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Vol. 19, No.

3 March 1997 V Small Animal Gastroenterology

Continuing Education Article

Refereed Peer Review

Canine and Feline

University of Tennessee
★Acquired megaesophagus
can result from numerous
Erick A. Mears, DVM
neuromuscular, endocrine, Christine C. Jenkins, DVM
or inflammatory disorders as
well as from obstructive lesions

in the esophagus.

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
■ Disruption of the afferent occurs as a congenital or secondary acquired disorder.1
pathway has been implicated Congenital megaesophagus is recognized at weaning and is believed to be
in the pathophysiology of caused by a lack of innervation of the esophagus.2,3 The mode of transmission
both congenital and adult- in most breeds of cats and dogs has not been well defined.4,5 However, congeni-
onset idiopathic canine tal megaesophagus is known to be inherited in wirehaired fox terriers and
megaesophagus. 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
■ Definitive diagnosis of either simple autosomal-dominant or a 60% penetrance autosomal-recessive trait.6–8
generalized or focal myasthenia A predisposition may exist in other canine breeds, including Great Danes, Ger-
gravis requires identification of man shepherds, Irish setters, Labrador retrievers, Newfoundlands, and Chinese
circulating antibodies against shar-peis.8 Feline breeds that may have a hereditary predisposition include the
acetylcholine receptors. Siamese and Siamese-related breeds.9
Acquired megaesophagus can result from numerous neuromuscular, en-
■ The most common endocrine docrine, or inflammatory disorders as well as from obstructive lesions in the
diseases associated with esophagus.4,5 Early diagnosis and elimination of predisposing diseases are essen-
megaesophagus are tial for successful management because prolonged dysfunction can cause irre-
hypoadrenocorticism and, versible distention.
possibly, hypothyroidism. Adult-onset idiopathic megaesophagus is associated with a poor to grave
prognosis. A high percentage of patients are euthanatized because of the pro-
■ Advanced techniques, gression of clinical signs and recurrent aspiration pneumonia.
including manometry and
nuclear scintigraphy, are ANATOMY
useful in evaluating esophageal The esophagus consists of the upper esophageal sphincter proximally, the
motility. 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 The Compendium March 1997

tone of the lower esophageal

Presence of food Afferent receptors (sensory) sphincter, the interdigitating
in the proximal esophageal and gastric rugal
esophagus folds, the diaphragmatic crus
Vagus/glossopharyngeal nerves (which serves as a muscular
sling), the oblique angle of the
distal esophagus as it enters the
stomach, and the compression
Nucleus solitarius exerted on the short intraabdom-
inal esophageal segment by posi-
Nucleus ambiguus Dorsal motor nucleus tive intraabdominal pressure.13
In dogs, the lower esophageal
sphincter contains fibers of both
Vagus nerve (motor) Vagus nerve (motor) striated and smooth muscle,
whereas in cats, it contains only
fibers of smooth muscle.
Neuromuscular junction Neuromuscular junction Esophageal contraction, or
peristalsis, follows swallowing
and the movement of food from
Striated muscle Striated and smooth muscle the pharyngeal area into the
esophagus. Sensory, or afferent,
receptors in the pharynx and
proximal esophagus are stimulat-
Esophageal contraction
ed by the presence of food. Solid
boluses are more effective than
Figure 1—Neural pathway for esophageal motility.
liquid in stimulating a swallow-
ing reflex.12 The afferent recep-
The esophageal body consists of two muscle layers tors stimulate the afferent nerve fibers of the vagus. The
that propel food via coordinated contractions from the origin of the vagus nerve (i.e., the nucleus ambiguus for
oral cavity to the stomach. The entire length of the ca- striated muscle and the dorsal motor nucleus for smooth
nine esophageal body is composed of two oblique layers muscle) initiates an efferent response via the somatic
of skeletal muscle, which contains predominantly type and parasympathetic nerve fibers of the vagus. This neu-
IIA fibers and is innervated by the somatic branches of ronal pathway ends at the myoneural junction with a
the vagus nerve.11 The two layers of skeletal muscle of coordinated contraction of the upper esophageal sphinc-
the esophagus in the cat are in an oblique orientation ter.12 This peristaltic wave propagates caudally through
in the proximal portion of the esophagus and become the body of the esophagus, passes through the lower
spiral in the distal portion, thus forming a longitudinal esophageal sphincter, and then moves into the stomach.
and circular pattern.12 Unlike the dog, the cat has an The initial wave that begins at the pharynx is called pri-
increased quantity of smooth muscle in the distal third mary peristalsis. Any remaining intraluminal ingesta
of the esophageal body. The striated muscle of the within the esophagus stimulates esophageal afferent re-
esophagus of the cat is also innervated by the vagus ceptors and initiates secondary peristalsis, which clears
nerve; however, the smooth muscle is innervated by the the lumen of the esophagus12 (Figure 1).
autonomic branches of the vagus nerve, which origi-
nates from the dorsal motor nucleus. PATHOGENESIS
The lower esophageal sphincter is considered a physi- Congenital
ologic sphincter and not a true anatomic sphincter be- The neural pathway of esophageal innervation has
cause of the absence of muscle mass at the sphincter been identified.12 Any lesion along this neural pathway
site.12 This sphincter separates the esophagus and the could alter the normal motility of the esophagus.4,5 A
cardia of the stomach and allows ingesta to pass into the study that evaluated the efferent pathway found that
stomach while preventing reflux of most stomach con- dogs with congenital idiopathic megaesophagus had
tents into the esophagus. Esophageal reflux is prevented normal vagal efferent innervation and decreased
by various contributing factors at the site of the lower esophageal motor function, possibly secondary to al-
esophageal sphincter. These factors include the resting 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-


