Diagnosis and Management of Feline Esophageal Disease
World Small Animal Veterinary Association World Congress Proceedings, 2001
Bob Sherding
United States

Clinical manifestations of esophageal disease include regurgitation, dysphagia, odynophagia (pain on swallowing), ptyalism, and exaggerated swallowing. Regurgitation is the passive expulsion of food or fluid from the esophagus and is influenced by mechanical events in the esophagus. Regurgitation must be distinguished from vomiting, a centrally mediated reflex in which the expelled material originates from the stomach (and duodenum). In contrast to regurgitation, vomiting is preceded by hypersalivation, retching, and abdominal contractions. Anorexia, cough, dyspnea, and fever may be seen with secondary aspiration pneumonia, esophageal perforation, or bronchoesophageal fistula.

The diagnosis of esophageal disease is usually established by the clinical history and the results of barium contrast radiography, and/or endoscopy of the esophagus. The esophagus is not normally seen on survey radiographs, but may be visualized when it contains gas, fluid, food, or foreign material. Thoracic radiographs also may demonstrate complications of esophageal disease, especially aspiration pneumonia. Barium sulfate paste (Esophotrast) dosed as 5–10 ml boluses is used for esophageal contrast studies. If perforation is suspected, iohexol (Omnipaque), a water-soluble non-ionic iodinated contrast agent, should be used instead, as it is less irritating to periesophageal tissues and more readily reabsorbed. Barium mixed with canned food may be preferable when a motility disorder or a stricture is suspected. In the distal one-third of the normal feline esophagus, prominent transverse folds form a distinctive herringbone mucosal pattern.

Endoscopic evaluation of the esophagus provides a noninvasive method for visually examining the esophageal mucosa and lumen and for obtaining specimens for biopsy, cytology, and culture. In addition, esophageal foreign body removal and dilation of esophageal strictures with endoscopy provides a therapeutic benefit.

Esophageal Hypomotility (Megaesophagus)

Esophageal hypomotility refers to a decrease in esophageal peristalsis. Megaesophagus is a flaccid dilated esophagus resulting from a severe diffuse motility disorder of the esophagus. Congenital and acquired forms of megaesophagus occur. A hereditary form of megaesophagus has been suspected in young cats, especially Siamese. Siamese cats with megaesophagus frequently have a concurrent gastric emptying disorder. The underlying cause of acquired megaesophagus is usually not identified. Occasionally, systemic neuromuscular disease is recognized as a cause of megaesophagus, for example, myasthenia gravis, polymyositis, lead poisoning, or dysautonomia. Loss of vagal innervation or primary CNS disease of the caudal brain stem can impair esophageal motility.

Clinical signs in cats with megaesophagus are typical of esophageal dysfunction. Regurgitation is the most consistent sign. Fever, dyspnea, and cough suggest aspiration pneumonia. If megaesophagus is secondary to a systemic neuromuscular disease, additional signs such as generalized muscle weakness, pain, or atrophy may be identified. CNS signs suggest a CNS disorder as the cause. Esophageal motility disorders are best evaluated with barium contrast fluoroscopy for assessing the intensity and coordination of esophageal peristalsis. With severe esophageal hypomotility, a dilated esophagus can be identified on routine survey and contrast radiographs. If a systemic neuromuscular disease is suspected, additional testing might include a serum acetycholine receptor autoantibody titer for myasthenia, electrodiagnostics (EMG, nerve conduction velocity), serum concentrations of muscle enzymes (CK, AST), and CSF analysis.

Treatment of esophageal hypomotility in cats is primarily supportive except in the rare case where a treatable underlying cause can be identified. The cat should be offered frequent small meals in an upright position. The cat may require a period of training to learn to eat from a platform. An upright position should be maintained for 10-15 minutes after eating so that gravity may assist entry of food into the stomach. Owners may accomplish this by holding the cat over their shoulder following meals. Moist or liquefied diets are usually better tolerated than dry foods. Cisapride (1 mg/kg q8h or 1.5 mg/kg q12h PO) is a GI prokinetic drug that increases motility of esophageal smooth muscle; however, since most of the esophagus is skeletal muscle its efficacy for treatment of idiopathic megaesophagus is questionable.

