You are on page 1of 38

549

26
Abnormalities of the upper airway
Norm G. Ducharme Jon Cheetham
performance by decreasing minute ventilation, exacerbating
exercise-induced hypoxemia, and decreasing maximal oxygen con-
sumption. While some obstructive diseases are static and evident at
rest, many obstructive lesions are dynamic and only apparent
during exercise. Furthermore, during exercise the coexistence of two
or more forms of upper airway obstruction has been reported in 30
to 70% of horses.
1,2
This emphasizes the need for dynamic examina-
tion to obtain the full identication of all the upper airway abnor-
malities in a given horse. A proper assessment including a complete
history, signalment, and physical examination, endoscopic exami-
nation of the upper airway, both at rest and during treadmill exer-
cise, will establish the etiology of the airway obstruction. In addition
to sound analysis, imaging modalities such as radiography, ultra-
sonography, computed tomography, and nuclear medicine can be
valuable in diagnosing performance-limiting lesions of the upper
airway.
Redundant alar folds
(alar fold collapse)
The alar fold is formed by a thick fold of skin and
mucous membrane extending rostrad from the ventral
nasal concha.
3
Redundant alar folds are a cause of abnormal respiratory
noise. In some horses they are also a cause of exercise
intolerance and respiratory noise in performance horses.
4,5

The prevalence has been reported to reach 9.6% in
Standardbred racehorses.
It is seen more commonly in Standardbreds but is also seen
in others breeds such as coldblooded trotters and
Thoroughbreds.
2,4
The diagnosis is made by manually holding the alar folds
open during exercise testing, on treadmill exam or securing
the alar folds dorsally to document decreased respiratory
noise and improved exercise intolerance.
2,4
Treatment includes tying the alar folds out of the airway
during exercise or alar fold resection.
4
Not all horses with alar fold collapse have airway
obstruction and therefore improvement in the abnormal
noise is not necessarily associated with improvement in
performance.
CHAPTER CONTENTS
Introduction 549
Redundant alar folds (alar fold collapse) 549
Mycotic rhinitis 552
Progressive ethmoid hematoma (PEH) 553
Sinusitis 554
Nasopharyngeal collapse 556
Retropharyngeal abscesses 557
Dorsal displacement of the soft palate (DDSP) 559
Epiglottic entrapment 562
Epiglottic retroversion 564
Subepiglottic cyst 565
Medial deviation of the aryepiglottic folds
(previously termed axial deviation) 566
Epiglottitis 567
Laryngeal hemiplegia 568
Arytenoid chondritis 572
Rostral displacement of the palatopharyngeal
arch (fourth and sixth branchial arch defect,
also known as 4-BAD, or cricopharyngeal-
laryngeal dysplasia) 575
Guttural pouch mycosis 576
Avulsion of the longus capitis/rectus capitis
ventralis muscles 578
Temporohyoid osteoarthropathy 579
Tracheal obstructive disease 580
References 582
Introduction
Upper airway obstructive diseases result in resistive breathing (an
increase in resistance to passage of air through the upper airways)
causing either an abnormal upper respiratory noise, exercise intoler-
ance, or both. Upper airway resistive breathing limits the athletic
Respiratory system
3
550
Fig 26.1 The nose of a horse with rings through the alar folds. The
string is used to tie the rings together, pulling the alar fold out of the
airway.
Recognition
History and presenting complaint
Most horses with redundant alar folds make an expiratory uttering
noise during exercise and a smaller percentage might be exercise
intolerant. Horses exhibit no clinical signs at rest.
2,4
Physical examination
No abnormalities are apparent at rest.
Special examination
Other causes of respiratory noise and exercise intolerance should
be eliminated by performing an endoscopic examination of the
upper airway and evaluating both nasal passages. Conrmation that
redundant alar folds are the cause of the airway noise is made by
alleviating the abnormal noise by placing a temporary suture
through the skin of each nostril, the alar folds, and tying it over the
bridge of the nose while the horse exercises (Fig. 26.1).
4
The alar
folds can also be held out of the nasal passage manually or with
clips.
2
Because dorsal displacement of the soft palate is seen in
association with this abnormality, dynamic endoscopic exam
during exercise is also indicated.
Laboratory examination
None is indicated.
Diagnostic conrmation
Absence of noise and improved exercise tolerance during exercise
with the alar folds secured out of the nasal passage conrms the
diagnosis.
2,4
Differential diagnoses for alar fold collapse include
obstructive airway diseases that cause exercise intolerance and
abnormal respiratory noise during exercise (Table 26.1). Paralysis
or paresis of the levator nasolabialis muscle associated with a tight
nose band or caveson can allow collapse of the lateral wall of the
nostril and could be confused with alar fold paralysis.
Treatment and prognosis
Therapeutic aims
The goal of treatment is to remove or secure the alar folds in an
open position during exercise. This can be achieved by suturing the
alar folds in an open (i.e. abducted) position during exercise, place-
ment of a nasal insert, or surgically resecting the alar fold. The rst
two treatments are not permitted in all racing jurisdictions.
Therapy
The procedure is most commonly done under general anesthesia in
dorsal recumbency or with the horse standing after a bilateral infra-
orbital nerve block. The alar fold is exposed by retracting or by
incising the lateral wall of the nostril. To provide hemostasis in this
vascular area, a Glassman intestinal clamp is placed on the dorsal
section of the alar fold. Using a blade adjacent to the clamp, the
dorsal part of the alar fold is excised, starting immediately caudal
to the alar cartilage (Fig. 26.2) and extending caudally along the
dorsal limit of the nasal cavity up to the V shape junction of the
incisive and nasal bones. At this time a simple continuous pattern
uniting the nasal mucosa to the skin at the remnant of the alar fold
is done. The Glassman clamp is then placed at the junction of the
ventral limit of the alar fold to the ventro-lateral limit of the nasal
cavity. A rostral-to-caudal incision completes the alar fold resec-
tion.
4
Usually, 12 cm of the cartilaginous portion of the ventral
nasal concha is excised. The ventral nasal mucosa and the skin of
the ventral nasal diverticulum is re-apposed as was done dorsally.
If the lateral nasal ala is incised to expose the alar fold, it is closed
in two layers.
4
Prognosis
Reportedly, respiratory tract noise improves in 71% of horses fol-
lowing alar fold resection and 88% of horses race after surgery.
4

Horses with small nares and narrow nasal passages have a poorer
prognosis for performance.
2,4
As mentioned earlier, alar fold
utters can result in an abnormal noise not necessarily an airway
obstruction.
Prevention
There is generally no known prevention.
Fig 26.2 Intraoperative view of the left alar fold. The lateral wall of the
nostril has been incised and a Glassman forceps is placed on the
dorsal aspect of the alar fold.
26
Abnormalities of the upper airway
551
D
I
S
E
A
S
E
P
a
O
2
P
a
C
O
2
T
I
P
T
E
P
Z
i
u
Z
e
u
I
F
E
F
R
F
V
T

V
E
N
o
r
m
a
l
1
3
2
7
1
.
7

(
1
.
6
)
5
4
.
7

(
1
.
9
)

4
2
.
9

(
2
.
8
)
9
.
2

(
3
.
8
)
0
.
5
3

(
0
.
0
2
)
0
.
1
4

(
0
.
0
6
)
8
0
.
4

(
4
.
2
)
6
6
.
6

(
4
.
3
)
8
4

(
4
)
2
2
.
2

(
1
.
6
)
1
8
5
8

(
1
0
9
)
N
o
r
m
a
l
5
1
7
5

(
2
.
3
)
5
5

(
2
.
3
)

3
9

(
3
.
3
)
1
2

(
1
.
4
)
0
.
4
2

(
0
.
0
5
)
0
.
1
8

(
0
.
0
2
)
9
0

(
5
.
2
)
9
1

(
4
.
1
)
1
0
9

(
1
1
.
7
)
1
7
.
1

(
1
.
7
)
1
6
9
0

(
1
3
0
)
P
h
a
r
y
n
g
e
a
l

c
o
l
l
a
p
s
e
1
3
1

4
0
.
8

(
4
.
4
)
2
2
.
0

(
6
.
6
)
0
.
7
3

(
0
.
0
2
)
0
.
4
6

(
0
.
1
9
)
5
4
.
2

(
4
.
0
)
5
5
.
6

(
4
.
1
)
7
6

(
4
.
0
)
1
6
.
8
1
1
5
9
.
4

(
9
4
.
1
)
D
D
S
P
4
8

1
8
.
6

(
7
.
6
)
3
6
.
2

(
1
1
.
3
)
0
.
4
1

(
0
.
1
1
)
0
.
8
8

(
0
.
3
8
)
4
4
.
5

(
9
.
0
)
4
6
.
7

(
1
0
.
4
)
5
7

(
9
.
8
)
1
5

(
3
.
3
1
)
8
7
5
.
2

(
1
1
4
.
5
)
D
D
S
P
5
1
6
4

(
3
.
6
)
6
6

(
4
.
9
)

2
9

(
3
.
4
)
3
5

(
6
.
7
)
0
.
3
3

(
0
.
0
5
)
0
.
6
6

(
0
.
1
1
)
6
6

(
3
.
8
)
6
9

(
3
.
4
)
9
8

(
8
.
2
)
1
3
.
6

(
2
.
5
)
1
2
6
5

(
3
1
5
)
I
L
H
6
4
5
3
5
8

(
8
.
3
)

5
9
.
4
2
1
.
3

(
0
.
4
7
)
1
.
5
2
0
.
4
9

(
9
.
0
)
4
2
.
6
4
2
.
7

(
9
)
7
0
1
1
0
6
.
5

(
1
9
1
.
5
)
L
a
r
y
n
g
o
p
l
a
s
t
y

+

v
e
n
t
r
i
c
u
l
o
c
o
r
d
e
c
t
o
m
y
6
4
8
3
3
9

4
5
.
1

(
8
.
4
)
0
.
8
2

(
0
.
1
4
)
5
5
.
5

(
5
.
0
)
7
7

(
2
0
)
1
2
1
1
.
5

(
9
5
.
4
)
A
r
y
t
e
n
o
i
d
e
c
t
o
m
y

+

v
e
n
t
r
i
c
u
l
e
c
t
o
m
y
8
8

4
0
.
0

(
4
.
4
)
0
.
8
1

(
0
.
1
0
)
4
8
.
0

(
2
.
0
)
1
1
7
8
.
5

(
3
8
.
6
)
E
p
i
g
l
o
t
t
i
c

r
e
t
r
o
v
e
r
s
i
o
n
6
0

3
5
.
7

(
3
.
8
0
)
1
3
.
3

(
2
.
4
)
5
8

(
5
)
T
I
P
,

t
r
a
c
h
e
a
l

i
n
s
p
i
r
a
t
o
r
y

p
r
e
s
s
u
r
e

(
c
m
H
2
O
)
:

T
E
P
,

t
r
a
c
h
e
a
l

e
x
p
i
r
a
t
o
r
y

p
r
e
s
s
u
r
e

(
c
m
H
2
O
)
;

Z
i
u
,

i
n
s
p
i
r
a
t
o
r
y

i
m
p
e
d
a
n
c
e

(
c
m
H
2
O
/
L
/
s
)
;

Z
e
u
,

e
x
p
i
r
a
t
o
r
y

i
m
p
e
d
a
n
c
e

(
c
m
H
2
O
/
L
/
s
)
;

I
F
,

p
e
a
k

i
n
s
p
i
r
a
t
o
r
y

o
w

(
L
)
;

E
F
,

p
e
a
k

e
x
p
i
r
a
t
o
r
y

o
w

(
L
)
;

R
F
,

r
e
s
p
i
r
a
t
o
r
y

f
r
e
q
u
e
n
c
y

(
b
r
e
a
t
h
s
/
m
i
n
)
;

V
T
,

t
i
d
a
l

v
o
l
u
m
e

(
L
)
;

V
E
,

m
i
n
u
t
e

v
e
n
t
i
l
a
t
i
o
n

(
L
/
m
i
n
)
;

v
a
l
u
e
s

i
n

p
a
r
e
n
t
h
e
s
e
s

a
r
e

s
t
a
n
d
a
r
d

e
r
r
o
r

o
f

t
h
e

m
e
a
n
.
T
a
b
l
e

2
6
.
1

U
p
p
e
r

a
i
r
w
a
y

m
e
c
h
a
n
i
c
s

m
e
a
s
u
r
e
m
e
n
t
s

a
n
d

b
l
o
o
d

g
a
s

v
a
r
i
a
b
l
e
s

i
n

h
o
r
s
e
s

w
i
t
h

o
b
s
t
r
u
c
t
i
v
e

u
p
p
e
r

a
i
r
w
a
y

d
i
s
e
a
s
e
s
Respiratory system
3
552
Laboratory examination
Laboratory tests are generally not warranted, but if the infection is
chronic, hyperbrinogenemia might be present.
Diagnostic conrmation
The diagnosis of fungal rhinitis is conrmed by biopsy and culture
of the plaque or mass. Fungi that have been reported to cause
mycotic rhinitis in horses include Conidiobolus coronatus, Cryptococ-
cus, Rhinosporidium, Aspergillus fumigatus and A. boydii, Coccidioides,
and Pseudallescheria.
49
The presence of septate hyphae or fungal
mycelium on cytological examination is indicative of fungal
infection.
Treatment and prognosis
Therapeutic aims
The goal of therapy is to eradicate the fungus from the nasal passage.
Therapy
Surgical debridement of granulomas and lesions followed by topical
antifungal lesions have been reported to be effective in the treat-
ment of mycotic rhinitis.
5
For example, Aspergillus fumigatus is sensi-
tive to natamycin solution applied topically.
6
Nystatin can be added
to the natamycin and used topically or intralesionally.
6
Topical and
intralesional injection of amphotericin B and intravenous sodium
iodide or oral potassium iodide has been used in the past to treat
Conidiobolus coronatus infection, but recurrence has been reported.
7

Long-term systemic antifungal therapy has also been effective; oral
itraconazole, 3 mg/kg, orally, twice daily, for 3.54 months also
results in the resolution of Aspergillus sp. infection.
8
Alternatively a
1% solution of enilconazole applied topically twice daily for 7 days
has been reported to be successful for the treatment of fungal
rhinitis.
5
Prognosis
Mycotic rhinitis due to Aspergillus sp. resolves with treatment and
recurrence is low.
5,6
Conidiobolus coronatus resolves with surgical
and medical treatment, but does recur.
7,8
Cryptococcus sp. is an inva-
sive fungus that can infect the paranasal sinuses and invade the
brain and meninges, and the prognosis is generally poor for
resolution.
7,10
Prevention
No method of prevention is known.
Etiology and pathophysiology
Etiology
Fungi isolated from the nasal cavity of affected horses include
Conidiobolus spp., Cryptococcus spp., Rhinosporidium, Aspergillus spp.,
Coccidioides, and Pseudallescheria.
Pathophysiology
Inhalation of fungal spores and colonization of the nasal mucosa
is the most likely route of infection, resulting in mycotic rhinitis.
Epidemiology
Mycotic rhinitis is rare (reported to represent less than 0.1% of all
21 160 admitted patients to a hospital
5
), but is most commonly
seen in hot, humid climates, such as the southeastern USA and
tropical areas.
Etiology and pathophysiology
Etiology
The etiology of redundant alar folds is unknown, but might involve
narrow nasal passages and inappropriate function of the transversus
nasi muscles.
Pathophysiology
A thick fold of skin forms the alar fold and mucous membrane
extending rostrad from the ventral nasal concha.
3
The space dorsal
to the alar fold is the false nostril or diverticulum of the nostril
while the true nostril that continues caudally to the nasal passage
is ventral to the alar fold. When the nostril is dilated, the alar fold
is tensed, obliterating the nasal diverticulum.
4
Excessive alar fold
tissue or inappropriate nostril dilation can cause the alar fold to
collapse across the nostril, causing airway obstruction and exercise
intolerance during inhalation, and a uttering noise during
exhalation.
Epidemiology
Standardbred, Scandinavian coldblooded trotters, and American
Saddlebreds might be predisposed to this condition.
2,4
Mycotic rhinitis
Rare fungal infection of the nasal cavity.
Often due to Aspergillus spp.
Diagnosis by endoscopy and laboratory identication of
fungus.
Treatment involves local debridement and topical application
of antifungal agent
Recognition
History and presenting complaint
Mycotic rhinitis is rare in horses and occurs most frequently in
warm, humid climates. The most common clinical signs include
nasal discharge that can be foul smelling, sneezing, and intermittent
epistaxis.
4,5,
Horses with nasal granulomas might make an abnor-
mal respiratory noise during exercise and show signs of exercise
intolerance. If the fungal infection is invasive and involves the
paranasal sinuses, extension to the brain and meninges can occur,
resulting in cerebral signs such as depression, dementia, ataxia, and
recumbency.
Physical examination
Horses with mycotic rhinitis generally have nasal discharge that is
malodorous, and if chronic, they can have alopecia along the
ventral aspect of the affected naris.
4,6
If a nasal granuloma is causing
airway obstruction, decreased airow through the affected nostril is
detected by holding the hands over each nostril.
Special examination
Endoscopic examination of the affected nasal passage reveals fungal
plaques or granulomas affecting the mucocutaneous junction of the
nostril, or mucous membrane of the nasal septum and concha.
4,5

Ulceration of the mucosa surrounding the plaque or granuloma can
also be seen.
6
If the primary site of infection is the paranasal sinus
region, exudate at the nasomaxillary opening within the middle
meatus can be evident.
26
Abnormalities of the upper airway
553
paranasal sinus region.
10,11
If the mass is conned to the maxillary
or frontal sinus, sero-sanguineous uid will be evident at the naso-
maxillary opening, yet the mass can be obscured from view.
10,11

Differential diagnoses for progressive ethmoid hematoma include
fungal granulomas, neoplasia, and nasal polyps which can be con-
rmed by biopsy.
Lateral, dorsoventral, and oblique radiographic projections of the
paranasal sinus region are taken to dene the anatomic limits of
the expansile mass (Fig. 26.4).
12
A discrete, round density overlying
the ethmoid labyrinth or within the maxillary or frontal sinus is
suggestive of progressive ethmoid hematoma.
13
Fluid lines in the
sinuses can be present if secondary sinusitis has occurred. Com-
puted tomography is useful to dene the extent of the mass prior
to surgical excision (Fig. 26.5).
12
Laboratory examination
Rarely, horses will have evidence of mild, regenerative anemia,
though generally blood loss from ethmoid hemotoma is minimal.
Depending on the duration, size of the mass, and inammatory
reaction, hyperbrinogenemia can be present.
13
Diagnostic conrmation
Differential diagnoses for PEH include neoplasia, fungal granu-
loma, nasal polyp, sinus cyst or abscess. Denitive diagnosis is
made based on the histopathology of the mass. Ethmoid hematoma
is a non-neoplastic angiomatous mass covered by respiratory epi-
thelium and brous tissue.
11,12
The parenchyma of the mass is com-
posed of blood, brous tissue, hemosiderin-laden macrophages,
neutrophils and necrotic debris, especially in large, chronic masses,
with occasional calcareous deposits.
Treatment and prognosis
Therapeutic aims
The goal of treatment is elimination of the mass. This can be
achieved by surgical excision, laser photo ablation, or chemical
ablation.
10,11,13,14
Most commonly, PEH is chemically ablated by
intralesional injection of formalin.
14,15
In the standing, sedated
horse, the mass is injected with 4% formaldehyde or neutral
Progressive ethmoid
hematoma (PEH)
Clinical signs include unilateral epistaxis and respiratory
stridor.
Endoscopy of the nasal passage and inspection of the
ethmoid region demonstrate ethmoid hematoma.
The diagnosis is conrmed by histopathology of the mass.
Most ethmoid hematoma originate at the ethmoid turbinate,
but can originate from any of the paranasal sinuses.
Treatment options include surgical excision, either sharply or
with a laser, or chemical ablation.
Recurrence is approximately 43%.
Recognition
History and presenting complaint
Horses with progressive ethmoid hematoma (PEH) have unilateral
or bilateral epistaxis, which can progress to respiratory stridor and
variable facial deformity depending on the duration of the condi-
tion, and decreased airow through the affected nostril.
10
Physical examination
Unilateral nasal obstruction can be diagnosed by holding the hands
over each nostril and detecting reduced airow from the affected
nostril. Facial deformity can also be observed as asymmetric convex-
ity of the facial bones, medial and rostral to the orbit.
Special examination
Endoscopic examination of the upper airway, including both
nasal passages, is frequently diagnostic for progressive ethmoid
hematoma. Ethmoid hematomas originate from the ethmoid tur-
binate region or paranasal sinuses (Fig. 26.3). The masses are
smooth, green to purple in color and can be small and discrete or
expansile, invading the entire nasal passage, nasopharynx, or
Fig 26.3 Endoscopic image of an ethmoid hematoma.
Ethmoid turbinate
Ethmoid hematoma
Nasal septum
Fig 26.4 Lateral radiograph of the paranasal sinus region of a horse.
The large arrow points to the ethmoid hematoma and the small arrow
points to the ethmoid turbinates.
Respiratory system
3
554
sinuses. Progressive expansion of the mass occurs due to recurrent
hemorrhage and local invasion of tissues. Masses can expand rostro-
ventrally into the nasal passage or nasopharynx, or within the para-
nasal sinuses.
Epidemiology
Progressive ethmoid hematomas have been reported in horses from
6 months to 20 years old, but are most commonly diagnosed in
middle-aged and older horses.
10,16
Thoroughbred horses are over-
represented in case series, though the disease has been reported in
many breeds. Bilateral lesions occur 15% of the time.
10,16
Sinusitis
The paranasal sinuses include the frontal, maxillary,
sphenopalatine, and dorsal and ventral conchal sinuses.
Sinusitis can be primary or secondary, and is most commonly
associated with dental disease, masses, and trauma.
Clinical signs of sinusitis include nasal discharge and facial
swelling.
Surgical debridement of the sinus is frequently recommended
for treatment of primary or secondary sinusitis.
Recognition
History and presenting complaint
Horses with sinusitis frequently have unilateral or bilateral nasal
discharge. Sinusitis can be primary if no underlying disease is
present or secondary if the sinusitis is due to dental disease or
fungal infection.
15
In the latter case the discharge can be foul smell-
ing and is more likely to be bilateral as compared to secondary
sinusitis.
15,16
Horses with primary sinusitis frequently have a history
of recent upper respiratory tract infection. If the sinusitis is second-
ary to a cyst or neoplastic mass, facial swelling and deformity of
facial bones can be detected as the mass expands within the
sinus.
15,16
Physical examination
Rarely are horses febrile. Facial swelling can be detected and can be
painful to palpation.
15,16
Deformity of facial bones overlying the
sinus can be evident, especially in chronic cases of expansile masses
such as sinus cysts and neoplasia.
1516
Increased respiratory rate and
effort is detected if the airway is obstructed. This occurs when the
ventral conchal sinus is affected and compresses the ventral meatus
16

or secondary to intrasinus lesions such as cyst or neoplasia.
15
Airow
obstruction is diagnosed by holding the hands over each nostril and
detecting reduced airow from the affected nostril. Submandibular
lymphadenopathy has been reported in 7883% of affected horses.
16