Small Animal The Compendium March 1997

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


Small Animal The Compendium March 1997

pressures following swallowing. ing cause. Endocrine testing

Manometry is used to evaluate (thyroxine [T4] level, thyroid-
subtle motility abnormalities stimulating hormone [TSH]
that may not be evident on fluo- assay, adrenocorticotropic
roscopy.66 Baseline manometric hormone [ACTH] stimula-
measurements of the esophagus tion); neuromuscular evalua-
for both dogs and cats have been tion (acetylcholine antibody,
evaluated.67,68 antinuclear antibodies [ANA],
Esophageal scintigraphy is a muscle biopsy, creatinine
newer technique that is used in phosphokinase [CPK]); and
humans to quantitatively evalu- toxin screening (lead, botu-
ate esophageal motility. This linum) are done to identify
technique involves the use of a the more common secondary
gamma camera to monitor radio- causes. The diagnosis, howev-
labeled food as it moves through er, is often idiopathic mega-
the esophagus. Transit time of esophagus.5
the food bolus through various Definitive diagnosis of either
regions of interest along the generalized or focal myasthe-
length of the esophagus is deter- nia gravis requires the identi-
mined (Figure 4). Time activity fication of circulating anti-
curves are then plotted to evalu- bodies against acetylcholine
ate the movement of the food receptors. The immunopre-
bolus through the esophagus cipitation radioimmunoassay
(Figures 5 and 6). is very specific and sensitive
Esophageal scintigraphy may for demonstrating circulating
be a more accurate measure of antibodies. This test does not
motility because it evaluates the give false-positive results.
response of the esophagus to a However, false-negative re-
food bolus without the influence sults (less than 5% of cases
of foreign material, such as bari- Figure 3A tested 32) may occur and in-
um or an esophageal catheter.69 dicate either the presence of
Recently, scintigraphy was used autoantibodies against other
to evaluate the effect of meto- components of the motor
clopramide and cisapride on end-plate or the presence of
esophageal motility in normal high-affinity antibodies. Oth-
beagles.68 er diagnostic tests that are
In most cases of megaesopha- available to support a diagno-
gus, manometric and scinti- sis of myasthenia gravis in-
graphic studies are not necessary clude the edrophonium chlo-
for a diagnosis. These tests can ride challenge and repetitive
be used to identify those animals nerve stimulation.
with subtle esophageal motility
abnormalities and consistent MANAGEMENT
clinical signs but with no identi- Management of idiopathic
fiable abnormality on routine Figure 3B megaesophagus, unresolved
radiographic imaging. Both Figure 3—(A) Ventral dorsal and (B) right lateral megaesophagus, or of esoph-
manometry and scintigraphy thoracic radiographs taken after administration of a ageal hypomotility involves
also provide a quantitative mea- barium meal. The entire thoracic portion of the feeding small amounts of
sure of esophageal motility pa- esophagus in this dog is distended, and the esopha- food to an animal in an up-
rameters. gus has displaced the trachea ventrally. A right medi- right position. The ability of
Once megaesophagus has been astinal shift has displaced the heart. An alveolar in- patients with megaesophagus
filtrate is present within the right middle and left
identified, additional testing is to swallow foods of differing
cranial lung lobes.
necessary to identify an underly- consistencies varies. A barium


