3 CE Credits

Megaesophagus
Sacha Mace, BA, DVM, DACVIM (Small Animal Internal Medicine)
Veterinary Specialty Center of the Hudson Valley

G. Diane Shelton, DVM, PhD, DACVIM (Internal Medicine)

University of California, San Diego

Susan Eddlestone, DVM, DACVIM (Small Animal Internal Medicine)*

Louisiana State University

Abstract: Megaesophagus is a disorder of the esophagus characterized by diffuse dilation and decreased peristalsis. It is classified into
congenital and acquired forms. Gastrointestinal, endocrine, immune-mediated, neuromuscular, paraneoplastic, and toxic disorders
have been associated with acquired megaesophagus. Common clinical signs of megaesophagus are regurgitation, weight loss, coughing,
and halitosis. Most cases of megaesophagus can be diagnosed using thoracic radiography; however, diagnosing the underlying cause
requires a thorough history and additional diagnostics. The treatment, management, and prognosis of megaesophagus vary greatly
depending on the underlying cause.

M
egaesophagus is defined as a disorder of the esophagus In these cases, acquired megaesophagus should be suspected.1
characterized by diffuse esophageal dilation and decreased Other concerns owners may report are weight loss, coughing, and
peristalsis.1 It may be congenital or acquired1; acquired halitosis. Weight loss due to megaesophagus results from regurgitant
megaesophagus is subclassified into idiopathic and secondary forms. loss of caloric intake.1 Coughing occurs with aspiration pneumonia,
Congenital and idiopathic acquired megaesophagus disorders are and halitosis is a sequela of chronic retention and regurgitation
suspected to be due to a combination of neurologic dysfunction of ingesta.
within the afferent arm of the swallowing reflex, altered esophageal
viscoelastic properties, and poor vagal responsiveness to intralu- Signalment
minal esophageal distention.1,2 Secondary acquired megaesophagus Congenital megaesophagus is documented in Newfoundlands,
can be caused by any disease that inhibits esophageal peristalsis Parson Russell terriers, Samoyeds, springer spaniels, smooth fox
by disrupting central, efferent, or afferent nerve pathways or by terriers, and shar-peis.1,2 These dogs typically present at the time of
any disease of the esophageal musculature, including immune- weaning with signs of regurgitation.1 Smooth fox terriers that have
mediated, infectious, and preneoplastic etiologies.3 megaesophagus secondary to congenital myasthenia gravis (MG)
present between 4 and 9 weeks of age.4 Irish setters, Great Danes,
Clinical Signs German shepherds, Labrador retrievers, miniature schnauzers,
In uncomplicated cases of megaesophagus, patients may present and Newfoundlands have an increased prevalence for acquired
with only regurgitation and weight loss. Other patients may present megaesophagus.1,2,5 Dogs with acquired megaesophagus present
with additional clinical signs that hint at the underlying cause of from 7 to 15 years of age.1 In Newfoundlands, acquired mega-
megaesophagus.1 The most common complication of megaesoph- esophagus and MG occur at a much younger age (≤2 years).
agus is aspiration pneumonia; often, these patients present with a These dogs do not have a history of congenital megaesophagus.6
moist cough, dyspnea, or fever.1 Congenital and acquired megaesophagus have been documented
in cats, with a familial disposition for the congenital form in the
History Siamese breed.1
The index of suspicion for megaesophagus should be high when
a patient presents for regurgitation. Regurgitation that occurs in Congenital Megaesophagus
a young patient at the time of weaning and conversion to solid The suspected etiology for congenital megaesophagus is esophageal
food is likely due to congenital megaesophagus. In older patients, hypomotility.7 In some patients, this hypomotility is due to delayed
the frequency of regurgitation and timing may be more variable. maturation of esophageal function that may or may not improve
*Dr. Eddlestone discloses that she has received financial benefits from Bayer Animal Health and IDEXX, Inc. with age.7 Congenital MG is an inherited autosomal recessive

