Vol. 19, No.
3 March 1997 V Small Animal Gastroenterology
Continuing Education Article
Refereed Peer Review
FOCAL POINT
★Acquired megaesophagus
can result from numerous
neuromuscular, endocrine,
or inflammatory disorders as
well as from obstructive lesions
KEY FACTS
in the esophagus.
■ Disruption of the afferent
pathway has been implicated
in the pathophysiology of
both congenital and adult-
onset idiopathic canine
megaesophagus.
■ Definitive diagnosis of either
generalized or focal myasthenia
gravis requires identification of
circulating antibodies against
acetylcholine receptors.
■ The most common endocrine
diseases associated with
megaesophagus are
hypoadrenocorticism and,
possibly, hypothyroidism.
■ Advanced techniques,
including manometry and
nuclear scintigraphy, are
useful in evaluating esophageal
motility.
Canine and Feline
Megaesophagus
University of Tennessee
Erick A. Mears, DVM
Christine C. Jenkins, DVM
M egaesophagus refers to a diffusely dilated esophagus with decreased
or absent motor function. Canine megaesophagus can occur as a
congenital disorder (with signs first appearing before or soon after
weaning), as an acquired disorder (secondary to an underlying primary condi-
tion), or as an adult-onset idiopathic disease. Feline megaesophagus is rare and
occurs as a congenital or secondary acquired disorder.1
Congenital megaesophagus is recognized at weaning and is believed to be
caused by a lack of innervation of the esophagus.2,3 The mode of transmission
in most breeds of cats and dogs has not been well defined.4,5 However, congeni-
tal megaesophagus is known to be inherited in wirehaired fox terriers and
miniature schnauzers.6,7 It is transmitted in wirehaired fox terriers as a simple
autosomal-recessive trait, whereas in miniature schnauzers, it is transmitted as a
simple autosomal-dominant or a 60% penetrance autosomal-recessive trait.6–8
A predisposition may exist in other canine breeds, including Great Danes, Ger-
man shepherds, Irish setters, Labrador retrievers, Newfoundlands, and Chinese
shar-peis.8 Feline breeds that may have a hereditary predisposition include the
Siamese and Siamese-related breeds.9
Acquired megaesophagus can result from numerous neuromuscular, en-
docrine, or inflammatory disorders as well as from obstructive lesions in the
esophagus.4,5 Early diagnosis and elimination of predisposing diseases are essen-
tial for successful management because prolonged dysfunction can cause irre-
versible distention.
Adult-onset idiopathic megaesophagus is associated with a poor to grave
prognosis. A high percentage of patients are euthanatized because of the pro-
gression of clinical signs and recurrent aspiration pneumonia.
ANATOMY
The esophagus consists of the upper esophageal sphincter proximally, the
esophageal body, and the lower esophageal sphincter distally. The upper
esophageal sphincter separates the pharynx from the body of the esophagus
and indirectly prevents aspiration of ingesta into the respiratory tract. This
sphincter is composed of striated muscle and is innervated by the somatic
branches (glossopharyngeal, pharyngeal, and recurrent laryngeal) of the vagus
nerve, which originates from the brain stem nucleus ambiguus.10
Small Animal
Presence of food Afferent receptors (sensory)
in the proximal
esophagus
Vagus/glossopharyngeal nerves
Nucleus solitarius
Nucleus ambiguus Dorsal motor nucleus
Vagus nerve (motor) Vagus nerve (motor)
Neuromuscular junction Neuromuscular junction
Striated muscle Striated and smooth muscle
Esophageal contraction
Figure 1—Neural pathway for esophageal motility.
The esophageal body consists of two muscle layers
that propel food via coordinated contractions from the
oral cavity to the stomach. The entire length of the ca-
nine esophageal body is composed of two oblique layers
of skeletal muscle, which contains predominantly type
IIA fibers and is innervated by the somatic branches of
the vagus nerve.11 The two layers of skeletal muscle of
the esophagus in the cat are in an oblique orientation
in the proximal portion of the esophagus and become
spiral in the distal portion, thus forming a longitudinal
and circular pattern.12 Unlike the dog, the cat has an
increased quantity of smooth muscle in the distal third
of the esophageal body. The striated muscle of the
esophagus of the cat is also innervated by the vagus
nerve; however, the smooth muscle is innervated by the
autonomic branches of the vagus nerve, which origi-
nates from the dorsal motor nucleus.