The Compendium March 1997 Small Animal

contrast study may help in every 4 to 6 weeks and ther-

the decision as to whether apy adjusted accordingly. If
to use liquid, canned, or dry clinical remission occurs, all
food. medications may be discon-
If the patient is difficult tinued; however, the disease
to feed, gastrostomy tubes may recur.73 Esophageal di-
can be placed to facilitate latation has been shown to
feeding. Surgical, percuta- resolve in both dogs and cats
neous endoscopic, and blind after appropriate therapy.45,73
(nonendoscopic) percuta- Various drug therapies
neous techniques for gas- have been used in an at-
trostomy tube placement Figure 4—Esophageal scintigraphic images were obtained 20 tempt to improve esoph-
have been described else- minutes after intravenous injection of pertechnetate, a ra- ageal motility in dogs with
where.b,70–72 dioactive substance. A bolus of food labeled with 99mtech- megaesophagus. Calcium-
Aspiration pneumonia netium was administered orally, and a series of images were channel blockers, such as
should be treated with obtained during esophageal transit of the radiolabeled food. nifedipine, have been used
broad-spectrum antibiotics The image shown here is a summation of the dynamic im- in dogs with suspected acha-
while culture and sensitivity ages; the course through the entire esophagus is shown. lasia or asynchrony of the
results from a transtracheal Pertechnetate localizes in the stomach and thyroid gland, al- lower esophageal sphincter
wash are pending. Identified lowing for visualization of esophageal landmarks. Note the function and esophageal
residual pertechnetate at the injection site on the forelimb.
causes of secondary mega- peristalsis. 74 Response to
The open circles represent regions of interest (see Figure 5)
esophagus should be treated over different areas of the esophagus. nifedipine in dogs, if any, is
promptly and appropriately transient.
to optimize resolution of Metoclopramide is a pro-
esophageal dysfunction. kinetic drug that has been
If the diagnosis of myas- used without success in dogs
thenia gravis is confirmed, with megaesophagus.19 Meto-
treatment should include clopramide may be indicated
the administration of long- in dogs with esophageal hypo-
acting anticholinesterase motility caused by reflux
drugs. Both pyridostigmine esophagitis because it in-
bromide (0.5 to 1.0 mg/kg creases lower esophageal
orally every 8 to 12 hours) sphincter tone.
and neostigmine (0.04 mg/kg Cisapride is another pro-
intramuscularly every 6 hours) kinetic drug that increases
are effective. Because myas- motility of the gastrointesti-
thenia gravis is an immune- nal tract by promoting the
mediated disease, cortico- release of acetylcholine. Ex-
s teroids may be useful; perimentally, cisapride has
Figure 5—An esophageal scintigraphic study of a 10-week-
however, their use is contro- been shown to alter esoph-
old schnauzer. The images above the graph are portions of
versial, and a complete evalu- ageal peristalsis in cats. 75
the dynamic acquisition and were obtained after swallow-
ation of the respiratory tract ing of a radiolabeled food bolus. Note that the food bolus Anecdotal reports indicate
for aspiration pneumonia is remains in the proximal esophagus. The numbers above possible clinical improve-
recommended before using each image represent time in seconds. The graph is a time ment in some dogs with
corticosteroids.73 Treatment activity curve that represents changes in esophageal activity megaesophagus.76
is considered successful if at specified regions of interest (ROI) over time. Normally, Other reports have ques-
clinical signs improve and the time activity curve should show a peak as the radioac- tioned the beneficial effects
the acetylcholine receptor tive bolus passes through the ROI. Note the relatively flat of cisapride or metoclo-
antibody level decreases. appearance of the proximal esophageal time activity curve, pramide in dogs with
This level should be checked which is the result of the lack of movement of the bolus megaesophagus.75 In normal
bSee the article in this issue by
from the proximal esophagus (Prox Esop = proximal esoph- dogs, cisapride decreased or
agus, Thx Inlet = thoracic inlet, Dist Esop = distal esopha-
Dr. Kathryn Michel on guide- gus). slowed the transit rate of a
lines for gastrostomy tubes. food bolus through the