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 Megaesophagus

condition in Parson Russell terriers, springer spaniels, and smooth rickettsial, spirochetal, and
fox terriers that results in a deficiency or functional abnormality of fungal infections can be as- Key Points
acetylcholine receptors (AChRs) at the neuromuscular junction.8 sociated with myositis. Pre-
The long-term prognosis for congenital MG is poor because of neoplastic syndromes differ t
Incidental esophageal dilation
the mechanism of the condition, lack of a specific treatment, and from paraneoplastic syn- is associated with excitement,
high complication rate of aspiration pneumonia. Congenital MG dromes in timing. Preneo- aerophagia, general anesthesia,
patients usually present with generalized weakness in addition to plastic syndromes occur and vomiting.
megaesophagus. Congenital MG patients generally succumb with occult cancer. Preneo- t
Measurement of acetylcholine
within 1 year; however, there are reports of some cats and Parson plastic syndromes that can receptor antibody titer is not a
Russell terriers that have survived for several years.8 cause myositis include bron- diagnostic tool for congenital MG.
chogenic carcinoma, lym-
Acquired Megaesophagus phoma, myeloid leukemia, t
The best food consistency to
The etiology for acquired idiopathic megaesophagus is unknown. and tonsillar carcinoma.14 minimize regurgitation varies
The current theory is that a defect in the afferent neural pathway Megaesophagus associ- with each patient.
causes reduced responsiveness to esophageal distention.1 ated with distemper is due
The diffuse neuromuscular dysfunction of acquired secondary to demyelination.19 Neuro-
megaesophagus can be caused by a variety of neuromuscular, logic signs can develop 1 to 3 weeks or even months after initial
immune-mediated, endocrine, gastrointestinal, paraneoplastic, recovery. The nerve damage is due to an inflammatory response
and toxic diseases.1,2,9–12 to the viral antigens in neurons and glial cells.20 This results in
gray matter damage and demyelination.20 Dogs with clinical signs
Neuromuscular and Immune-Mediated Causes of nasal and footpad hyperkeratosis are more likely to develop
The most common neuromuscular disorders associated with mega- central nervous system disease.21
esophagus include MG and generalized inflammatory myopathies Generalized tetanus is known to cause esophageal dysfunction
such as polymyositis and those associated with infectious diseases.13,14 in dogs and humans.22 Classic clinical signs in dogs include a stiff
Less common neuromuscular disorders associated with mega- gait, an outstretched or dorsally curved tail, the “joker’s smile”
esophagus include myopathies such as muscular dystrophies, (erect ears, drawn-back lips, wrinkled forehead), protrusion of
dysautonomia, storage diseases, and neurogenic muscular atro- the third eyelids, enophthalmos, trismus, increased salivation,
phy.13,14 Because the canine esophagus is composed predominantly and a strong response to stimuli.22
of striated muscle, any neuromuscular disease that affects limb Although dysautonomia is rare, megaesophagus is a common