Vascular Ring Anomalies

Vascular ring anomalies are congenital malformations of the great vessels and their branches that entrap the intrathoracic esophagus and cause clinical signs of esophageal obstruction. Persistent right aortic arch (PRAA) accounts for 95% of vascular ring malformations and occurs when the embryonic right rather than the left fourth aortic arch becomes the functional adult aorta. The ligamentum arteriosum continues to develop from the left side, thus forming a band that crosses over the esophagus to connect the main pulmonary artery and the anomalous aorta. Esophageal compression occurs by the aorta on the right, the ligamentum dorsolaterally on the left, the pulmonary trunk on the left, and the base of the heart ventrally.

Affected cats are usually presented as kittens for regurgitation of solid food that began at the time of weaning. Most cats are presented before six months of age. Regurgitation of undigested food usually occurs immediately after eating but is sometimes delayed as ingesta is retained in a large esophageal pouch that develops cranial to the obstruction. Liquids and semisolid food are preferentially retained. On physical examination, most cats are underweight.

The dilated esophagus appears as a food or fluid-filled density cranial to the base of the heart. On the ventrodorsal view, the normal bulge of the aortic arch to the left is absent. A barium esophagram can confirm the location of esophageal obstruction and the severity of secondary esophageal distention. Endoscopy shows extraluminal compression by the ligamentum.

Definitive therapy for PRAA is surgical ligation and transection of the ligamentum arteriosum. Clinical improvement is usually noted after surgery; however, mild esophageal distention may persist, especially if a large pouch was present prior to surgery. Recovery of normal esophageal function is best when the surgery is performed at an early age.

Esophageal Foreign Body

Esophageal foreign bodies are an occasional problem of cats. Exposure usually occurs because of their hunting and playing behavior. The most common foreign bodies (FB) are string, needles, fishhooks, pins, hairballs, and bones (especially V-shaped avian bones). Esophageal FBs usually lodge at the thoracic inlet, the base of the heart, or the hiatus of the diaphragm because of the constricting effect of surrounding soft tissue structures in these areas. The extent of secondary esophageal damage depends on the type of object, its size and shape, and the duration of time in contact with the mucosa. Potential complications of esophageal FB include esophagitis, perforation with mediastinitis or abscess, stricture, and rarely, bronchoesophageal fistula. Abnormal esophageal motility may predispose to recurrent esophageal hairballs.

Cats with esophageal FB are usually presented for acute onset of gagging, retching, salivation, dysphagia, repeated swallowing, or regurgitation. Signs of depression, anorexia, fever, cough, and dyspnea may suggest secondary aspiration pneumonia or esophageal perforation. A history of recent FB ingestion may be elicited from the owners. With needles, an attached thread may be found wrapped around the base of the tongue. Foreign bodies in the cervical esophagus may be palpable. Survey cervical or thoracic radiographs are usually diagnostic for metal or bone FBs. Thoracic radiographs should be evaluated for secondary aspiration pneumonia. Findings of pneumomediastinum, pneumothorax, mediastinitis, or pleural effusion suggest esophageal perforation (see following section). Contrast radiography may be necessary to identify radiolucent objects. Most esophageal FBs can be extracted endoscopically or pushed into the stomach for easier surgical extraction via gastrotomy or for dissolution (in the case of bones). Esophageal FBs should be considered an emergency and removal should not be delayed, because the likelihood of complications increases with time.

Once the object is removed, the mucosa is assessed for hemorrhage, erosions, lacerations, or perforations. Following an uncomplicated FB retrieval, oral food and water are withheld for 24 to 48 hours and parenteral fluids are administered. If the mucosa is damaged, parenteral broad-spectrum antibiotics such as amoxicillin should be given to control bacterial contamination of the damaged mucosa. Small amounts of soft food are gradually introduced.


Causes of esophagitis in cats include esophageal foreign bodies, ingestion of chemical irritants, thermal injury from ingestion of overheated (microwaved) food, and gastroesophageal (GE) reflux secondary to general anesthesia, persistent vomiting, hiatal hernia, or indwelling nasogastric tubes. Although the fastidious eating habits of cats makes ingestion of caustic chemicals unlikely, chemical contaminants on the haircoat may be ingested during grooming behavior. Retention of highly acidic medications such as doxycycline in the esophagus may cause severe irritation.

