Diagnosing and treating esophageal diseases in dogs and cats (Proceedings)

Basic anatomy and Physiology

The basic anatomical structures of the esophagus are the upper esophageal sphincter (UES), the body of the esophagus and the lower esophageal sphincter (LES). The entire canine esophagus is composed of two layers of striated muscle, while the distal third of the feline esophagus is composed of striated muscle1, 2. The esophagus is innervated by the vagus nerve and its branches (glossopharyngeal, pharyngeal, recurrent laryngeal nerves) 1. The UES, composed of the cricopharyngeus and thyropharyngeus muscles and the cricoid cartilage, remains closed at all times, relaxing momentarily to allow passage of a bolus 2. The LES is a physiologic rather than a true anatomic sphincter2. It is composed of an outer longitudinal muscle layer and an inner smooth muscle layer 2. In health, the LES remains closed except to allow passage of a bolus and prevents reflux of stomach contents into the esophagus 2. Esophageal peristalsis is stimulated by the oropharyngeal stage of swallowing and the movement of a bolus across the UES (primary peristalsis) as well as by distension of the body of the esophagus by the bolus (secondary peristalsis) 2.

Clinical signs of Esophageal Disease

Regurgitation is the hallmark clinical sign of esophageal disease. Differentiation of regurgitation from vomiting is essential. Regurgitation is the passive, retrograde movement of ingested material, usually before it reaches the stomach. Food and fluid move in an orad direction by force of gravity. Regurgitated material is expelled with minimal or no premonitory signs of nausea, distress or retching / abdominal effort. The regurgitant material originates from the oral cavity, pharynx or esophagus and as such is usually undigested. Regurgitation may occur immediately after intake of food but is often delayed for several hours or more. Additional clinical signs can include repeated attempts to swallow a single bolus, painful swallowing and failure to thrive or loss of body condition. Aspiration pneumonia, (dyspnea, cough, nasal discharge, fever, moist crackles on thoracic auscultation) is a common complication1.

Persistent right aortic arch (PRAA)

Vascular ring anomalies are congenital malformations of the major vessels of the heart that entrap the esophagus and cause esophageal obstruction1. The most common vascular ring anomaly in dogs and cats is persistence of the right aortic arch. The esophagus and trachea are entrapped by the pulmonary artery / heart base on the left and ventrally, the aorta on the right, and the ligamentum arteriosum dorsolaterally on the left1. Clinical signs of regurgitation and failure to thrive (stunted growth, thin body condition) most commonly develop at the time of weaning, when the animal first attempts to ingest solid food. Respiratory signs such as cough, dyspnea, nasal discharge and fever signal secondary aspiration pneumonia. Plain thoracic radiographs are potentially diagnostic and may reveal: (1) Lateral: esophageal body dilation cranial to the base of the heart and possibly ventral curvature of the trachea cranial to the heart; (2) VD or DV: Leftward deviation of the trachea cranial to the cranial border of the cardiac silhouette is a reliable sign of PRAA in dogs.1,3 Abrupt attenuation of the barium column at the base of the heart and cranial esophageal dilatation is expected on barium contrast esophagram. Thoracic radiographs must be carefully evaluated for other intrathoracic pathology or anomalies and evidence of secondary aspiration pneumonia. In some cases, fluoroscopic or computed tomography evaluation may be necessary. Definitive treatment is surgical ligation and transection of the ligamentum arteriosum1. Supportive care may need to include treatment of aspiration pneumonia (broad spectrum antibiotics, supplemental oxygen, nebulization, etc) and gastrotomy tube feeding. 90% of animals display significant clinical improvement post-operatively1. Some degree of esophageal hypomotility and regurgitation may persist post-operatively, especially if clinical signs were severe and / or longstanding. Early diagnosis and prompt treated is recommended1.