muscles can affect the esophagus.8 finding in these patients.23 Dysautonomia is an idiopathic autonomic
Of all acquired megaesophagus cases, approximately 25% are nerve disorder of cats and dogs that is suspected to be immune
secondary to MG.1 Acquired MG is a disorder of neuromuscular mediated. All ganglia and sympathetic and parasympathetic
transmission due to immune-mediated destruction of postsynaptic nerves are affected, with neuronal cell body damage and axonal
AChRs in skeletal muscle by AChR antibodies.2 Acquired MG degeneration.24 Within 1 to 7 days, patients experience a fulminant
can present in focal, generalized, and acute fulminating forms.8 loss of autonomic nervous system function, followed by constipation,
Focal MG can present with various degrees of esophageal, facial, dry mucous membranes, pupillary dilation, prolapsed nictitating
laryngeal, or pharyngeal dysfunction.8 Ninety percent of dogs membranes, diminished pupillary light response, bradycardia,
with generalized MG have megaesophagus.8 Although acquired areflexic anus, and bladder atony.23
MG can affect dogs of any age older than a couple of months, most Glycogen storage diseases (GSDs) are inborn errors of glycogen
affected dogs are between 2 and 3 years of age or older than 9 metabolism.25 Of the eight human GSD types, small animal
years.15 Acquired MG occurs most often in German shepherds and equivalents have been published for GSD I A (glucose-6-phos-
golden retrievers.3 Akitas and Scottish terriers have an increased phatase deficiency), GSD II (α-glucosidase deficiency), GSD III
relative risk for MG.16 Familial and breed-associated forms have (debrancher enzyme amylo-1,6-glucosidase deficiency), GSD IV
been described in Newfoundlands and Great Danes.6,17 Affected (branching enzyme α–1,4-D-glucan), and GSD VII (phospho-
feline breeds include the Abyssinian, Somali, and Siamese.1,18 fructokinase deficiency).26 Only GSD II, which is documented in
Approximately 14% of dogs with diagnosed generalized inflam- Swedish Lapland dogs, has been associated with megaesophagus.25
matory myopathies present with megaesophagus.14 Patients A clinical presentation of megaesophagus associated with gait
presenting with generalized weakness, stiff gait, dysphagia, or diffuse abnormalities and laryngeal paralysis is suggestive of laryngeal
muscle atrophy may have myositis.14 Serum creatine kinase (CK) paralysis–polyneuropathy complex (LP-PNC).13 Megaesophagus
activities may or may not be elevated, so a normal CK activity does is documented in most dogs that are affected with LP-PNC,
not rule out myositis. Generalized inflammatory myopathy is a which is due to neurogenic muscular atrophy.13 The intrinsic
comprehensive term used to group causes of diffuse myositis. laryngeal and appendicular skeletal muscles are affected. LP-PNC
Generalized inflammatory myopathies can have immune-mediated is documented in Dalmatians, Leonbergers, Pyrenean mountain
(polymyositis), infectious, or preneoplastic etiologies.14 Protozoal, dogs, and rottweilers.13 Puppies usually present between 2 and 6

