancer harboured disease ultimately amenable to curative resection. Among those patients
301

who underwent curative resection, a median survival of 26 months and 5 year actuarial survival of
38% were observed (31).

Nodal spread is one of the most important factors for poor survival 5-year survival in node-negative
patients was 58%, versus 0% in node-positive patients. (32).

Figure- Percutaneous transhepatic biliary drainage in a patients with advanced gallbladder carcinoma with
obstructive jaundice

Indian experience with major resections in advanced gallbladder cancer (30).

ERH- Extended right hepatectomy; HPD- Hepatopancreaticoduodenectomy

Hilar Cholangiocarcinoma
In Hilar Cholangiocarcinoma preoperative evaluation must address the following four crucial
determinants of resectability
Extent of tumour within the biliary tree
Vascular involvement
Hepatic lobar atrophy
Metastatic disease
302

Substantial evidence supports the argument that partial hepatectomy usually is required to achieve
the goal of R0 resection (40). Bile duct excision with partial hepatectomy, often with enbloc caudate
lobectomy is frequently necessary to achieve negative margins. Several studies show a parallel
between the number of patients undergoing partial hepatectomy and negative resection margin.

Pre Operative portal vein Embolization may be indicated in some patients planned for extensive liver
resections. The purpose of portal vein Embolization is to initiate compensatory hypertrophy in the
future liver remnant to minimize postoperative liver dysfunction and prevent liver failure.

REFERENCES:
1.

Mallet Guy. P. Value of preoperative manometric and roentographic

Examination in the diagnosis

of pathological changes and functional diseases of the biliary tract. Surg Gynecol Obstet . 1952,
94: 385-393.
2.

Karsten TM. Morphological changes of extrahepatic ducts during obstruction and subsequent
decompression by endoprosthesis. Surgery 1991, 111;562-568

3.

Koeppel et al. extrahepatic biliary obstruction impairs microvascular circulation. Hepatology 1997,
26: 1085-1091

4.

Jacob G et al. Cardiac function and responsiveness - adrenoreceptor

agonists in rats with

obstructive jaundice. Am J Physiol 1993, 265:G314-G320


5.

Padillo et al. Improved cardiac function in patients with obstructive jaundice after biliary drainage.
Ann Surg 2001, 234:652-656

6.

Dietch et al. Obstructive jaundice promotes bacterial translocation from the gut . Am J Surg 1990,
159:79-84

7.

Grande et al. Obstructive jaundice and wound healing. Br J Surg 1990, 77:440-442

8.

Liu TH et al. Patient evaluation and management with selective use of MRC and ERCP before
laparoscopic cholecystectomy. Ann Surg 2001;234:33-40.

9.

Eisen GM. An annotated algorithm for evaluation of choledocholithiasis. Gastrointest

Endosc

2001; 53: 864-866


10. Contractor QQ. Abnormal Common bile duct sonography: the best predictor of cholelithiasis
before laparoscopic cholecystectomy. J Clin Gastroenterol 1997;25:429-432.
11. Laing FC : Biliary Dilatation: Defining the level and cause by real time US. Radiology 160:3942,1986
12. Fulcher AS. MRCP and ERCP in the diagnosis of common bile duct stones. Gastrointest Endosc
2002;56: S178-182
13. Hann LE: Cholangiocarcimoma at the hepatic hilus: Sonographic findings AJR; 168: 985-989.
14. Park MS. Differentiation of extrahepatic bile duct cholangiocarcinoma from

Benign strictures:

findings at MRCP vs. ERCP. Radiology 2004; 233:234-240.


15. Rao ND. 3D CT Cholangiography with minimum intensity projection in gall bladder carcinoma with
obstructive jaundice: comparison with MRCP and PTC. Gastroenterol. Hepatol. 2005;20: 304-308
16. Mark DH. Evidence based assessment of diagnostic modalities for common bile duct stones.
Gastrointest Endosc 2002;56: S190-194
17. Ellison EC. Whats new in general surgery : Gastrointestinal conditions. J Am Coll Surg 2005;
199:409-417

303

18. Petelin JB. Surgical management of common bile duct stones. Gastrointest Endosc 2002; 56: S
183-189
19. Shackelfords Surgery of the Alimentary Tract; 6th edition Pg No.1483. Saunders Elsevier
20. Surgery of the Liver, Biliary Tract, and Pancreas; 4th edition, Pg No. 519. Saunders Elsevier
21. Maingots Abdominal Operations. 11th edition, Pg No.877. McGraw Hill Medical
22. de Aretxabala X. Choledochoduodenostomy for common bile duct stones. World J Surgery 1998;
22:1171-74
23. Panis Y. Long term results of choledochoduodenostomy and choledochojejunostomy for
Choledocholithiasis. The French Association for Surgical Research. Surg Gynecol Obstet 1993;
177:33-37.
24. Sgourakis

G,

Karaliotas

(2002)

Laparoscopic

common

bile

duct

exploration

and

cholecystectomy versus endoscopic stone extraction and Laparoscopic cholecystectomy for


choledocholithiasis. A prospective randomized study. MinervaChirurgica 57:467-474