The lower esophageal sphincter is considered a physi-
ologic sphincter and not a true anatomic sphincter be-
cause of the absence of muscle mass at the sphincter
site.12 This sphincter separates the esophagus and the
cardia of the stomach and allows ingesta to pass into the
stomach while preventing reflux of most stomach con-
tents into the esophagus. Esophageal reflux is prevented
by various contributing factors at the site of the lower
esophageal sphincter. These factors include the resting
ANATOMY ■ ESOPHAGEAL MOTILITY ■ NEURAL PATHWAYS
The Compendium March 1997
tone of the lower esophageal
sphincter, the interdigitating
esophageal and gastric rugal
folds, the diaphragmatic crus
(which serves as a muscular
sling), the oblique angle of the
distal esophagus as it enters the
stomach, and the compression
exerted on the short intraabdom-
inal esophageal segment by posi-
tive intraabdominal pressure.13
In dogs, the lower esophageal
sphincter contains fibers of both
striated and smooth muscle,
whereas in cats, it contains only
fibers of smooth muscle.
Esophageal contraction, or
peristalsis, follows swallowing
and the movement of food from
the pharyngeal area into the
esophagus. Sensory, or afferent,
receptors in the pharynx and
proximal esophagus are stimulat-
ed by the presence of food. Solid
boluses are more effective than
liquid in stimulating a swallow-
ing reflex.12 The afferent recep-
tors stimulate the afferent nerve fibers of the vagus. The
origin of the vagus nerve (i.e., the nucleus ambiguus for
striated muscle and the dorsal motor nucleus for smooth
muscle) initiates an efferent response via the somatic
and parasympathetic nerve fibers of the vagus. This neu-
ronal pathway ends at the myoneural junction with a
coordinated contraction of the upper esophageal sphinc-
ter.12 This peristaltic wave propagates caudally through
the body of the esophagus, passes through the lower
esophageal sphincter, and then moves into the stomach.
The initial wave that begins at the pharynx is called pri-
mary peristalsis. Any remaining intraluminal ingesta
within the esophagus stimulates esophageal afferent re-
ceptors and initiates secondary peristalsis, which clears
the lumen of the esophagus12 (Figure 1).
PATHOGENESIS
Congenital
The neural pathway of esophageal innervation has
been identified.12 Any lesion along this neural pathway
could alter the normal motility of the esophagus.4,5 A
study that evaluated the efferent pathway found that
dogs with congenital idiopathic megaesophagus had
normal vagal efferent innervation and decreased
esophageal motor function, possibly secondary to al-
tered biomechanical or viscoelastic properties of the
The Compendium March 1997 Small Animal

esophagus.14,15 Two other studies confirmed a

normal efferent limb and implicated a disrup-
Disorders that Cause Megaesophagus
tion of the afferent limb of the neural pathway
Central Nervous System Esophageal Musculature
as the cause of congenital canine megaesopha-
gus.16,17 ■ Distemper7,20 ■ Systemic lupus
■ Cervical vertebral erythematosus20,37
Adult-Onset Idiopathic instability with ■ Glycogen storage
In an evaluation of the afferent nerve pathway leukomalacia20 disease38
in adult dogs with acquired idiopathic mega- ■ Brain stem lesions20 ■ Polymyositis20,39
esophagus, pressure measurements were taken ■ Neoplasia20 ■ Dermatomyositis40
from the upper esophageal sphincter, the ■ Trauma20 ■ Cachexia26
esophageal body, and the lower esophageal ■ Trypanosomiasis41
sphincter after both swallowing and intraluminal Peripheral Neuropathies
■ Hypoadrenocorticism20
distention.18 Pressure measurements of the lower ■ Polyradiculoneuritis20
■ Hypothyroidism (?)