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 Megaesophagus

Esophageal obstructions can be caused by esophageal foreign

bodies, neoplasia, strictures, or vascular ring anomalies. Foreign
bodies can cause a partial or complete mechanical obstruction.
Peristaltic spasms over the retained foreign object cause tissue
edema and mucosal abrasions. Although possible in any small
dog, there seems to be a higher incidence of esophageal foreign
bodies in young terriers. Because these terriers are young, this
may be a condition of delayed esophageal maturation.7
Foreign bodies or chronic gastroesophageal reflux (GER) can
cause esophageal strictures, which occur secondary to mucosal
healing attempts.32,33 Esophageal damage that penetrates the sub-
mucosa and muscularis layers causes inflammation resulting in
collagen deposition and fibrous connective tissue stricture.32,33
Extraluminal esophageal obstruction is most commonly associ-
ated with vascular anomalies. In 95% of patients with secondary
megaesophagus due to a vascular ring anomaly, the cause is a
Figure 1. Radiographic appearance of a dilated esophagus (lateral abdominal view; persistent right aortic arch.34 Other vascular anomalies associated
arrows). Megaesophagus was an incidental finding. This patient was diagnosed with secondary megaesophagus include persistent right or left
with esophagitis associated with chronic inflammatory bowel disease and subclavian arteries, double aortic arch, persistent right dorsal aorta,
gastrointestinal reflux. Courtesy of Dr. J. Kramer, Huntington Animal Hospital,
left aortic arch, right ligamentum arteriosum, aberrant intercostal
Huntington Station, NY.
arteries, and persistent left cranial vena cava.34,35
Dogs with chronic or recurrent gastric dilatation with or
months of age13; however, in Leonbergers, onset is delayed to 1 to without volvulus have an increased risk of developing mega-
9 years of age.13 A demyelinating polyneuropathy has been reported esophagus.28 In these dogs, megaesophagus is due to decreased
in a family of miniature schnauzer dogs presenting with predom- lower esophageal sphincter (LES) tone caused by a combination
inantly respiratory dysfunction associated with laryngeal paralysis of esophagitis from chronic GER or vomiting; chronic intermittent
and esophageal dilatation.27 obstruction of the LES; increased intragastric and intraabdominal
pressures; and delayed gastric emptying.7,28
Endocrine Causes In patients with hiatal hernia, the esophagus is essentially
Hypoadrenocorticism and hypothyroidism are associated with obstructed. Four types of hiatal hernias have been described in
reversible megaesophagus. Patients with hypoadrenocorticism may humans.10 Two of these types are applicable to animals. Type I is
have megaesophagus due to electrolyte imbalances and a cortisol the “sliding” hernia, defined as intermittent cranial displacement
deficiency. Electrolyte imbalances cause altered membrane poten- of the abdominal esophagus, LES, and gastric cardia through the
tials, which results in decreased neuromuscular function. In hiatus.10 Type II is the paraesophageal hernia, in which the gastro-
addition, muscle weakness is a consequence of deficient cortisol.28 esophageal junction remains in its normal anatomic position;
The association between megaesophagus and hypothyroidism however, the stomach and abdominal organs enter the caudal
has yet to be understood. Hypothyroidism is prevalent in some mediastinum through a defect adjacent to the esophageal hiatus.10
breeds that are predisposed to megaesophagus and laryngeal
paralysis.1,29,30 Megaesophagus occurs in 3% of hypothyroid dogs.29 Paraneoplastic Causes
Resolution of megaesophagus once the thyroid is regulated has According to one study, megaesophagus was present in 40% of
been reported.31 Aspiration pneumonia may cause a sick euthyroid dogs with thymoma.36 The incidence of thymoma in dogs with MG
syndrome that may be misdiagnosed as hypothyroidism.29 is 3%; in cats with MG, the incidence is 26%.16,18 In humans, thy-
momas have increased production of CD4+CD8+ T cells and lack
Gastrointestinal Causes antigen-presenting cells that function for negative selection. This
Gastrointestinal disorders associated with acquired megaesophagus combination results in autoimmune disease.37 The prognosis for
include esophagitis, esophageal obstruction, gastric dilatation– nonresectable thymoma in a dog with MG and megaesophagus is
volvulus, and hiatal hernia. In cats, acquired secondary mega- poor. However, complete thymic resection can result in resolution
esophagus is due to pyloric dysfunction.1 of megaesophagus and a decrease in AChR antibody titer.8,38
Esophagitis is a common finding associated with megaesoph-
agus.1 It may or may not precede megaesophagus. In patients with Toxic Causes
esophagitis, secondary megaesophagus develops due to chemical Toxic substances that can cause megaesophagus include lead,
or obstructive irritation. Gastric reflux contains gastric acid, pepsin, organophosphates, and snake venom.3,28 Low-level lead exposure
bile salts, and trypsin, all of which cause esophageal inflammation causes severe abdominal pain, vomiting, diarrhea, and mega-
and ultimately decrease esophageal motility7 (FIGURE 1). esophagus.39 Lead intoxication can occur from ingestion of batteries,

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 Megaesophagus

Figure 3. Endoscopic appearance of the esophagus following endoscopic retrieval of

a rawhide that had been lodged in the distal esophagus. Note the severe multifocal
Figure 2. Radiographic appearance of a dilated esophagus (arrows). Note the mucosal abrasions. The patient (a terrier) was treated with liquid sucralfate and
radiopaque walls of the esophagus and luminal dilation with air on both sides of broad-spectrum antibiotics. Fortunately, follow-up endoscopy revealed that no
the diaphragmatic silhouette. stricture developed.