Small Animal The Compendium March 1997

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.

1. Hoenig M, Mahaffey MB, Parnell PG, Styles ME: Mega-
esophagus in two cats. JAVMA 196(5):763, 1990.
2. Diamant N, Szczepanski M: Idiopathic megaesophagus in
the dog: Reasons for spontaneous improvement and a possi-
Figure 6—A follow-up (16 weeks) esophageal scintigraphic ble method of medical therapy. Can Vet J 15:66–71, 1974.
study of the dog shown in Figure 5. The images above the 3. Diamant N, Szczepanski M, Nui H: Manometrtic character-
graph are portions of the dynamic acquisition. Note the istics of idiopathic megaesophagus in the dog: An unsuitable
movement of the radioactive bolus through the esophagus animal model for achalasia in man. Gastroenterology 65:216–
(unlike the lack of movement in Figure 5). The time activity 223, 1973.
4. Strombeck DR, Guilford WG: Diseases of swallowing, in
curve is more normal in appearance, with well-defined peaks Guilford WG, Center SA, Strombeck DR, et al (eds):
as the bolus traverses the esophageal regions of interest Strombeck’s Small Animal Gastroenterology, ed 3. Philadel-
(ROI). The residual activity in the distal esophagus may phia, WB Saunders Co, 1990, pp 216–238.
represent mild esophageal dysfunction. The improvement in 5. Twedt DC: Diseases of the esophagus, in Ettinger SJ, Feld-
esophageal function is probably related to the resolution of man EC (eds): Textbook of Veterinary Internal Medicine, ed
congenital megaesophagus (Prox Esop = proximal esophagus, 4. Philadelphia, WB Saunders Co, 1995, pp 1124–1142.
6. Cox VS, Wallace LJ, Anderson VE, Rushmer RA: Heredi-
Thx Inlet = thoracic inlet, Dist Esop = distal esophagus).
tary esophageal dysfunction in the miniature schnauzer dog.
Am J Vet Res 41(3):326, 1980.
7. Osborne CA, Clifford DH, Jessen C: Hereditary esophageal
esophagus.68 Therefore, cisapride and other current achalasia in dogs. JAVMA 151:572–581, 1967.
prokinetic drugs cannot be recommended to improve 8. Guilford WG: Megaesophagus in the dog and cat. Semin
esophageal motility in a patient with primary mega- Vet Med Surg Small Anim 5(1):37, 1990.
9. Clifford DH, Soifer FK, Wilson CF, et al: Congenital achala-
esophagus. Because it increases the pressure of the low- sia of the esophagus in four cats of common ancestry. JAVMA
er esophageal sphincter, however, cisapride (like meto- 158(9):1554, 1971.
clopramide) may help decrease reflux esophagitis. The 10. Washabau RJ: Pathogenesis of canine megaesophagus: Neu-
result is fewer episodes of regurgitation and subsequent ropathy Proc 14th ACVIM Forum:583–584, 1996.
11. Hudson LC: Histochemical identification of the striated
esophagitis, both of which may exacerbate megaesopha- muscle of the canine esophagus. Anat Histol Embryol 22(2):
gus.8 101–104, 1993.
12. Strombeck DR, Guilford WG: Pharynx and esophagus:
SUMMARY Normal structure and function, in Guilford WG, Center
SA, Strombeck DR, et al (eds): Strombeck’s Small Animal
Megaesophagus can be congenital, secondary to nu- Gastroenterology, ed 3. Philadelphia, WB Saunders Co, 1990,
merous disorders, or idiopathic. Diagnosis of mega- pp 202–210.
esophagus is based on consistent historical and physical 13. Watrous BJ, Suter PF: Normal swallowing in the dog: A cin-
examination findings in conjunction with the results of eradiographic study. Vet Radiol 20:99–109, 1979.
14. Holland CT, Satchell PM, Farrow BRH: Oesophageal com-
imaging techniques. Motility disorders that cannot be pliance in naturally occurring canine megaoesophagus. Aust
identified with traditional radiographic techniques may Vet J 70(11):414–420, 1993.
require manometric and scintigraphic evaluation. Sec- 15. Holland CT, Satchell PM, Farrow BRH: Vagal esophago-
ondary megaesophagus has the best prognosis if the motor nerve function and esophageal motor performance in
dogs with congenital idiopathic megaesophagus. Am J Vet
underlying cause can be determined and effectively Res 57(6):906, 1996.
treated. Treatment of congenital or idiopathic mega- 16. Tan BJ, Diamant NE: Assessment of the neural defect in a
esophagus is at best supportive. dog with idiopathic megaesophagus. Dig Dis Sci 32:76, 1987.