esophageal sphincter after swallowing were nor- ■ Dysautonomiaa,21,22
mal and indicated appropriate relaxation of the ■ Ganglioradiculitis23 Obstructive Lesions
sphincter,18,19 thus suggesting a normal efferent ■ Giant cell axonal ■ Neoplasia
pathway. However, measurements taken after in- neuropathy24 ■ Granulomas
traluminal distention of the esophagus revealed ■ Spinal muscular atrophy25 ■ Vascular ring
failure of the lower esophageal sphincter to relax.18 ■ Polyneuritis26
Therefore, a defect probably exists in the afferent anomalies
■ Thallium toxicity27 ■ Strictures
pathway of dogs with both congenital and adult-
onset idiopathic megaesophagus. Similar studies ■ Lead toxicitya,28 ■ Foreign body
have not been done in cats. ■ Acrylamide toxicity29
■ Mediastinitis30 Miscellaneous
Secondary Acquired ■ Bronchoesophageal ■ Pyloric stenosisa,42
Megaesophagus can be caused by any disease fistula30 ■ Gastric dilatation volvulus
that inhibits esophageal body peristalsis by dis- ■ Bilateral vagal damage ■ Gastric heterotopiaa,43
rupting central, efferent, or afferent neural ■ Pituitary dwarfism
pathways or esophageal musculature.8 The vari- Neuromuscular Junction
■ Thymomaa
ous causes and their proposed mechanisms will ■ Myasthenia gravisa,20,31–33
■ Familial reflex clonus
be discussed in the following section. ■ Botulism34,35
■ Dystrophin deficiencya,44
■ Tetanus5
CAUSES ■ Anticholinesterase
Congenital toxicity36
The neurologic dysfunction that results in a
Diagnosed in cats.
diffuse megaesophagus is unclear. It has been
hypothesized that the innervation of the esophagus is cal obstruction and possibly generalized esophageal dis-
incomplete in congenital megaesophagus and that in- tention.
nervation may improve with maturity.2,3
Myasthenia Gravis
Secondary Acquired Myasthenia gravis is a common cause of secondary
The list of specific diseases that cause megaesophagus megaesophagus in dogs and, although rare in cats, has
is extensive. Broad disease categories include central been reported to cause proximal esophageal dilatation.45
and peripheral neuropathies, diseases of the neuromus- Myasthenia gravis can be either congenital or acquired,
cular junction, myopathies, and obstructive lesions of and both can result in megaesophagus.31 Because con-
the esophagus (see Disorders that Cause Megaesopha- genital myasthenia gravis is less common, it will not be
gus20–44). The following discussion focuses on several of addressed in this article.
the most common specific diseases—myasthenia gravis, Acquired myasthenia gravis is a disorder of neuro-
a disorder of the neuromuscular junction; hypoadreno- muscular transmission in which autoantibodies against
corticism (and possibly hypothyroidism), which alter nicotinic acetylcholine receptors at the neuromuscular
the function of the esophageal musculature; and all junction result in a reduction of acetylcholine receptors
types of obstructive lesions, which cause focal mechani- and subsequent muscle weakness.46 Two forms of ac-

AFFERENT PATHWAY DEFECT ■ SECONDARY DISORDERS ■ MYASTHENIA GRAVIS

Small Animal
quired myasthenia gravis (generalized and focal) have
been identified. Generalized myasthenia gravis causes
muscle weakness that worsens after exercise and im-
proves with rest. Most dogs with generalized myasthe-
nia gravis and muscle weakness have concurrent mega-
esophagus. One report showed that two of four cats
with generalized myasthenia gravis had a dilated proxi-
mal esophagus, possibly the result of the proximal dis-
tribution of skeletal muscle.45
Focal myasthenia gravis in dogs has been recognized
to cause weakness involving the esophageal, pharyngeal,
and/or facial muscles.33 One study found that 40 of
152 (26%) dogs with a diagnosis of “idiopathic”
megaesophagus had focal myasthenia gravis. Forty-
eight percent of these dogs showed clinical improve-
ment or remission of clinical signs, which was associat-
ed in all cases with decreased titers of antibody to
acetylcholine receptors. Another more recent study re-
vealed that 36% of dogs diagnosed with acquired myas-
thenia gravis had focal disease with megaesophagus but
without evidence of general muscle weakness.32
Hypoadrenocorticism and Hypothyroidism
The most common endocrine diseases associated
with megaesophagus are hypoadrenocorticism47,48 and,
possibly, hypothyroidism.49 With hypoadrenocorticism,
it is suspected that megaesophagus results from impair-
ment of muscle carbohydrate metabolism due to gluco-
corticoid insufficiency. In addition, depleted muscle
glycogen stores and decreased catecholamine activity
may play a role.32 In one case report, atypical Addison’s
disease was diagnosed and subsequent therapy with
prednisone resolved the megaesophagus.48
The cause-and-effect relationship between hypothy-
roidism and megaesophagus is controversial. Hypothy-
roidism has been implicated in the pathogenesis of vari-
ous myopathies and neuropathies.33,49,50 The results of
treating hypothyroid dogs with megaesophagus have
been equivocal.49,50 In a retrospective study of 29 dogs
with hypothyroidism, 4 had megaesophagus. After ap-
propriate thyroxine supplementation, the clinical signs
improved in only one dog; however, all four continued
to have radiographic evidence of a dilated esophagus.49
Another study identified five dogs with neurologic ab-
normalities; all five had myasthenia gravis and signs
consistent with hypothyroidism.50 These dogs showed
clinical signs and radiographic evidence of megaesopha-
gus. Clinical signs resolved in two of the five dogs after
administration of thyroid hormone.