fishing line weights, lead-based paint, linoleum, and plumbing or mechanical obstruction. Barium accumulates within the distended
solder supplies. Organophosphate toxicosis should be suspected esophagus. Focal narrowing of the esophagus at the cardiac base is
if a patient presents with concurrent weakness and cerebellar suggestive of a vascular ring anomaly.1,34 However, the diagnostic
signs.40 Organophosphates exist in flea collars and insecticides. benefit of a contrast study should be weighed against the potential
They irreversibly bind to acetylcholinesterase, causing a cholinergic for aspiration of contrast agent.
crisis (salivation, lacrimation, urination, defecation). Australian Fluoroscopy evaluates pharyngeal motility and the presence
tiger snake envenomation causes a rapidly progressing myopathy and intensity of esophageal peristalsis. However, this diagnostic
of skeletal muscle.3 If not lethal, Australian tiger snake envenom- modality is not essential for diagnosis of megaesophagus and
ation has a 75% recovery rate for normal esophageal function.3 may not be readily available. It can be helpful in cases of MG or
esophagitis. MG can selectively affect only the pharyngeal and
Diagnosis esophageal musculature without more overt clinical signs. Also, in
Diagnostic Imaging cases of mild esophagitis, fluoroscopy may be of greater diagnostic
Thoracic radiography is diagnostic for most cases of megaesoph- value than a contrast esophagram in detecting hypomotility.
agus.1,3 Common findings include a prominent, dilated esophagus Esophagoscopy is rarely indicated for a diagnosis of mega-
that can be filled with air or ingesta2 (FIGURE 2). The degree of esophagus, but it can be helpful for suspected cases of obstructive
esophageal dilation has no diagnostic value in determining the disease or reflux esophagitis34 (FIGURE 3). Esophagoscopy may
etiology.2 Underlying causes of megaesophagus that may be revealed identify an esophageal stricture due to a vascular ring anomaly,
by radiography include neoplasia, foreign body, vascular ring but it cannot differentiate the type of vascular ring anomaly.34
anomaly, gastric dilatation–volvulus, and hiatal hernia. Normal
midline tracheal location does not exclude a vascular ring anomaly; Laboratory Testing
however, focal leftward deviation of the trachea near the cranial A complete blood count (CBC), serum chemistry panel that includes
border of the heart on a dorsoventral or ventrodorsal view is a CK activity, and urinalysis should be performed for all regurgi-
reliable sign of persistent right aortic arch in young dogs that tating patients and those in which megaesophagus is suspected.
regurgitate after eating solid food.34,35 Radiographic findings of In addition, an AChR antibody titer test should be performed in
megaesophagus with concurrent aspiration pneumonia or a dis- all cases of acquired megaesophagus. AChR antibody testing is
tended stomach, small bowel, or urinary bladder should raise performed by the Comparative Neuromuscular Laboratory in
suspicion for dysautonomia.23 Incidental esophageal dilation does the School of Medicine at the University of California, San Diego.
occur and is associated with excitement, aerophagia, general Information regarding sample submission can be obtained
anesthesia, and vomiting.2 at http://vetneuromuscular.ucsd.edu/. Corticosteroid therapy at
If thoracic radiographic findings of megaesophagus are ques- immunosuppressive dosages for longer than 7 to 10 days lowers
tionable, a barium contrast esophagram can confirm dilation and AChR antibody levels, so a pre-corticosteroid serum sample is

