The most common cause of regurgitation in dogs is idiopathic megaesophagus, although the etiology of the problem is unclear. The condition is characterized by moderate to severe dilation of the esophagus and ineffective esophageal muscle contractility (peristalsis). Several forms of the syndrome have been described:

Congenital idiopathic megaesophagus is a generalized dilation and hypomotility of the esophagus causing regurgitation and failure to thrive in puppies shortly after weaning. An increased breed incidence has been reported in the Boston terrier, Chinese shar-pei, great Dane, German shepherd, white German shepherd, golden retriever, greyhound, Irish setter, Labrador retriever, mastiff, Newfoundland, and Rhodesian ridgeback breeds, but heritability has been proven only in the miniature schnauzer and wire-haired fox terrier breeds. The underlying cause is not completely understood, but appears to be a defect in the sympathetic (vagal) nerve supply to the esophagus.

Acquired secondary megaesophagus may occur in association with a number of other conditions. Myasthenia gravis accounts for at least 25% of these cases. In some myasthenia gravis cases, regurgitation and weight loss may be the only presenting signs of the disease.

Acquired idiopathic megaesophagus is the form of disease seen in most adult onset cases. It appears spontaneously in adult dogs between 7-15 years of age, and there is no sex or breed predilection. The disorder is not the same as esophageal achalasia in humans. While the responses of the upper and lower esophageal sphincters to swallowing appear to be intact, esophageal distension does not initiate peristaltic contractions in affected animals. The exact site of this abnormality in the nerve response has not yet been determined.

Routine laboratory testing should be performed to investigate possible secondary causes of megaesophagus such as hypothyroidism, polymyositis, and hypoadrenocorticism (Addison’s disease). X-rays including contrast studies should be made to confirm the diagnosis, evaluate motility, and exclude foreign bodies or obstruction as the cause of the megaesophagus.

Animals with secondary acquired megaesophagus should be treated for the associated underlying condition. For hypothyroid dogs, therapy with thyroxine should be given twice daily at least an hour before or three hours after a meal to ensure proper absorption. If the thyroid condition is autoimmune thyroiditis, the animal should not be used for breeding, although having megaesophagus is another reason to not breed the dog.

Affected animals should be fed a high-calorie diet, in small frequent feedings, from an elevated or upright position to take advantage of gravity drainage through a non-peristaltic esophagus. While medical therapies have been advocated for treating dogs with megaesophagus, clinical results have failed to show efficacy in improving esophageal peristalsis in affected dogs.

Animals with congenital idiopathic megaesophagus have a fair prognosis if adequate nutrition is provided and every effort is made to prevent aspiration pneumonia. Many of these dogs will develop improved esophageal motility over the course of several months.

By contrast, the morbidity and mortality of acquired idiopathic megaesophagus remain unacceptably high, and lead to a poor overall prognosis. Many animals eventually succumb to the effects of chronic malnutrition and repeated episodes of aspiration pneumonia. Animals with acquired secondary megaesophagus have a more favorable prognosis if the underlying disease (e.g. hypothyroidism) can be promptly identified and successfully managed. In a retrospective study of 29 dogs with neurologic signs and hypothyroidism, four cases had megaesophagus. Of these, three dogs had good clinical remission with occasional regurgitation and one dog did not improve. In one published case study, the treatment for concomitant hypothyroidism resulted in total regression of the megaoesophagus, which completely disappeared clinically and radiographically for at least two years of followup. However, although resolution following therapy with thyroxine is highly suggestive of a causal relationship between megaesophagus and hypothyroidism, it does not prove it.

References: Jaggy et al. JVIM 8: 328-336, 1994; Dodds. Adv Vet Sci Comp Med 39: 29-96, 1995; Gaynor, Shofer, Washabau. JAVMA 211:1406-1412, 1997; Huber et al. Sch Arch Tier 148: 512-514, 2001; Washabau. Proc. WSAVA Congress, Vancouver, BC, 2001, 5 pp.