The tenuous association between hypothyroidism and
megaesophagus is often complicated by the current lack
of both sensitive and specific diagnostic tests for hypothy-
roidism.51 In addition, many patients with megaesophagus
ENDOCRINE DISEASES ■ VASCULAR RING ANOMALY ■ SURGICAL LIGATION
The Compendium March 1997
have underlying or concurrent diseases that may interfere
with the evaluation of the hypothalamic-pituitary-thyroid
axis. Some hypothyroid dogs with megaesophagus have
improved with thyroxine supplementation.49,50 However,
spontaneous improvement of megaesophagus has been
previously documented.52 In addition, a recent retrospec-
tive megaesophagus risk factor analysis showed that hy-
pothyroidism is not a significant risk factor.a Until a cor-
relation between hypothyroidism and megaesophagus is
established, “hypothyroid” dogs with megaesophagus
should be monitored closely while under treatment.
Obstructive Lesions
Lesions that cause focal mechanical obstruction
(e.g., vascular ring anomalies, tumors, granulomas,
strictures, and foreign bodies) can progress to general-
ized esophageal distention. Constricting vascular ring
anomalies are the most common cause of segmental ob-
structive megaesophagus in young animals. These in-
clude persistent right aortic arch, double aortic arch,
left aortic arch and right ligamentum arteriosum, per-
sistent left or right subclavian arteries, ductus arteriosus
with normal aortic arch, persistent right dorsal aorta,
and aberrant intercostal arteries.5 Persistent right aortic
arch is the most common vascular ring anomaly in
both dogs and cats.53,54 The right, instead of the left,
fourth aortic arch becomes functional. As a result, the
trachea and esophagus are encircled by the base of the
heart ventrally, the aortic arch to the right, the dorsal
aorta dorsally, and the ligamentum arteriosum and
pulmonary artery to the left.55
Clinical signs associated with secondary megaesopha-
gus usually become evident at the time of weaning to
solid food. They are apparent in 90% of animals by 6
months of age.56 Diagnosis is confirmed by barium
contrast radiography, which demonstrates an esopha-
geal dilatation cranial to the base of the heart. Esopha-
goscopy may help rule out primary esophageal stricture
or a foreign body but is often unnecessary.
The treatment of choice is early surgical ligation of
the aberrant vessels or ligamentum arteriosum to release
the esophageal stricture.57 Although the primary defect
is corrected, many animals continue to have abnormal
esophageal motility and some continue to have clinical
signs.58 In one study, postsurgical fluoroscopy showed
that all surgically corrected patients had abnormal
motility; 58% occasionally exhibited clinical signs.59
Although esophageal cancer in dogs and cats is rare,
squamous cell carcinoma, leiomyosarcoma, fibrosarco-
ma, and osteosarcoma have been reported.60 Benign tu-
aGaynor A, Shofer F, Washabau RJ: Personal communica-
tion, School of Veterinary Medicine, University of Pennsylva-
nia, 1996.
The Compendium March 1997 Small Animal

mors, including leiomyoma requires the identification of a

and plasmacytoma, can oc- Diagnostic Tests for Megaesophagus dilated esophagus on survey
cur.60–62 Early identification thoracic radiographs (Figure
Minimum Data Base
and/or resolution of the ob- 2) or a barium esophagogram.