The Compendium March 1997 Small Animal

17. Holland CT, Satchell PM, Farrow BRH: Vagal afferent dys- 42. Pearson H, Gaskell CJ, Gibbs C, Waterman A: Pyloric and
function in naturally occurring canine esophageal motility oesophageal dysfunction in the cat. J Small Anim Pract
disorder. Dig Dis Sci 39(10):2090–2098, 1994. 15:487, 1974.
18. Washabau RJ: Pathogenesis and therapy of canine mega- 43. Bishop LM, Kelly DF, Gibbs C, et al: Megaloesophagus and
esophagus. Proc 10th ACVIM Forum:671–674, 1992. associated gastric heterotopia in the cat. Vet Pathol 16:444–
19. Magne ML: Esophageal motility disorders in the dog. Proc 449, 1979.
4th ACVIM Forum 12(9):9–13, 1986. 44. Gaschen FP, Hoffman EP, Gorospe JR, et al: Dystrophin
20. Boudrieau RJ, Rogers WA: Megaesophagus in the dog: A re- deficiency causes a lethal muscle hypertrophy in cats. J Neurol
view of 50 cases. JAAHA 21:33, 1985. Sci 110(1–2):149–159, 1992.
21. Schrauwen E, Van Ham L, Maenhout T, Desmidt M: Ca- 45. Joseph RJ, Carrillo JM, Lennon VA: Myasthenia gravis in
nine dysautonomia: A case report. Vet Rec 128:524, 1991. the cat. J Vet Intern Med 2(2):75, 1988.
22. Canton DD, Sharp NJH, Aguirre GD: Dysautonomia in a 46. Lindstrom J, Shelton D, Fujii Y: Myasthenia gravis. Adv
cat. JAAHA 192(9):1293, 1988. Immunol 42:233–284, 1987.
23. Cummings JF, DeLahunta A, Mitchell WJ: Ganglioradiculi- 47. Feldman EC, Nelson RW: Hypoadrenocorticism, in Feld-
tis in the dog. Acta Neuropathol 60:29–39, 1983. man EC, Nelson RW (eds): Canine and Feline Endocrinology
24. Duncan ID, Griffith IR: Canine giant axonal neuropathy; and Reproduction. Philadelphia, WB Saunders Co, 1996, pp
Some aspects of its clinical, pathological and comparative 266–306.
features. J Small Anim Pract 22:491–501, 1981. 48. Bartges JW, Nielson DL: Reversible megaesophagus associ-
25. Shell LG, Jortner BS, Leib MS: Spinal muscular atrophy in ated with atypical primary hypoadrenocorticism in a dog.
two Rottweiler littermates. JAVMA 190:878–880, 1987. JAVMA 201(6):889, 1992.
26. Watrous BJ: Esophageal disease, in Ettinger SJ (ed): Text- 49. Jaggy A, Oliver JE, Ferguson DC, et al: Neurological mani-
book of Veterinary Internal Medicine. Philadelphia, WB festations of hypothyroidism: A retrospective study of 29
Saunders Co, 1983, pp 1191–1233. dogs. J Vet Intern Med 8(5):328, 1994.
27. Zook BD, Gilmore CE: Thallium poisoning in dogs. JAVMA 50. Dewey CW, Shelton GD, Bailey CS, et al: Neuromuscular
151:206–217, 1967. dysfunction in five dogs with acquired myasthenia gravis and
28. Zook BC: The pathologic anatomy of lead poisoning in presumptive hypothyroidism. Prog Vet Neurol 6(4):117,
dogs. Vet Pathol 9:310–327, 1972. 1995.
29. Satchell PM: The neuropathic oesophagus. A radiographic 51. Greene R: Thyroid testing: The full circle. Int Symp Canine
and manometric study on the evolution of megaoesophagus Hypothyroid:4–5, August 1996.
in dogs with developing axonal neuropathy. Res Vet Sci 52. Hendricks JC, Maggio-Price L, Dougherty JF: Transient
48:249, 1990. esophageal dysfunction mimicking megaesophagus in three
30. Van Ee RT, Dodd VM, Pope ER, Henry GA: Broncho- dogs. JAVMA 185(1):90, 1984.
esophageal fistula and transient megaesophagus in a dog. 53. Buchanon JW: Symposium: Thoracic surgery on the dog
