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Veterinary Voice, September 2012 – Megaesophagus: Etiologies are Immeasurable – It’s not always MG

Jan 06, 2013


September 2012, Issue 47

AMVS Event Updates!

  September was a great month for Aspen Meadow Veterinary
Specialists. The Homeward Bound Harvest had a great turn out and raised a
whopping $113,000 dollars for the Longmont Humane Society. The Longmont
Artwalk was great as well, despite the darkness there was a great turn
out and the kids especially enjoyed the glow sticks! It's great to have
the opportunity to catchup with our local patients and their parents.


Upcoming Events!

On Saturday, October 20th, AMVS will
be sponsoring Wildlands Restoration Volunteers (WRV) in the aid of the
St. Vrain Lafarge project. Volunteers will spend the day removing
invasive Russian Olive Trees, creating fish habitat reef structures and
planting 400 to 500 native Riparian Trees.


Upcoming CE's

Animal Emergency and Critical Care is offering the first of many planned CE opportunities:

This lecture will cover how to treat some common and not so common
toxicities. The lecture will focus on 4 primary toxins, albuterol,
marijuana, xylitol, and baclofen. Following the lecture, there will be a
one hour question and answer session with the doctors. There will be 3
additional lecturers present, each one with further information on one
of these toxins. Doctors will be set up in stations and attendees will
be able to ask each of these doctors further questions on their specific

Hosted by

Animal Emergency and Critical Care

104 South Main Street

Longmont, CO 80501


Close Encounters: Emergency Toxicities


Dana Dietrich, DVM (Primary Speaker)

Date and Time

Thursday, October 25, 2012

6:30pm Registration, Appetizers, and Drinks

7:00-8:00pm Lecture

8:00-9:00 Question and Answer Portion


Front Range Community College- Community Room

2121 Miller Drive

Longmont, CO 80501



Megaesophagus: Etiologies are Immeasurable - It's not always MG

By: Sacha Mace, DVM Internal Medicine Specialist

Practice Points:

  • Regurgitation is the most common clinical sign of megaesophagus at presentation
  • Megaesophagus is common in dogs and less common in cats
  • Diagnosis of megaesophagus is made radiographically, and the primary
    cause should be evaluated with appropriate diagnostic testing
  • Management of megaesophagus is supportive unless an underlying cause is identified
  • The prognosis for megaesophagus depends on the presence of aspiration pneumonia and the underlying condition

Some Etiologies for Megaesophagus:

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

Acquired megaesophagus is sub classified into idiopathic and secondary
forms. Congenital and idiopathic acquired megaesophagus disorders are
suspected to be due to a combination of neurologic dysfunction.
Secondary acquired megaesophagus can be caused by any disease that
inhibits esophageal peristalsis by disrupting central, efferent, or
afferent nerve pathways or by any disease of the esophageal musculature,
including immune-mediated, infectious, and preneoplastic etiologies.

Congenital megaesophagus is documented in Newfoundlands, Parson Russell
terriers, Samoyeds, Springer spaniels, smooth fox terriers, and
Shar-Peis. These dogs typically present at the time of weaning with
signs of regurgitation. Irish setters, Great Danes, German shepherds,
Labrador retrievers, miniature schnauzers, and Newfoundlands have an
increased prevalence for acquired megaesophagus. Dogs with acquired
megaesophagus present from 7 to 15 years of age. In Newfoundlands,
acquired megaesophagus and MG occur at a much younger age (≤2 years),
and these dogs do not have a history of congenital megaesophagus.

Congenital and acquired megaesophagus has been documented in cats, with
a familial disposition for the congenital form in the Siamese breed.

The suspected etiology for congenital megaesophagus is esophageal
hypomotility. In some patients, this hypomotility is due to delayed
maturation of esophageal function that may or may not improve with age.
Congenital MG is an inherited autosomal recessive condition in Parson
Russell terriers, Springer spaniels, and smooth fox terriers that
results in a deficiency or functional abnormality of acetylcholine
receptors (AChRs) at the neuromuscular junction. The long-term prognosis
for congenital MG is poor and patients generally succumb within 1 year.
Congenital MG patients usually present with generalized weakness in
addition to megaesophagus.