Epiphora occurs in horses with sinusitis if the nasolacrimal duct is
compressed by a mass or swelling in the surrounding tissues.
16
Hair
loss can be detected on the horses face if the epiphora is chronic.
Special examination
Techniques used to diagnose sinusitis include radiography, com-
puted tomography, sinoscopy, endoscopy, and nuclear medicine.
16,17

Generally at least four views of the skull are taken if sinusitis is
expected, including the left and right oblique, lateral, and dorso-
ventral views. The left and right oblique views help to conrm
which side of the head is affected. Fluid lines (Fig. 26.6), masses
within the sinuses (Fig. 26.7) and periapical tooth root absces-
sation and abnormal alveolar bone can frequently be detected
buffered 10% formalin until the mass distends using a trans-
endoscopic 23-gauge retractable needle (Mill-Rose Laboratories,
Inc., Mentor, OH) or through an injection apparatus constructed
from polyethylene tubing and a 22- or 25-gauge needle.
13,14
Treat-
ments are repeated every 34 weeks until the lesion is obliterated,
requiring 118 treatments.
15
If the lesion is very large especially
if invaded the sinuses surgical excision of progressive ethmoid
hematoma is required
10,1519
Laser excision is rarely indicated.
11

Copious hemorrhage is expected (especially under general anesthe-
sia) and controlled using cold saline and pressure applied with
sterile gauze packing.
Complications from surgical excision include severe hemor-
rhage, chronic sinusitis, surgical site infection, and osteomyelitis
of the bone ap.
10
Complications following formalin injection
include laminitis, dysphagia, and neurologic disease, if the ethmoid
hematoma has eroded through the cribiform plate.
13,14
Prognosis
Recurrence following surgical excision is 43%, necessitating peri-
odic re-evaluation should the mass recur. Recurrence is slightly
higher in horses with bilateral progressive ethmoid hematomas.
1012,15
Prevention
There are no known preventive measures.
Etiology and pathophysiology
Etiology
The etiology of PEH is unknown.
Pathophysiology
Progressive ethmoid hematoma is an expanding angiomatous mass
originating from the mucosa of the ethmoid conchae or paranasal
Fig 26.5 Coronal slice of a computed tomographic image of a horse
with an ethmoid hematoma. Notice the left sinus region is occupied
by the ethmoid hematoma. E = normal ethmoid turbinate;
ET = endotracheal tube; M = molars.
Ethmoid
hematoma
M
M
ET
E
26
Abnormalities of the upper airway
555
gained from the computed tomographic scan aids in surgical plan-
ning and the surgical approach. Sinoscopy is performed in the
sedated, standing horse by inserting a exible endoscope or arthro-
scope through a trephine in the frontal, rostral maxillary, or caudal
maxillary sinus.
17
Fluid is aspirated from the sinus and submitted
for culture and cytology and the sinus can be irrigated to evacuate
exudate. The sinuses can be explored and masses or tooth root
abscesses identied and biopsied by use of this technique. Endo-
scopic examination of the nasal passages is useful in cases of sinusi-
tis to conrm that the exudate is coming from the naso-maxillary
opening of the middle meatus. The specic origin of the exudate
and inciting cause cannot be determined by endoscopy alone.
Despite radiography and computed tomography, identifying the
affected tooth can at times be difcult. Nuclear medicine is rarely
used in cases of sinusitis, but can be used to conrm infected apical
tooth root.
Laboratory examination
The results of laboratory tests on blood are generally normal. Fluid
aspirates are submitted for culture and sensitivity.
Diagnostic conrmation
The diagnosis of primary sinusitis is made based on a history of
previous upper respiratory tract infection, nasal discharge originat-
ing from the paranasal sinus region, evidence of uid within the
sinuses on radiographs or computed tomography, and the absence
of a secondary cause of the sinusitis.
1516
Secondary sinusitis is
diagnosed based on the presence of an inciting cause of the sinusi-
tis, such as apical tooth root abscess, sinus cyst, neoplastic mass,
ethmoid hematoma, mycotic granuloma, polyp, or trauma and
facial bone fracture into the sinus.
1516
Conrmation of the etiology
of secondary sinusitis is made by sinoscopy, biopsy, or surgical
exploration of the sinuses.
Treatment and prognosis
Therapeutic aims
The goal of therapy is to rid the sinus of infection and remove the
inciting cause in cases of secondary sinusitis.
Therapy
The results of culture and sensitivity of uid aspirated from the
sinus dictate the appropriate antimicrobial therapy. Because primary
sinusitis frequently is a sequela to upper respiratory tract infection,
Streptococcus spp. are frequently isolated. Penicillin or trimethoprim
sulfonamides are appropriate antibiotics to use in the treatment of
primary sinusitis, prior to receipt of culture results. In addition to
systemic antibiotics, repeated lavage of the sinus with balanced
polyionic solution decreases the exudate and dilutes the organisms
and inammatory mediators within the sinus.
1516
A chronic irriga-
tion system can be placed following sinus centesis. Sinus centesis
can be performed at the cranial or caudal maxillary sinus or frontal
sinus. A point 2.53 cm dorsal to the facial crest and 3 cm rostral
to the medial canthus marks the placement for centesis of the
caudal maxillary sinus;
1516
2.53 cm dorsal to the facial crest and
3 cm caudal to the infraorbital foramen permits access to the cranial
maxillary sinus. Centesis of the frontal sinus is performed at a site
midway between the medial canthus of the eye and the midline of
the head. Following aseptic preparation, a 23 mL bleb of local
anesthetic is injected subcutaneously. A stab incision is made
through the skin and subcutaneous tissue and a 2 mm Steinmann
pin in a Jacobs chuck is used to drill a hole into the sinus. Sterile
radiographically. Computed tomography is performed to localize
the lesion more accurately in cases of secondary sinusitis. Sinus
cysts, dental disease, neoplasia, ethmoid hematoma, mycotic granu-
lomas, polyps, and epidermal inclusion cysts can cause secondary
sinusitis and frequently require surgical removal.
16
The information
Fig 26.6 Lateral radiograph of the paranasal sinus region of a horse
with sinusitis illustrating the uid line (arrow) within the maxillary sinus.
Fig 26.7 Lateral radiograph of the paranasal sinus region of a horse
with a mass (arrow) within the maxillary sinus.
Respiratory system
3
556
Horses with hyperkalemic periodic paralysis are at increased
risk for developing nasopharyngeal collapse.
Recognition
History and presenting complaint
Various degrees of nasopharyngeal collapse can cause exercise intol-
erance and respiratory noise in exercising horses.
Physical examination
This is normal in the resting horse.
Special examination
In affected horses, endoscopic examination of the nasopharynx and
larynx at rest is generally normal unless a pharyngitis is present. At
rest during nasal occlusion the lateral walls, dorsal aspect of the
nasopharynx, or rostral portion of the soft palate can collapse into
the airway to an abnormal degree in affected horses, especially
horses with hyperkalemic periodic paralysis (HYPP).
22,23
Be aware
that sedation and topical application of local anesthetic can create
nasopharyngeal collapse. Some horses show signs of nasopharyn-
geal collapse during resting endoscopic examination, and have
normal nasopharyngeal function during exercise.
Dynamic examination is required to conrm the diagnosis (Fig.
26.8). The interpretation of the endoscopic image at exercise is
obvious for lateral wall collapse. The interpretation of billowing of
the oor of the nasopharynx (i.e rostral nasopharyngeal collapse)
as well as the roof of the nasopharynx (i.e dorsal nasopharyngeal
collapse) must be made with caution. Normally, the roof of
the nasopharynx minimally projects ventrally at the end of expira-
tion due to positive end-expiratory pressure within the guttural
pouches resulting in some degree of dorsal pharyngeal collapse at
the end of expiration.
24
Dorsal nasopharyngeal collapse has recently
been proposed to be articially created in the dressage horse by the
excessive thoraco-cervical and atlanto-occipal hyperexion (i.e.
rollkur).
25
Dorsal nasopharyngeal collapse is also reported to be
secondary to subclinical tympany of the guttural pouch present only
during head exion.
26
Billowing of the rostral palate can be due to
a ventral position of the endoscope in the most rostral aspect of the
nasopharynx or caudal aspect of nasal passage during exercise will
visually amplify the normal billowing of the rostral palate and cause
an inaccurate identication of this condition.
Laboratory examination
None is indicated.
Diagnostic conrmation
The diagnosis is best conrmed by dynamic endoscopic exam
during exercise.
Treatment and prognosis
Therapeutic aims
The goal of treatment is to resolve the nasopharyngeal collapse.
Therapy
Horses with nasopharyngeal collapse may be given local or systemic
anti-inammatory agent if upper airway inammation is present.
Horses that are HYPP positive respond to acetazolamide therapy.
Horses with dorsal nasopharyngeal collapse may respond to fenes-
tration of the guttural pouches or removal of plica salpingopharyn-
geal membrane.
26
polyethylene tubing is fed through the centesis site and uid is
aspirated using a needle and syringe attached to the tubing. If
elected, a chronic irrigation system can be sutured in place. The
chronic irrigation system permits irrigation of the sinus with 13
liters of solution two to four times daily until exudate is no longer
produced.
The goal of treating secondary sinusitis is to treat the primary
cause. Depending upon the location, sinus cysts, ethmoid hemato-
mas, neoplasia, polyps, and infected teeth can be approached sur-
gically through a maxillary bone ap or frontal nasal bone ap.
15,18

Standing surgery reduces the amount of the bleeding compared
to sinusotomy under general anesthesia. Hemorrhage is controlled
during surgery by lavaging the site with cold saline and applying
pressure to the bleeding area. Occasionally, but rarely, vessels can
be located and ligated. After the mass has been removed, continu-
ous pressure is applied to the area using gauze (within a stocki-
nette) or roll gauze packing placed within the sinus. The end of
the packing is exited through a hole in the dorsal or ventral
conchal sinus and then out the nose or through a trephine opening
in the caudal maxillary sinus. The packing is pulled in 36 to
48 hours.
Prognosis
The prognosis for recovery from primary sinusitis, sinus cysts,
trauma, and dental disease is good.
15,19,20
Complications can include
chronic drainage from the sinus, recurrence of the cyst if a portion
of the cystic lining was left within the sinus, oral nasal stulas from
tooth extraction, incisional infection and sequestration of the bone
ap overlying the sinus. Prognosis for most neoplastic masses
within the sinus resulting in sinusitis is poor due to the expansile,
invasive, and metastatic nature of the tumors.
Prevention
There is no known prevention.
Etiology and pathophysiology
Etiology
Sinusitis can result from a primary infection within the sinus, fre-
quently secondary to an upper respiratory tract infection. Sinusitis
can also occur secondary to an apical tooth root abscess, sinus cyst,
neoplasia, trauma and fracture of facial bones, ethmoid hematoma,
and fungal granuloma.
15,16
Epidemiology
The prevalence of sinusitis ranges from 0.4 to 1.06%.
2021
Nasopharyngeal collapse
Horses with nasopharyngeal collapse are usually normal
at rest.
The diagnosis of nasopharyngeal collapse is made during
exercise (overground or treadmill) endoscopic examination.
Dorsal nasopharyngeal collapse can be a consequence of
excessive thoraco-cervical and atlanto-occipal hyperexion.
Dorsal nasopharyngeal collapse can be a manifestation of
subclinical guttural pouch tympany and treated by addressing
the latter surgically.
Clinical signs of nasopharyngeal collapse, in young horses or
in horses with pharyngitis, can resolve with time.
26
Abnormalities of the upper airway
557
Prognosis
The prognosis is usually unfavorable, especially in horses with
underlying disease such as HYPP. The condition resolves in some
horses.
Prevention
There is no known prevention.
Etiology and pathophysiology
Etiology
In most cases the etiology of pharyngeal collapse is not known.
However in some cases the disease is associated with pharyngitis or
HYPP and in foal with muscle disease.
Pathophysiology
Nasopharyngeal collapse can result from some form of exercise-
induced guttural pouch tympany or neuromuscular lesion involv-
ing the muscles that support the dorsal nasopharynx.
23,26
Horses
should be evaluated for neuromuscular or primary muscle disor-
ders, such as equine protozoal neuropathy, selenium and vitamin
E deciency, hyperkalemic periodic paralysis, or upper respiratory
inammatory disease.
22
Epidemiology
The epidemiology of this condition has not been described.
However, this disease is most frequently diagnosed in young race-
horses, which can be due to the speed and intensity at which they
compete. Nasopharyngeal collapse is also frequently recognized in
horses with HYPP, and rather than being a distinct entity, represents
a muscle group affected by the disorder.
Retropharyngeal abscesses
Recognition
History and presenting complaint
Horses with retropharyngeal abscessation frequently have palpable
swelling in the throat region, nasal discharge, abnormal respiratory
noise during exercise, dorsal displacement of the soft palate, and
exercise intolerance. If the airway obstruction is severe, horses can
show signs of respiratory distress at rest.
27,28
Additional clinical signs
include dysphagia, inappetance, and depression.
27
Physical examination
Palpation of the throat in the area of Viborgs triangle can reveal
swelling that can be painful and lead to stridorous upper airway
noise. If the horse is dysphagic, feed material and saliva can be seen
at the nares. If the horse is in respiratory distress, stridorous breath-
ing and increased respiratory effort might be apparent.
Special examination
Radiography of the throat area reveals soft tissue density in the
retropharyngeal region, dorsal to the pharynx and on the oor of
the guttural pouch (Fig. 26.9). Compression of the dorsal nasophar-
ynx by the abscessed retropharyngeal lymph node is evident during
endoscopic examination of the upper airway (Fig. 26.10). The
enlarged lymph node can be best seen within the guttural pouch,
on the oor of the medial compartment (Fig. 26.11).
Fig 26.8 Endoscopic images of the nasopharynx of an exercising
horse showing progressive nasopharyngeal collapse. Collapse is
apparent in the rst frame (A) and increases with increasing duration
of exercise on the treadmill (B, C).
A
B
C
Respiratory system
3
558
the surface protein (SeM) has been used as an epidemiological tool
to identify geographically linked outbreak.
30
Treatment and prognosis
Therapeutic aims
The goal of therapy is resolution of the abscess.
Therapy
Emergency tracheotomy
If the horse is in respiratory distress, an emergency tracheotomy is
performed in the mid cervical area. After inltration with local
anesthetic and aseptic preparation, a 1012 cm linear incision is
made through the skin, subcutaneous tissue, and cutaneous trunci
with a scalpel along the midline. The fascial plane dividing the right
and left sternohyoid muscles is sharply incised with a scalpel,
Metzenbaum scissors exposing the tracheal rings. A scalpel is
inserted through the tracheal ligament parallel to and in between
two tracheal rings. Approximately 40% of the ventral aspect of the
tracheal ligament is incised and the tracheostomy tube inserted. The
tube must be secured such that when the horse moves its head and
neck, the tube lumen is not obstructed and the tube is not dislodged
from the trachea.
Because most retropharyngeal lymph node abscesses are caused
by streptococcal species, penicillin, 22 00044 000 IU/kg, or
sulfamethoxazole-trimethoprim, 15 mg/kg, is administered for
710 days. Judicious use of non-steroidal anti-inammatory medi-
cation is appropriate. If the lymph nodes are large, surgical drainage
can be required. Following general anesthesia, the horse is posi-
tioned in dorsal recumbency. A modied Whitehouse approach is
performed on the affected side, exposing the abscessed lymph node.
Conrmation of the abscess is made by inserting a needle into the
mass and aspirating material from the lymph node that can be
submitted for culture and antibiotic sensitivity. A stab incision is
then made in the lymph node and the purulent material evacuated.
Ultrasonographic examination of the throat will show increased
soft tissue density containing hyperechoic uid, or purulent
exudates.
Laboratory examination
Results of complete blood count frequently show leukocytosis and
neutrophilia with regenerative left shift, and lymphocytosis. Some
horses will have hyperbrinogenemia.
Diagnostic conrmation
The diagnosis is conrmed by aspiration of material from the
affected lymph node and real-time PCR or culture of the exudate.
29

Retropharyngeal lymph node abscesses are most frequently caused
by Streptococcus spp., particularly Streptococcus equi. Sequencing of
Fig 26.9 Lateral radiograph of the pharyngeal region of a horse with
an abscessed retropharyngeal lymph node causing collapse of the
dorsal nasopharynx.
Mass
Nasopharynx
Fig 26.10 Endoscopic image of the nasopharynx of a horse with
abscessed retropharyngeal lymph nodes. Notice how the dorsal
nasopharynx is collapsed, such that the larynx cannot be seen.
E = epiglottis.
Dorsal nasopharynx
Soft palate
E
Fig 26.11 Endoscopic image of the medial compartment of the
guttural pouch. Notice the abscessed retropharyngeal lymph node.
Abscessed retropharyngeal
lymph node
Medial compartment
Longus capitis
26
Abnormalities of the upper airway
559
is dependent on the activity of the horse. DDSP in show horses
generally affects the horses performance because of the noise pro-
duction or coughing, although poor performance is also reported.
32

Horses that perform with the head and neck exed, such as upper-
level dressage horses and Saddlebreds, suffer exercise intolerance
with DDSP due to the more negative inspiratory pressure and
airway resistance that occurs with head and neck exion.
33
These
horses must be differentiated from horses with collapse of the roof
of the nasopharynx, which can also cause a similar abnormal noise
and impairment in performance. Dorsal displacement of the soft
palate is more common in racehorses, especially 24-year-olds.
34,35

