Megaesophagus may be due to a congenital defect or may be an adult-onset, acquired disorder. Congenital defects that may result in megaesophagus include vascular ring anomalies, esophageal diverticula, congenital myasthenia gravis, and an idiopathic form. (Also see Congenital and Inherited Anomalies of the Esophagus Congenital and Inherited Anomalies of the Esophagus Clinically significant esophageal disorders generally manifest themselves as swallowing dysfunction and regurgitation, especially when puppies or kittens are weaned and begin to eat solid food... read more .) Adult-onset megaesophagus may be primary (idiopathic) or secondary to systemic disease. Secondary megaesophagus may be due to myasthenia gravis, systemic lupus erythematosus, polymyositis, hypoadrenocorticism, heavy metal (lead) toxicity, thallium toxicity, glycogen storage disease, neurotoxin-induced cholinesterase inhibition, dysautonomia, CNS disorders including neoplasia, and possibly hypothyroidism. Esophageal dilatation may also develop cranial to an esophageal lesion such as an esophageal stricture, foreign body, neoplasia, or extraesophageal compression.
The cardinal sign is regurgitation. A puppy with congenital megaesophagus characteristically begins to regurgitate at weaning when it starts to eat solid food. Affected pups are generally unthrifty and smaller than their littermates. Pressure applied to the abdomen may cause ballooning of the esophagus at the thoracic inlet. Aspiration pneumonia is a complication with associated signs of cough, fever, and sometimes nasal discharge. Adult animals that develop megaesophagus also start to regurgitate and ultimately lose weight. Respiratory signs may predominate, with little or no apparent regurgitation. Thoracic radiographs reveal air, fluid, or food in a dilated esophagus. The esophagus is usually uniformly dilated. A large ventral deviation may be present cranial to the heart. Megaesophagus secondary to a stricture, foreign body, neoplasia, or vascular ring anomaly is visualized as a dilatation of the esophagus cranial to the defect only. Strictures, foreign bodies, or vascular ring anomalies can be excluded with an esophagram and/or esophagoscopy.
In adult dogs, associated diseases (eg, myasthenia gravis) should be excluded or, if found, treated. Surgery is indicated for a vascular ring anomaly. Surgery may not successfully resolve the clinical signs in longstanding cases with severe esophageal dilatation cranial to the anomaly. Medical management is indicated for congenital or acquired idiopathic megaesophagus. Congenital megaesophagus may resolve as the animal ages, usually by 6 mo of age. The consistency of the diet that best prevents regurgitation varies from dog to dog; a soft gruel works for some, while dry food works for others. Another possibility is canned food formed into a meatball shape. Frequent, small meals work best for most dogs. Feeding from an elevated position with the forelimbs higher than the hindlimbs and holding that position for at least 10–15 min after eating allows gravity to assist food passage into the stomach. Neither surgery nor medications improve esophageal function. Ultimately, most animals succumb to aspiration pneumonia.