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Vol. 19, No.

3 March 1997 V Small Animal Gastroenterology

Continuing Education Article


Refereed Peer Review

Canine and Feline


Megaesophagus
FOCAL POINT
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

KEY FACTS
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

ANATOMY ■ ESOPHAGEAL MOTILITY ■ NEURAL PATHWAYS


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 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.

ENDOCRINE DISEASES ■ VASCULAR RING ANOMALY ■ SURGICAL LIGATION


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 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

ESOPHAGEAL SCINTIGRAPHY ■ DIAGNOSTIC TESTS ■ MYASTHENIA GRAVIS DIAGNOSIS


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

FEEDING ■ DRUG THERAPY ■ METOCLOPRAMIDE ■ CISAPRIDE


Small Animal 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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