The exercise intolerance is often described by trainers and riders or
drivers as choking down or hitting a wall because DDSP causes
signicant expiratory obstruction that limits minute ventilation.
Mouth breathing during exhalation is recognized by uttering of
the cheeks as air is diverted underneath the soft palate through the
mouth. Occasionally, coughing during exercise is reported in asso-
ciation with the disease; this complaint is more common in sport
horses.
Physical examination
Because intermittent DDSP is a dynamic obstructive airway disease
that occurs during exercise, most horses are normal at rest. If the
soft palate displacement is persistent and associated with dysphagia,
feed material can accumulate in the airway, the horse can cough,
and have clinical signs of aspiration pneumonia. The primary com-
plaint in these horses is dysphagia and aspiration. This is quite
different in horses with intermittent DDSP, where exercise intoler-
ance and respiratory noise are seen.
Some horses with intermittent DDSP have a history of upper
respiratory infection. These horses can have nasal discharge, cough-
ing, and enlarged retropharyngeal and submandibular lymph
nodes.
Special examination
Intermittent DDSP
Watching and listening to the horse exercise at a racetrack and wit-
nessing the described abnormal noise, open mouth breathing
during exhalation and exercise intolerance can be helpful in diag-
nosing DDSP. The noise is somewhat specic in that it occurs during
expiration and has a snoring character, quite different from inspira-
tory noises associated with laryngeal hemiplegia and other dynamic
inspiratory airway abnormalities.
Endoscopic examination of the nasopharynx and larynx at rest in
unsedated horses is important to assess nasopharyngeal function
and rule in or out other causes of abnormal airway noise and exer-
cise intolerance, such as laryngeal hemiplegia/hemiparesis or epi-
glottic entrapment. Examination of both guttural pouches can be
helpful if dysphagia present. Dorsal displacement of the soft palate
is recognized by the dorsal position of the caudal edge of the soft
palate obstructing the view of the epiglottis (Fig. 26.12). Occluding
the horses nares for 2060 seconds, forcing the horse to breathe
against the obstruction, can stimulate increased activity in upper
airway muscles and induce DDSP. The observation of induced
DDSP during nasal occlusion or resting endoscopy is predictive of
DDSP at exercise although it is an insensitive test.
36,37
Indeed, the
observation of DDSP at rest, coupled with a history of abnormal
respiratory noise at exercise, is only correct in approximately half
the horses.
36
After withdrawing the endoscope, the caudal edge of
the soft palate can be examined for evidence of ulcers (Fig. 26.13),
or prior staphylectomy. Ideally a laryngeal forceps is used to elevate
the epiglottic cartilage to better examine the caudal edge of the soft
palate (Fig. 26.14) and the subepiglottic tissue for ulcers, cysts,
The incision is left open, to heal by second intention, and the site
is lavaged with saline or dilute iodine solution twice daily.
Prognosis
The prognosis for return to normal function within 45 months
following retropharyngeal lymph node abscess is excellent, or
approximately 90%.
27
Prevention
Decreased exposure to horses infected with Streptococcus equi mini-
mizes the occurrence of retropharyngeal lymph node abscess forma-
tion. Prophylactic vaccination against S. equi can limit lymph node
abscess formation, but vaccination is not without risk.
Etiology
Etiology
Most retropharyngeal lymph node abscesses are caused by strepto-
coccal species, principally S. equi.
Epidemiology
Retropharyngeal lymph node abscesses are most commonly seen in
horses less than 1 year old, and in horses infected with S. equi.
Dorsal displacement of the soft
palate (DDSP)
Recognition
History and presenting complaint
Horses with intermittent dorsal displacement of the soft palate
(DDSP) are exercise intolerant and often make an abnormal expira-
tory noise during exercise. The displaced soft palate billows dorsally
during exhalation as air ows beneath the soft palate (Fig. 26.12).
The noise associated with DDSP is a gurgling or snoring noise, and
is caused by uttering of the caudal margin of the soft palate. In
approximately 2030% of horses with DDSP, noise is not heard.
31

The importance of either noise production or exercise intolerance
Fig 26.12 Endoscopic image of a horse with dorsal displacement
of the soft palate while exercising on a treadmill. Notice how the soft
palate billows dorsally in the airway, obstructing the rima glottidis.
Arrow, caudal free margin of the soft palate.
Soft palate
Respiratory system
3
560
Persistent DDSP
It is important to evaluate the epiglottis morphology; for instance,
subepiglottic masses and epiglottic deformity can result in DDSP.
If persistent displacement is present, there are a few techniques that
can be used to evaluate the structure and integrity of the epiglottis.
Sometimes removing the twitch will relax the horse and allow it to
reposition the soft palate appropriately. Sedation can permit
replacement of the soft palate.
38
Following application of local anes-
thetic to the nasopharynx, a laryngeal forceps can be passed in one
nostril and used to un-entrap the epiglottis from the soft palate.
Evaluation of the epiglottic cartilage and the position of the soft
palate can be performed using radiography (Fig. 26.15). Finally, an
oral endoscopic examination can be performed on the horse fol-
lowing sedation or general anesthesia and application of a mouth
speculum. If the horse is anesthetized, manual palpation of the
epiglottic cartilage and soft palate can also be performed.
Diagnostic conrmation
Because horses with intermittent DDSP are generally normal at rest
(with clinical signs occurring only during exercise) the diagnosis
can be very difcult to conrm. DDSP is best diagnosed by a
dynamic endoscopic examination.
Treatment and prognosis
Therapeutic aims
The goal of therapy is to prevent DDSP from occurring. Because the
etiology of DDSP is varied, treatment should be directed at the
cause.
Therapy
The following discussion should be noted with the concerns
expressed in a systemic review
39
recently performed where no treat-
ment could be determined to be superior. This is because most
reports in the literature failed to report control or when controls
were present, the health status of the control are unknown.
39,40

granulomas, or swollen aryepiglottic membrane indicative of inter-
mittent aryepiglottic entrapment. During endoscopy, the observa-
tions suggestive of DDSP are (1) the ease with which DDSP can be
induced by nasal occlusion, (2) more than one swallow is required
to correct the DDSP, and (3) ulceration on the caudal edge of the
soft palate. Dynamic endoscopic examination of the upper airway
is the gold standard to diagnose DDSP.
36,37
Diagnosis is made by
observation of DDSP during strenuous exercise or by observation
of palatal instability with accid epiglottis (presumably both are a
reection of caudal retraction of the larynx). Palatal instability (PI)
is interpreted as prodromal to DDSP.
36,37
Fig 26.13 Endoscopic image of the nasopharynx of a horse with
dorsal displacement of the soft palate. Note the ulcer (arrow) at the
caudal free margin of the soft palate.
Soft palate
Fig 26.14 Epiglottic cartilage is being lifted with an equine laryngeal
forceps, revealing an ulcer on the caudal free edge of the soft palate.
Fig 26.15 Lateral radiograph of the pharyngeal region of a horse with
persistent dorsal displacement of the soft palate. Notice the epiglottis
(small arrow) positioned ventral to the soft palate (large arrow).
Nasopharynx
26
Abnormalities of the upper airway
561
and muscle is resected bilaterally. The incision is left open to
heal or can be sutured if desired. Complications are usually minor
and include incisional seromas or abscesses requiring appropriate
drainage. However, in experimental horses with normal airway
function, resection of the sternothyroid and sternohyoid muscles
has been observed to result in a less dynamically stable nasophar-
ynx at exercise as measured by an increase in inspiratory tracheal
pressure.
63
Laryngeal tie-forward is based on an experimental model of inter-
mittent DDSP caused by bilateral resection of the thyrohyoideus
muscles which was corrected using a suture.
59
This was then shown
to be effective in 3 subsequent trials in restoring earnings post-
operatively in horses with a clinical diagnosis of DDSP.
58,59,61
Under
general anesthesia in dorsal recumbency, a ventral midline incision
is made from the base of the lingual process extending 1 cm caudal
to the cricoid cartilage. A non-absorbable suture (No. 5 USP) is
passed 34 times in the caudal edge of the thyroid cartilage over a
1 cm span immediately ventral to the ventral limit of the ST tendon.
Both sutures are then passed dorsal to the basihyoid bone with the
trailer end of the suture emerging adjacent to the base of the lingual
process on the contralateral side while the leading end of the suture
emerged adjacent to the base of the lingual process on the ipsilateral
side. The procedure is repeated on the contralateral side. The ventral
sutures are then tied rst advancing the rostral edge of the thyroid
cartilage dorsal to the basihyoid bone with an overlap of approxi-
mately 1.5 cm. The dorsal sutures are then tied together.
Prognosis
The prognosis following treatment ranged from 53 to
80%.
39, 4350, 5255,5961
These results must be taken with a grain of salt
as all outcomes are using some indices of performance as surrogate
of success and not actual resolution of the disease. The reported
success rate after bilateral tenectomy/myotomy of the sternothyroid
muscle is 60%.
45,46
Anecdotally recurrence can occur 36 months
after surgery. Following laryngeal tie-forward the success rate is
1020% higher than after bilateral sternothyroid muscle/tendon
transection.
5961
Etiology and pathophysiology
Etiology
Intermittent DDSP has a multifactorial etiology. Anecdotally physi-
cal obstruction (i.e subepiglottic and palatal masses, granulomas,
cysts) interferes with the subepiglottic position of the soft palate.
Furthermore, epiglottic malformation or chondritis can result in
permanent or persistent DDSP.
64
Damage of the innervation of the soft palate (i.e palatinus and
palatopharyngeus muscles),
64
dysfunction of the neuromusculature
of the extrinsic laryngeal muscles such as thyrohyoideus muscles,
65

and of the hypoglossal nerves
66
have all, alone, been sufcient to
create dorsal displacement of the soft palate.
The innervation of the soft palate is through the pharyngeal
branch of the vagus nerve, which with the glossopharyngeal and
hypoglossal nerves which course through the guttural pouch and
therefore are susceptible to disease processes that specically affect
the lymph node in the oor of the guttural pouches. The pharyngeal
branch of the vagus nerve provides motor innervation to the palati-
nus and palatopharyngeus muscles, two muscles that control the
position of the caudal portion of the soft palate. Experimentally
desensitizing the pharyngeal branch of the vagus nerve bilaterally
causes persistent DDSP at rest with dysphagia.
65
The thyrohyoideus
is a at rectangular muscle attached to the lateral surface of the
thyroid cartilage lamina that inserts on the caudal part of the
Therapy is directed to the likely cause of the DDSP. Pharyngitis has
been associated with DDSP due to inammation of the nerves and
perhaps muscles that stabilize the soft palate.
64
Upper airway inam-
mation is treated in a plethora of different ways, including systemic
administration of corticosteroids (dexamethasone), non-steroidal
anti-inammatory medication, topical anti-inammatory throat
sprays, systemic administration of interferon, and guttural pouch
lavage with balanced polyionic solutions with or without dimethyl
sulfoxide and corticosteroids. Oral interferon alpha (50200 IU/day
for 10 days to two weeks) is sometimes prescribed. An appropriate
treatment regimen for moderate-to-severe nasopharyngeal inam-
mation, without bacterial infection, might include treatment rst
with systemic corticosteroids such as prednisolone or dexametha-
sone and a topical anti-inammatory throat spray for 24 weeks. A
common throat spray administered at the rate of 20 cc, orally, every
12 hours consists of: glycerin 250 mL, 250 mL DMSO 90%, nitro-
furazone 500 mL, prednisolone 50 mL (25 mg/mL). Horses should
be rested (light training without fast speed work) for 1030 days
and the upper airway function re-evaluated periodically.
If there is a structural abnormality, such as epiglottic deformity,
entrapment, subepiglottic or soft palate cyst or mass, present then
these abnormalities should be addressed. Cysts should be removed
either through laser surgery or sharp dissection through a laryn-
gotomy. Granulomas are treated with local anti-inammatory
agents as described above or rarely through resection. Horses with
deformed epiglottic cartilage are more difcult to address. In some
cases the epiglottic deformity is worsened by partial entrapment by
subepiglottic tissues. Those can be released with laser surgery
Whether secondary to an inammatory process in the upper
airways, structural abnormalities and when no structural causes are
found, tack modications such as the use of a bit that keeps the
tongue under it (i.e., a W bit, Serena song bit), tongue-ties and the
gure-eight noseband are traditional approaches (although
unproven) that might be of value in reducing the occurrence of
DDSP. There is some circumstantial evidence to support the use of
a tongue-tie in the prevention of DDSP or improvement of airway
mechanics in exercising horses.
40,41
Finally the use of an external
device which positions the larynx in a more forward and dorsal
position has been shown to prevent DDSP during treadmill exercise
in an experimental model.
42
(Conict of interest disclosure: one of
the authors (N.G.D.) is listed as inventor on a patent owned by
both authors employer, i.e Cornell University).
Many surgical treatments have been reported, including sta-
phylectomy, various bilateral strap muscle resections (sternohyoid,
sternothyroid, and omohyoid alone or in combination), epiglottic
cartilage augmentation, and various tension or thermal palatoplasty
procedures.
4350
These procedures are performed by some surgeons
alone or in various combinations.
49,50
When comparing the results
of these surgical treatments to the results of conservative treatment
with or without case-control studies, they appear to be little or no
advantage to the above procedures.
5155
Two recent studies looked
at the biomechanical/histological results following procedure aims
to stiffens the soft palate with laser or injection of sclerosing
agent.
5658
The authors believe that there are two surgical treatments
to be considered for treatment of intermittent DDSP: bilateral ster-
nothyroid muscle tenectomy/myotomy transection
46
and laryngeal
tie-forward.
5861
The goal of the bilateral resection of the tendon of the sternothy-
roideus (ST) muscles is to prevent caudal retraction of the larynx
from the caudal edge of the soft palate.
46
Through a ventral midline
incision centered on the cricoid cartilage, the sternothyroideus
tendon/muscle is identied and clamped caudal to the cricoid car-
tilage to avoid damaging the cricothyroid muscles which can lead
to vocal cord collapse at exercise.
62
A 24 cm section of ST tendon
Respiratory system
3
562
radiographically. If the soft palate is persistently displaced, due
to or associated with the entrapment, a laryngeal forceps can be
used to either retract the soft palate, or undisplace the soft palate
so that the entrapping membrane can be observed. Alternatively an
oral exam during general anesthesia will identify the entrapment.
thyrohyoid bone. It is innervated by the hypoglossal nerve and
moves the hyoid bone caudally or the larynx rostrally and dorsally.
Experimentally bilateral resection of the thyrohyoideus muscles
causes intermittent DDSP during exercise in horses.
60
Finally appli-
cation of local anesthetic around each hypoglossal nerve at the level
of the ceratohyoid bone also resulted in DDSP at exercise in experi-
mental horses.
66
Pathophysiology
Dorsal displacement of the soft palate is an expiratory obstructive
syndrome that causes increased expiratory impedance, decreased
minute ventilation, hypoxia, and hypercarbia (Table 26.1).
65,67-69

During inhalation, the soft palate is located ventrally (still dorsal
to the epiglottis). During exhalation, the soft palate displaces dor-
sally, thus diverting the ow of air through the oropharynx and
mouth. This ow pattern is associated with more negative peak
tracheal pressure and increased expiratory impedance.
65,68,69
Prevention
Preventing DDSP is difcult because the etiology of this disease is
unknown. However, timely treatment of upper airway inamma-
tion and appropriate vaccination against upper respiratory tract
viruses can decrease the chances of horses developing intermittent
DDSP.
Epidemiology
Dorsal displacement of the soft palate (DDSP) is a performance-
limiting upper airway condition in horses that was reported to be
present in 1020% of racehorses.
51
Epiglottic entrapment
Epiglottic entrapment occurs when redundant aryepiglottic
tissue envelops the epiglottis.
Epiglottic entrapment can be an incidental nding during
endoscopic examination of the larynx and not associated with
clinical signs.
The entrapping aryepiglottic tissue can be smooth or
edematous and ulcerated.
Recognition
History and presenting complaint
Horses with epiglottic entrapment can have exercise intolerance and
make an abnormal respiratory noise during exercise. It must be
realized that the performance of some horses with epiglottic entrap-
ment is unaffected
70,71
and therefore treatment may not be needed.
Physical examination
External physical exam is generally normal. On rare occasion,
horses with severely ulcerated, swollen entrapping aryepiglottic
membrane can be lead to coughing, dysphagia and have signs of
aspiration pneumonia.
Special examination
Endoscopic examination reveals that the epiglottis is in its normal
position dorsal to the soft palate but is encased in the aryepiglottic
membrane so that the normal serrated edge of the epiglottis and
its vascular pattern are not visible. The aryepiglottic tissue can
be smooth, tting tightly around the epiglottis, or swollen and
ulcerated (Fig. 26.16A, B). The entrapment can also be observed
Fig 26.16 (A) Endoscopic image of the larynx of a horse with
epiglottic entrapment. Note that the epiglottis is encased in the
aryepiglottic membrane such that the vascular pattern on the dorsal
surface of the epiglottis and the serrated margin of the epiglottis is not
visible. (B) Endoscopic image of the larynx of a horse with an
epiglottic entrapment. Note the ulcerated area (arrow) of the
entrapping aryepiglottic tissue.
Epiglottic entrapment
A
B
26
Abnormalities of the upper airway
563
anesthesia through a laryngotomy incision, after everting the epi-
glottic cartilage in the larynx.
73
Following midline division of the aryepiglottic membrane, topical
and systemic anti-inammatory therapies are recommended to
prevent re-entrapment of the epiglottis. A topical anti-inammatory
solution (throat spray) is applied twice daily using a soft rubber
tube (i.e. 12 Fr infant feeding tube) placed in alternating nostrils.
In addition, dexamethasone (20 mg, IV, SID for 3 days) and an oral
phenylbutazone or unixin meglumine is recommended for
710 days.
Occasionally, the epiglottis is entrapped intermittently, during exer-
cise or immediately after swallowing only. In these cases, the diag-
nosis can be made by dynamic endoscopic examination during
exercise.
Laboratory examination
Laboratory examination is normal, but none is usually indicated.
Diagnostic conrmation
Differential diagnoses for epiglottic entrapment include dynamic
upper airway lesions that cause exercise intolerance and abnor-
mal respiratory noise during exercise. A denitive diagnosis of
epiglottic entrapment is made by static or dynamic endoscopic
examination.
Treatment and prognosis
Therapeutic aims
The goal of treatment is to relieve the entrapment. Chronic entrap-
ment can result in epiglottic chondritis and/or deformity.
Therapy
Midline division of the entrapping aryepiglottic membrane can be
performed standing by passing a shielded hook bistoury intra-
nasally
72
or by use of a hooked bistoury through the mouth with
the horse under general anesthesia (Fig. 26.17).
73,74
It is ill-advised
to use an unshielded hooked bistoury transnasally on standing,
even on sedated horses, because it exposes the horse to unnecessary
morbidity (possibly career ending) such as palatal, esophageal or
guttural pouch laceration if the horse swallows or moves. The
entrapping membrane can also be divided with the laser.
75
The
laser must not come into contact with the epiglottic cartilage, so it
is advisable to use a laryngeal forceps or blunt hook to elevate
the epiglottic membrane prior to division (Fig. 26.18A,B). The
advantage of the laser over the hooked bistoury is that if the aryepi-
glottic membrane is ulcerated and swollen, the membrane can be
resected. Alternatively this resection can be done under general
Fig 26.17 Endoscopic image through the oropharynx of a horse
where an entrapping aryepiglottic membrane is being excised using a
hooked bistoury (arrow) with the horse under general anesthesia.
Epiglottic entrapment
Fig 26.18 (A) Endoscopic image of an epiglottic entrapment being elevated by a blunt laryngeal forceps to protect the epiglottic cartilage
from inadvertent contact with the laser. The laser rst cut is an horizontal incision to allow the blunt hook to come through the membrane.
(B) Endoscopic image of the laser-assited midline division of the aryepiglottic membrane.
A B
Respiratory system
3
564
retroversion is observed when an exceptionally large subepiglottic
cyst is swallowed into the esophagus (see subepiglottic cyst). The
horse can then become dyspneic.
Laboratory examination
Laboratory examination is normal, though none is usually
indicated.
Diagnostic conrmation
Differential diagnosis of epiglottic retroversion includes those dis-
eases that cause abnormal respiratory noise during inhalation at
exercise and can result in exercise intolerance (Table 26.1). The
diagnosis of epiglottic retroversion is denitively made during
endoscopic examination during exercise.
Treatment and prognosis
Therapeutic aims
The goal of treatment is to stabilize the epiglottis and prevent it
from obstructing the airway during inspiration.
Therapy
Little is described in the treatment for epiglottic retroversion. Treat-
ment of two horses is described, with one horse racing successfully
after epiglottic augmentation with polytetrauoroethylene (Teon),
and another horse showing no improvement.
81
The author has
performed different xation (epiglottic tie-down) in ve cases
(four to basihyoid and one to thyroid cartilage) and only one
responded to treatment. Currently better results have been obtained
using facilitated ankylosis of the thyroepiglottic articulation.
Prognosis
Prognosis is excellent for life, but guarded for athletic
endeavors.
80,81
Prognosis
Seventy-four to 82% of horses have a positive outcome following
transoral axial division of the aryepiglottic tissue; 510% of horses
have recurrence of the entrapment after surgery, and 1015% of
horses develop dorsal displacement of the soft palate following
correction of epiglottic entrapment.
7275
Prevention
There is no known preventive measure.
Etiology and pathophysiology
Etiology
The etiology is unknown.
Pathophysiology
Aryepiglottic tissue is areolar, mucous membrane that attaches
along the ventral margin of the epiglottis and continues between
the lateral edges of the epiglottis to the corniculate processes of the
arytenoid cartilages. The manner by which the entrapment occurs
is unknown, but it can be precipitated by airway inammation and,
specically, inammation of the aryepiglottic tissue. It has been
suggested that horses with epiglottic hypoplasia, diagnosed by use
of endoscopy or radiographic measurement of the thyroepiglottic
length, are predisposed to epiglottic entrapment.
73
Epidemiology
Between 0.74 and 3% of racehorses have epiglottic
entrapment.
70,71,7679
Epiglottic retroversion
Epiglottic retroversion is a rare cause of exercise intolerance
and abnormal respiratory noise in horses.
Epiglottic retroversion is diagnosed during dynamic
examination during exercise.
When the epiglottis retroverts, it prolapses through the rima
glottides during inhalation, causing airway obstruction.
Epiglottic retroversion is probably due to damage to the
hyoepiglotticus muscle or the hypoglossal nerve or some of its
branches.
Recognition
History and presenting complaint
Epiglottic retroversion is a rare condition that causes abnormal
respiratory noise during exercise and exercise intolerance.
Physical examination
The physical examination is normal.
Special examination
Epiglottic retroversion is diagnosed during dynamic endoscopic
examination at exercise.
80,81
At rest, the nasopharynx and larynx of
affected horses are almost always normal during endoscopic exami-
nation. During exercise endoscopy, the epiglottis retroverts such
that the ventral surface of the epiglottis faces rostrally (Fig. 26.19).
In some horses, the epiglottic retroversion is increased by traction
on the lines or reins. Epiglottic retroversion causes dynamic airway
obstruction in affected horses (Table 26.1). A rare form of epiglottic
Fig 26.19 Endoscopic image of the larynx of a horse running on a
treadmill. Note that the epiglottis (arrow) is retroverted through the
rima glottidis, exposing the ventral surface of the epiglottis.
26
Abnormalities of the upper airway
565
Treatment and prognosis
Therapeutic aims
The goal of treatment is removal of the cyst.
Therapy
Subepiglottic cysts are usually excised with the horse using laser in
standing sedated horses.
82
If the cyst is large it may need to be
excised under general anesthesia to allow the procedure to be
carried out through the oropharynx. The cyst can also be excised
Prevention
There are no known preventive measures, though care should be
taken when performing surgery ventral to the epiglottis (i.e pharyn-
gotomy) so as not to damage nerve supply or muscles in this area.
In addition, injections lateral to the larynx commonly termed
palatal injection can result in injury to the hypoglossal nerve or its
branches to the hyoepiglotticus muscle(s).
Etiology and pathophysiology
Etiology
Aside from iatrogenic damage to the hyoepiglotticus muscle or its
innervation as described above, the cause of epiglottic retroversion
is unknown.
Pathophysiology
Epiglottic retroversion has been produced experimentally by bilater-
ally anesthetizing the hypoglossal nerves, suggesting that trauma or
dysfunction of the hyoepiglotticus or geniohyoideus muscle are
implicated in the pathogenesis of epiglottic retroversion.
82
Epidemiology
Because so few cases have been reported, the epidemiology of this
disease is unknown.
Subepiglottic cyst
Recognition
History and presenting complaint
Coughing, abnormal respiratory noise, and exercise intolerance are
clinical signs of subepiglottic cysts in mature horses. Dysphagia can
occur in foals or horses with a very large cyst.
Physical examination
Physical examination is usually normal. If the horse is dysphagic,
coughing and aspiration pneumonia can be evident.
Special examination
Endoscopic examination of the larynx and nasopharynx is generally
diagnostic for a subepiglottic cyst (Fig. 26.20). The cyst is round,
pale pink to red, covered with mucosa, and generally seen beneath
the epiglottis and average in size, 34 cm.
83,84
Occasionally, the cyst
is not visible as it rests in the oropharynx and can only be seen
briey in the nasopharynx during swallowing or intermittently
during exercise. Most rarely the cyst can be swallowed in the esopha-
gus, leading to epiglottic retroversion at rest and obstruction of the
rima glottidis and complete airway obstruction (Fig. 26.21).
84
Laboratory examination
None is indicated unless there is a suspicion of aspiration
pneumonia.
Diagnostic conrmation
Endoscopic examination is diagnostic for a subepiglottic cyst. Fol-
lowing resection, the cyst can be submitted for histopathologic
analysis if there is any concern that the cyst can instead be a neo-
plastic mass.
Fig 26.20 Endoscopic image of the epiglottis of a horse with a
subepiglottic cyst.
Epiglottis
Cyst
Fig 26.21 Endoscopic image of a horse that has swallowed its
subepiglottic cyst into the esophagus. The glottis is obscured by the
ventral aspect of the epiglottic cartilage.
Respiratory system
3
566
Recognition
History and presenting complaint
Horses with medial deviation of the aryepiglottic folds are exercise
intolerant and make an abnormal respiratory noise during
exercise.
87
Physical examination
Physical examination is normal.
Special examination
Medial deviation of the aryepiglottic folds is only diagnosed during
endoscopic examination of horses during exercise (Fig. 26.22).
During intense exercise, the vertical component of the aryepiglottic
tissue which connects the corniculate portions of the arytenoid
cartilages to the lateral edge of the epiglottis collapses medially
across the rima glottidis during inhalation.
87
The obstruction is
dynamic and worsens as exercise intensity increases. In some horses
the medial collapse is seen prior to an imminent occurrence
of DDSP.
Laboratory examination
Laboratory examination is normal; none is usually indicated.
Diagnostic conrmation
The denitive diagnosis of medial deviation of the aryepiglottic
folds is made during dynamic endoscopic examination.
87,88
Treatment and prognosis
Therapeutic aims
The goal of treatment is to alleviate the dynamic airway obstruction
by stabilizing the aryepiglottic folds.
Therapy
Treatment for medial deviation of the aryepiglottic folds is pre-
dominately by surgical resection of the aryepiglottic tissue between
the lateral edge of the epiglottis and the corniculate processes of
the arytenoid cartilages (Fig. 26.23). This is accomplished
using a laser, with the horse sedated and standing. Alternatively,
along with the overlying mucosa by application of a snare device
made with obstetrical wire threaded through an infusion pipette.
80