The etiology for acquired idiopathic megaesophagus is unknown. The
diffuse neuromuscular dysfunction of acquired secondary megaesophagus
can be caused by a variety of neuromuscular, immune-mediated, endocrine,
gastrointestinal, paraneoplastic, and toxic diseases. The most common
neuromuscular disorders associated with megaesophagus include MG and
generalized inflammatory myopathies such as polymyositis and those
associated with infectious diseases (Protozoal, rickettsial,
spirochetal, fungal, Distemper, Tetanus infections). Less common
neuromuscular disorders associated with megaesophagus include myopathies
such as muscular dystrophies, dysautonomia, storage diseases, and
neurogenic muscular atrophy. Because the canine esophagus is composed
predominantly of striated muscle, any neuromuscular disease that affects
limb muscles can affect the esophagus.

Of all acquired megaesophagus cases, approximately 25% are secondary to
MG. Acquired MG can present in focal, generalized, and acute
fulminating forms. Focal MG can present with various degrees of
esophageal, facial, laryngeal, or pharyngeal dysfunction. Ninety percent
of dogs with generalized MG have megaesophagus. Although acquired MG
can affect dogs of any age older than a couple of months, most affected
dogs are between 2 and 3 years of age or older than 9 years. Acquired MG
occurs most often in German shepherds and golden retrievers. Affected
feline breeds include the Abyssinian, Somali, and Siamese.

Preneoplastic syndromes differ from paraneoplastic syndromes in timing.
Preneoplastic syndromes occur with occult cancer. Preneoplastic
syndromes that can cause myositis include bronchogenic carcinoma,
lymphoma, myeloid leukemia, and tonsillar carcinoma.

Megaesophagus associated with distemper is due to demyelination.
Neurologic signs can develop 1 to 3 weeks or even months after initial

Although dysautonomia is rare, megaesophagus is a common finding in
these patients. Dysautonomia is an idiopathic autonomic nerve disorder
of cats and dogs that is suspected to be immune mediated. Within 1 to 7
days, patients experience a fulminant loss of autonomic nervous system
function, followed by constipation, dry mucous membranes, pupillary
dilation, prolapsed nictitating membranes, diminished pupillary light
response, bradycardia, areflexic anus, and bladder atony.

Glycogen storage diseases (GSDs) are inborn errors of glycogen
metabolism. Only GSD II, which is documented in Swedish Lapland dogs,
has been associated with megaesophagus.

A clinical presentation of megaesophagus associated with gait
abnormalities and laryngeal paralysis is suggestive of laryngeal
paralysis-polyneuropathy complex (LP-PNC). Megaesophagus is documented
in most dogs that are affected with LP-PNC. LP-PNC is documented in
Dalmatians, Leonbergers, Pyrenean mountain dogs, and Rottweilers.
Puppies usually present between 2 and 6 months of age; however, in
Leonbergers, onset is delayed to 1 to 9 years of age.

Endocrine causes

Hypoadrenocorticism and hypothyroidism are associated with
reversible megaesophagus. Patients with hypoadrenocorticism may have
megaesophagus due to electrolyte imbalances and a cortisol deficiency.
Electrolyte imbalances cause altered membrane potentials, which results
in decreased neuromuscular function. In addition, muscle weakness is a
consequence of deficient cortisol.

The association between megaesophagus and hypothyroidism has yet to be
understood. Hypothyroidism is prevalent in some breeds that are
predisposed to megaesophagus and laryngeal paralysis. Megaesophagus
occurs in 3% of hypothyroid dogs. Resolution of megaesophagus once the
thyroid is regulated has been reported. Aspiration pneumonia may cause a
sick euthyroid syndrome that may be misdiagnosed as hypothyroidism.

Gastrointestinal Causes

Gastrointestinal disorders associated with acquired megaesophagus
include esophagitis, esophageal obstruction, gastric
dilatation-volvulus, and hiatal hernia. In cats, acquired secondary
megaesophagus is due to pyloric dysfunction. Esophagitis is a common
finding associated with megaesophagus. It may or may not precede
megaesophagus. In patients with esophagitis, secondary megaesophagus
develops due to chemical or obstructive irritation. Gastric reflux
contains gastric acid, pepsin, bile salts, and trypsin, all of which
cause esophageal inflammation and ultimately decrease esophageal

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

Foreign bodies or chronic gastroesophageal reflux (GER) can cause
esophageal strictures, which occur secondary to mucosal healing
attempts. Esophageal damage that penetrates the submucosa and muscularis
layers causes inflammation resulting in collagen deposition and fibrous
connective tissue stricture.