JAVMA 188(8):874, 1986. and cat. III. Patent ductus arteriosus and persistent right aor-
31. Shelton GD: Canine myasthenia gravis, in Kirk RW, tic arch surgery in dogs. J Small Anim Pract 9:409–428,
Bonagura JD (eds): Current Veterinary Therapy. XI. Philadel- 1968.
phia, WB Saunders Co, 1992, pp 1039–1042. 54. Wheaton LG, Blevine WE, Weirich WE: Persistent right
32. Shelton GD: Pathogenesis of canine megaesophagus: Neuro- aortic arch associated with other vascular anomalies in two
muscular disorders. Proc 14th ACVIM Forum:581–582, cats. JAVMA 184(7):848–851, 1984.
1996. 55. Eyster GE, Probst M: Basic cardiac procedures, in Slatter
33. Shelton GD, Willard MD, Cardinet GH, Lindstrom J: Ac- DH (ed): Textbook of Small Animal Surgery. Philadelphia,
quired myasthenia gravis: Selective involvement of esopha- WB Saunders Co, 1985, pp 1107–1131.
geal, pharyngeal, and facial muscles. J Vet Intern Med 56. Patterson DF: Canine congenital heart disease: Epidemiolo-
4(6):281, 1990. gy and etiological hypothesis. J Small Anim Pract 12:263–
34. Darke PGG, Roberts TA, Smart JL, et al: Suspected bot- 287, 1971.
ulism in foxhounds. Vet Rec 99:98–100, 1976. 57. Van Gundy T: Vascular ring anomalies. Compend Contin
35. Van Ness JJ: Electrophysiological evidence of peripheral Educ Pract Vet 11(1):36–48, 1989.
nerve dysfunction in six dogs with botulism type C. Res Vet 58. Shire PK, Liu W: Persistent right aortic arch in dogs: A
Sci 40:372–376, 1986. longterm follow-up after surgical correction. JAAHA 17:
36. Harris LD, Ashworth WD, Ingelfinger FJ: Esophageal aperi- 773–776, 1981.
stalsis and achalasia produced in dogs by prolonged
59. Komtebedde J, Koblik P, Mattoon J, Moore A: Preoperative
cholinesterase inhibition. J Clin Invest 39:1744–1751, 1960.
and postoperative fluoroscopy in dogs with persistent right
37. Krum SH, Cardinet GH, Anderson BC, et al: Polymyositis
and polyarthritis associated with systemic lupus erythemato- aortic arch. Vet Surg 20:340, 1991.
sus in a dog. JAVMA 170:61–64, 1977. 60. Withrow SJ: Esophageal cancer, in Withrow SJ, MacEwen
38. Walvort HC, VanNess JJ, Stokhof AA, et al: Canine glyco- EG (eds): Small Animal Clinical Oncology, ed 2. Philadel-
gen storage disease type II: A clinical study of four affected phia, WB Saunders Co, 1996, pp 241–243.
Lapland dogs. JAAHA 20:279–286, 1984. 61. Culbertson R, Branam JE, Rosenblatt LS: Esophageal/gastric
39. Kornegay JN, Gorgacz EJ, Dawe DL, et al: Polymyositis in leiomyoma in the laboratory beagle. JAVMA 183:1168–
dogs. JAVMA 176:431–438, 1980. 1171, 1983.
40. Haupt KH, Prieur DJ, Moore MP, et al: Familial canine 62. Hamilton TA, Carpenter JL: Esophageal plasmacytoma in a
dermatomyositis: Clinical, electrodiagnostic, and genetic dog. JAVMA 204:1210–1211, 1994.
studies. Am J Vet Res 46:1861–1869, 1985. 63. Strombeck DR, Troya L: Evaluation of lower motor neuron
41. Marsden PD, Hagstrom JWC: Experimental Trypanosoma function in two dogs with megaesophagus. JAVMA 169(4):
cruzi infection in beagle puppies. Trans R Soc Trop Med Hyg 411, 1976.
62(Abstract):816, 1968. 64. Rogers WA, Fenner WR, Sherding RG: Electromyographic
Small Animal The Compendium March 1997