Alternatively,the cyst can be excised through a laryngotomy inci-
sion, with the horse in dorsal recumbency under general anesthe-
sia.
80
The cyst is positioned beneath the laryngotomy incision by
retroverting the epiglottis. The aryepiglottic mucosa is incised and
the cyst is dissected free and removed. In all cases, care must be
taken to remove the entire cyst and a minimal amount of aryepiglot-
tic tissue.
Sclerotherapy is an alternative treatment where the cyst is injected
with ethanol
85
or formalin.
86
This treatment option should be
reserved for cases where economic limitation is present, as the pos-
sibility of recurrence and morbidity from excessive brosis could
lead to dysphagia or displacement of the soft palate.
Prognosis
The prognosis for return to function and resolution of coughing is
good to excellent. Occasionally a partial or complete epiglottic
entrapment is seen a few weeks postoperatively. Recurrence of the
cyst is rare, unless the entire cyst was not removed.
Prevention
There is no known preventive measure.
Etiology and pathophysiology
Etiology
Subepiglottic cysts can be either acquired, especially in older horses,
or congenital, as in foals. The cysts can develop from remnants of
thyroglossal ducts in humans,
85
but this has not been proven in
horses.
Pathophysiology
Airway obstruction and abnormal respiratory noise results from the
cyst ipping dorsally across the rima glottidis, causing airway
obstruction or leading to DDSP, which results in upper airway
obstruction during exhalation.
Epidemiology
Subepiglottic cysts are most frequently diagnosed in young racing
horses, both Standardbreds and Thoroughbreds, but have been
identied in foals and older horses. There is no known breed
predisposition.
80
Medial deviation of the
aryepiglottic folds (previously
termed axial deviation)
Medial deviation of the aryepiglottic folds has been
diagnosed in racing Thoroughbreds, Standardbreds, and
Arabians.
87,88
Diagnosis is made during endoscopic
examination of the horse running on a treadmill.
Medial deviation is sometimes seen prior to DDSP at
exercise.
Medial deviation is usually bilateral except when seen in a
horse with partial or complete arytenoid collapse where
contralateral medial collapse is seen.
89
Treatment includes rest and anti-inammatory therapy or
surgical removal of the aryepiglottic folds.
Fig 26.22 Endoscopic image of the larynx of a horse with bilateral
medial deviation of the aryepiglottic fold collapse during exercise.
26
Abnormalities of the upper airway
567
Recognition
History and presenting complaint
Most horses have a history of exercise intolerance, abnormal
respiratory noise during exercise, and coughing. Occasionally,
horses have evidence of airway obstruction at rest, dysphagia, and
anorexia.
90
Physical examination
Generally, physical examination is normal, unless the horse is dys-
phagic or coughing.
90,91
Coughing can be easily elicited by laryngeal
palpation. Dysphagic horses can have clinical signs of aspiration
pneumonia or rhinitis.
90
Special examination
Epiglottitis is diagnosed by endoscopic examination. The epiglottis
and subepiglottic tissue are swollen and dark pink to purple and
can be ulcerated. Occasionally, the tip of the epiglottic cartilage is
visible and is surrounded by granulation tissue. To identify the
lesion, exploration with laryngeal forceps under endoscopic control
might be needed.
92
Laboratory examination
Complete blood count and serum chemistry values are usually
normal. When chondritis is present, bacterial culture can help direct
antimicrobial therapy.
Diagnostic conrmation
Differential diagnosis of epiglottitis includes epiglottic entrapment,
chondritis of the epiglottis, and subepiglottic cyst and granuloma.
Treatment and prognosis
Therapeutic aims
The goal of treatment is to resolve inammation of the epiglottis.
Therapy
Horses should be rested for a minimum of 14 days. Topical admin-
istration of throat spray is applied transnasally twice daily for 10
days to 2 weeks.
90,91
In addition, systemic anti-inammatory medi-
cation such as phenylbutazone is recommended for 10 to 14 days.
If aspiration pneumonia is suspected, broad-spectrum antimicro-
bial therapy is recommended.
90
Endoscopic examination of the
airway should be repeated in 2 weeks.
If signicant loss/deformity of epiglottic cartilage is present
redundant aryepiglottic membrane may be needed to treat medial
deviation of the aryepiglottic fold.
92
Additionally a laryngeal tie-
forward can be recommended if DDSP is observed.
92
Prognosis
Prognosis for return to performance is excellent unless epiglottic
chondritis is present. Complications resulting from epiglottitis
occur in approximately 28% of cases and include epiglottic deform-
ity, which can occur if the epiglottic cartilage is exposed and chon-
dritis occurs.
90
Also, epiglottic entrapment, medial deviation of the
aryepiglottic folds and DDSP can occur following epiglottitis due
to the subepiglottic inammation.
9093
Prevention
There is no known prevention.
the procedure can be carried out after performing a laryngotomy
under general anesthesia and retroverting the epiglottic cartilage
to access the left and right aryepiglottic fold. A very small percentage
of horses respond to rest and local treatment with topical
anti-inammatory throat spray and systemic anti-inammatory
medication.
87
If the disease is seen in association with DDSP, it is not always
necessary to treat the condition if treatment of the DDSP is done.
Prognosis
Seventy-ve percent of horses that have surgery have objective
improvement in performance.
89
Prevention
There is no known method of prevention.
Etiology and pathophysiology
Etiology
The cause of this condition is unknown.
Pathophysiology
The aryepiglottic tissue that attaches the lateral aspect of the cor-
niculate process of the arytenoid cartilage to the lateral edge of the
epiglottis collapses dynamically across the rima glottidis during
intense exercise, resulting in inspiratory airway obstruction. Com-
puter modeling studies have revealed that the contralateral aryepi-
glottic fold in a horse with unilateral laryngeal collapse (or partial
abduction) is subjected to more negative inspiratory pressure.
89
Epidemiology
Medial deviation of the aryepiglottic folds has been diagnosed in
racing Thoroughbreds, Standardbreds, and Arabians.
87
Epiglottitis
Epiglottis is inammation of the epiglottic mucosa, and at
times, the tip of the epiglottic cartilage.
Treatment includes rest and systemic and topical anti-
inammatory therapy.
The prognosis worsens when epiglottic cartilage chondritis is
present,.
Complications of epiglottitis include epiglottic entrapment,
DDSP, and deformity of the epiglottic cartilage.
Fig 26.23 Endoscopic image of the larynx of a horse during resection
of left aryepiglottic fold.
Respiratory system
3
568
results from perivascular injection of caustic substances or trauma
involving the jugular furrow, due to the close proximity of the
jugular vein, recurrent laryngeal nerve, and vagosympathetic trunk.
Horners syndrome is recognized based upon clinical signs of uni-
lateral ptosis, miosis, dropped eyelid, and sweating near the base of
the ear, due to loss of sympathetic innervation. An important char-
acteristic of Horners syndrome is dilation of the vascular bed of the
ipsilateral nasal cavity. Sympathetic nerve damage causes the horse
to lose its ability to constrict the nasal vascular bed, leading to
reduced airow that can be detected manually.
The larynx is palpated for evidence of atrophy of the cricoaryte-
noid dorsalis (CAD) muscle. This is done by using the index ngers
to palpate the dorsal aspect of the cricoid cartilage and muscular
processes for symmetry (Fig. 26.24) The laryngeal musculature is
best evaluated using external and/or esophageal ultrasound.
99
Historically, the absence of arytenoid cartilage adductor move-
ment can be identied by the thoracolaryngeal reex (slap test).
100

While standing on the left side of the horse, one could place two
ngers of the left hand on the lateral aspect of the larynx, and using
the right hand, slap the wither area. A positive slap test will elicit a
contraction of the adductor muscles and a twitching can be felt
over the contralateral side of the larynx. Horses with RLN tend to
make a grunt sound and/or a hoarse whistling noise during
inspiration.
Etiology and pathophysiology
Etiology
The etiology of epiglottitis is unknown, though speculative causes
include trauma due to poor-quality hay, the presence of a foreign
body, respiratory tract infection, and allergic reaction.
Pathophysiology
Respiratory noise and dysphagia are caused by swelling of the epi-
glottis with subsequent partial occlusion of the airway and abnor-
mal function of the epiglottis.
Epidemiology
Epiglottitis is diagnosed frequently in racehorses but has been seen
in older brood mares.
90
Laryngeal hemiplegia
Laryngeal hemiplegia is more commonly a bilateral
mononeuropathy affecting more severely the left recurrent
laryngeal nerve: thus it is referred to commonly as recurrent
laryngeal neuropathy (RLN).
93
Others causes of laryngeal hemiplegia include trauma,
arytenoid chondritis, and fourth branchial arch defect.RLN is
a distal axonopathy leading to preferential loss of ber type
2x with clinical implications predominantly on the left
side.
9395
Laryngeal hemiplegia (grade IV) is frequently diagnosed
during endoscopic examination of the larynx at rest, but
exercise endoscopy can be required to identify laryngeal
collapse on hemiparesis (grade IIII).
The current surgical therapy of choice includes laryngoplasty
with ventriculocordectomy for treatment of poor performance
and unilateral or bilateral ventriculocordectomy for treatment
of abnormal noise.
Recognition
History and presenting complaint
Horses with RLN or roarers have a history of making an inspiratory
noise during exercise and/or poor performance. The term roaring
describes an unnatural sound rattling, snoring, and whistling
during inspiration.
96,97
The noise is heard only during exercise,
immediately after exercise during hyperpnea, or when the horse is
startled (grunt test). These horses also have abnormal vocalization.
Many sport horses are unaffected until 56 years of age such that a
history of normal breathing during exercise followed by progres-
sively more noisy breathing is often reported. Exercise intolerance
experienced by horses with RLN is associated with decreased venti-
lation due to laryngeal collapse.
89,98
The degree of impairment
reects a combination of factors such as degree of laryngeal col-
lapse, athletic capacity, and the length and intensity of competition.
The major complaint of horses performing lower levels of work,
such as show hunters and trail horses, is the presence of an abnor-
mal inspiratory noise during exercise.
Physical examination
A thorough examination can help to identify the causes of the
disease, though the majority of cases of RLN are idiopathic. The
throat and cervical areas are inspected for signs of trauma or deform-
ity. Horners syndrome can accompany laryngeal hemiplegia that Fig 26.24 Illustration of laryngeal palpation technique.
26
Abnormalities of the upper airway
569
access to videoendoscopy. RLN is identied by the presence of
sound throughout inhalation and exhalation and the presence of
three frequency bands centered on 0.3 kHz, 1.6 kHz, and 3.8 kHz
are seen during inhalation (Fig. 26.28A, B).
31
Laryngeal ultrasound is becoming one of the most useful diag-
nostic modalities in identifying horses with RLN and differentiating
them from chondritis. First described in 2006,
99
percutaneous
Special examination
Endoscopic exam at rest allows assessment of the laryngeal anatomy
as well as some indication of function by categorizing the degree of
arytenoid movement and synchrony (see Table 26.2).
101,102
The diag-
nosis of RLN with complete paralysis (grade IV) is made by endo-
scopic examination of the larynx at rest and observation of a midline
or paramedian position of the corniculate process without morpho-
logical evidence of enlargement or deformation of the cartilage (i.e.
arytenoid chondritis). A clinical diagnosis of RLN must not be made
solely by observation of motion abnormalities (such as weak,
paretic, partially paralyzed, utter, and/or hesitation) of the aryte-
noid cartilage at rest. If one suspects laryngeal collapse (arytenoid
cartilage collapse [ACC] (Fig. 26.25) or vocal cord collapse [VCC]
(Fig. 26.26)), dynamic videoendoscopy (treadmill or overground)
is necessary to conrm the diagnosis and identify concomitant
obstruction.
1,37,103105
During exercise, the laryngeal grade can also
be classied as grade A, B, or C (Fig. 26.27).
101
Exercise endoscopy
allows the precise diagnosis of collapse as well as co-morbid obstruc-
tion such that the optimum treatment can be prescribed. For
example, horses with partial arytenoid collapse during exercise often
have the same or better degree of arytenoid abduction than that
obtained after a laryngoplasty. These horses frequently have vocal
cord collapse obstructing the ventral aspect of the rima glottidis,
with little collapse of the arytenoid cartilage. Therefore ventriculo-
cordectomy might alleviate the obstruction.
106
If a dynamic exam at
exercise is not possible, there is a reasonable correlation between
laryngeal grade as show in Table 26.2 and laryngeal grade at exercise
(Fig. 26.27);
103
horses with a resting laryngeal grade of I or II have
a 7% prevalence of laryngeal collapse, while horses with laryngeal
grade of III.1, III.2, and III.3 have a prevalence of laryngeal collapse
at 44%, 83%, and 100%, respectively.
Another modality less frequently used now that dynamic endos-
copy can be done is sound analysis.
31
Frequency analysis of airway
sounds during exercise can help quantitate the upper airway sounds
of horses such that RLN can be diagnosed during exercise without
Table 26.2 Consensus grading system of laryngeal function performed in the standing unsedated horse
104
GRADE DESCRIPTION

SUB-GRADE
I All arytenoid cartilage movements are synchronous
and symmetrical and full arytenoid cartilage
abduction can be achieved and maintained
II Arytenoid cartilage movements are asynchronous
and/or asymmetrical but full arytenoid cartilage
abduction can be achieved and maintained
1. Transient asynchrony, utter or delayed movements is seen
2. There is asymmetry of the rima glottidis much of the time due to
reduced mobility of the affected arytenoid and vocal fold but there
are occasions, typically after swallowing or nasal occlusion, when
full symmetrical abduction is achieved and maintained
III Arytenoid cartilage movements are asynchronous
and/or asymmetrical but full arytenoid cartilage
abduction cannot be achieved and maintained
1. There is asymmetry of the rima glottidis much of the time due to
reduced mobility of the arytenoid and vocal fold but there are
occasions, typically after swallowing or nasal occlusion, when full
symmetrical abduction is achieved but not maintained
2. Obvious arytenoid abductor decit and arytenoid asymmetry. Full
abduction is never achieved
3. Marked but not total arytenoid abductor decit and asymmetry with
little arytenoid movement. Full abduction is never achieved
IV Complete immobility of the arytenoid cartilage and
vocal fold
Description generally refers to the left arytenoid cartilage in reference to the right. However, this grading system can apply to the right side (i.e. right grade
III.1).)
Fig 26.25 Endoscopic image of the larynx of a horse with grade IV
idiopathic laryngeal hemiplegia while the horse is running on the
treadmill. Notice how the left arytenoid collapses across the rima
glottidis (arrow).
Respiratory system
3
570
Fig 26.26 Endoscopic image of the larynx of a horse with grade III
idiopathic laryngeal hemiplegia and vocal fold collapse. Notice how the
left vocal fold collapses across the rima glottidis (arrow) as well as mild
collapse of right aryepiglottic fold.
Fig 26.27 Endoscopic image of a larynx showing the position of the
corniculate process of the arytenoids cartilage for each grade of
laryngeal position. Zone A represents the position (maximal abduction)
for grades I and II; Zone B represents the position for grade III (partial
abduction); Zone C represents the position for grade IV laryngeal
hemiplegia, or complete paralysis with no abduction.
A
B
C
Fig 26.28 (A) Spectrogram of respiratory sounds from a horse with
normal upper airway function. Time is on the abscissa, frequency on
the ordinate. Sound level increases with brightness of the color (black
indicates no sound). Inspiration is indicated by a star, expiration by an
arrow. The top line of the graph is sound pressure level, a measure of
sound intensity. (B) Spectrogram of respiratory sounds for a horse
with laryngeal hemiplegia. Note the formants of inspiratory noise
centered at 0.3, 1.6, and 3.8 kHz.
4 kHz
2 kHz
+
+
+
+ +
+
3 4 s s 5 s
A
4 kHz
2 kHz
5 s s s s 6 7 8
+
+
+
+ +
+
+
+
B
assessment of the cricoarytenoid lateralis through the caudo-lateral
window (Fig. 26.29 A,B) is used as a sentinel for RLN as the adduc-
tor muscles are affected earlier and more severely than the abductor
muscles.
107
Increase in CAL echogenicity has been shown to corre-
late with laryngeal collapse at exercise with a sensitivity and speci-
city of 90 and 98%, respectively.
108
In sports medicine clinics, airway mechanics can be measured,
accurately assessing the degree of laryngeal function and dysfunc-
tion.
109,110
In addition, blood gas measurements can help to deter-
mine the degree of ventilation compromise caused by laryngeal
hemiplegia.
110
Finally electrodiagnostic testing of the thoracolaryn-
geal reex latency and velocity has been shown to have no correla-
tion with endoscopic examination and, therefore, is not useful in
the assessment of laryngeal function.
111
However preliminary work
with nerve conduction velocity suggests that this methodology
might be useful in identifying early forms of RLN.
112
Treatment and prognosis
Therapeutic aims
The goal of therapy is to restore the diameter of the rima glottidis
and to prevent dynamic collapse of the vocal cord and arytenoid
26
Abnormalities of the upper airway
571
nerve.
124,125
Laryngeal reinnervation returns upper airway mechanics
during exercise to normal, but the time required for successful rein-
nervation is 912 months.
125
Therefore, this procedure is generally
reserved for yearling racehorses or sport horses.
125
Most recently
electrical stimulation of the laryngeal recurrent nerve
126
or the CAD
muscle
127
is opening the possibility of early return to function with
a more physiological treatment, thus minimizing or eliminating the
morbidity of the current treatment.
Prognosis
The clinical results of treatment of laryngeal hemiplegia with col-
lapse of the upper airway (grade III and IV) are highly dependent
on the activity of the horse. Horses used for show and jumping have
a 90% chance of returning to their same level of function, while the
prognosis is worse for racehorses, approximately 6070%.
116119,128

