Introduction

Megaesophagus (ME) is characterized by generalized dilatation of the esophagus. It is the most common cause of regurgitation and a common esophageal disease in dogs. Causes of acquired megaesophagus include: idiopathic ME, myasthenia gravis (MG) - generalized or focal, esophagitis, endocrine diseases, toxicosis (e.g., lead). Less common causes include: other neurologic diseases (botulism, tetanus, dysautonomia, rabies), systemic lupus erythematosus.

Clinical Presentation

Clinical signs consistent with esophageal disease include: regurgitation, dysphagia, swallowing attempts “on empty,” halitosis, ravenous appetite, tachypnea, dyspnea, cough, exercise intolerance, fever (in case of aspiration pneumonia).

Diagnostic Approach

The first step in the diagnostic approach is to rule out esophageal obstruction (foreign body, stricture) by taking a detailed history, and getting good quality thoracic radiographs. A generalized dilatation of the esophagus is usually easily identified on the thoracic films. Generalized dilatation is typically due to functional disease whereas segmental dilation is more commonly associated with foreign body, infiltrative disease (neoplasia or inflammation, hiatal diseases, segmental motor disease, stricture, ring anomaly, and redundant esophagus). Radiographically, the dilated esophagus can be gas or fluid opaque depending on the disease process. Radiographic signs include visualization of the esophagus, dilatation with gas, retention of food or fluid, tracheal stripe sign, ventral displacement of the intrathoracic trachea, and ventral displacement of the heart. In addition, it is important to carefully check for aspiration pneumonia in these patients.

The systematic approach is continued by screening animals for primary, underlying diseases associated with secondary megaesophagus. A minimal database consisting of CBC, biochemistry panel (including serum creatine kinase), and urinalysis is recommended. Then, screening for endocrinopathies (resting cortisol or ACTH stimulation test, serum thyroxine, and endogenous TSH), and search for opacities in the cranial mediastinum (looking for possible thymoma associated with myasthenia gravis [MG]) are recommended. A sensitive and specific serum assay documenting the presence of autoantibodies against nicotinic acetylcholine receptors is available for the diagnosis of MG http://vetneuromuscular.ucsd.edu. Endoscopic examination of the esophagus may be useful in unclear cases and to allow visualization of extent and severity of esophagitis, if present. In cases with suspected polymyositis or polyneuropathy electrodiagnostics (EMG, nerve conductions studies) and collection of muscle and nerve biopsies for histopathologic evaluation should be considered. In endemic lesions, infection with the parasite Spirocerca lupi should be ruled out (see esophagitis lecture).

Management

Dietary management is of central importance - it is important to try various options such as dry food kibbles, canned food in meatballs and food blended with water in different consistencies (thick or thin slurry) because each animal may respond differently. Dogs and cats with ME should be fed a caloric-dense diet in a vertical position and be maintained in that position for 10–15 minutes after the meal in order to use gravity to facilitate aboral movement of the food bolus. Small dogs can be held on a person’s lap for that time. Medium size and large dogs can be fed on stairs and maintained with their front limbs higher than their hind limbs. The Bailey chair is a useful device to keep medium size and large dogs in a vertical position during and after meals. This aspect of treatment can be a challenge for dogs with pre-existing orthopedic diseases such as coxofemoral arthritis. In severe cases, placement of a gastrostomy tube may be beneficial to ensure appropriate nutrition and timely delivery of oral medications to the stomach, and to prevent aspiration pneumonia.

Identified underlying diseases need to be treated. For instance, recommended treatment of MG includes administration of acetylcholinesterase inhibitor pyridostigmine (1–3 mg/kg PO q12h, start with a low dose to minimize risk of cholinergic crisis) and immunosuppressive doses of prednisone or prednisolone (1–2 mg/kg PO q12h). Gastric prokinetic drugs do not significantly influence esophageal motility, while some of them increase LES tone in dogs (cisapride, erythromycin). Bethanechol is a cholinergic agent that has been shown to increase esophageal motility in some dogs and can be used in the management of clinical cases of idiopathic ME (5 to 15 mg/dog PO q8h, start with a low dose to minimize risk of cholinergic crisis). Because of the high prevalence of esophagitis in patients with ME, sucralfate suspension should be administered to facilitate mucosal healing (0.5–1 g/dog q8h). Treatment of aspiration pneumonia is mostly supportive. If secondary bacterial infection is suspected, antibiotic treatment is best based on culture and sensitivity from a tracheal or bronchial wash, however, empiric treatment with a broad-spectrum antibiotic may be necessary in some cases (e.g., amoxicillin and clavulanic acid, ampicillin, and sulbactam).

Home management of pets with megaesophagus is complex and time-consuming. Owners may feel overwhelmed and discouraged at first. Therefore, optimal communication between the veterinary care team and the animal’s owners is essential for successful management of this condition, and web-based (e.g., Facebook) support groups may be very helpful.

Prognosis

Studies from Scotland and Germany reported a short median survival time of 3 months after diagnosis regardless of the etiology in dogs with ME. In the Glasgow study, 41% of dogs survived 1 year, 31% were alive at 2 years, and 22% survived for 5 years. Identified risk factors for shorter survival were dogs older than 13 months of age at the time of diagnosis and presence of aspiration pneumonia at diagnosis. Megaesophagus may be reversible when associated with endocrinopathies, but this represents only a small percentage of dogs with ME.