struction via surgical or en- ■ Complete blood count Radiographs may show an
doscopic intervention is war- ■ Chemistry panel esophagus filled with air, flu-
ranted to prevent further ■ Electrolytes id, or ingested material. Tho-
damage. ■ Urinalysis racic radiographs are also indi-
■ Thoracic radiographs and/or barium cated to evaluate for evidence
CLINICAL SIGNS esophagogram of aspiration pneumonia. If
The most common clinical ■ Acetylcholine antibody test megaesophagus is diagnosed
sign associated with mega- ■ Adrenocorticotropic hormone (ACTH) stimulation on survey radiographs, an
esophagus is regurgitation, esophagogram is generally un-
■ Thyroxine (T4) level
which is defined as the pas- necessary and may pose a
sive evacuation of undigested ■ Thyroid-stimulating hormone (TSH) assay greater risk for aspiration.
food from the esophagus. Additional Tests A minimum data base that
The regurgitated material ■ Lead level includes a complete blood
may contain mucus as well as count, serum chemistries,
■ Botulinum test
undigested food but is gener- and a urinalysis is necessary
■ Antinuclear antibody (ANA) test
ally not bile stained. In con- to identify any underlying
trast to vomiting, there is no ■ Muscle biopsy metabolic abnormalities. In
prodromal phase; regurgita- ■ Creatinine phosphokinase (CPK) cases of esophageal hypo-
tion may occur soon after ■ Endoscopy motility without significant
eating or have a lag phase of ■ Manometry esophageal dilatation, barium
many hours. Frequency of ■ Scintigraphy contrast, alone or with food,
regurgitation varies, and ani- may be necessary to identify
mals may regurgitate food and/or liquids. Other clini- mild esophageal dilatation or to outline an obstructive le-
cal signs observed with megaesophagus include vomit- sion (Figure 3). The response of the esophagus is based
ing, ptyalism, halitosis, gurgling noises from the on the consistency of the diet.12
esophagus, and respiratory signs associated with aspira- Fluoroscopy is available in referral institutions and
tion pneumonia. An absent respiratory reflex has been may be used to visualize esophageal motility. Esopha-
identified in dogs with idiopathic megaesophagus and goscopy can aid in the diagnosis of reflux esophagitis,
may increase the risk of aspiration.63 which may cause abnormal motility and distention of
the esophagus.8
PHYSICAL In humans, esophageal
EXAMINATION motility is evaluated with
Physical examination fluoroscopy and esophageal
findings may include appar- manometry. In veterinary
ent ventral neck swelling medicine, the use of esoph-
due to esophageal disten- ageal manometry is limited
tion. Patients with mega- to teaching institutions and
esophagus may also be cachec- research facilities. 19,64,65
tic from poor nutritional Esophageal motility mano-
intake. If aspiration pneu- metric studies are best done
monia is present, fever, on awake animals because of
harsh rales, and/or mucopu- the effects of anesthetics on
rulent nasal discharge may normal esophageal moti-
be observed. lity. 65 Manometry utilizes
a catheter passed into
DIAGNOSIS Figure 2—Right lateral thoracic radiograph of a 10-year-old the esophageal lumen for
Definitive diagnosis of dog with idiopathic megaesophagus. The air-filled, diffuse- dynamic measurement of
megaesophagus (see Diagnos- ly dilated esophagus has resulted in ventral displacement of esophageal pressure, transit
the trachea.
tic Tests for Megaesophagus) rate, and lower esophageal

REGURGITATION ■ THORACIC RADIOGRAPHS ■ MANOMETRY

Small Animal
pressures following swallowing.
Manometry is used to evaluate
subtle motility abnormalities
that may not be evident on fluo-
roscopy.66 Baseline manometric
measurements of the esophagus
for both dogs and cats have been
evaluated.67,68
Esophageal scintigraphy is a
newer technique that is used in
humans to quantitatively evalu-
ate esophageal motility. This
technique involves the use of a
gamma camera to monitor radio-
labeled food as it moves through
the esophagus. Transit time of
the food bolus through various
regions of interest along the
length of the esophagus is deter-
mined (Figure 4). Time activity
curves are then plotted to evalu-
ate the movement of the food
bolus through the esophagus
(Figures 5 and 6).
Esophageal scintigraphy may
be a more accurate measure of
motility because it evaluates the
response of the esophagus to a
food bolus without the influence
of foreign material, such as bari-
um or an esophageal catheter.69
Recently, scintigraphy was used
to evaluate the effect of meto-
clopramide and cisapride on
esophageal motility in normal
beagles.68
In most cases of megaesopha-
gus, manometric and scinti-
graphic studies are not necessary
for a diagnosis. These tests can
be used to identify those animals
with subtle esophageal motility
abnormalities and consistent
clinical signs but with no identi-
fiable abnormality on routine
radiographic imaging. Both
manometry and scintigraphy
also provide a quantitative mea-
sure of esophageal motility pa-
rameters.
