Diseases of the esophagus (Proceedings)


Esophagitis may be caused by chemical injury from ingested substances, gastroesophageal reflux (secondary to general anesthesia, hiatal defects, persistent vomiting, malpositioned nasoesophageal/pharyngostomy tubes), or esophageal foreign bodies.


Esophagitis may be caused by chemical injury from ingested substances, gastroesophageal reflux (secondary to general anesthesia, hiatal defects, persistent vomiting, malpositioned nasoesophageal/pharyngostomy tubes), or esophageal foreign bodies. Disturbances in esophageal motility may accompany esophagitis regardless of the cause. The reported prevalence of acute esophagitis is low; however, this is likely an underestimation due the subtlety of clinical signs and radiographic findings associated with this disorder. Clinical signs vary as to the type of chemical injury, severity of inflammation, and extent of esophageal involvement. Esophagitis is an endoscopic diagnosis that does not require mucosal biopsy. Mucosal abnormalities that may be observed include increased erythema, erosions, and alterations in mucosal texture. Lesions are usually evident in the distal esophagus, adjacent to and including the LES.

Treatment - Mild esophagitis frequently resolves with minimal treatment other than dietary management. Provide frequent, smaller-sized meals of a low-fat, high-protein content to enhance LES tone and to minimize reflux. Animals having more severe esophagitis will require drug therapy and gastrostomy tube feeding. Sulcralfate suspension (0.5-1.0 g PO TID) is the most beneficial and specific therapy for reflux esophagitis. Administer metoclopramide (0.1-0.2 mg/lb per os, SC, TID) or cisapride (0.05-0.25 mg/lb per os BID) to decrease esophageal reflux (by increasing LES pressure) and to promote gastric emptying. Gastric acid secretory inhibitors (ranitidine 0.5 -1.0 mg/lb PO or IV BID; famotidine 0.25-0.5 mg/lb PO SID; omeprazole 0.35 mg/lb PO SID) should be given to decrease acidity of gastric juice. The duration of drug therapy is empirical and varies with severity of signs and endoscopic lesions. Mild lesions are treated for 5-7 days; moderate-to-severe esophagitis is treated for 2-3 weeks. The prognosis in most cases of esophagitis is good with appropriate medical therapy. Animals having severe disease warrant a guarded prognosis as stricture or segmental or generalized hypomotility may occur.

Esophageal Foreign Bodies

Foreign bodies are a common cause for esophageal dysphagia in the dog but are rare in cats. They usually lodge at points of minimal esophageal distension including the thoracic inlet, at the base of the heart, or at the diaphragmatic hiatus. The most common objects ingested are bones, fish hooks, needles, sticks, and play toys. Retained foreign bodies cause partial or complete mechanical obstruction. Muscle spasm and tissue edema occur around the foreign body making passage of the object down the esophagus more difficult. Mucosal abrasion, laceration, and perforation may occur with sharp or angular objects which are lodged intraluminally. The severity of clinical signs is related to the size of the foreign body and duration of esophageal obstruction. Most dogs and cats with large esophageal foreign bodies are presented for evaluation of acute onset of regurgitation, dysphagia, odynophagia, gagging, and excessive salivation. Survey and contrast radiology show the presence of the foreign material, aspiration pneumonia and/or evidence of perforation. Esophagoscopy should be performed to confirm the diagnosis and to assess secondary mucosal damage.

Treatment - Esophageal foreign bodies are medical emergencies and should be promptly removed. Endoscopic removal of foreign bodies using a flexible instrument which accommodates a variety of retrieval (grasping) instruments is usually successful. Thoroughly evaluate the esophageal mucosa following foreign body extraction for hemorrhage, lacerations, and perforations. Obtain post-procedural thoracic radiographs to access for pneumomediastinum/pneumothorax. Restrict food or water for 24 hours depending on the extent of esophageal trauma. Animals with severe mucosal damage will require complete esophageal rest and gastrostomy tube feedings. Initiate medical therapy for esophagitis. Esophageal perforations are successfully treated with broad-spectrum antibiotics such as ampicillin (11 mg/lb SC, IM, IV TID). The prognosis after endoscopic foreign body removal is generally excellent. Significant esophageal trauma or large perforation carries a guarded prognosis.

Esophageal Stricture

Esophageal stricture occurs secondary to severe esophagitis. Following mucosal injury, inflammation extends beyond the mucosa into the muscular layer and heals by fibrosis. Fibrotic changes in the esophageal wall cause lumenal narrowing. Strictures may occur at any point along the length of the esophagus. The time period from severe esophagitis to lumenal stenosis is approximately 1-3 weeks. The most important causes for stricture are gastroesophageal reflux and trauma from esophageal foreign bodies. Classical signs include regurgitation, dysphagia, ptyalism and tend to be progressive. A ravenous appetite with weight loss is common because of the inability to transport food past the strictured site. A diagnosis of stricture is often suggested by clinical history. Survey thoracic radiographs are usually normal. Contrast studies are useful in accessing the number, location, and length of strictures. Most animals have a single esophageal stricture. Esophagoscopy confirms stricture and permits differentiation of benign from malignant stricture via mucosal biopsy/cytology.

Treatment - Benign strictures are best treated by mechanical dilatation using a balloon catheter under endoscopic guidance. Balloon catheter dilatation is the current treatment standard for stricture. A polyethylene catheter (Ridgiflex Dilator, Microvasive Inc.) is carefully advanced adjacent to the endoscope and centered in the stricture for dilatation. Dilatations are usually performed 2-4 times at intervals of 2-3 days since re-stricture occurs rapidly. Strictures associated with active esophagitis will require a greater number of dilatation procedures. Medical therapy of esophagitis is required following mechanical dilatation. Withhold feedings for 24 hours, or place a gastrostomy tube for enteral feedings in animals with severe mucosal trauma. Corticosteroids (prednisone 0.5 -1.0 mg/lb PO divided BID for 10-14 days) may prevent stricture recurrence. The prognosis for benign strictures is good with successful dilatation.