Complications of the laryngoplasty include (1) continued exercise
intolerance and respiratory noise in 30 to 40% of horses during
exercise, (2) chronic coughing due to abduction of the left arytenoid
cartilage and the resulting inability of the larynx to protect the
trachea from aspiration of ingesta in 20 to 40% of horses, and
(3) loosening of the prosthetic suture(s) and loss of an initial degree
of abduction in approximately 10% of horses.
116119,128
Etiology and pathophysiology
Anatomical considerations
The recurrent laryngeal nerve exits the caudal brainstem as part of
the vagus nerve (cranial nerve X) and descends along the trachea
dorsal to the common carotid artery with a different course between
the left and right recurrent laryngeal nerves. The right recurrent
laryngeal nerve leaves the vagus nerve at the level of the second rib
turning around the costo-cervical trunk before ascending toward the
larynx. The left recurrent laryngeal nerve leaves the vagus nerve as
the latter crosses the aortic arch.. Both recurrent laryngeal nerves
ascend cranially, ventral to the common carotid artery, to innervate
all intrinsic muscles of the larynx except for the cricothyroid
muscles, which are innervated by the ipsilateral external branch of
the cranial laryngeal nerve.
Fig 26.29 Percutaneous ultrasound image showing (A) right cricoarytenoid lateralis (CAL) muscle between the thyroid (Th) and arytenoid (Ar)
and immediately rostral to the cricoid (Cr) cartilages. Note similar muscle echogenicity between CAL and cricothyroid (CT) muscles. (B) Left
cricoarytenoid lateralis (CAL) muscle between the thyroid (Th) and arytenoid (Ar) and immediately rostral to cricoid (Cr) cartilages. Note the
increased muscle echogenicity compared to right CAL and right and left cricothyroid (CT) muscles.
A B
cartilage during inspiration. The problem resides in the fact that the
larynx has both digestive and respiratory functions. The arytenoid
cartilage must fully abduct (larynx must be fully dilated) during
strenuous exercise and fully adducted (larynx must fully close)
during swallowing. Therefore, treatments aimed at permanently
increasing the diameter of the rima glottidis tend to interfere with
laryngeal adduction during swallowing and protection of the airway.
Therapy
The value of surgical therapy for RLN depends on whether the
complaint is exercise intolerance, noise production, or both.
Ventriculocordectomy is effective in reducing airway noise and
stabilizing the arytenoid cartilage during exercise, but does not
improve airway mechanics as well as other surgical procedures.
113

Also, ventriculocordectomy or cordectomy is the surgical treatment
of choice for horses with vocal fold collapse as seen in early cases
of RLN.
106
Laryngoprosthesis with unilateral ventriculocordectomy is the
current standard surgical treatment for horses with arytenoid col-
lapse at exercise.
114119
Laryngoplasty reduces the high inspiratory
upper airway impedance measured in horses with experimentally
induced left laryngeal hemiplegia.
1
Partial arytenoidectomy
120
is performed in some horses for treat-
ment of RLN but these horses fail to return to their previous level
of competition or at the same level as control horses although the
return rate into competition can be higher than after laryngo-
plasty.
121,122
This is probably because, although airway mechanics
measurements are improved following partial arytenoidectomy,
impedance values are signicantly higher than those of horses
treated with laryngoplasty or those of normal horses.
115,123
In
summary, partial arytenoidectomy is an alternative to laryngoplasty
in sport horses and in racehorses where return rate to racing is more
important than the level of performance.
124
The neuromuscular pedicle graft procedure was introduced as a
more physiological surgical treatment for RLN and is performed by
grafting neuromuscular bundles composed of the rst or second
cervical nerve and omohyoideus muscle to the atrophied cricoary-
tenoideus dorsalis muscle or by anastomosing branches of the rst
cervical nerve to the abductor branch of the left recurrent laryngeal
Respiratory system
3
572
Once the arytenoid cartilage is abscessed and deformed, the
treatment is surgical resection by arytenoidectomy.
Recognition
History and presenting complaint
Horses affected only with ulcerative lesions of the mucosa on the
axial surface of the corniculate processes of the arytenoid cartilages
(Fig. 26.30) are generally asymptomatic at rest and during exercise.
These lesions are identied during endoscopic examination for
reasons unrelated to abnormal airway function. Horses with granu-
lation tissue originating from the arytenoid cartilage and protruding
into the lumen of the rima glottidis (Fig. 26.31A, B) or horses with
severe arytenoid cartilage abscessation and deformity (Fig. 26.32)
have clinical signs of exercise intolerance and upper respiratory
noise very similar to horses with laryngeal hemiplegia. If the abscess
within the cartilage is large enough, the arytenoid cartilage can be
deformed such that it causes severe obstruction of the rima
glottidis.
Physical examination
Palpation of the throat and larynx is usually normal. The larynx has
a normal contour and asymmetry of the cricoarytenoideus dorsalis
muscles is not detected, as in idiopathic laryngeal hemiplegia.
Rarely will there be perilaryngeal swelling associated with infection
of the arytenoid cartilage.
Horses with arytenoid chondritis characterized by granulation
tissue formation protruding from the arytenoid cartilage, with or
without cartilage deformity, can be exercise intolerant and make an
abnormal inspiratory noise during exercise. Depending upon the
severity of respiratory distress, a tracheostomy can be warranted
before further diagnostic evaluation is performed.
Special examination
Endoscopic examination of the larynx is frequently diagnostic for
arytenoid chondritis. The morphology of the arytenoid cartilages
Fig 26.30 Endoscopic image of the larynx of a horse with kissing
lesions on the axial aspect of the mucosa covering the corniculate
processes of the left arytenoid cartilage (arrow).
Pathology
Idiopathic RLN is a peripheral neuropathy characterized by a distal
loss of large myelinated bers (distal axonopathy), is a bilateral
mononeuropathy, leading to neurogenic atrophy of the intrinsic
laryngeal muscles supplied by the recurrent laryngeal nerve.
95,107,129,130

Histologically, sections of the cricoarytenoideus dorsalis muscle
exhibit ber type grouping intermixed with atrophic bers, sugges-
tive of denervation and reinnervation.
94,107,129
Interestingly, there is
a preferential atrophy of the adductor muscles in some horses
so adductor decit of the left arytenoid cartilage is observed
despite normal abductor function in affected horses.
107
In addition,
although the disease affects preferentially the left recurrent laryn-
geal nerve, there are some mild pathological lesions found in the
right recurrent laryngeal nerve and associated right intrinsic laryn-
geal muscles.
130
There is a signicant and reasonable correlation (r = 0.75)
between muscle histopathology and clinical disease (as in Table
26.2) or the degree of arytenoid dysfunction.
131
Horses with a clini-
cal laryngeal grade IV RLN have marked pathological lesions. Horses
with left-sided RLN can have histopathologic evidence of right-
sided lesions without right-sided clinical signs.
131
This subclinical
disease and its progression are not well understood. The progres-
sion from laryngeal grade I to grade IV is variable. Some horses
show no progression in their laryngeal grade and stay at laryngeal
grade III for years while others progress over a period of 24 months
from normal to grade IV.
132,133
Etiology
The etiology of RLN is unknown. Anatomically, the course of the
left recurrent laryngeal nerve around the aorta, combined with the
pathological appearance of the nerve, is suggestive of a compressive
lesion, and led to the theory that the aortic pulse against the recur-
rent laryngeal nerve might be involved in the pathological process.
Experimentally, constricting sutures were placed around the recur-
rent laryngeal nerve and a mixed array of abductor and adductor
axons were affected along the course of the nerve, which is quite
different than what is seen in the clinical disease.
95,134
Risk factors for RLN include gender, breed, size, and perhaps
genetics.
135138
Male horses are over-represented, as are Thorough-
bred and draft horses.
135137
Horses greater than 16 hands have a
higher incidence of RLN and the disease is rarely reported in
ponies.
136138
Additional causes of ILH included perivascular injections with
caustic substances, heart base tumors or other thoracic masses,
exposure to organophosphates or lead, thiamine deciency, and
guttural pouch infections, and various neurologic diseases such as
equine lower motor neuron disease.
Arytenoid chondritis
Arytenoid chondritis has three clinical presentations: simple
mucosal ulceration, granulation tissue formation (i.e.
granulomas), and cartilage deformity.
The size of the granulomas or of the enlargement of the body
of the arytenoid determines the presence and severity of the
airway obstruction.
Clinical signs during exercise mimic those seen in idiopathic
RLN.
Endoscopic examination is diagnostic for arytenoid
chondritis.
Ultrasound exam identies involvement of the body of the
arytenoid cartilage.
26
Abnormalities of the upper airway
573
and the integrity of the overlying mucosa should be evaluated, as
well as any purulent exudates draining from the cartilage. In addi-
tion, it is important to assess the degree of arytenoid movement. If
a tracheostomy has been performed, the endoscope can be passed
retrograde through the tracheostomy site to further evaluate the
morphology of the arytenoid cartilage (Fig. 26.33).
Fig 26.31 Endoscopic image of the larynx of two horse with arytenoid chondritis. (A) Note the granulation tissue (arrow) protruding from the left
arytenoids. (B) A bilateral lesion, where the second smaller lesion (arrow) is thought to secondary to trauma from right granulomas.
A B
Fig 26.32 Endoscopic image of the larynx of a horse with severe
arytenoid chondritis. Note the severely deformed left arytenoid
cartilage, with medialization of the corniculate process exposing the
palatopharyngeal arch (arrow).
Fig 26.33 Endoscopic image of the lumen of the larynx of a horse
with right arytenoid chondritis. Note the abscessed arytenoid cartilage
bulging into the laryngeal lumen. The image was taken by passing the
endoscope retrograde, through the tracheotomy site.
Tracheal
lumen
Chondritic
arytenoid
cartilage
The most useful technique to identify a lesion extending in the
body of the arytenoid is laryngeal ultrasound. Using a caudo-lateral
window, an irregular and enlarged body of the arytenoid cartilage
(Fig. 26.34) can be detected as well as perilaryngeal abscess if
present. In the vast majority of cases the CAL and CAD muscles
remain normal in terms of echogenicity (Fig. 26.34). Radiographic
Respiratory system
3
574
through the stab incision and the cricothyroid membrane into
the lumen of the larynx. An 18-gauge needle is placed through the
mucosal defect into the arytenoid cartilage in the area where
the granulation tissue was resected. A curette is used to enlarge the
opening, initiating drainage of purulent exudate. Following drain-
age of the abscess, the lesion can regress completely with return of
full cartilage abduction.
In chronic cases of arytenoid chondritis or if following drainage
of the abscess, the arytenoid cartilage function failed to return, an
arytenoidectomy is performed. Two types of arytenoidectomy can
be performed: partial and subtotal arytenoidectomy.
142144
Partial
arytenoidectomy
142,143
includes removal of all portions of the aryte-
noid cartilage except the muscular process of the arytenoid cartilage.
Subtotal arytenoidectomy involves removal of the body of the ary-
tenoid cartilage, leaving the muscular and corniculate processes.
Subtotal arytenoidectomy has been shown to yield minimal
improvement in airway diameter because the unsupported cornicu-
late process collapses into the rima glottidis during inhalation.
144

