Many diseases have been associated with acquired megaesophagus, and generally fall into categories of myopathies, peripheral
neuropathies, other disorders of the neuromuscular junction, or obstructive diseases such as strictures, foreign bodies, granulomas
or tumors (Spirocerca lupi). Among the myopathies linked to megaesophagus are inflammatory myopathies of infectious or non-infectious (immune-mediated)
origin (polymyositis, systemic lupus erythematosis, dermatomyositis). Some neuropathies tied to acquired megaesophagus include
polyradiculoneuritis, bilateral vagal nerve injury, dysautonomia, and lead and thallium toxicity. Other neuromuscular junction
diseases with the potential to cause megaesophagus include botulism, tetanus and anticholinesterase toxicities (e.g. organophosphates).
Central nervous system disease (e.g. brain stem lesions, neoplasia, trauma) has also been associated with megaesophagus.
Myasthenia gravis (MG) is considered one of the most common causes of acquired megaesophagus in dogs; dogs with MG may have
megaesophagus as the only manifestation of neuromuscular junction disease, or may have more classical appendicular weakness.
Gaynor et al retrospectively studied a large number of dogs with megaesophagus to identify risk factors associated with the
disease. In their series of 136 dogs, the most common risk factor identified was MG; other risk factors found in this study
included esophagitis and peripheral nerve disease. Despite being commonly cited as a risk factor for acquired megaesophagus,
the Gaynor study did not find any association between megaesophagus and hypothyroidism.
Esophagitis is another cause of acquired megaesophagus in dogs; esophagitis itself can be the result of a number of other
diseases. Some of the more important causes of esophagitis include gastroesophageal reflux, and chronic vomiting. Gastroesophageal
reflux appears to be a common event during anesthetic procedures. In a study by Wilson et al, more than half (51/90) of dogs
undergoing surgical procedures with either halothane, isoflurane or sevoflurane had evidence of esophageal reflux (as assessed
by continuous monitoring of esophageal pH throughout the procedure) during the anesthetic period, and most dogs experiencing
esophageal reflux had low esophageal pH for prolonged periods of time. The inhalant anesthetic used, or the type of premedication
administered, did not appear to alter the risk of reflux during anesthesia. While the number of clinical cases that emerge
from anesthetic-related esophagitis/megaesophagus is fortunately small, the failure to consider that the dog "vomiting" post-operatively
may in fact be regurgitating could result in treatment errors and more serious consequences (e.g. strictures).
Animals with megaesophagus may also have difficulty swallowing, excessive salivation, pain with swallowing, or if pulmonary
aspiration has occurred, cough or alterations in respiratory rate and pattern. Vomiting may also be a component of the clinical
presentation potentially confounding the recognition of regurgitation as an element of the animal's clinical presentation;
vomiting can accompany megaesophagus if vomiting (usually chronic) has led to esophagitis. Animals with esophagitis or aspiration
may also have fever. Prolonged regurgitation is likely to lead to weight loss.
Physical examination abnormalities in patients with megaesophagus can include poor body condition, distension (which can be
dynamic) of the left ventral neck area, and fever and pulmonary crackles if aspiration pneumonitis is present. Patients with
MG may have evidence of peripheral weakness, although this will not be appreciated in all patients.
Once the problem of regurgitation is suspected, megaesophagus is often easily demonstrated on plain thoracic radiographs on
which an air (or sometimes fluid)-filled esophagus is readily seen. Occasionally, animals with megaesophagus will not have
an obvious air-filled esophagus apparent on thoracic radiographs, and esophageal hypomotility may be demonstrated during a
contrast esophogram. There is a risk of the patient aspirating contrast material during a contrast esophogram.
Once megaesophagus has been identified, revisiting the physical examination to carefully screen the patient for other signs
of neuromuscular disease can be helpful in prioritizing differential diagnoses.