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 Megaesophagus

recommended.41 Addition- hormone, and low free T4 levels confirm the diagnosis of hypo-
al diagnostics are per- thyroidism.44
formed based on the his- Dogs with typical or atypical hypoadrenocorticism can present
tory, physical examination, with megaesophagus. Hyperkalemia and hyponatremia are sug-
and preliminary laboratory gestive of typical hypoadrenocorticism. A low sodium:potassium
findings.1 The diagnostic ratio is not definitive for hypoadrenocorticism, even with studies
objective is to determine that found a sodium:potassium ratio <15 to be more diagnostic
whether the megaesophagus for hypoadrenocorticism than a ratio of 27:1.45 Typical and atypical
is associated with a poten- hypoadrenocorticism are diagnosed with an ACTH stimulation
tially treatable disorder. For test.45
example, MG, hypothy- Nucleated erythrocytes without anemia or basophilic stippling
roidism, hypoadrenocorti- of red blood cells is suggestive of lead poisoning. These abnormalities
cism, polymyositis, and lead are caused by transportation of lead to bone marrow.46 Serum
poisoning all have specific blood lead tests are commercially available.
treatments, whereas treat- Organophosphate toxicosis can be excluded by measuring
ment for idiopathic mega- cholinesterase in a whole blood sample. A cholinesterase activity
esophagus is limited to sup- less than 25% to 50% of normal is suggestive of organophosphate
portive and symptomatic toxicosis.47
Figure 4. This specially made feeding chair was management. Additional diagnostic tests may include antibody titers for
designed by an owner of a megaesophagus Although CBC, chem- Toxoplasma gondii, Neospora caninum, Borrelia burgdorferi, Ehrlichia
patient. The chair aids in feeding and in istry panel, and urinalysis canis, and Rickettsia rickettsii; electromyography; measurement of
maintaining a postprandial upright position.
results do not provide de- nerve conduction velocity; and muscle and nerve biopsies to exclude
finitive information regard- myopathic and neuropathic disorders. Atropine, histamine, or pilo-
ing MG, they may exclude other causes of muscle weakness or carpine tests can be performed to exclude dysautonomia.1,2,9,13,14,23,48
help identify a concurrent disease.15 Elevated serum CK activity Atropine is administered IV (0.02 mg/kg) or SC (0.04 mg/kg);
occurs with muscle damage associated with some myopathies lack of an increase in heart rate is supportive of dysautonomia.23
(inflammatory, necrotizing, and dystrophic) and muscle trauma When the intradermal histamine test (0.01375 mg per dog) is
and may be mildly elevated in patients in extended recumbency or used, absence of a wheal and flare within 15 minutes is supportive
after intramuscular injections.42 Definitive diagnosis of acquired of dysautonomia.23 The histamine test has limited value in cats, as
MG requires an AChR antibody titer test.8 However, this test is there is no significant difference in the histamine response between
not useful in diagnosing congenital MG, which is a result of dysautonomic and control cats.24 If miosis does not occur after
structural or functional AChR abnormalities and not immune- topical ophthalmic administration of pilocarpine 0.1%, a presump-
mediated damage. Therefore, congenitally affected dogs and cats tive diagnosis of dysautonomia can be made.23
do not have measurable circulating AChR antibodies.2,8 In the
future, diagnosis of congenital MG will depend on mutational Treatment
analysis of candidate genes. Treatment for idiopathic megaesophagus is largely supportive
Edrophonium chloride, a short-acting acetylcholinesterase and symptomatic with periodic rechecks. Thoracic radiography
drug, can be administered to support a presumptive diagnosis of is advised to monitor progress of esophageal dilation and aspiration
congenital or acquired MG.8 Before administration of the edro- pneumonia. Treatment for acquired secondary megaesophagus
phonium, the patient is exercised until fatigued. The appearance depends on managing the underlying specific disease process in
of MG fatigue can include weakness, stiff gait, collapse, inspiratory addition to providing supportive and symptomatic care. Medications
stridor, or a reduced palpebral reflex.43 After fatigue is induced, should be in liquid (not pill) form to enhance movement to the
edrophonium is administered IV (0.1 to 0.2 mg/kg).8 A positive stomach and avoid accumulation within the esophagus, which
response is characterized by improved muscle strength. This can lead to esophageal irritation and nontherapeutic medication
commonly occurs within 30 seconds of the edrophonium injection, levels. If accumulated medication passes into the stomach, over-
and weakness returns within 5 minutes. Temporary improve- dose may occur.
ment of generalized muscle weakness is suggestive of, but not
definitive for, MG.8 The degree of megaesophagus is not affected Supportive and Symptomatic Care
by this test; however, improvement in motility may be observed Nutrition
if evaluated by fluoroscopy after administration of contrast agent. Nutritional needs must be met and regurgitation minimized.
Hypercholesterolemia, hypertriglyceridemia, and hyponatremia This can be accomplished by frequent feeding of small, high-calorie
with or without the presence of a normochromic, normocytic, meals with the patient in a cranially elevated position (FIGURE 4).
nonregenerative anemia is suggestive of hypothyroidism.44 In This position uses gravity to help move the ingesta to the stomach.1
most cases, low total T4, elevated canine thyroid stimulating The optimal food consistency to minimize regurgitation varies