However, it best preserves the protective mechanism of the larynx
and is associated with less aspiration of feed material. Partial aryte-
noidectomy provides the best improvement in airway diameter,
with a small risk of aspiration of feed material.
143
Following aryte-
noidectomy, the horses should be fed and watered from the ground
to minimize tracheal contamination.
Prognosis
The prognosis for resolution of mucosal ulcers with medical therapy,
without the progression to arytenoid chondritis, is excellent. Horses
treated with medical therapy for granulation tissue protruding from
the arytenoid have a 30% chance of developing arytenoid chondri-
tis. The prognosis for pasture soundness or light riding following
arytenoidectomy is very good.
142
In rare cases, tracheal aspiration of
feed material occurs at times, resulting in aspiration pneumonia.
Bilateral arytenoidectomy has a less favorable prognosis because the
potential for aspiration of feed and laryngeal stenosis is increased.
145
Recent data indicated that in term of resolution of exercise intol-
erance, the prognosis is good.
121,146
Etiology and pathophysiology
Etiology
The arytenoid cartilage has two processes: the vocal process where
the vocal ligament is attached and the muscular process where the
cricoarytenoid dorsalis muscle (the laryngeal abductor muscle)
inserts (Fig. 26.35).
3
The comma-shaped corniculate process is
attached to the apex of the arytenoid cartilage and forms the dorsal
border of the rima glottidis.
Arytenoid chondritis develops following trauma to the mucosa
of the arytenoid cartilage and invasion of bacteria into the cartilage.
In humans, cattle, and presumably horses, trauma occurs following
severe coughing episodes where the arytenoid cartilages contact
each other during these marked adduction episodes, creating
contact ulcers.
147,148
Other causes include iatrogenic damage to the
and MRI examination can also help to identify enlarged or mineral-
ized arytenoid cartilage but are rarely needed to identify or treat a
horse with chondritis.
Treatment and prognosis
Therapeutic aims
If mucosal ulceration of the arytenoid cartilage is the only abnor-
mality and the morphology and function of the arytenoids are
normal, the goal of treatment is to reduce the local inammation
and prevent bacterial invasion of the arytenoid cartilage. Systemic
and topical anti-inammatory and antimicrobial therapy form the
basis of treatment in these cases. Granulation tissue protruding
from the arytenoid cartilage is removed sharply or with a laser, and
if no abnormality of the arytenoid cartilage or its function is
detected, systemic and topical anti-inammatory and antimicrobial
therapy is prescribed.
139141
In chronic cases where the arytenoid
cartilage is deformed, abscessed, and dysfunctional, the goal of
treatment is to restore the diameter of the rima glottidis by surgical
removal of the granuloma and the arytenoid cartilage.
142
Therapy
Ulceration of the mucosa covering the arytenoid cartilage is a sub-
clinical nding that is important because the ulcer can serve as an
entrance for bacterial invasion into the arytenoid cartilage, poten-
tially leading to abscessation and deformity of the arytenoids. Treat-
ment consists of local therapy with an anti-inammatory throat
spray applied twice daily. Systemic antibiotics are prescribed for 23
weeks (trimethoprim sulfa, 15 mg/kg, p.o. q 12 h) and a non-
steroidal anti-inammatory drug (phenylbutazone or unixin meg-
lumine) for 710 days.
Protruding buds of granulation tissue with normal arytenoid
cartilage abduction are treated with surgical resection of the lesion
and medical treatment of the resulting mucosal defect as described
above. Endoscopic re-evaluation should be performed to determine
if the lesion recurs or the process extends into the arytenoid carti-
lage, resulting in chondritis and cartilage deformity.
In acute cases of unilateral arytenoid chondritis, medical treat-
ment as described above is initiated. The abscessed cartilage is
probed to determine if surgical drainage is possible.
140
To accom-
plish this, the horse is sedated and, via endoscopy, local anesthetic
is liberally applied to the laryngeal mucosa. Under endoscopic
control, a No. 15 blade is used to make a stab incision through the
skin, muscle, and cricothyroid membrane. A 5 mm trocar is placed
Fig 26.34 Percutaneous ultrasound image using left caudo-lateral
window showing enlarged and irregular body of the left arytenoid
cartilage. Note that similar to Fig. 26.29A and unlike Fig. 26.29B the
cricoarytenoid lateralis (CAL) muscle remains of normal echogenicity.
Thyroid cartilage = TH, arytenoid cartilage = AR, cricoid cartilage = Cr,
and cricothyroid muscle = CT. Fig 26.35 Illustration of the anatomy of the arytenoid cartilage.
Muscular process
of the arytenoid
Cricoid
articular surface
Vocal process
Corniculate cartilage
Medial view Lateral view
26
Abnormalities of the upper airway
575
endoscopic examination of the larynx in yearling horses. Clinical
signs include poor performance and an inspiratory noise, the sever-
ity of which is related to the severity of the congenital malforma-
tion. The character of the inspiratory noise resembles that heard in
horses with laryngeal hemiplegia except that it is generally less
intense and shorter in duration. In a review of 60 cases, 83% of
horses made abnormal inspiratory noise, 22% had involuntary aer-
ophagia, 17% had nasal discharge and coughing, and 3% reported
tympanic colic.
150
Physical examination
The most common cause of rostral displacement of the palatopha-
ryngeal arch is congenital malformation of the laryngeal cartilages.
The most common abnormality is deformation of the wing(s) of
the thyroid cartilage.
150
The larynx should therefore be palpated to
detect a gap between the thyroid and cricoid cartilages. In addition
it is important to palpate the muscular processes of the arytenoid
cartilages because a less prominent or impalpable muscular process
suggests arytenoid and/or thyroid cartilage malformation. Para-
laryngeal cysts can also be present and cause bulging of the lamina
of the thyroid cartilage that can be felt unilaterally or bilaterally
around the larynx.
Special examination
The position of the palatopharyngeal arch rostral to the corniculate
process of the arytenoid cartilage is pathognomonic for rostral dis-
placement of the palatopharyngeal arch (Fig. 26.36). In a signicant
proportion of horses affected with rostral displacement of the pal-
atopharyngeal arch, incomplete abduction of one arytenoid carti-
lage (usually the right) is seen. Dynamic endoscopic examination
is performed to assess which airway abnormalities are associated
with this malformation.
Radiography of the throat is helpful because horses with rostral
displacement of the palatopharyngeal arch frequently have an
mucosa of the arytenoid cartilage by coarse feed material, from kick
back on dirt tract, or during medical procedures such as nasogastric
intubation and endoscopy.
148
Pathophysiology
Arytenoid chondritis has three clinical presentations affecting one
or both arytenoid cartilages: mucosal ulceration, granulation tissue
projecting in the lumen of the larynx, and arytenoid cartilage
abscessation leading to deformity and dysfunction. Following ulcer-
ation of the arytenoid cartilage mucosa, local bacterial invasion of
the body of the arytenoid cartilage causes a supercial chondritis
resulting in the production of granulation tissues and a stulous
tract. If the infection extends deeper in the body of the cartilage, an
abscess can form, and enlargement and deformation of the aryten-
oid cartilage, and lack of movement results.
The physical presence of the granulation tissue protruding into
the rima glottidis causes a static luminal obstruction during both
inspiration and expiration. When the cartilage is deformed and
immobile, dynamic inspiratory obstruction occurs.
Prevention
Prevention of this syndrome is difcult. Preventing trauma to the
arytenoid cartilage by minimizing trauma during nasogastric intuba-
tion and endoscopic examination is prudent. Treatment of mucosal
ulceration and granulation tissue can prevent further bacterial inva-
sion of the cartilage and more severe chondritis from developing.
There has been one report of an association in Thoroughbred
horses of equine lymphocyte antigen A9 and chondritis, suggesting
a possible genetic predisposition to this disease.
149
Rostral displacement of the
palatopharyngeal arch (fourth
and sixth branchial arch defect,
also known as 4-BAD, or
cricopharyngeal-laryngeal
dysplasia)
Rostral displacement of the palatopharyngeal arch results
most commonly from laryngeal cartilage malformation.
Rarely are horses affected at rest but they show signs of
exercise intolerance and abnormal respiratory noise during
exercise.
Three types of obstruction can be seen with this deformity
due to failure of abduction of ipsilateral arytenoid cartilage,
DDSP, and collapse of palatopharyngeal arch or its
continuation the aryepiglottic fold during inhalation.
Surgical restoration of the arytenoid cartilage by simple
laryngoplasty is usually unsuccessful due to the cartilage
deformity, which most commonly involves the thyroid
cartilage and the cricothyroid articulation.
Rostral displacement of the palatopharyngeal arch can also
occur secondarily in horses with arytenoid chondritis, due to
deformity of the arytenoid cartilage.
Recognition
History and presenting complaint
Horses affected with rostral displacement of the palatopharyngeal
arch are usually asymptomatic at rest but this condition can be
diagnosed at rest during routine palpation of the larynx or
Fig 26.36 Endoscopic image of the larynx of a horse with rostralg
displacement of the palatopharyngeal arch. Note how the
palatopharyngeal arch (arrow) protrudes over the corniculate
processes of the arytenoid cartilages.
Respiratory system
3
576
laryngeal from the sixth branchial arch. The epiglottic cartilage
develops separately as it originates from the hypobranchial
eminence.
Abnormalities seen with this congenital disease include absence
of cricopharyngeal muscles, deformed thyroid cartilage resulting in
an increased space between the thyroid and cricoid cartilage, abnor-
mality of the cricopharyngeus and thyropharyngeus muscles,
absence or small muscular process of the arytenoid cartilage, pres-
ence of paralaryngeal cyst(s) and associated deformation of laryn-
geal cartilage.
150,151
Vertical displacement of the lamina of the thyroid
cartilage over the muscular process of the arytenoid cartilage can
occur, and this deformity prevents arytenoid cartilage abduction.
The right side of the larynx is most frequently affected but the
deformities can occur bilaterally or on the left side.
150
Rostral displacement of the palatopharyngeal arch can also be
seen unilaterally with arytenoid chondritis or following partial ary-
tenoidectomy. This is thought to be due to the physical loss of the
corniculate process of the arytenoid cartilage, caudal to which the
palatopharyngeal arch membrane normally sits.
Pathophysiology
Most of the clinical signs associated with rostral displacement of
the palatopharyngeal arch are respiratory in origin and are due to
obstruction of the rima glottidis. More rarely, associated abnormal-
ity of the cricopharyngeal sphincter leads to dysphagia and aero-
phagia, which can cause tympanic colic in some horses.
Airway obstruction is caused by one or more of the following
abnormalities: collapse of one of the arytenoid cartilage, collapse
of the palatopharyngeal arch, medial collapse of the aryepiglottic
fold and/or DDSP.
150,155157
Failure of abduction occurs for several
reasons including the absence of the muscular process of the aryte-
noid cartilage, or thyroid cartilage physical obstruction of the ary-
tenoid preventing abduction of the arytenoid cartilage. The absence
of the cricothyroid articulation leads to caudal displacement of the
arytenoid cartilage instead of abduction.
150
Vertical displacement of
the thyroid lamina prevents caudo-lateral displacement of the mus-
cular process of the arytenoid cartilage, a process needed for abduc-
tion of the arytenoid cartilage.
When rostral displacement of the palatopharyngeal arch occurs
following partial arytenoidectomy, this presentation is unlikely to
be of any clinical signicance. Decreased performance in horses
treated with partial arytenoidectomy can justify dynamic endo-
scopic examination of the larynx to determine if there is dynamic
obstruction of the airway due to unilateral collapse of the palat-
opharyngeal arch membrane or the remnant of its extension the
aryepiglottic membrane.
The digestive dysfunction is rare and caused by regurgitation of
esophageal contents back into the nasopharynx due to deciency
in the musculature of the cricopharyngeal sphincter. Regurgitation
of feed material back into the nasopharynx and trachea can result
in coughing and nasal discharge.
150,
In addition, aerophagia created
by the decient cricopharyngeal sphincter has been reported to
result in tympanic colic.
150
Guttural pouch mycosis
Associated with a fungal infection usually near or on
the internal carotid artery but can extend to the maxillary
artery.
Most commonly recognized by unilateral epistaxis as the
lesion erodes in the internal and/or maxillary arteries.
Medical treatment is risky as horses can die during the next
epistaxis episode.
anomaly of the cricopharyngeal sphincter, which is seen radio-
graphically as a continuous column of air between the nasopharynx
and the esophagus. The presence of redundant tissue dorsal to the
corniculate processes of the arytenoid cartilages on radiographs is
suggestive of rostral displacement of the palatopharyngeal arch.
Laryngeal ultrasound allows the observation of missing crico-
thyroid articulation. Computer tomography can help identify carti-
lage malformation such as dorsal border of the thyroid cartilage
extending dorsally over the muscular process and also detect para-
laryngeal cysts. However MRI exam gives the most detailed evalua-
tion of the abnormal cartilage and muscle such as abnormal
cricopharyngeal sphinter and perilaryngeal muscle such as
thyrohyoideus.
151
Diagnostic conrmation
The diagnosis is made by a combination of laryngeal palpation,
videoendoscopic examination and imaging of the upper airway.
Treatment and prognosis
Therapeutic aims
The goal of therapy is to restore airway patency during strenuous
exercise. It is important to assess which of the possible conse-
quences of 4 BAD contributes to an airway obstruction. DDSP can
be treated by laryngeal tie-forward, the redundant palatopharyngeal
arch can be resected. If one of the arytenoid cartilages cannot
abduct, laryngoplasty used to treat horses with RLN will be ineffec-
tive in this instance because the cartilages are malformed; proper
resection of a section of the thyroid lamina may be needed to allow
abduction of the arytenoid after placement of the laryngoprosthesis.
Alternatively a partial arytenoidectomy may need to be performed.
If a laryngeal cyst is causing the cartilage malformation, the cyst can
be removed.
Therapy
Laryngeal cyts are removed using the lateral laryngeal approach
used for laryngoplasty. However, cyst removal does not ensure
return of normal abductor function of the arytenoid cartilage. This
is because multiple concomitant laryngeal deformations are usually
present. Partial arytenoidectomy can be performed in an attempt to
maximize the lumen of the airway. Laryngoplasty is generally unsuc-
cessful at abducting the arytenoid cartilage because deformities
diminish any abductory movement at the arytenoid cricoid
articulation.
Prognosis
The prognosis for athleticism is guarded, and is related to the degree
of laryngeal cartilage malformation.
Prevention
Because this congenital malformation is probably heritable, avoid-
ing breeding affected horses will limit occurrence.
Etiology and pathophysiology
Etiology
There is little information on the embryology of horses as it relates
to formation of the larynx and nasopharynx.
152
It is, however,
well known that the human larynx and its intrinsic musculature,
and laryngeal nerves, originate from a combination of the fourth
and sixth branchial arches.
153,154
Specically, the cranial laryngeal
nerve originates from the fourth branchial arch and the recurrent
26
Abnormalities of the upper airway
577
Laboratory examination
Horses can be anemic if guttural pouch hemorrhage is severe or if
multiple bleeding episodes have occurred.
Diagnostic conrmation
Differential diagnosis for guttural pouch mycosis includes other
conditions that would result in guttural pouch hemorrhage, the
most common being avulsion of the longus capitis muscle from the
basisphenoid bone, or trauma.
163
Biopsy and culture of the fungal
plaque conrms the diagnosis.
Treatment and prognosis
Therapeutic aims
The goals of treatment are to prevent life-ending hemorrhage and
eradicate the fungal infection from the guttural pouch.
Therapy
Medical treatment of guttural pouch mycosis includes topical appli-
cation of non-irritating antifungal agents that are effective against
Aspergillus spp., such as itraconazole, micozadole, and enilcona-
zole.
164,165
Medical therapy consists of miconazole 70 mg diluted
in 10 mL isotonic saline or in a 400 mg gynecological prepara-
tion (must be warmed) administered through a female urinary
catheter. The preparation is administered under endoscopic control
at the following schedule: Week 1: once a day, Week 2: EOD,
and Week 34: twice a week. Medical therapy can be justied
if hemorrhage has not occurred and the fungal plaques do not
involve any blood vessels or if nancial constraint prevents surgical
options.
If vascular structures are involved, which is most common, the
goal of surgical therapy is to occlude the affected arteries.
158,161
Most
simply, the internal carotid artery on the affected side can be ligated.
This can decrease the hemorrhage, but horses are still at risk for fatal
hemorrhage due to collateral circulation through the circle of Willis
and the palatine arteries.
161
Alternatively, a combination of internal,
external and palatine artery ligation and balloon angioplasty using
venous thrombectomy catheters, coil embolization, or nitinol vas-
cular occlusion plugs can be performed.
158,159,161,166,167
These tech-
niques alleviate the possibility of continued hemorrhage through
retrograde ow. Following occlusion of the rostral portion of the
internal carotid artery, embolization coils/balloon/coils are then
placed in the caudal portion of the vessels to prevent normograde
blood ow. If the external carotid or maxillary arteries are affected,
embolization coil vascular occlusion is performed in the maxillary
artery just before the alar foramen, and in the external carotid artery,
just after it bifurcates from the linguofacial artery. When obstructing
ow into the maxillary artery one should not ligate the palatine
artery; instead it should be catheterized so that the obstruction is
located at the caudal aspect of the palatine bone; otherwise, blind-
ness can occur due to steal phenomena.
168
Prognosis
Approximately 50% of horses that bleed severely die from fatal
hemorrhage. If appropriate vascular occlusion is successful,
the prognosis for life is excellent. Fungal plaques generally
resolve without antifungal medication, 30 to 60 days following
vascular occlusion. Dysphagia, unilateral laryngeal hemiplegia,
and Horners syndrome can resolve over 6 to 8 months, or can be
permanent. Potential complications related to the surgical proce-
dures include unilateral blindness, cerebral ischemia, and recurrent
hemorrhage.
158,161,169
Simple ligation at the cardiac side does not always prevent
continued epistaxis episodes because of retrograde ow from
the circle of Willis.
Embolization of the vessels is needed to prevent retrograde
ow.
Recognition
History and presenting complaint
The most common clinical sign of guttural pouch mycosis is severe
epistaxis caused by erosion of the internal carotid artery, external
carotid artery and/or maxillary artery. Other clinical signs include
mucopurulent or hemorrhagic nasal discharge, coughing, dysphagia
caused by cranial nerve damage (IX and X), unilateral laryngeal
hemiplegia, Horners syndrome, parotid pain, tongue paresis, and
head shaking.
158161
Endoscopic examination of the nasopharynx can
reveal hemorrhage from one or both nasopharyngeal openings.
Physical examination
Physical examination ndings vary depending upon the chronicity
of the hemorrhage. If the horse has recently bled severely due to
erosion of a major artery within the guttural pouch by a mycotic
plaque, the horse will show clinical signs of hypovolemic shock,
including sweating, tachycardia, weak peripheral pulses, pale
mucous membranes, and cold ears and muzzle. Occasionally, if the
mycotic plaque forms over cranial nerves, such as branches of the
vagus nerve or the sympathetic trunk, the horse can have clinical
evidence of dysphagia and aspiration pneumonia or Horners
syndrome.
158161
Tongue paresis can occur due to hypoglossal nerve
involvement.
162
Special examination
Endoscopic examination of the nasopharynx and guttural pouches
is diagnostic for guttural pouch mycosis. Following hemorrhage, a
blood clot will protrude from the affected pouch. If the disease is
bilateral or the fungus has eroded through the median septum, clots
can form at both guttural pouch openings. Inspection of the affected
guttural pouch reveals a single fungal plaque or multiple plaques
associated with the major arteries of the guttural pouch, including
most commonly the internal carotid artery, but also the external
carotid artery, and the maxillary artery (Fig. 26.37).
158,161
Fig 26.37 Endoscopic image of the guttural pouch of a horse with
guttural pouch mycosis. Note the gray-to-black mycotic lesion (arrow).
Stylohyoid
bone
Respiratory system
3
578
Prevention
There is no known method of prevention.
Etiology and pathophysiology
Etiology
The etiology is unknown, but Aspergillus spp. is frequently cultured
from the diphtheritic plaques.
165
Pathophysiology
The fungal plaques grow within the guttural pouch, and if they
erode through the walls of the internal, external, or maxillary arter-
ies, life-threatening hemorrhage can ensue.
Epidemiology
There is neither a known geographical predisposition nor age,
breed, sex, or occupational predilection for guttural pouch mycosis.
Avulsion of the longus capitis/
rectus capitis ventralis muscles
Recognition
History and presenting complaint
Horses with avulsion or rupture of the longus capitis and rectus
capitis ventralis muscles usually have a history of trauma, such as
falling over or being tied and pulling free.
163
Occasionally (one case)
the trauma can occur as a result of the horse throwing its head and
neck overzealously. Affected horses can have bilateral epistaxis,
swelling or thickening in the throatlatch area, and can be ataxic or
exhibit other signs of neurologic dysfunction.
163
Physical examination
Horses will often have bilateral epistaxis, may be ataxic or have
cranial nerve decits, and swelling in the area of Viborgs triangle.
163