Once megaesophagus has been
identified, additional testing is
necessary to identify an underly-
ESOPHAGEAL SCINTIGRAPHY ■ DIAGNOSTIC TESTS ■ MYASTHENIA GRAVIS DIAGNOSIS
The Compendium March 1997
ing cause. Endocrine testing
(thyroxine [T4] level, thyroid-
stimulating hormone [TSH]
assay, adrenocorticotropic
hormone [ACTH] stimula-
tion); neuromuscular evalua-
tion (acetylcholine antibody,
antinuclear antibodies [ANA],
muscle biopsy, creatinine
phosphokinase [CPK]); and
toxin screening (lead, botu-
linum) are done to identify
the more common secondary
causes. The diagnosis, howev-
er, is often idiopathic mega-
esophagus.5
Definitive diagnosis of either
generalized or focal myasthe-
nia gravis requires the identi-
fication of circulating anti-
bodies against acetylcholine
receptors. The immunopre-
cipitation radioimmunoassay
is very specific and sensitive
for demonstrating circulating
antibodies. This test does not
give false-positive results.
However, false-negative re-
sults (less than 5% of cases
Figure 3A tested 32) may occur and in-
dicate either the presence of
autoantibodies against other
components of the motor
end-plate or the presence of
high-affinity antibodies. Oth-
er diagnostic tests that are
available to support a diagno-
sis of myasthenia gravis in-
clude the edrophonium chlo-
ride challenge and repetitive
nerve stimulation.
MANAGEMENT
Management of idiopathic
Figure 3B megaesophagus, unresolved
Figure 3—(A) Ventral dorsal and (B) right lateral megaesophagus, or of esoph-
thoracic radiographs taken after administration of a ageal hypomotility involves
barium meal. The entire thoracic portion of the feeding small amounts of
esophagus in this dog is distended, and the esopha- food to an animal in an up-
gus has displaced the trachea ventrally. A right medi- right position. The ability of
astinal shift has displaced the heart. An alveolar in- patients with megaesophagus
filtrate is present within the right middle and left
to swallow foods of differing
cranial lung lobes.
consistencies varies. A barium
The Compendium March 1997
contrast study may help in
the decision as to whether
to use liquid, canned, or dry
food.
If the patient is difficult
to feed, gastrostomy tubes
can be placed to facilitate
feeding. Surgical, percuta-
neous endoscopic, and blind
(nonendoscopic) percuta-
neous techniques for gas-
trostomy tube placement
have been described else-
where.b,70–72
Aspiration pneumonia
should be treated with
broad-spectrum antibiotics
while culture and sensitivity
results from a transtracheal
wash are pending. Identified
causes of secondary mega-
esophagus should be treated
promptly and appropriately
to optimize resolution of
esophageal dysfunction.
If the diagnosis of myas-
thenia gravis is confirmed,
treatment should include
the administration of long-
acting anticholinesterase
drugs. Both pyridostigmine
bromide (0.5 to 1.0 mg/kg
orally every 8 to 12 hours)
and neostigmine (0.04 mg/kg
intramuscularly every 6 hours)
are effective. Because myas-
thenia gravis is an immune-
mediated disease, cortico-
s teroids may be useful;
however, their use is contro-
versial, and a complete evalu-
ation of the respiratory tract
for aspiration pneumonia is
recommended before using
corticosteroids.73 Treatment
is considered successful if
clinical signs improve and
the acetylcholine receptor
antibody level decreases.
This level should be checked
bSee the article in this issue by
Dr. Kathryn Michel on guide- gus).
lines for gastrostomy tubes.
