Screen Shot 2019-05-29 at 12.25.59 PM.png — Megaesophagus in a Dog

Anne Desrochers DVM DACVIM

Patient Information:

Age: 13 year-old

Gender: Neutered Male

Species: Canine

Breed: German Shephard

History:

History of regurgitation/gagging of 10-day duration. Bloodwork showed slight increased white blood cell count.Alk Phos was low <10 (23-212)

Image Interpretation:

Ultrasound of the left lateral cervical region was performed: the esophagus appeared flattened throughout its length with poor contractility. In addition, the esophagus was moderately distended with gas and fluid secretion and Its wall thickness appeared thinner than normal measuring 1.7mm.

Thoracic ultrasound was performed: no evidence of peripheral lesions, mass or effusion was detected. The visceral pleural surface was smooth and regular with normal gliding motion bilaterally. The cranial mediastinal space and thoracic inlet had a normal sonographic appearance.

Acquired esophageal dysfunction was suspected and testing for myasthenia gravis was recommended.

Additional Testing:

Acetylcholine Receptor Ab-Myasthenia Gravis

Lab Result (in nmol/l) : 3.30

Reference Values in dogs:

< 0.6 nmol/L Normal serum titer.

> 0.6 nmol/L Positive serum titer, diagnostic of acquired myasthenia gravis.Fine-needle biopsies of the pancreas mass and spleen were collected and submitted Fine-needle biopsies of the pancreas mass and spleen were collected and submitted Fine-needle biopsies of the pancreas mass and spleen were collected and submitted

Diagnosis:

Megaesophagus is defined as dilatation of the esophagus due to weakness of the esophageal musculature from any cause. Dogs and cats of any age or sex can be affected. Congenital megaesophagus most commonly affected Siamese, German shepherds, Great Danes, Labrador retrievers, miniature schnauzers, Irish setters, sharpeis, fox terriers, Newfoundlands. Acquired megaesophagus in dogs most often occurs in black standard poodles (secondary to hypoadrenocorticism) but there are numerous potential causes of megaesophagus in the adult dog. Myasthenia gravis, caused by autoantibody production against nicotinic acetylcholine receptors at neuromuscular junctions, is common and responsible for up to 30% of cases.

Myasthenia gravis is treated with pyridostigmine bromide (1-3mg/kg PO q8-12 hours), and antibody concentrations should be checked every 4-6 weeks; if antibody titers return to normal, treatment can be discontinued. Clinicians should monitor for both relapses and progression from focal to generalized myasthenia gravis. In cases not responding to pyridostigmine, immunosuppressive therapy (prednisone, azathioprine) can be instituted. In addition, supportive care with the therapy goals of minimizing regurgitation, providing ample nutrition, and resolving and/or preventing aspiration pneumonia should be provided. Dogs with myasthenia gravis should also be spayed/neutered to prevent breeding, and because heat cycles and pregnancy can exacerbate clinical signs. Risk assessment should also be used when considering vaccines for any dogs with myasthenia gravis as immune stimulation may worsen their clinical signs.

Outcome:

A week following the ultrasound examination, the patient was referred to the internal medicine services for further management and treatment. At this point, humane euthanasia was elected due to complications from aspiration pneumonia.