Megaesophagus and Esophageal Hypomotility

Megaesophagus is characterized by diffuse esophageal dilation and aperistalsis. This syndrome may occur as a congenital idiopathic disorder (uncommon), or it may manifest in adult animals as an idiopathic (common) or acquired lesion. A familial predisposition for congenital megaesophagus has been suggested for the Irish Setter, Great Dane, German shepherd, Labrador retriever, Chinese Shar Pei, Newfoundland, miniature schnauzer, and fox terrier breeds. The pathogenesis of congenital idiopathic megaesophagus may involve a defect in vagal afferent innervation of the esophagus.

The underlying pathophysiologic mechanism for acquired idiopathic megaesophagus is unknown. Acquired secondary megaesophagus may result from many disorders, especially diseases causing diffuse neuromuscular dysfunction. Myasthenia gravis accounts for at least 25 percent of the acquired causes in dogs. Other causes of segmental or diffuse esophageal hypomotility include foreign bodies, stricture, vascular ring anomalies, and esophagitis. Esophageal dysfunction in Chinese Shar Peis may also result from segmental hypomotility and esophageal redundancy. Regurgitation is the salient clinical sign seen with megaesophagus. There is considerable variability in the frequency and timing of regurgitation episodes following meal ingestion. Respiratory distress (moist cough, dyspnea) and fever indicate aspiration pneumonia which is the most common complication of megaesophagus. Suspect megaesophagus in any adult animal, particularly dogs, with a history of regurgitation. Survey radiographs of the cervical neck and thorax usually reveal the presence of a dilated air-, fluid-, or ingesta-filled esophagus. An acetylcholine receptor antibody titer should be performed to evaluate for acquired myasthenia gravis (MG), even in the absence of generalized muscle weakness, since MG may mimic idiopathic megaesophagus. Additional laboratory tests are performed on the basis of clinical suspicion.

Treatment - Animals with acquired secondary megaesophagus are treated specifically for the disorder causing esophageal hypomotility. Treatment of idiopathic megaesophagus and those acquired forms that fail to respond to specific medical therapy is primarily supportive and symptomatic. Animals which are severely malnourished or that have aspiration pneumonia should have a gastrostomy tube placed for enteral nutrition. Give broad-spectrum antibiotics for treatment of aspiration pneumonia.

The prognosis with acquired idiopathic megaesphagus is generally poor. These animals usually succumb to repeated episodes of aspiration pneumonia or are euthanized because of their irreversible disease. Animals with acquired secondary megaesophagus may respond to specific drug therapy. The prognosis in dogs with megaesophagus caused by acquired myasthenia gravis is favorable with 50 percent of dogs responding to therapy.

Vascular Ring Anomaly

Vascular ring anomalies are congenital malformations of the major arteries of the heart that entrap the intrathoracic esophagus and cause esophageal obstruction. Persistent right aortic arch (PRAA) is the best documented anomaly in both dogs and cats. This anomaly is considered to have a familial tendency since German shepherds and Irish setters appear to be predisposed. Affected animals present for regurgitation of solid foods at the time of weaning. Weight loss despite a good appetite is commonly observed. The presence of a moist cough, dyspnea, and fever suggest aspiration pneumonia. Vascular ring anomalies should be differentiated from other causes of regurgitation in young animals such as congenital idiopathic megaesophagus, esophageal foreign body, and cricopharyngeal dysphagia. The signalment and a compatible history of regurgitation since weaning are very suggestive of a vascular ring anomaly. Survey thoracic radiographs usually demonstrate esophageal body dilation cranial to the base of the heart. A barium esophagram should be performed to confirm the location of esophageal obstruction and severity of esophageal distension.

Treatment - Definitive therapy for PRAA is surgical ligation and transection of the ligamentum arteriosum. Animals with severe debilitation from malnutrition will require enteral nutritional support via gastrostomy tube feedings. Aspiration pneumonia should be effectively treated with broad-spectrum antibiotics before surgery. The best prognosis for return of normal esophageal function is obtained with early diagnosis and prompt surgical intervention. Progressive esophageal dilatation may occur if a diagnosis is not made at an early age.

Esophageal Neoplasia

Tumors of the esophagus are rare. Neoplasms may be of primary esophageal, periesophageal, or metastatic origin. Esophageal fibrosarcoma and osteosarcoma are the most common malignant tumors in dogs. Squamous cell carcinoma is the most commonly diagnosed primary esophageal tumor in cats. Animals with esophageal neoplasia have signs consistent with progressive esophageal obstruction including chronic regurgitation dysphagia, odynophagia, and pytalism. Anorexia, weight loss, and depression are more typical of advanced disease (metastasis, systemic effects of cancer) and malnutrition resulting from the inability to retain food. Consider a diagnosis of esophageal neoplasia in middle-aged and older animals having chronic progressive signs of obstructive esophageal disease. Survey thoracic radiographs may be normal or reveal variable esophageal dilatation, an intraluminal mass, or evidence of a periesophageal lesion displacing the esophagus. A barium esophagram typically confirms the presence of an intraluminal mass or obstructive lesion. Esophagoscopy with mucosal biopsy/exfoliative cytology is required for definitive diagnosis.

Treatment. Successful treatment of malignant esophageal neoplasia is uncommon because the disease is often well advanced at the time of diagnosis. Chemotherapy, radiation therapy, and surgery are palliative techniques for treatment of malignant tumors.


1. Jergens AE. Diseases of the Esophagus. In: Textbook of Veterinary Internal Medicine, 6th ed, Ettinger

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