and esophagomanometric findings in clinically normal dogs 70. Van Sluijs FJ, Happe RP: Surgical disease: The stomach, in
and in dogs with idiopathic megaesophagus. JAVMA 174(2): Slatter DH (ed): Textbook of Small Animal Surgery. Philadel-
181, 1979. phia, WB Saunders Co, 1985, pp 684–717.
65. Strombeck DR, Harrold D: Effects of acepromazine, meper- 71. Bright RM, Burrows CF: Percutaneous endoscopic tube gas-
idine, and xylazine on gastroesophageal sphincter pressure in trostomy in dogs. Am J Vet Res 49:629, 1988.
the dog. Am J Vet Res 46(4):963–965, 1985. 72. Mauterer JV, Abbod SK, Buffington CA, et al: New tech-
66. Maurer AH, Fisher RS: Scintigraphy. Atlas of Gastrointesti- nique and management guidelines for percutaneous nonen-
nal Motility in Health and Disease. Baltimore, Williams & doscopic tube gastrostomy. JAVMA 205:574–579, 1994.
Wilkins, 1993, pp 85–104. 73. Shelton GD: Megaesophagus secondary to acquired myas-
67. Correnti FS, Little AG, Calleja IJ, et al: Manometric evalua- thenia gravis, in Kirk RW, Bonagura JD (eds): Current Vet-
tion of the feline esophagus. J Surg Res 41(3):312–318, erinary Therapy. XI. Philadelphia, WB Saunders Co, 1992,
1986. pp 580–583.
68. Mears EA, Jenkins C, Daniel G, et al: The effect of cisapride 74. Chandra NC, McLeod CG, Hess JL: Nifedipine: A tempo-
and metoclopramide on esophageal motility in normal bea- rizing therapeutic option for the treatment of megaesopha-
gles. Proc 14th ACVIM Forum:738(Abstract), 1996. gus in adult dogs. JAAHA 25:175, 1989.
69. Taillefer R, Jadliwalla M, Pellerin E, et al: Radionuclide 75. Washabau RJ, Hall JA: Cisapride. JAVMA 207(10):1285–
esophageal transit in detection of esophageal motor dysfunc- 1288, 1995.
tion: Comparison with motility studies (manometry). J Nucl 76. Tams TR: Cisapride: Clinical experience with the newest GI
Med 31(12):1921–1926, 1990. prokinetic drug. Proc 12th ACVIM Forum:100–102, 1994.