Additional diagnostic steps often performed early in patients with megaesophagus include a CBC, biochemical profile and urinalysis
to screen for inflammatory, or endocrine (hypoadrenocorticism) disease, anti-acetylcholine receptor antibodies, and if evidence
supports hypoadrenocorticism, an ACTH stimulation test. A positive test for Ach-receptor antibodies confirms a diagnosis of
MG, but a negative result does not exclude a diagnosis of MG as it is known that some dogs with MG can be antibody negative;
this may be particularly true of focal forms of myasthenia in which only the esophagus may be affected. Other tests that may
be indicated in occasional patients include ANA titers, serum CK activity, blood lead concentrations, and if there is evidence
of dysfunction in other muscles, EMG and muscle biopsies for histopathological examination.
Endoscopic examination of the esophagus is not commonly performed in animals with megaesophagus, but is probably underutilized.
Esophagoscopy is a sensitive means of detecting esophagitis, which can lead to acquired megaesophagus. In animals whose history
includes risk factors for esophagitis (e.g. recent general anesthesia) or suggests the possibility of concurrent vomiting,
endoscopic examination of the esophagus and other parts of the intestinal tract may reveal lesions suggestive of esophagitis
or other gastrointestinal disease and allows for biopsy of the gastrointestinal mucosa to help define the underlying cause
of vomiting. Another benefit of endoscopic examination is the opportunity it provides to place gastrostomy tubes, which can
be very helpful in the provision of nutritional support in addition to insuring reliable delivery of medications.
Ancillary testing that can be important for some patients is sampling of the respiratory tract for cytology and microbial
culture. Culture of respiratory washes (transtracheal, bronchial or bronchoalveolar lavage) is more important in those animals
that have been treated for long periods of time with antibiotics, or that have received multiple different antibiotics.
Treatment of megaesophagus centers on identification and treatment of underlying diseases when identified. Patients with MG
should receive an acetylcholinesterase inhibitor such as pyridostigmine and are often candidates for immunosuppressive therapy
with glucocorticoids and/or azathioprine. The timing of implementation of immunosuppressive treatment in the face of pulmonary
aspiration is based on clinical judgment, but the author will typically try to wait, when possible, until there has been clinical
and radiographic resolution of pneumonia before implementing immunosuppressive therapy. Some animals that exhibit good responses
can be maintained with immunosuppressive drugs alone. The optimal dosage of glucocorticoids for animals with MG has not been
established. Avoiding immunosuppressive dosages is advocated by some to lessen the risk of exacerbating muscle weakness.
Esophagitis can be treated with H2 receptor blockers such as famotidine, and a sucralfate slurry. Metoclopramide, which increases
lower esophageal sphincter tone, probably should not be given in the face of overt esophageal hypomotility. It may be reasonable
to empirically treat for esophagitis while awaiting Ach receptor antibody test results, or if the owner refuses to allow diagnostic
investigation for financial or other concerns. Causes of vomiting or predispositions to esophagitis should be identified and
treated when possible. Resolution of megaesophagus can be appreciated in some patients with correction of underlying causes.
Animals with evidence of aspiration pneumonitis are usually candidates for antimicrobial treatment, which should be broad-spectrum
if treatment is done without benefit of respiratory wash cultures. Antibiotics should be continued for a week beyond radiographic
resolution of pulmonary injury.
The prognosis associated with acquired megaesophagus varies with the underlying cause. For patients that have treatable primary
disorders (e.g. MG; esophagitis), resolution of megaesophagus and associated clinical signs is possible, and the prognosis
can be fair to good. The prognosis for patients with megaesophagus secondary to obstructive disease seems to be a function
of the length of time that the esophagus has been obstructed; the longer the esophagus has been obstructed, the less likely
there will be return of normal esophageal function. Animals with idiopathic megaesophagus often have a poor prognosis as these
patients are susceptible to repeated bouts of aspiration, weight loss, and continued regurgitation, all of which can prove
extremely frustrating for owners.
Kogan DA, et al. Clinical, clinicopathologic, and radiographic finding in dogs with aspiration pneumonia: 88 cases (2004-2006).
J Am Vet Med Assoc 2008; 233:1742.
Kogan DA, et al. Etiology and clinical outcome in dogs with aspiration pneumonia: 88 cases (2004-2006). J Am Vet Med Assoc 2008; 233:1748.