Extraluminal esophageal obstruction is most commonly associated with
vascular anomalies. In 95% of patients with secondary megaesophagus due
to a vascular ring anomaly, the cause is a persistent right aortic arch.
Other vascular anomalies associated with secondary megaesophagus
include persistent right or left subclavian arteries, double aortic
arch, persistent right dorsal aorta, left aortic arch, right ligamentum
arteriosum, aberrant intercostal arteries, and persistent left cranial
vena cava.

Dogs with chronic or recurrent gastric dilatation with or without
volvulus have an increased risk of developing megaesophagus. In these
dogs, megaesophagus is due to decreased lower esophageal sphincter (LES)
tone caused by a combination of esophagitis from chronic GER or
vomiting; chronic intermittent obstruction of the LES; increased
intragastric and intra-abdominal pressures; and delayed gastric

In patients with hiatal hernia, the esophagus is essentially
obstructed. Four types of hiatal hernias have been described in humans.
Two of these types are applicable to animals. Type I is the "sliding"
hernia, defined as intermittent cranial displacement of the abdominal
esophagus, LES, and gastric cardia through the hiatus. Type II is the
paraesophageal hernia, in which the gastroesophageal junction remains in
its normal anatomic position; however, the stomach and abdominal organs
enter the caudal mediastinum through a defect adjacent to the
esophageal hiatus.

Paraneoplastic Causes

According to one study, megaesophagus was present in 40% of dogs with
thymoma. The incidence of thymoma in dogs with MG is 3%; in cats with
MG, the incidence is 26%. In humans, thymomas have increased production
of CD4+CD8+ T cells and lack antigen-presenting cells that function for
negative selection. This combination results in autoimmune disease. The
prognosis for nonresectable thymoma in a dog with MG and megaesophagus
is poor. However, complete thymic resection can result in resolution of
megaesophagus and a decrease in AChR antibody titer.

Toxic Causes

Toxic substances that can cause megaesophagus include lead,
organophosphates, and snake venom. Low-level lead exposure causes severe
abdominal pain, vomiting, diarrhea, and megaesophagus. Lead
intoxication can occur from ingestion of batteries, fishing line
weights, lead-based paint, linoleum, and plumbing or solder supplies.
Organophosphate toxicosis should be suspected if a patient presents with
concurrent weakness and cerebellar signs. Organophosphates exist in
flea collars and insecticides. They irreversibly bind to
acetylcholinesterase, causing a cholinergic crisis (salivation,
lacrimation, urination, defecation). Australian tiger snake envenomation
causes a rapidly progressing myopathy of skeletal muscle. If not
lethal, Australian tiger snake envenomation has a 75% recovery rate for
normal esophageal function.

Diagnostics for ME:



Thoracic radiography is diagnostic for most cases of megaesophagus. The
degree of esophageal dilation has no diagnostic value in determining
the etiology. Underlying causes of megaesophagus that may be revealed by
radiography include neoplasia, foreign body, vascular ring anomaly,
gastric dilatation-volvulus, and hiatal hernia. Normal midline tracheal
location does not exclude a vascular ring anomaly; however, focal
leftward deviation of the trachea near the cranial border of the heart
on a dorso-ventral or ventro-dorsal view is a reliable sign of
persistent right aortic arch in young dogs that regurgitate after eating
solid food. Radiographic findings of megaesophagus with concurrent
aspiration pneumonia or a distended stomach, small bowel, or urinary
bladder should raise suspicion for dysautonomia. Incidental esophageal
dilation does occur and is associated with excitement, aerophagia,
general anesthesia, and vomiting.