Affected horses may have signs of vestibular disease (head tilt,
falling, ipsilateral weakness, circling), facial nerve injury (palsy of
facial muscles, inability to blink, creased lacrimation and keratitis
sicca) and cerebral dysfunction (depressed mentation).
Special examination
Endoscopic examination of the nasopharynx reveals collapse of the
dorsal nasopharynx due to the hematoma formation within the
dorsal and medial tissues of the guttural pouch and blood or blood
clots at the nasopharyngeal openings of the guttural pouches.
Within the guttural pouch, hemorrhage and hematoma formation
are evident along the medial wall (Fig. 26.38). Lateral radiographic
projections of the guttural pouch region show soft tissue density
within the guttural pouch compression of the dorsal nasopharynx,
and avulsion fracture of the basisphenoid bone (Fig. 26.39).
Laboratory examination
Laboratory examination is normal or there is evidence of
hemorrhage.
Diagnostic conrmation
Differential diagnosis for avulsion of the longus capitis and rectus
capitis ventralis muscles is guttural pouch mycosis. The history of
trauma and the appearance of the hematoma within the medial
wall of the guttural pouch are diagnostic for this condition.
Fig 26.38 Endoscopic image of the guttural pouch of a horse that
avulsed the longus capitis and rectus capitis muscles from the
basisphenoid and basioccipitus bones at the base of the skull. Note
the large hematoma (arrow) within the medial compartment of the
guttural pouch.
Fig 26.39 Lateral radiograph of the guttural pouch region of a horse
that avulsed the longus capitis and rectus capitis muscles from the
basisphenoid and basioccipitus bones at the base of the skull. Note
the bone fragment (arrow) and the hemorrhage within the guttural
pouch.
Hemorrhage within
guttural pouch
26
Abnormalities of the upper airway
579
Recognition
History and presenting complaint: most horses with temporohyoid
osteoarthropathy (THO) have clinical signs suggestive of facial
nerve (cranial nerve VII) and/or vestibulocochlear nerve (cranial
nerve VIII) decits. Presenting complaints include facial nerve paral-
ysis and lip droop, head tilt, ataxia or falling, difculty eating,
corneal ulceration/keratitis, nasal discharge, and head shaking/
tossing.
170174
Physical examination
Physical examination ndings include fever, facial and vestibuloco-
chlear nerve decits, including vestibular signs that can resemble
ataxia, pain with manipulation of the jaw or opening the mouth,
blepharospasm and corneal ulceration.
170174
Special examination
The diagnosis of THO is made based on physical examination nd-
ings and endoscopic examination of the guttural pouches. Skull
radiographs and computed tomography are sometimes used to help
conrm the diagnosis or more fully describe the lesion at the tem-
porohyoid articulation. Osseous proliferation at the proximal
aspect of the stylohyoid bone is seen during endoscopic examina-
tion of the guttural pouch on the affected side (Fig. 26.40). Dorso-
ventral radiographic projections of the skull can show enlargement
of the temporohyoid region. Computed tomographic scans can
show fusion of the temporohyoid joint and osseous proliferation
of the proximal portion of the stylohyoid bone. Occasionally, frac-
ture of the stylohyoid or ceratohyoid bones can be seen. Schirmer
tear test can be performed to assess tear production from the
affected eye, especially if signs of facial neuropathy are present.
CT examination allows the most precise assessment of the condi-
tion which will inuence or facilitate the surgery by characterizing
the plane of the ceratohyoidstylohyoid articulation, extent of
disease on ceratohyoid bone and unilateral or bilateral disease.
175,176
Treatment and prognosis
Therapeutic aims
The goal of therapy is to provide supportive care if the horse has
neurologic signs and conne the horse to minimize the risk of
further hemorrhage.
Therapy
Two to three months of stall rest and broad-spectrum antimicrobial
therapy are warranted due to the hematoma formation within the
guttural pouch.
163
Judicious use of non-steroidal anti-inammatory
therapy for analgesia is recommended. If neurologic signs are severe
and the horse is unable to rise, subdural hemorrhage involving the
brainstem and cerebral cortex should be suspected and euthanasia
is warranted.
Prognosis
The prognosis for return to function is good unless neurologic de-
cits are severe.
163
Prevention
There is no known method of prevention.
Etiology and pathophysiology
Etiology
Avulsion of the rectus capitis muscles usually occurs as a result of
trauma.
Pathophysiology
Three muscles that ex the head and neck include the large longus
capitis muscle and two small muscles, rectus capitis ventralis and
rectus capitis lateralis, which course ventrally between the guttural
pouches. Simultaneous contraction of these muscles as the horse
falls over backwards would lead to avulsion fracture from the basi-
sphenoid and occipital bones, resulting in hemorrhage from the
guttural pouch and hematoma formation.
Epidemiology
Horses most commonly affected are young animals early in their
training or breaking program. The disease is less common in older
horses because they are less likely to fall over backwards or pull
back violently when tied.
Temporohyoid osteoarthropathy
Degenerative disease of unknown cause leading to fusion of
the temporohyoid articulation.
169
The disease can be unilateral or bilateral.
Enlargment of the temporohyoid articulation leads to
compression of the VII and VIII cranial nerves.
170
Clinical signs are associated with decit of the cranial nerves
VII and VIII as well as pain upon movement of the stylohyoid
bone by movement of the tongue or pressure on the
basihyoid bone.
Fusion of the temporohyoid articulation can lead to petrous
bone fracture and acute death.
Treatment includes removal of the lever arm action of the
stylohyoid bone by removal of the ceratohyoid bone.
Fig 26.40 Endoscopic image of the articulation of the stylohyoid
bone and the petrous portion of the temporal bone in a horse with
temporohyoid osteoarthropathy. Note the enlarged region (arrow)
of the proximal aspect of the stylohyoid bone.
Respiratory system
3
580
Tracheal obstructive disease
Primary obstructive tracheal disease in horses is rare, and includes
tracheal collapse, fungal granulomas, chondritis, trauma, and
foreign bodies. The equine trachea has an oval shape and measures
approximately 5 by 7 cm, dorsoventrally to transversely, respec-
tively. It is composed of 48 to 60 incomplete hyaline cartilage rings
interspersed by broelastic annular ligaments. The dorsal area is
made up of brous tissue and the trachealis muscle, which is
attached to the concave surface of each cartilage ring. The trachealis
muscle allows for changes in diameter of the trachea during inhala-
tion and exhalation, while the bro-elastic annular ligaments
permit unimpeded exion and extension of the head and neck,
important in running horses.
Recognition
History and presenting complaint
Horses with primary tracheal obstructive disease are exercise
intolerant, make an abnormal respiratory noise during exercise or
sometimes at rest, which is characterized as a honking sound,
and have bilateral nasal discharge that can be mucopurulent or
hemorrhagic.
Physical examination
Physical examination is usually normal. If tracheal trauma has
occurred, palpation of the ventral cervical region can reveal a con-
cavity in the area of previous trauma, swelling, or scar tissue. Thick-
ened or abnormal tracheal rings can be palpable in the proximal to
middle region of the cervical area if the rings have been traumatized
or are chondritic. If the trachea is perforated, subcutaneous emphy-
sema is noted along the neck, withers, and shoulders.
Special examination
Endoscopy, radiography, and ultrasonography can be useful to
assess tracheal abnormalities. If the tracheal lesion is caused by a
static mass, such as a fungal granuloma, chondritic cartilage, or
persistently deformed trachea, endoscopic examination of the
trachea at rest will be useful in assessing the tracheal lumen (Fig.
26.41). If dynamic tracheal collapse occurs during exercise, endo-
scopic examination of the trachea during treadmill exercise is
required to diagnose the dynamic collapse.
178
Lateral radiographs
of the trachea are useful in assessing extraluminal masses that
can cause intraluminal obstruction, as well as the position and
extent of the tracheal lesion, if it is cranial to the thoracic inlet.
Ultrasonography is also used to evaluate soft tissue densities exter-
nal to the trachea that can impinge on the tracheal lumen such as
abscesses, hematomas, or neoplastic lesions or fracture of the tra-
cheal ring (Fig. 26.42).
Laboratory examination
Complete blood count and serum chemistry values are usually
normal.
Diagnostic conrmation
The diagnosis is conrmed based on endoscopic examination of the
trachea at rest. Intraluminal masses, such as fungal granulomas, are
biopsied and submitted for culture and cytology.
179
Granulomatous
tracheitis caused by Conidiobolus coronatus can also be conrmed by
agar gel immunodiffusion assay performed at the Centers for
Disease Control and Prevention, Atlanta, GA.
179
Lesions of the tra-
cheal rings, such as chondritis, are diagnosed based upon endo-
scopic examination, history of tracheal trauma or injection, and
Laboratory examination
Most frequently, clinical laboratory examination is normal. Leuko-
cytosis, lymphopenia, anemia, and hyperbrinogenemia can occur.
Diagnostic conrmation
Endoscopic, radiographic, or computed tomographic evidence of
temporohyoid fusion or enlargement are diagnostic for temporohy-
oid osteoarthropathy.
Treatment and prognosis
Therapeutic aims
The goals of therapy include resolution of the vestibular and facial
nerve decits, removing pain associated with swallowing, treatment
or prevention of corneal ulceration, and protecting the horse from
further trauma resulting from its vestibular disease. Most horses
are treated with antibiotics and non-steroidal anti-inammatory
drugs, including trimethoprim sulfa, enrooxacin, or penicillin
and gentamicin for 30 days, and oral phenylbutazone or unixin
meglumine.
171174
Surgical treatment involves removing the cerato-
hyoid bone to minimize motion at the temporohyoid articula-
tion.
177
Corneal ulcers are treated with topical medication, and if
the eyelid is not functional, a tarsorrhaphy can be performed to
protect the cornea until facial neuropathy resolves or improves.
Ocular lubricants can be applied to affected eyes several times daily
if the cornea is healthy but eyelid function is abnormal.
Prognosis
Following temporohyoid osteoarthropathy, pain is alleviated
usually within 2448 hours: 63% of horses return to athletic activ-
ity and most horses return to their intended use, although you may
need to maintain the tarsorrhaphy to prevent eye lesions from desic-
cation. Rehabilitation time can be long, up to 2 years, though many
clinical signs will abate within 30 to 60 days.
170,172, 173,174,
Prevention
There are no known preventive measures.
Etiology and pathophysiology
Etiology
The etiology is unknown.
Pathophysiology
THO is probably the result of primary generative osteoarthritis of
the temporohyoid joint associated with age.
169173
Alternatively, it
can be the sequela to otitis media/interna that develops secondary
to hematogenous spread of bacteria, ascending infection from the
respiratory tract, otitis externa, or extension of guttural pouch
empyema.
170,172
The infection and inammatory reaction of the
tympanic bulla, temporohyoid joint, and stylohyoid bone resolves,
leaving bony proliferation of the proximal stylohyoid bone and
fusion of the temporohyoid joint. Vestibular disease and facial nerve
paralysis occur when osseous proliferation impinges on cranial
nerves VII (facial) and VIII (vestibulocochlear) or if the petrous
temporal bone fractures. The condition is usually unilateral but can
be bilateral.
Epidemiology
Temporohyoid osteoarthropathy affects horses of all ages and sex
and does not have a geographic predilection.
26
Abnormalities of the upper airway
581
possibly localization of an abscess within the body of the tracheal
cartilage. Dynamic tracheal collapse is diagnosed by endoscopic
examination of the trachea during exercise if clinical signs are not
apparent at rest and endoscopic examination of the upper airway
and trachea is normal at rest.
Treatment and prognosis
Therapeutic aims
The goal of treatment is to ameliorate the tracheal obstruction.
Therapy
Discrete intraluminal tracheal masses can be excised by use of
transendoscopic laser or sharply through a tracheotomy incision if
the mass is within an accessible area of the trachea. Treatment of
tracheal trauma includes systemic antimicrobial and non-steroidal
anti-inammatory therapy. Individual tracheal rings that have been
traumatically damaged or are chondritic and cause airway obstruc-
tion can be resected. Treatment of tracheal collapse is dependent
upon the length and accessibility of the trachea involved. Some
forms of tracheal collapse can be treated by stenting individual
tracheal rings (Fig. 26.43), tracheal prosthesis, or resection and
anastomosis of the affected area.
180
Granulomatous tracheitis
caused by Conidiobolus coronatus was successfully treated by intrave-
nous administration of sodium iodide 20%, 44 mg/kg, once daily
for 7 days followed by 1.3 mg/kg organic iodide 4.57%, twice daily
for 1 year.
179
Prognosis
Prognosis for removal of discrete intraluminal masses within the
trachea and return to function is excellent.
Prevention
There is no known method of prevention of tracheal obstruction.
Etiology and pathophysiology
Etiology
Chondritis of tracheal cartilages can occur following intratracheal
injections or transtracheal aspiration, if a tracheal ring is perforated
during the injection, trauma, or idiopathically. Alternatively, direct
trauma can fracture one or more tracheal rings. Finally, a degenera-
tive process leads to tracheal collapse in miniature horses and
ponies.
Pathophysiology
The pathophysiology of tracheal obstruction is based upon the type
of obstruction.
Epidemiology
Tracheal obstruction is rare in athletic horses.
With thanks to Susan J. Holcombe, who co-created the original chapter
in the rst edition.
Fig 26.41 Endoscopic image of the lumen of the trachea of a horse
with tracheal collapse during exercise.
Courtesy of Dr. Gary Priest, Kentucky.
Fig 26.42 Percutaneous ultrasound exam ination of a Thoroughbred
lly with an old fracture of the rst cervical ring. Note the rounded
edge of tracheal cartilage at the side.
A
Fig 26.43 Intraoperative view of treatment of a ventral tracheal
collapse in a Thoroughbred. (A) Tracheal collapse is being repaired by
a titanium mesh sutured to the tracheal ring proximal and distal to the
collapse area. (B) Titanium mesh is then reinforced by PMMA cement
to prevent folding of the mesh.
B
Respiratory system
3
582
References
1. Lane JG, Bladon B, Little DR, et al.
Dynamic obstructions of the equine
upper respiratory tract. Part 1:
observations during high-speed
treadmill endoscopy of 600
Thoroughbred racehorses. Equine Vet J
2006;38:3939.
2. Strand E, Fjordbakk CT, Sundberg K,
et al. Relative prevalence of upper
respiratory tract obstructive disorders in
two breeds of harness racehorses (185
cases: 19982006). Equine Vet J 2011.
doi: 10.1111/j.20423306.2011.00517.x.
[Epub ahead of print]
3. Sisson S. Equine respiratory system. In:
Getty R, editor. Sisson and Grossmans
the anatomy of domestic animals. 5th
ed. Philadelphia: WB Saunders; 1975.
p. 4989.
4. Hawkins JF, Tulleners EP, Evans LH,
et al. Alar fold resection in horses: 24
cases (19791992). J Am Vet Med Assoc
1995;206(12):191316.
5. Kendall A, Brjer J, Karlstam E, et al.
Enilconazole treatment of horses with
supercial Aspergillus spp. rhinitis. J Vet
Intern Med 2008;22(5):1239342.
6. Greet T. Nasal aspergillosis in three
horses. Vet Record 1982;109(22):4879.
7. Zamos DT, Schumacher J, Lay JK.
Nasopharyngeal conidiobolomycosis in
a horse. J Am Vet Med Assoc 1996;
208(1):1001.
8. Korenek NL, Legendre AM, Andres FM,
et al. Treatment of mycotic rhinitis with
itraconazole in three horses. J Vet Intern
Med 1994;8(3):2247.
9. Watt DA. A case of cryptococcal
granuloma in the nasal cavity of a
horse. Aust Vet J 1970;46(10):4935.
10. Nickels FA. Nasal Passages. In: Auer JA,
Stick JA, editors. Equine surgery. 2nd ed.
Philadelphia: WB Saunders; 1992.
p. 32636.
11. Rothaug PG, Tulleners EP.
Neodymium:yttrium-aluminum-garnet
laser-assisted excision of progressive
ethmoid hematomas in horses: 20 cases
(19861996). J Am Vet Med Assoc
1999;214(7):103741.
12. Gasser IS, Love NE, Tate LP.
Radiographic diagnosis ethmoid
hematoma. Vet Radiol Ultrasound
2000;41(3): 2479.
13. Frees KE, Vaughan EM, Lillick JD. Severe
complication after administration of
formalin for treatment of progressive
ethmoidal hematoma in a horse. J Am
Vet Med Assoc 2001;219(7):9502.
14. Schumacher J, Yarborough T, Pasco J,
et al. Transendoscopic chemical
ablation of progressive ethmoidal
hematoma in standing horses. Vet Surg
1998;27:17581.
15. Dixon PM, Parkin TD, Collins N, et al.
Equine paranasal sinus disease: a
long-term study of 200 cases
(19972009): treatments and long-term
results of treatments. Eq Vet J 2011;10:
20423306.
16. Tremaine WH, Dixon PM. A long-term
study of 277 cases of equine sinonasal
disease. Part 1: details of horses,
historical, clinical and ancillary
diagnostic ndings. Equine Vet J
2001;33(3):27482.
17. Ruggles AJ, Ross MW, Freeman DE.
Endoscopic examination of normal
paranasal sinuses in horses. Vet Surg
1991;20:41822.
18. Freeman DE, Orsini PG, Ross MW, et al.
A large frontonasal bone ap for sinus
surgery in the horse. Vet Surg
1990;19(2):12230.
19. Tremaine WH, Dixon PM. A long-term
study of 277 cases of equine sinonasal
disease. Part 2: treatments and results of
treatments. Equine Vet J 2001;33(3):
2839.
20. Boulton C. Equine nasal cavity and
paranasal sinus disease: A review of 85
cases. Equine Vet Sci 1985;5:26871.
21. Author unknown. British Equine
Veterinary Association: a survey of
equine diseases (19621963). Vet
Record 1965;77:52837.
22. Ducharme N. Pharynx. In: Auer JA, Stick
JA, editors. Equine surgery. 4th ed.
St. Louis: Elsevier; 2012. p. 56991.
23. Carr EA, Spier SJ, Kortz GD, et al.
Laryngeal and pharyngeal dysfunction
in horses homozygous for hyperkalemic
periodic paralysis. J Am Vet Med Assoc
1996;209(4):798803.
24. Rehder RS. Equine upper airway and
guttural pouch pressures during
exercise. MS thesis, Cornell University;
1992.
25. Cehak A, Rohn K, Barton AK, et al.
Effect of head and neck position on
pharyngeal diameter in horses. Vet
Radiol Ultrasound 2010;51(5):4917.
26. Barton AK, Cehak A, Ohnesorge B.
Transendoscopic laser surgery of a
transient pharyngeal collapse in exed
position of the head in 7 horses.
Proceedings WEAS 2009, 2005.
27. Golland LC, Hodgson DR, Davis RE.
Retropharyngeal lymph node infection
in horses: 46 cases (19771992). Aust
Vet J 1995;72(5):1614.
28. Boyle A. Streptococcus equi subspecies
equi infection (strangles) in horses.
Compend Contin Educ Vet
2011;33(3):E18.
29. Bverud V, Johansson SK, Aspan A.
Real-time PCR for detection and
differentiation of Streptococcus equi
subsp. equi and Streptococcus equi
subsp. zooepidemicus. Vet Microbiol
2007;124(34):21929.
30. Ivens PA, Matthews D, Webb K, et al.
Molecular characterisation of strangles
outbreaks in the UK: the use of
M-protein typing of Streptococcus equi
ssp. equi. Equine Vet J 2011;43(3):
35964.
31. Derksen FJ. Spectrum analysis of
respiratory sounds in exercising horses
with experimentally induced laryngeal
hemiplegia or dorsal displacement of
the soft palate. Am J Vet Res 2001;62:
65964.
32. Davidson EJ, Martin BB, Boston RC,
et al. Exercising upper respiratory
videoendoscopic evaluation of 100
nonracing performance horses with
abnormal respiratory noise and/
or poor performance. Equine Vet J
2011;43(1):38.
33. Petsche VM, Derksen FJ, Berney CE,
et al. Effect of head position on upper
airway function in exercising horses.
Equine Vet J Suppl 1995;18:1822.
34. Parente EJ, Martin BB, Tulleners EP,
et al. Upper respiratory dysfunctions in
horses during high-speed exercise. Proc
Am Assoc Equine Pract 1994;40:812.
35. Hackett RP, Ducharme NG, Rehder RS.
Use of the high-speed treadmill in
management of horses with dorsal
displacement of the soft palate. Proc
Am Assoc Equine Pract 1992;38:1534.
36. Barakzai SZ, Dixon PM. Correlation of
resting and exercising endoscopic
ndings for horses with dynamic
laryngeal collapse and palatal
dysfunction. Equine Vet J
2011;43(1):1823.
37. Lane JG, Bladon B, Little DR, et al.
Dynamic obstructions of the equine
upper respiratory tract. Part 2:
comparison of endoscopic ndings at
rest and during high-speed treadmill
exercise of 600 Thoroughbred
racehorses. Equine Vet J 2006;38(5):
4017.
38. Duggan VE, MacAllister CG, Davis MS.
Xylazine-induced attenuation of
dorsal displacement of the soft palate
associated with epiglottic dysfunction in
a horse. J Am Vet Med Assoc 2002;221:
399401.
39. Allen KJ, Christley RM, Birchall MA,
et al. A systematic review of the
efcacy of interventions for dynamic
intermittent dorsal displacement of the
soft palate. Equine Vet J 2012:44:
25966.
40. Franklin SH, Naylor JR, Lane JG. The
effect of a tongue-tie in horses with
dorsal displacement of the soft palate.
Equine Vet J Suppl 2002;34:4303.
41. Barakzai SZ, Finnegan C, Boden LA.
Effect of tongue tie use on racing
performance of Thoroughbreds in the
United Kingdom. Equine Vet J
2009;41(8):81216.
42. Woodie JB, Ducharme NG, Hackett RP,
et al. Can an external device prevent
dorsal displacement of the soft palate
26
Abnormalities of the upper airway
583
during strenuous exercise? Equine Vet J
2005;37(5):4259.
43. Ahern TJ. Oral palatopharyngoplasty; a
survey of one hundred post-operative
raced horses. Equine Vet Sci 1993;13:
6702.
44. Ordidge RM. Thermal cautery of the
equine soft palate as a treatment for
displacement of the soft palate during
exercise. Proceedings of the 7th World
Congress, 2001. p. 287.
45. Harrison IW, Raker CW.
Sternothyrohyoideus myectomy in
horses: 17 cases (19841985). J Am Vet
Med Assoc 1988;193(10):12991302.
46. Llewellyn HR. Sternothyroideus
myotomy for the treatment of dorsal
displacement of the soft palate. Proc
Am Assoc Equine Pract 1997;43:
23943.
47. Peloso JG, Stick JA, Nickels FA, et al.
Epiglottic augmentation by use of
polytetrauoroethylene to correct dorsal
displacement of the soft palate in a
Standardbred horse. J Am Vet Med
Assoc 1992;201:13935.
48. Hogan PM, Palmer SE. Transendoscopic
laser cauterization of the soft palate as
an adjunctive treatment for dorsal