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 Megaesophagus

with each patient, so experimentation is encouraged.1 The use of remission in the absence of immunosuppression.54 Before immuno-
enteral feeding may be needed in weak patients or in patients in suppressive therapy is used, pneumonia or any other infectious
which regurgitation cannot be controlled by other methods.8 In disease should be completely resolved.
these cases, a gastrotomy tube should be placed.15 In our clinical
experience, a percutaneous endoscopic gastrostomy tube or low- Prognosis
profile gastrotomy tube is effective. Nasoesophageal or esophageal The prognosis for megaesophagus varies with the underlying
tubes are not advised because they increase regurgitant volume, etiology and presence of secondary complications. Aspiration
raising the risk of aspiration pneumonia. pneumonia, dehydration, and malnutrition can significantly
worsen the prognosis. Congenital megaesophagus has a guarded
Treatment of Secondary Complications to poor prognosis; however, there is potential for improvement
Aspiration pneumonia and esophagitis are the most common of esophageal motility with maturity up to 1 year of age.7,10 The
complications of megaesophagus.1 For aspiration pneumonia, prognosis for congenital MG is poor due to the mechanism of
administration of a broad-spectrum antibiotic is advised.8 Culture the condition, lack of a specific treatment, and high complication
and sensitivity testing of a transtracheal wash or bronchoalveolar rate of aspiration pneumonia. Acquired idiopathic megaesophagus
lavage sample can be helpful in choosing an antibiotic; however, in general has a guarded to poor prognosis due to the common
the risk of obtaining the sample should be considered. occurrence of aspiration pneumonia and malnutrition. Morbidity
Esophagitis can result in esophageal stricture within 1 to 3 weeks; and mortality depend on the degree and nature of the underlying
therefore, eliminating further mucosal damage and allowing the disease and client compliance.1 In the absence of severe aspira-
mucosa to heal are important considerations.33 Liquid sucralfate tion pneumonia or thymoma, the success rate for acquired MG
is advised because it binds to eroded mucosa, allowing it to can be good with early diagnosis and appropriate management.53
heal.1,33 For megaesophagus secondary to esophagitis, addressing Spontaneous remission of acquired MG with resolution of mega-
the underlying cause of GER is the key to improvement. Antacids esophagus can also occur within an average of 6 months.54 How-
(e.g., calcium carbonate), H2-blockers, and proton-pump inhibitors ever, many myasthenic dogs die of aspiration pneumonia during
are all used to lower gastric acidity and may prevent esophagitis the first month after diagnosis, so the overall prognosis is still
due to GER.33 guarded. With the exception of the acute fulminating form of
Promotility drugs (e.g., metoclopramide, cisapride) have no myasthenia,55 there is no association between the severity of MG
current documented benefit in managing canine megaesophagus and the possibility of remission.54
but may have a role in managing feline megaesophagus. This is In one study, 39% of dogs with immune-mediated polymyositis
due to the differences in feline and canine anatomy and the had clinical improvement of their megaesophagus with continued
mechanism of action of these drugs. Metoclopramide and cisapride medical management.14 However, early diagnosis and initiation
act on smooth muscle. They have no effect on striated muscle. of appropriate therapy are key to a good clinical outcome. Evaluation
The canine esophagus has striated muscle its entire length.1,33 Cats of muscle biopsy samples early in the course of the disease to establish
have smooth muscle within the distal esophagus, so cisapride may a diagnosis is critical. The prognosis for pre- and paraneoplastic
improve lower esophageal smooth muscle motility in cats.33,49 myositis is poor due to the underlying cancer.14 Dysautonomia is
Metoclopramide and cisapride are not advised in canine mega- progressive, with a survival rate of <25% in cats over 18 months.24
esophagus patients because these drugs increase the LES tone, Prognostic indicators include showing response to therapy (e.g.,
which slows esophageal emptying and contributes to further maintenance of body weight with oral feedings, fecal and urinary
regurgitation.42,49–52 Bethanecol may be a better option for dogs as continence) within 7 to 10 days.24
it is documented to stimulate esophageal propagating contractions
in skeletal muscle by stimulating cholinergic receptors.1 Conclusion
Megaesophagus is common in dogs and less common in cats.
Acquired Secondary Megaesophagus Regurgitation is the most common clinical sign of megaesophagus
Treatment for acquired secondary megaesophagus is based on a
at presentation. Diagnosis of megaesophagus is made radio-
definitive diagnosis. For example, the cornerstone of treatment
graphically, and the primary cause should be evaluated with
for this form of MG is anticholinesterase drugs.8 If an animal is
appropriate diagnostic testing. Idiopathic megaesophagus is a
confirmed by positive AChR antibody titer as having MG and
diagnosis of exclusion. Management of megaesophagus is supportive
pyridostigmine alone does not control the clinical signs, then
unless an underlying cause is identified. The prognosis for mega-
other agents are indicated. These can include either low-dose
esophagus depends on the presence of aspiration pneumonia
prednisone (not an immunosuppressive dosage, which can worsen
and the underlying condition.
the weakness) or immunosuppressants such as azathioprine, myco-
phenolate mofetil, or cyclosporine.53 Although anticholinesterase
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 Megaesophagus