If thoracic radiographic findings of megaesophagus are questionable, a
barium contrast esophagram can confirm dilation and mechanical
obstruction. Barium accumulates within the distended esophagus. Focal
narrowing of the esophagus at the cardiac base is suggestive of a
vascular ring anomaly. However, the diagnostic benefit of a contrast
study should be weighed against the potential for aspiration of contrast

Fluoroscopy evaluates pharyngeal motility and the presence and
intensity of esophageal peristalsis. However, this diagnostic modality
is not essential for diagnosis of megaesophagus. It can be helpful in
cases of MG or esophagitis. MG can selectively affect only the
pharyngeal and esophageal musculature without more overt clinical signs.
Also, in cases of mild esophagitis, fluoroscopy may be of greater
diagnostic value than a contrast esophagram in detecting hypomotility.

Esophagoscopy is rarely indicated for a diagnosis of megaesophagus, but
it can be helpful for suspected cases of obstructive disease or reflux
esophagitis. Esophagoscopy may identify an esophageal stricture due to a
vascular ring anomaly, but it cannot differentiate the type of vascular
ring anomaly.

Laboratory Testing

A complete blood count (CBC), serum chemistry panel that includes CK
activity, and urinalysis should be performed for all regurgitating
patients and those in which megaesophagus is suspected. In addition, an
AChR antibody titer test should be performed in all cases of acquired
megaesophagus. AChR antibody testing is performed by the Comparative
Neuromuscular Laboratory in the School of Medicine at the University of
California, San Diego. Information regarding sample submission can be
obtained at
Corticosteroid therapy at immunosuppressive dosages for longer than 7
to 10 days lowers AChR antibody levels, so a pre-corticosteroid serum
sample is recommended.

Additional diagnostics are performed based on the history, physical
examination, and preliminary laboratory findings. The diagnostic
objective is to determine whether the megaesophagus is associated with a
potentially treatable disorder. For example, MG, hypothyroidism,
hypoadrenocorticism, polymyositis, and lead poisoning all have specific
treatments, whereas treatment for idiopathic megaesophagus is limited to
supportive and symptomatic management.

Elevated serum CK activity occurs with muscle damage associated with
some myopathies (inflammatory, necrotizing, and dystrophic) and muscle
trauma and may be mildly elevated in patients in extended recumbency or
after intramuscular injections.

Definitive diagnosis of acquired MG requires an AChR antibody titer
test. However, this test is not useful in diagnosing congenital MG,
which is a result of structural or functional AChR abnormalities and not
immune-mediated damage. Therefore, congenitally affected dogs and cats
do not have measurable circulating AChR antibodies.

Edrophonium chloride, a short-acting acetylcholinesterase drug, can be
administered to support a presumptive diagnosis of congenital or
acquired MG. Before administering the edrophonium be sure to exercise
your patient until fatigued. The appearance of MG fatigue can include
weakness, stiff gait, collapse, inspiratory stridor, or a reduced
palpebral reflex. After fatigue is induced, edrophonium is administered
IV (0.1 to 0.2 mg/kg). A positive response is characterized by improved
muscle strength. This commonly occurs within 30 seconds of the
edrophonium injection, and weakness returns within 5 minutes. Temporary
improvement of generalized muscle weakness is suggestive of, but not
definitive for, MG. The degree of megaesophagus is not affected by this
test; however, improvement in motility may be observed if evaluated by
fluoroscopy after administration of contrast agent.

Hypercholesterolemia, hypertriglyceridemia, and hyponatremia with or
without the presence of a normochromic, normocytic, nonregenerative
anemia is suggestive of hypothyroidism. In most cases, low total T4,
elevated canine thyroid stimulating hormone, and low free T4 levels
confirm the diagnosis of hypothyroidism.

Dogs with typical or atypical hypoadrenocorticism can present with
megaesophagus. Hyperkalemia and hyponatremia are suggestive of typical
hypoadrenocorticism. A low sodium to potassium ratio is not definitive
for hypoadrenocorticism, even with studies that found a sodium to
potassium ratio <15 to be more diagnostic for hypoadrenocorticism
than a ratio of 27:1. Typical and atypical hypoadrenocorticism are
diagnosed with an ACTH stimulation test.

Nucleated erythrocytes, without anemia or basophilic stippling of red
blood cells, suggests lead poisoning. These abnormalities are caused by
transportation of lead to bone marrow. Serum blood lead tests are
commercially available.