FEEDING ■ DRUG THERAPY ■ METOCLOPRAMIDE ■ CISAPRIDE
Small Animal
every 4 to 6 weeks and ther-
apy adjusted accordingly. If
clinical remission occurs, all
medications may be discon-
tinued; however, the disease
may recur.73 Esophageal di-
latation has been shown to
resolve in both dogs and cats
after appropriate therapy.45,73
Various drug therapies
have been used in an at-
Figure 4—Esophageal scintigraphic images were obtained 20 tempt to improve esoph-
minutes after intravenous injection of pertechnetate, a ra- ageal motility in dogs with
dioactive substance. A bolus of food labeled with 99mtech- megaesophagus. Calcium-
netium was administered orally, and a series of images were channel blockers, such as
obtained during esophageal transit of the radiolabeled food. nifedipine, have been used
The image shown here is a summation of the dynamic im- in dogs with suspected acha-
ages; the course through the entire esophagus is shown. lasia or asynchrony of the
Pertechnetate localizes in the stomach and thyroid gland, al- lower esophageal sphincter
lowing for visualization of esophageal landmarks. Note the function and esophageal
residual pertechnetate at the injection site on the forelimb.
peristalsis. 74 Response to
The open circles represent regions of interest (see Figure 5)
over different areas of the esophagus. nifedipine in dogs, if any, is
transient.
Metoclopramide is a pro-
kinetic drug that has been
used without success in dogs
with megaesophagus.19 Meto-
clopramide may be indicated
in dogs with esophageal hypo-
motility caused by reflux
esophagitis because it in-
creases lower esophageal
sphincter tone.
Cisapride is another pro-
kinetic drug that increases
motility of the gastrointesti-
nal tract by promoting the
release of acetylcholine. Ex-
perimentally, cisapride has
Figure 5—An esophageal scintigraphic study of a 10-week-
been shown to alter esoph-
old schnauzer. The images above the graph are portions of
ageal peristalsis in cats. 75
the dynamic acquisition and were obtained after swallow-
ing of a radiolabeled food bolus. Note that the food bolus Anecdotal reports indicate
remains in the proximal esophagus. The numbers above possible clinical improve-
each image represent time in seconds. The graph is a time ment in some dogs with
activity curve that represents changes in esophageal activity megaesophagus.76
at specified regions of interest (ROI) over time. Normally, Other reports have ques-
the time activity curve should show a peak as the radioac- tioned the beneficial effects
tive bolus passes through the ROI. Note the relatively flat of cisapride or metoclo-
appearance of the proximal esophageal time activity curve, pramide in dogs with
which is the result of the lack of movement of the bolus megaesophagus.75 In normal
from the proximal esophagus (Prox Esop = proximal esoph- dogs, cisapride decreased or
agus, Thx Inlet = thoracic inlet, Dist Esop = distal esopha-
slowed the transit rate of a
food bolus through the
Small Animal
Figure 6—A follow-up (16 weeks) esophageal scintigraphic
study of the dog shown in Figure 5. The images above the
graph are portions of the dynamic acquisition. Note the
movement of the radioactive bolus through the esophagus
(unlike the lack of movement in Figure 5). The time activity
curve is more normal in appearance, with well-defined peaks
as the bolus traverses the esophageal regions of interest
(ROI). The residual activity in the distal esophagus may
represent mild esophageal dysfunction. The improvement in
esophageal function is probably related to the resolution of
congenital megaesophagus (Prox Esop = proximal esophagus,
Thx Inlet = thoracic inlet, Dist Esop = distal esophagus).
esophagus.68 Therefore, cisapride and other current
prokinetic drugs cannot be recommended to improve
esophageal motility in a patient with primary mega-
esophagus. Because it increases the pressure of the low-
er esophageal sphincter, however, cisapride (like meto-
clopramide) may help decrease reflux esophagitis. The
result is fewer episodes of regurgitation and subsequent
esophagitis, both of which may exacerbate megaesopha-
gus.8
SUMMARY
Megaesophagus can be congenital, secondary to nu-
merous disorders, or idiopathic. Diagnosis of mega-
esophagus is based on consistent historical and physical
examination findings in conjunction with the results of
imaging techniques. Motility disorders that cannot be
identified with traditional radiographic techniques may
require manometric and scintigraphic evaluation. Sec-
ondary megaesophagus has the best prognosis if the
underlying cause can be determined and effectively
treated. Treatment of congenital or idiopathic mega-
esophagus is at best supportive.
SCINTIGRAPHIC STUDY ■ REFLUX ESOPHAGITIS
The Compendium March 1997
ACKNOWLEDGMENT
The authors thank Dr. Greg Daniel, of the College of
Veterinary Medicine, University of Tennessee, for pro-
viding Figures 2 through 6.
About the Authors
Drs. Mears and Jenkins are affiliated with the Department
of Small Animal Clinical Sciences, College of Veterinary
Medicine, University of Tennessee, Knoxville, Tennessee.
They are Diplomates of the American College of Veteri-
nary Internal Medicine.
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