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1. _________ is not a clinical sign of megaesophagus. 6. Which statement regarding MG is true?

a. Regurgitation a. All dogs with generalized MG have megaesophagus.
b. Halitosis b. Acquired MG occurs more often in German shepherds
c. Weight gain and golden retrievers than in other canine breeds.

d. Coughing c. Definitive diagnosis of congenital MG requires an AChR

antibody test.
2. Which condition is matched with the wrong clinical signs? d. Dogs with acquired MG do not have measurable circulating
a. congenital megaesophagus: regurgitation at time of weaning anti-AChR antibodies.
b. pneumonia: moist cough, dyspnea, and fever
7. Which CBC/serum chemistry result is not correctly matched
c. myositis: generalized weakness, stiff gait, and dysphagia with an appropriate etiology?
d. organophosphate toxicosis: stiff gait, erect ears, and a. hypercholesterolemia and hyponatremia: hypothyroidism
strong response to stimuli
b. hyperkalemia and hyponatremia: hyperadrenocorticism
3. In which breed is congenital megaesophagus not commonly c. normochromic, normocytic, nonregenerative anemia:
documented? hypothyroidism
a. Parson Russell terrier d. nucleated erythrocytes without anemia: lead poisoning
b. Malinois
8. Which therapy is not recommended as supportive care for
c. Newfoundland megaesophagus?
d. Samoyed a. enteral feeding with an esophageal tube

4. Which statement regarding feline megaesophagus is false? b. broad-spectrum antibiotics

a. Congenital and acquired megaesophagus occur in cats. c. liquid sucralfate

b. Abyssinian, Somali, and Siamese cats may have a familial d. antacids and H2 blockers
predisposition for megaesophagus.
9. Which statement is true regarding medication administration
c. In cats, acquired secondary megaesophagus is not due for a patient with diagnosed megaesophagus?
to pyloric dysfunction.
a. Formulation (liquid or pill) does not matter.
d. Metoclopramide may have a role in managing feline
b. Pills cannot result in subtherapeutic medication levels.
megaesophagus.
c. Pills cannot result in overdose.
5. Which statement is true regarding diagnosing d. Pills can lead to esophageal irritation.
megaesophagus?
a. Thoracic radiography is diagnostic for most cases of 10. Which statement regarding megaesophagus prognosis is true?
megaesophagus. a. The prognosis for congenital MG is good.
b. Radiography is never useful in revealing underlying b. Aspiration pneumonia contributes to a poor prognosis.
causes of megaesophagus. c. Malnutrition does not contribute to the prognosis.
c. Normal midline tracheal location excludes a vascular d. Congenital idiopathic megaesophagus has a good prognosis.
ring anomaly.
d. Incidental esophageal dilation does not occur.

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