Organophosphate toxicosis can be excluded by measuring cholinesterase
in a whole blood sample. A cholinesterase activity less than 25% to 50%
of normal is suggestive of organophosphate toxicosis.

Additional diagnostic tests may include antibody titers for Toxoplasma
gondii, Neospora caninum, Borrelia burgdorferi, Ehrlichia canis, and
Rickettsia rickettsii; electromyography; measurement of nerve conduction
velocity; and muscle and nerve biopsies to exclude myopathic and
neuropathic disorders. Atropine, histamine, or pilocarpine tests can be
performed to exclude dysautonomia. Atropine is administered IV (0.02
mg/kg) or SC (0.04 mg/kg); lack of an increase in heart rate is
supportive of dysautonomia. When the intradermal histamine test (0.01 mg
per dog) is used, absence of a wheal and flare within 15 minutes is
supportive of dysautonomia. The histamine test has limited value in
cats, as there is no significant difference in the histamine response
between dysautonomic and control cats. If miosis does not occur after
topical ophthalmic administration of pilocarpine 0.1%, a presumptive
diagnosis of dysautonomia can be made.


Treatment for idiopathic megaesophagus is largely supportive
and symptomatic with periodic rechecks. Thoracic radiography is advised
to monitor progress of esophageal dilation and aspiration pneumonia.
Treatment for acquired secondary megaesophagus depends on managing the
underlying specific disease process in addition to providing supportive
and symptomatic care. Medications should be in liquid (not pill) form to
enhance movement to the stomach and avoid accumulation within the
esophagus, which can lead to esophageal irritation and nontherapeutic
medication levels. If accumulated medication passes into the stomach,
overdose may occur. Nutritional needs must be met and regurgitation
minimized. This can be accomplished by frequent feeding of small,
high-calorie meals with the patient in a cranially elevated position
(FIGURE 1). The optimal food consistency to minimize regurgitation
varies with each patient, so experimentation is encouraged.
Nasoesophageal or esophageal tubes are not advised because they increase
regurgitant volume, raising the risk of aspiration pneumonia.
Aspiration pneumonia and esophagitis are the most common complications
of megaesophagus.


The prognosis for megaesophagus varies with the underlying
etiology and presence of secondary complications. Aspiration pneumonia,
dehydration, and malnutrition can significantly worsen the prognosis.
Congenital megaesophagus has a guarded to poor prognosis; however, there
is potential for improvement of esophageal motility with maturity up to
1 year of age. The prognosis for congenital MG is poor due to the
mechanism of the condition, lack of a specific treatment, and high
complication rate of aspiration pneumonia. Acquired idiopathic
megaesophagus in general has a guarded to poor prognosis due to the
common occurrence of aspiration pneumonia and malnutrition. Morbidity
and mortality depend on the degree and nature of the underlying disease
and client compliance. In the absence of severe aspiration pneumonia or
thymoma, the success rate for acquired MG can be good with early
diagnosis and appropriate management. Spontaneous remission of acquired
MG with resolution of megaesophagus can also occur within an average of 6
months. However, many myasthenic dogs die of aspiration pneumonia
during the first month after diagnosis, so the overall prognosis is
still guarded. With the exception of the acute fulminating form of
myasthenia, there is no association between the severity of MG and the
possibility of remission. In one study, 39% of dogs with immune-mediated
polymyositis had clinical improvement of their megaesophagus with
continued medical management. However, early diagnosis and initiation of
appropriate therapy are key to a good clinical outcome. Evaluation of
muscle biopsy samples early in the course of the disease to establish a
diagnosis is critical. The prognosis for pre- and paraneoplastic
myositis is poor due to the underlying cancer. Dysautonomia is
progressive, with a survival rate of <25% in cats over 18 months.
Prognostic indicators include showing response to therapy (e.g.,
maintenance of body weight with oral feedings, fecal and urinary
continence) within 7 to 10 days.

The original Bailey chair creator, Donna Koch, offers free Bailey chair building instructions: &

They also have a web group site at: 


Thank you for your continued support!

-Aspen Meadow Veterinary Specialists

104 S. Main Street

Longmont, CO 80501

303-678-8844 (p)

303-678-8855 (f)