Esophageal damage caused by GE reflux is primarily attributed to mucosal contact with gastric acid, pepsin, bile salts, and pancreatic proteolytic enzymes. Intermittent GE reflux probably occurs normally in many animals, but is not associated with signs because of efficient esophageal clearance mechanisms. General anesthesia has been associated with reflux esophagitis and subsequent esophageal stricture in cats. Reflux esophagitis may also result from impaired GES function caused by hiatal hernia (see later section). Once esophagitis occurs from any cause, it may be perpetuated by GE reflux resulting from a reversible decrease in GE sphincter (GES) pressure.

Clinical signs of esophagitis are similar to other esophageal diseases, including dysphagia, regurgitation, odynophagia, repeated swallowing, and excessive salivation. With mild esophagitis, signs may be absent. Vomiting and regurgitation can be observed concurrently when esophagitis is associated with a hiatal hernia or secondary to persistent vomiting. When esophagitis occurs secondary to anesthesia, signs usually begin two to 14 days post-anesthesia. Concomitant stomatitis and oral ulcerations may suggest ingestion of a caustic chemical as the cause.

Survey radiographs are usually unremarkable; however, small amounts of gas may be seen in the esophagus and mild, focal esophageal dilatation may be present due to delayed motility. Contrast studies are often normal, but when esophagitis is severe and deep, the mucosal surface may appear irregular and the lumen may be segmentally narrowed. This radiographic appearance can be difficult to distinguish from a fibrous stricture.

Endoscopy is the most sensitive method for detecting esophagitis. Findings include mucosal erythema, hemorrhage, increased friability, erosions or ulcers, and pseudomembranes. If gastroesophageal reflux is the underlying cause of esophagitis, lesions are most severe in the distal esophagus and the gastroesophageal junction may appear wide open.

Mild esophagitis may resolve on its own without therapy, especially when the underlying cause (e.g., foreign body) is gone. General treatment recommendations for esophagitis are as follows: 1) maintain adequate nutrition using frequent, small amounts of a non-abrasive soft food, or indwelling gastrostomy tube feeding in severe cases; 2) control mucosal bacteria with antibiotics such as amoxicillin, or amoxicillin-clavulanate; 3) decrease GE reflux and promote gastric emptying using either cisapride (Propulsid®) at 1 mg/kg q8h PO, or metoclopramide at 0.2–0.4 mg/kg q8h PO or 1-2 mg/kg per 24 hr by constant rate IV infusion; 4) decrease gastric acidity using omeprazole or an H2 blocker such as cimetidine, ranitidine, or famotidine; and 5) provide mucosal cytoprotection using sucralfate suspension (Carafate®) 250 mg (2.5 ml) per cat q8h PO. Corticosteroids may prevent fibrosis in severe cases.

Esophageal Stricture

An intramural esophageal stricture results when severe esophagitis involving the submucosa and muscularis heals by fibrosis. Strictures can be single or multiple. Although esophageal stricture can occur after any severe mucosal injury, it is most commonly a complication of reflux esophagitis after anesthesia and esophageal foreign bodies. Strictures may also occur after esophageal surgery, ingestion of caustic substances (including medications such as doxycycline), vomiting of large hairballs, and secondary reflux esophagitis associated with a hiatal hernia. Clinical signs of esophageal stricture usually include progressively worsening dysphagia of solid foods, regurgitation immediately after eating, and weight loss in spite of a ravenous appetite. Clinical signs from a stricture usually occur within five to 14 days after onset of esophageal injury.

Esophageal stricture can be diagnosed by either barium contrast radiography or endoscopy. Survey radiographs are often normal unless the esophagus is distended with food, fluid, or air proximal to the stricture. Secondary aspiration pneumonia may also be detected. The lumen is narrowed or obstructed on a contrast esophagram. Endoscopically, an esophageal stricture appears as a ridge, ring, or web of fibrous tissue, which narrows the lumen (average diameter is 3–4 mm) and fails to distend with insufflation. Over 75% are in thoracic esophagus and multiple strictures (two or three) are common. Adjacent mucosa may be inflamed, hemorrhagic, or ulcerated.