displacement of the soft palate. Proc
Am Assoc Equine Pract 2002;48:
22830.
49. Anderson JD, Tulleners EP, Johnston JK,
et al. Sternothyrohyoideus myectomy
or staphylectomy for treatment of
intermittent dorsal displacement of the
soft palate in racehorses: 209 cases
(19861991). J Am Vet Med Assoc
1995;206:19091912.
50. Barakzai SZ, Hawkes CS. Dorsal
displacement of the soft palate and
palatal instability. Equine Vet Educ
2010;22(5):25364.
51. Barakzai SZ, Johnson VS, Baird DH,
et al. Assessment of the efcacy of
composite surgery for the treatment of
dorsal displacement of the soft palate in
a group of 53 racing thoroughbreds
(19901996). Equine Vet J 2004;36(2):
1759.
52. Barakzai SZ, Dixon, PM. Conservative
treatment for thoroughbred racehorses
with intermittent dorsal displacement
of the soft palate. Vet Record 2005;157:
33740.
53. Reardon RJM, Fraser BSL, Heller J, et al.
The use of race winnings, ratings and a
performance index to assess the effect of
thermocautery of the soft palate for
treatment of horses with suspected
intermittent dorsal displacement. A
case-control study in 110 racing
Thoroughbreds. Equine Vet J 2008;40
(5):50813
54. Barakzai SZ, Boden LA, Hillyer MH,
et al. Efcacy of thermal cautery for
intermittent dorsal displacement
of the soft palate as compared to
conservatively treated horses: Results
from 78 treadmill diagnosed horses.
Equine Vet J 2009;41:659.
55. Alkabes KC, Jan F, Miller MA, et al.
Evaluation of the effects of
transendoscopic diode laser palatoplasty
on clinical, histologic, magnetic
resonance imaging, and biomechanical
ndings in horses. Am J Vet Res
2010;71:57582.
56. Muoz Ja, Marcoux M, Picandet V, et al.
Histological and biomechanical effects
of palatal sclerotherapy in the horse
using sodium tetradecyl sulfate. Vet J
2010;183:31621.
57. Ducharme NG, Hackett RP, Woodie JB,
et al. Investigation into the role of the
thyrohyoid muscles in the pathogenesis
of dorsal displacement of the soft palate
in horses. Equine Vet J
2003;35(3):25863.
58. Cheetham JC, Pigott JH, Thorson LM,
et al. Racing performance following the
laryngeal tie-forward procedure: a
case-controlled study. Equine Vet J
2008;40(5):5017.
59. Woodie JB, Ducharme NG, Kanter P,
et al. Surgical advancement of the
larynx (laryngeal tie-forward) as a
treatment for dorsal displacement of the
soft palate in horses: a prospective study
20012004. Equine Vet J 2005;37:
41823.
60. Franklin SH, McCluskie L, Woodford
SN, et al. A comparison of efcacy of
soft palate cautery and laryngeal
tie-forward procedure in thoroughbred
racehorses with a denitive diagnosis of
palatal dysfunction. Proceedings of the
Congress of the British Equine
Veterinary Association. Equine Vet J
2009;168.
61. Holcombe SJ, Rodriguez K, Lane J, et al.
Cricothyroid muscle function and vocal
fold stability in exercising horses. Vet
Surg 2006;35(6):495500.
62. Holcombe SJ, Beard WL, Hinchcliff KW,
et al. Effect of sternothyrohyoid
myectomy on upper airway mechanics
in normal horses. J Appl Physiol
1994;77:281216.
63. Infernuso T, Watts AE, Ducharme NG.
Septic epiglottic chondritis with
abscessation in 2 young Thoroughbred
racehorses. Can Vet J 2006;47:100710.
64. Holcombe SJ, Derksen FJ, Stick JA,
et al. Bilateral nerve blockade of the
pharyngeal branch of the vagus nerve
produces persistent soft palate
dysfunction in horses. Am J Vet Res
1998;59(4):5048.
65. Cheetham J, Pigott JH, Hermanson JW,
et al. Role of the hypoglossal nerve in
equine nasopharyngeal stability. J Appl
Phys 2009;107:4717.
66. Linford RL, OBrien TR, Wheat JD, et al.
Radiographic assessment of epiglottic
length and pharyngeal and laryngeal
diameters in the Thoroughbred. Am J
Vet Res 1983;44:16606.
67. Hackett RP, Ducharme NG, Ainsworth
DM, et al. Effects of extrathoracic airway
obstruction on intrathoracic pressure
and pulmonary artery pressure in
exercising horses. Am J Vet Res 1999;60:
48594.
68. Rehder R, Ducharme NG, Hackett RP,
et al. Measurement of upper airway
pressures in exercising horses with
dorsal displacement of the soft palate.
Am J Vet Res 1995;56:26974.
69. Saulez MN, Gummow B. Prevalence of
pharyngeal, laryngeal and tracheal
disorders in thoroughbred racehorses,
and effect on performance. Vet Rec
2009;165(15):4315.
70. Brown JA, Hinchcliff KW, Jackson MA,
et al. Prevalence of pharyngeal and
laryngeal abnormalities in
Thoroughbreds racing in Australia, and
association with performance. Equine
Vet J 2005;37(5):397401.
71. Lacourt M, Marcoux M. Treatment of
epiglottic entrapment by transnasal
axial division in standing sedated horses
using a shielded hook bistoury. Vet Surg
2011;40(3):299304.
72. Lumsden JM, Stick JA, Caron JP, et al.
Surgical treatment for epiglottic
entrapment in horses: 51 cases
(19811992). J Am Vet Med Assoc
1994;205(5):72935.
73. Honnas CM, Wheat JD. Epiglottic
entrapment: a transnasal surgical
approach to divide the aryepiglottic fold
axially in the standing horse. Vet Surg
1988;17:24651
74. Tulleners EP. Transendoscopic contact
neodymium:yttrium aluminum garnet
laser correction of epiglottic entrapment
in standing horses. J Am Vet Med Assoc
1990;196:197180.
75. Aitken MR, Parente EJ. Epiglottic
abnormalities in mature nonracehorses:
23 cases (19902009). J Am Vet Med
Assoc 2011;238(12):16348.
76. Raphel C. Endoscopic ndings in the
upper respiratory tract of 479 horses.
J Am Vet Med Assoc 1982;56:4704.
77. Sweeney CF, Maxson AD, Soma LR.
Endoscopic ndings in the upper
respiratory tract of 678 Thoroughbred
racehorses. J Am Vet Med Assoc
1991;198:10378.
78. Morris EA, Seeherman HJ. Clinical
evaluation of poor performance in the
racehorse: the results of 275
evaluations. Equine Vet J
1991;23:16974.
79. Stick JA. Larynx. In: Auer JA, Stick JA,
editors. Equine surgery. 3rd ed.
Philadelphia: WB Saunders, 2006.
p. 566.
80. Parente EJ, Martin BV, Tulleners EP.
Epiglottic retroversion as a cause of
poor performance in two horses. Equine
Vet J 1998;30:2702.
81. Holcombe SJ, Derksen FJ, Stick JA, et al.
Effect of bilateral hypoglossal and
Respiratory system
3
584
glossopharyngeal nerve blocks on
epiglottic and soft palate position in
exercising horses. Am J Vet Res
1997;58(9):10226.
82. Aitken MR, Parente EJ. Epiglottic
abnormalities in mature nonracehorses:
23 cases (19902009). J Am Vet Med
Assoc 2011;238:16348.
83. Hay WP, Baskett A, Abdy MJ. Complete
upper airway obstruction and syncope
caused by a subepiglottic cyst in a
horse. Eq Vet J 1997;97:756.
84. Chow TL, Choi CY, Yee-Hing Hui J.
Thyroglossal duct cysts in adults treated
by ethanol sclerotherapy: a pilot
study of a nonsurgical technique.
Laryngoscope 2012. doi: 10.1002/
lary.23254. [Epub ahead of print]
85. Dougherty SS, Palmer JL. Use of
intralesional formalin administration
for treatment of a subepiglottic cyst in a
horse. J Am Vet Med Assoc 2008;233:
4635.
86. King DS, Tulleners EP, Martin BB, et al.
Clinical experience with axial deviation
of the aryepiglottic folds in 52
racehorses. Vet Surg 2001;30:15160.
87. Priest DT, Cheetham J, Regner AL, et al.
Dynamic respiratory endoscopy of
Standardbred racehorses during
qualifying races. Equine Vet J 2012;
44(5):52934.
88. Rakesh V, Ducharme NG, Cheetham J,
et al. Implications of different degrees
of arytenoid cartilage abduction on
equine. Eq Vet J 2008;40:62935.
89. Hawkins JF, Tulleners EP. Epiglottitis in
horses: 20 cases (19881993). J Am Vet
Med Assoc 1994;205:15779.
90. Infernuso T, Watts AE, Ducharme NG.
Septic epiglottic chondritis with
abscessation in 2 young Thoroughbred
racehorses. Can Vet J 2006;47:100710.
91. Ortved KF, Cheetham J, Mitchell LM,
et al. Successful treatment of persistent
dorsal displacement of the soft palate
and evaluation of laryngohyoid position
in 15 racehorses. Eq Vet J 2010;42(1):
239.
92. Hahn CN, Matiasek K, Dixon PM, et al.
Histological and ultrastructural evidence
that recurrent laryngeal neuropathy is a
bilateral mononeuropathy limited to
recurrent laryngeal nerves. Equine Vet J
2008;40:66672.
93. Rhee HS, Steel CM, Derksen FJ, et al.
Immunohistochemical analysis of
laryngeal muscles in normal horses and
horses with subclinical recurrent
laryngeal neuropathy. J Histochem
Cytochem 2009;57:787800.
94. Duncan ID, Grifth IR. A light and
electron microscopic study of the
neuropathy of equine idiopathic
laryngeal hemiplegia. Acta Neuropathol
1978;4:483501.
95. Cardiot PJ. Roaring in horses: its
pathology and treatment. Swan
Sonnenschein 1892;778.
96. Witte SHP, Witte TH, Harriss F, et al.
Association of owner-reported noise
with ndings during dynamic
respiratory endoscopy in Thoroughbred
racehorses. Eq Vet J 2011;43:917.
97. Derksen JF, Stick JA, Scott EA, et al.
Effects of laryngeal hemiplegia and
laryngoplasty on airway ow mechanics
in exercising horses. Am J Vet Res
1986;47:1626.
98. Chalmers HJ, Cheetham J,Yeager AE,
et al. Ultrasonography of the equine
larynx. Vet Radiol 2006;47(5):47681.
99. Newton-Clarke MJ, Divers TJ, Valentine
BA. Evaluation of the thoraco-laryngeal
reex (slap test) as an indicator of
laryngeal adductor myopathy in the
horse. Equine Vet J 1994;26:3557.
100. Rakestraw PC, Hackett RP, Ducharme
NG, et al. Arytenoid cartilage movement
in resting and exercising horses. Vet
Surg 1991;20:1227.
101. Anon. Consensus statement on equine
laryngeal neuropathy. In: Havermeyer
workshop on equine laryngeal
neuropathy. Havermeyer monograph
series no 11, R& W Publications
(Newmarket) Ltd; 2003. p. 937.
102. Barakzai SZ, Dixon PM, Correlation of
resting and exercising endoscopic
ndings for horses with dynamic
laryngeal collapse and palatal
dysfunction. Equine Vet J 2011;43:
1823.
103. Desmaizieres L, Serraud N, Plainfosse B,
et al. Dynamic respiratory endoscopy
without treadmill in 68 performance
Standardbred, Thoroughbred and saddle
horses under natural training
conditions. Eq Vet J 2009;41:34752.
104. Pollock PJ, Reardon RJM, Parkin TDH,
et al. Dynamic respiratory endoscopy in
67 Thoroughbred racehorses training
under normal ridden exercise
conditions. Eq Vet J 2009;41:
354360.
105. Taylor SE, Barakzai SZ, Dixon P.
Ventriculocordectomy as the sole
treatment for recurrent laryngeal
neuropathy: long-term results
from ninety-two horses. Eq Vet J
2006;35:6537.
106. Duncan ID, Reifenrath P, Jackson KF,
et al. Preferential denervation of the
adductor muscles of the equine larynx.
II: Nerve pathology. Equine Vet J
1991;23:99103.
107. Garrett KS, Woodie JB, Embertson RM.
Association of treadmill upper airway
endoscopic evaluation with results of
ultrasonography and resting upper
airway endoscopic evaluation. Equine
Vet J 2011;43(3):36571.
108. Tetens J, Derksen JF, Stick JA, et al.
Efcacy of prosthetic laryngoplasty
with and without bilateral
ventriculocordectomy as treatments for
laryngeal hemiplegia in horses. Am J Vet
Res 1996;57:166873.
109. Ducharme NG, Hackett RP, Gleed RD,
et al. Measurements of pulmonary
capillary pressure in horses undergoing
alteration of intrathoracic pressure by
imposition of various upper airway
resistive loads. Equine Vet J Suppl
1999;30:2733.
110. Hawe C, Dixon PM, Canhew IG. A
study of an electrodiagnostic technique
for the evaluation of equine recurrent
laryngeal neuropathy. Equine Vet J
2001;33(5):45965.
111. Cheetham J, Pigott JH, Leal MT, et al.
Conduction velocity in horses with
normal arytenoid function. Proceedings
BEVA, 2008. p. 343.
112. Brown JA, Derksen FD, Stick JA, et al.
Ventriculocordectomy reduces
respiratory noise in horses with
laryngeal hemiplegia. Eq Vet J
2003;35(6):5704.
113. Shappel KK, Derksen FJ, Stick JA, et al.
Effects of ventriculectomy, prosthetic
laryngoplasty, and exercise on upper
airway function in horses with induced
left laryngeal hemiplegia. Am J Vet Res
1988;49:17606.
114. Lumsden JM, Derksen FJ, Stick JA, et al.
Evaluation of partial arytenoidectomy
as a treatment for equine laryngeal
hemiplegia. Equine Vet J 1994;24:
1259.
115. Russel AP, Slone DE. Performance
analysis after prosthetic laryngoplasty
and bilateral ventriculectomy for
laryngeal hemiplegia in horses: 70 cases
(19861991). J Am Vet Med Assoc
1994;204:123541.
116. Kidd JA, Slone DE. Treatment of
laryngeal hemiplegia in horses by
prosthetic laryngoplasty,
ventriculectomy and vocal cordectomy.
Vet Rec 2002;150:4814.
117. Strand E, Martin GS, Haynes PF, et al.
Career racing performance in
Thoroughbreds treated with prosthetic
laryngoplasty for laryngeal neuropathy:
52 cases (19811989). J Am Vet Med
Assoc 2000;217:168996.
118. Hawkins JF, Tulleners EP, Ross MW,
et al. Laryngoplasty with or without
ventriculectomy for treatment of left
laryngeal hemiplegia in 230 horses. Vet
Surg 1997;26:48491.
119. White NA, Blackwell RB. Partial
arytenoidectomy in the horse. Vet Surg
1980;9:512.
120. Witte TH, Mohammed HO, Radcliffe
CH, et al. Racing performance after
combined prosthetic laryngoplasty and
ipsilateral ventriculocordectomy or
partial arytenoidectomy: 135
Thoroughbred racehorses competing at
less than 2400 m (19972007). Eq Vet J
2009;41(1):705.
121. Parente E J, Tulleners E P, Southwood
LL. Long-term study of partial
arytenoidectomy with primary mucosal
closure in 76 Thoroughbred racehorses
26
Abnormalities of the upper airway
585
(19922006). Eq Vet J 2008;40(3):
21418.
122. Radcliffe CH, Woodie JB, Hackett RP
et al. A comparison of laryngoplasty
and modied partial arytenoidectomy
as treatments for laryngeal hemiplegia
in exercising horses. Vet Surg 2006;
35(7):64352.
123. Ducharme NG, Viel L, Partlow GD,
et al. Attempts to restore abduction
of the paralyzed equine arytenoid
cartilage: III. Nerve anastomosis. Can J
Vet Res 1989;53:21623.
124. Fulton IC, Derksen FJ, Stick JA, et al.
Treatment of left laryngeal hemiplegia
in Standardbreds using a nerve muscle
pedicle graft. Am J Vet Res 1991;52:
14616.
125. Ducharme NG, Cheetham J, Sanders I,
et al. Considerations for pacing of the
cricoarytenoid dorsalis muscle by
neuroprosthesis in horses. Equine Vet J
2010 42(6):53440.
126. Cheetham J, Regner A, Jarvis JC, et al.
Functional electrical stimulation of
intrinsic laryngeal muscles under
varying loads in exercising horses. PloS
one 2011;6(8):e24258.
127. Dixon PM, McGorum BC, Railton DI,
et al. Long-term survey of laryngoplasty
and ventriculocordectomy in an older,
mixed-breed population of 200 horses.
Part 2: Owners assessment of the value
of surgery. Equine Vet J 2003;35(4):
397401.
128. Duncan ID. The pathophysiology of
equine idiopathic laryngeal hemiplegia.
Proceedings International Neurology
Conference, 1997. p. 10810.
129. Hahn CN, Matiasek K, Dixon PM, et al.
Histological and ultrastructural evidence
that recurrent laryngeal neuropathy is a
bilateral mononeuropathy limited to
recurrent laryngeal nerves. Equine Vet J
2008;40(7):66672.
130. Collins N, Milne E, Hahn C, et al.
Correlation of the Havemeyer
endoscopic laryngeal grading system
with histopathological changes in
equine cricoarytenoideus dorsalis
muscles. Ir Vet J 2009;62(5):3348.
131. Baker GJ. Laryngeal asynchrony in the
horses: Denition and signicance.
In: Snow DH, Persson SHB, Rose RJ,
editors. Equine exercise physiology.
Cambridge: Granta; 1983. p. 4650.
132. Dixon PM, McGorum BC, Railton DI,
et al. Clinical and endoscopic evidence
of progression in 152 cases of equine
recurrent neuropathy. Equine Vet J
2002;34(1):2934.
133. Dyer KR, Duncan ID. The intraneural
distribution of myelinated bres in the
equine recurrent laryngeal nerve. Brain
1987;110(Pt 6):153143.
134. Ohnesorge B, Deegen E, Miesner K,
et al. [Laryngeal hemiplegia in warm
blood horses a study of stallions,
mares and their offspring]. Zentralbl
Veterinarmed A 1993;40:13454.
135. Bohanon TC, Beard WL, Robertson JT.
Laryngeal hemiplegia in draft horses. A
review of 27 cases. Vet Surg
1990;19(6):4569.
136. Poncet PA, Montavon S. A preliminary
report on the possible genetic basis of
laryngeal hemiplegia. Equine Vet J
1989;21:1378.
137. Dupuis MC, Zhang Z, Druet T, et al.
Results of a haplotype-based GWAS for
recurrent laryngeal neuropathy in the
horse. Mamm Genome 2011;22(910):
61320.
138. Kelly G, Lumsden JM, Dunkerly G, et al.
Idiopathic mucosal lesions of the
arytenoid cartilages of 21 Thoroughbred
yearlings: 19972001. Equine Vet J
2003;35(3):27681.
139. Sullins K. Endoscopically guided laser
debridement of arytenoid chondritis in
standing horses. Abstract 13. In:
Proceeding World Equine Airways
Society, 2001, CD.
140. Tulleners E, Harrison IW, Raker CW.
Management of arytenoid chondropathy
and failed laryngoplasty in horses: 75
cases (19791985). J Am Vet Med Assoc
1988;192:6705.
141. White NA, Blackwell RB. Partial
arytenoidectomy in the horse. Vet Surg
1980;9:512.
142. Lumsden JM, Derksen FJ, Stick JA, et al.
Evaluation of partial arytenoidectomy
as a treatment for laryngeal hemiplegia.
Equine Vet J 1994;26:1259.
143. Belknap JK, Derksen FJ, Nickels
FA, et al. Failure of subtotal
arytenoidectomy to improve upper
airway ow mechanics in exercising
Standardbreds with induced laryngeal
hemiplegia. Am J Vet Res 1990;51:
14816.
144. Harrison IW, Raker CW. Dorsal glottic
stenosis after bilateral arytenoidectomy
in two horses. J Am Vet Med Assoc
1988;192:2024.
145. Parente EJ, Tulleners EP, Southwood
LL. Long-term study of partial
arytenoidectomy with primary
mucosal closure in 76 Thoroughbred
racehorses (19922006). Equine Vet J
2008;40(3):21418.
146. Jensen R, Lauerman LH, Braddy PM,
et al. Laryngeal contact ulcers in feedlot
cattle. Vet Pathol 1980;17:66771.
147. Smith RL, Perkins, NR, Firth EC, et al.
Arytenoid mucosal injury in young
Thoroughbred horses investigation
of a proposed aetiology and clinical
signicance. N Z Vet J 2006;54(4):
1736.
148. McClure JJ, Koch C, Powell M, et al.
Association of arytenoid chondritis with
equine lymphocyte antigens but no
association with laryngeal hemiplegia,
umbilical hernias and cryptorchidism.
Anim Genet 1988;19:42733.
149. Lane GF. Fourth branchial arch defects
in Thoroughbred horses: 60 cases.
In: Proceeding of the World Equine
Airways Symposium, Edinburgh,
Scotland, 2001.
150. Garrett KS, Woodie JB, Embertson RM,
et al. Diagnosis of laryngeal dysplasia in
ve horses using magnetic resonance
imaging and ultrasonography. Equine
Vet J 2009;41(8):76671.
151. Baxter GM, Allen D, Farrel RL.
Paralaryngeal accessory bronchial
cyst as a cause of laryngeal hemiplegia
in a horse. Equine Vet J 1992;24:
679.
152. Wilson RG, Sutton RH, Groenendyk S.
Rostral displacement of
palatopharyngeal arch in a
Thoroughbred yearling. Aust Vet J
1986;63:99100.
153. Zaw-Tun HA, Burdi AR. Reexamination
of the origin and early development of
the human larynx. Acta Anat (Basel)
1985;122:16384.
154. Hast MH. Early development of the
human laryngeal muscles. Ann Otol
Rhino Laryngol 1972;81:52430.
155. Goulden BE, Anderson LJ, Davies AS,
et al. Rostral displacement of the
palatopharyngeal arch: a case report.
Equine Vet J 1976;8:958.
156. Blikslager AT, Tate LP, Tudor R.
Transendoscopic laser treatment
of rostral displacement of the
palatopharyngeal arch in four
horses. J Clin Laser Med Surg
1999;17:4952.
157. Lepage OM, Piccot-Crzollet C.
Transarterial coil embolisation in 31
horses (19992002) with guttural
pouch mycosis: a 2-year follow-up.
Equine Vet J 2005;37(5):4304.
158. Leveille R, Hardy J, Robertson JT, et al.
Transarterial coil embolization of the
internal and external carotid and
maxillary arteries for prevention of
hemorrhage from guttural pouch
mycosis in horses. Vet Surg 2000;29(5):
38997.
159. Greet TRC. Outcome of treatment in 35
cases of guttural pouch mycosis. Equine
Vet J 1987;19(5):4837.
160. Freeman DE, Ross MW, Dona wick WJ,
et al. Occlusion of the external carotid
and maxillary arteries in the horse to
prevent hemorrhage from guttural
pouch mycosis. Vet Surg 1989;18(1):
3947.
161. Kipper A, Frees K. Hypoglossal neuritis
with associated lingual hemiplegia
secondary to guttural pouch mycosis.
Vet Pathol 1993;30(6):54756.
162. Sweeney CR, Freeman DE, Sweeney RW,
et al. Hemorrhage into the guttural
pouch (auditory tube diverticulum)
associated with rupture of the
longus capitis muscle in three horses.
J Am Vet Med Assoc 1993;202(7):
112931.
Respiratory system
3
586
163. Ludwig A, Gatineau S, Reynaud MC,
et al. Fungal isolation and identication
in 21 cases of guttural pouch mycosis in
horses (19982002). Vet J 2005;169(3):
45761.
164. Davis EW, Legendre AM. Successful
treatment of guttural pouch mycosis
with itraconazole and topical
enilconazole in a horse. J Vet Intern
Med 1994;8(4):3045.
165. Delfs KC, Hawkins JF, Hogan DF.
Treatment of acute epistaxis secondary
to guttural pouch mycosis with
transarterial nitinol vascular occlusion
plugs in three equids. J Am Vet Med
Assoc 2009;235(2):18993.
166. Benredouane K, Lepage O. Trans-arterial
coil embolization of the internal carotid
artery in standing horses. Vet Surg
2012;41(3):4049.
167. Freeman DE, Ross MW, Dona wick WJ.
Steal phenomenon proposed as the
cause of blindness after arterial
occlusion for treatment of guttural
pouch mycosis in horses. J Am Vet Med
Assoc 1990;197(7):81112.
168. Naylor RJ, Perkins JD, Allen S, et al.
Histopathology and computed
tomography of age-associated
degeneration of the equine
temporohyoid joint. Equine Vet J
2010;42(5):42530.
169. Power HT, Watrous BJ, de Lahunta A.
Facial and vestibulocochlear nerve
disease in six horses. J Am Vet Med
Assoc 1983;183:107680.
170. Blythe LL, Watrous BJ, Shire MH.
Prophylactic partial stylohyoidostectomy
for horses with osteoarthropathy of the
temporohyoid joint. J Equine Vet Sci
1994;14:327.
171. Blythe LL. Otitis media and interna and
temporohyoid osteoarthropathy. Vet
Clin North Am Equine Pract 1997;13:
2142.
172. Divers TJ, Ducharme NG, de Lahunta A,
et al. Temporohyoid osteoarthropathy.
Clin Tech Equine Pract 2006;5:
1723.
173. Walker AM, Sellon DC, Cornellisse CJ,
et al. Temporohyoid osteoarthropathy
in horses: 33 cases (19932000).
J Vet Intern Med 2002;16(6):
697703.
174. Hilton H, Puchalski SM, Aleman M. The
computed tomographic appearance of
equine temporohyoid osteoarthropathy.
Vet Radiol Ultrasound 2009;50(2):
1516.
175. Pownder S, Scrivani PV, Bezuidenhout
A, et al. Computed tomography of
temporal bone fractures and temporal
region anatomy in horses. J Vet Intern
Med 2010;24(2):398406.
176. Pease AP, van Biervliet J, Dykes NL,
et al. Complication of partial
stylohyoidectomy for treatment of
temporohyoid osteoarthropathy and an
alternative surgical technique in three
cases. Equine Vet J 2004;36:54650.
177. Tetens J, Hubert JD, Eddy AL, et al.
Dynamic tracheal collapse as a cause of
exercise intolerance in a Thoroughbred.
J Am Vet Med Assoc 2000;216(5):
7224.
178. Steiger RR, Williams MA.
Granulomatous tracheitis caused by
Conidiobolus coronatus in a horse.
J Vet Intern Med 2000;14(3):31114.
179. Tate LP, Koch DB, Sembrat RF, et al.
Tracheal reconstruction by resection and
end-to-end anastomosis in the horse.
J Am Vet Med Assoc 1981;178(3):
2538.