Conservative management of esophageal strictures by endoscopically guided balloon dilation is effective in most cases. Mechanical dilation of the stricture is performed under general anesthesia with endoscopic visualization. Balloon catheters with a balloon size (when inflated) of 10 or 15 mm in diameter and 6 to 8 cm in length are used. The catheter diameter when deflated is 2.8 mm and can be passed through the lubricated operating channel of many endoscopes or it can be guided alongside the endoscope. The deflated balloon is inserted into the lumen of the stricture and then inflated to 40–50 psi for one to two minutes while pressure is monitored manometrically (Marsh gauge). The procedure is repeated at 3 to 5 day intervals for a minimum of three treatments. The total number of dilations is variable (averaging four times, ranging three to 10) and is determined by the severity of the stricture and the clinical response. Long term follow-up has found complete or partial resolution of clinical signs in 85% of dogs and cats with strictures treated by endoscopic balloon dilation. Serious complications (hemorrhage, perforation) are rare. During the course of dilations and for two to three weeks following the last dilation, therapy for esophagitis is used as described previously.

Hiatal Hernia and Gastroesophageal Intussusception

Hiatal hernia and gastroesophageal intussusception are uncommon in cats. A sliding hiatal hernia is a protrusion of any structure (usually the distal esophagus and stomach) through the esophageal hiatus of the diaphragm into the thorax. In GE intussusception, the stomach is prolapsed into the lumen of the distal esophagus. Both hiatal hernia and GE intussusception may be intermittent or persistent. Hiatal hernia can be congenital or acquired.

Cats with hiatal hernia or chronic intermittent GE intussusception usually present for both intermittent vomiting and regurgitation. Vomiting may occur immediately after eating or be unrelated to meals. Hypersalivation and weight loss may also be seen. Small hernias may not cause clinical signs and intermittent organ displacements may cause signs to be intermittent. Respiratory distress can be a prominent clinical sign with large hiatal hernias. The clinical signs of hiatal hernia are mostly because of secondary reflux esophagitis. Displacement of the GE junction into the thorax results in a loss of integrity of the GES mechanism, thus predisposing to reflux. GE intussusceptions can also cause esophageal obstruction.

Survey radiographs may demonstrate a soft tissue and gas density mass (the stomach) in the dorsocaudal mediastinum. An esophogram is usually required to confirm a hernia or intussusception. With a hiatal hernia, the gastroesophageal junction and gastric rugae are visible cranial to the diaphragm, but the linear relationship between the esophagus and stomach is preserved. Gastroesophageal reflux may also be demonstrated. With an intussusception, gastric rugae are seen within the esophageal lumen and esophageal obstruction is present. Endoscopy can assess secondary reflux esophagitis and identify intussusception.

The clinical significance of small intermittent hiatal hernias and intussusceptions is debatable; medical therapy for reflux esophagitis will usually control clinical signs. Surgery is the treatment of choice for large hiatal hernias and intussusceptions. Surgery is performed only after a thorough attempt has been made to exclude other causes of regurgitation and vomiting and after medical management of reflux esophagitis has not been beneficial. Megaesophagus with decreased esophageal contractions has been observed in dogs and cats with large hiatal hernias. Esophageal motility returns to normal within three months after surgical repair of the hernia and treatment for reflux esophagitis. However, when megaesophagus is diagnosed concurrently with GE intussusception, megaesophagus is more likely to be the cause rather than a consequence of the intussusception.

Esophageal Neoplasms

Primary esophageal neoplasms are rare. Squamous cell carcinoma of elderly cats is the most common primary esophageal neoplasm. Esophageal neoplasia causes chronic progressive signs of esophageal disease (regurgitation, dysphagia, ptyalism, weight loss, anorexia). Survey radiographs may be normal or may reveal a soft tissue mass in the region of the esophagus. With obstruction, the esophagus may be dilated with air, fluid, or food proximal to the tumor site. An irregular intraluminal filling defect on a barium esophagram is indicative of esophageal neoplasia. Endoscopically, squamous cell carcinoma usually appears as a focal proliferative mass, which may occlude the lumen. Surgical resection is not usually feasible or successful.

Periesophageal Masses

Mass lesions arising from periesophageal tissues may cause regurgitation because of compression of the esophagus with partial or complete obstruction. Mediastinal lymphoma is most common, although any large tumor or abscess arising from mediastinal structures (e.g., thymus, lymph node, lung) could potentially cause secondary esophageal compression. Lymphoma is mostly in young cats, whereas thymoma occurs in elderly cats. Survey and/or contrast thoracic radiography usually identifies the mass. Lymphoma is diagnosed by fluid or FNA cytology.

Speaker Information
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Robert Sherding
United States

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