Esophageal Foreign Body

Esophageal foreign bodies usually lodge at points of decreased esophageal diameter; namely the thoracic inlet, heart base and at the point where the esophagus traverses the diaphragm. In addition to mechanical obstruction, retained foreign bodies can also cause tissue edema, abrasion, laceration and perforation (either directly due to the potentially sharp nature of the object or secondary to tissue necrosis at the site of obstruction). Small breed dogs are most commonly affected5. Clinical signs relate to the size of the object, degree of obstruction (partial vs. complete), duration of obstruction, degree of associated esophageal damage and presence or absence of esophageal perforation. Most dogs are presented for evaluation of acute onset regurgitation, halitosis, gagging, hypersalivation, discomfort, anorexia and/or painful or exaggerated swallowing1. Known or observed ingestion of bones, toys, etc. may be a component of the medical history. Obstruction by smaller objects may go undiagnosed for a longer period of time due to milder clinical signs1. Partial obstruction may allow passage of liquids and small solids, while complete obstruction generally results in regurgitation of both liquids and solids. Coughing, dyspnea/tachypnea, nasal discharge, fever and lethargy are suggestive of aspiration pneumonia or esophageal perforation, with resultant pneumothorax (± pneumomediastinum) and/or pleural effusion ( ± mediastinitis). Most esophageal foreign bodies can be identified on plain thoracic radiographs. The entire esophagus should be evaluated for soft tissue or foreign body opacities, with special attention paid to the regions of the thoracic inlet, heart base and diaphragmatic hiatus. The esophagus may be dilated cranial to the foreign object. Thoracic radiographs must be carefully evaluated for evidence of aspiration pneumonia and esophageal perforation (pneumomediastinum, mediastinitis, pleural effusion) 1. Positive contrast esophagram (using a water soluble agent such as iohexol if esophageal perforation is suspected) or endoscopic exam is occasionally required to identify radiolucent objects (e.g. chicken bones) 1. Esophageal obstruction due to a foreign body is an urgent medical condition that must be dealt with promptly1. Endoscopic retrieval of the object is the treatment of choice. Objects may be retrieved through the mouth but distal esophageal foreign bodies may be pushed into the stomach1. Once in the stomach, the size and nature of the object will determine whether a gastrotomy is required. Immovable objects, objects that will cause significant esophageal damage if retrieved endoscopically or cases where esophageal perforation is suspected, require surgical retrieval via thoracotomy. Treatment after foreign body removal will depend on the degree of esophageal injury and can include restriction of food and water for 24-48 hours depending on the severity of esophageal injury1, standard treatment of esophagitis (see below) and antibiotics (in case of aspiration pneumonia or perforation). Gastrotomy tube feeding is generally required for medical management of esophageal perforations, post-esophageal surgery and for patients who are unable to maintain adequate nutrition due to complications such as severe esophagitis or esophageal stricture. The prognosis for full recovery following uncomplicated endocscopic retrieval is good to excellent1. Historically a more guarded prognosis was accorded to animals with severe esophageal injury, perforation or those requiring esophageal surgery. In a recent retrospective review of 14 dogs requiring surgical transthoracic esophageal foreign body retrieval, only 1 dog was euthanised at the time of surgery and 2 dogs experienced post-operative complications (pyothorax, seroma)5. Esophageal stricture formation may be more likely and mortality rate higher, in dogs with esophageal obstruction due to dental chew treat6.

Esophageal Stricture

An esophageal stricture is an abnormal circumferential narrowing of the esophageal lumen secondary to significant esophageal injury. Esophageal injury that extends beyond the mucosa and into the muscular layer may heal by fibrosis and cause narrowing of the lumen1.

The most important causes of esophageal stricture are gastroesophageal reflux (GER) under general anesthesia (most common), ingestion of caustic substance or medication (e.g. doxycycline in cats), trauma from esophageal foreign body or complication of esophageal surgery1. The time period between esophageal injury and development of a stricture is usually 1-3 weeks but can be as long as 4-6 weeks1. As such, clinical signs of esophageal dysfunction that occur within 6 weeks of a predisposing event are strongly suggestive of an esophageal stricture. Progressive clinical signs of esophageal obstruction predominate (see above). Depending on the size of the stricture, some animals may be able to swallow water or liquid meals but not solid foods. Complications such as aspiration pneumonia and loss of body condition are common. Survey thoracic radiographs are usually normal save for possible evidence of aspiration pneumonia. Barium (or barium mixed with food) positive contrast radiographs demonstrate narrowing of the esophageal lumen with or without esophageal dilation cranial to the stricture1. Balloon dilation under endoscopic guidance is generally considered the treatment of choice1 , although a recent report suggests bougienage is equally safe and effective7. A balloon catheter is passed through the endoscope to the level of the stricture and held inflated 2-3 minutes, generating a radial force that dilates the stricture1,8. To minimize stricture recurrence, balloon dilations are performed multiple times at intervals of 2-3 days1. In a retrospective study of canine and feline esophageal strictures, the median number of balloon procedures was 2, with a range of 1-59. Complications can include mucosal hemorrhage, stricture recurrence and esophageal rupture1, 9. Supportive care should include medical therapy for esophagitis (see below) and potentially gastric tube feeding. Oral prednisone (1 mg/kg q24 hrs) or triamcinolone injections at the stricture site immediately post-ballooning may decrease stricture recurrence by delaying healing by fibrosis1,8,9. There is currently insufficient data to routinely recommend the use of prednisone but data from the human medical suggests triamcinalone injections are effective. The prognosis for esophageal strictures is good with repeated balloon dilation and proper supportive care. An acceptable outcome (ability to eat without or with no more than 1 episode of regurgitation per week) was reported in 88% and 71% of patients treated by balloon dilation or bougienage, respectively7,9.

Neoplasia

Tumours of the esophagus are rare in the dog and cat. Neoplasms may be primary esophageal, periesophageal, or metastatic in origin1. Fibrosarcoma and osteosarcoma are the most common malignant tumours in dogs while squamous cell carcinoma the most common in cats1. Extraesophageal tumours can arise from lymph nodes, thyroid, thymus, heart base, etc.

Megaesophagus

Megaesophagus is a term used to describe generalized esophageal dilation and aperistalsis1. Congenital megaesophagus is uncommon. Breed predispositions, clinical signs and diagnostic evaluation are similar to the acquired condition, except that the age of presentation is generally < 3 months2. As the etiology is unknown, treatment is limited to conservative medical management and the prognosis is poor. Acquired megaesophagus is more common in dogs that in cats. Predisposed breeds may include the Irish setter, Great Dane, German shepherd, Labrador retriever, Chinese Shar Pei, Newfoundland, miniature schnauzer, fox terrier and Siamese cat1,2. Animals typically present with clinical signs of esophageal dysfunction, weight loss and /or aspiration pneumonia. Importantly, some animals will present with clinical evidence of aspiration pneumonia without a history of regurgitation; suggesting the animal is swallowing/aspirating the material without expelling it from the oral cavity. Esophageal distension from retained food and fluid is occasionally palpable as a swelling of the ventral cervical region at the thoracic inlet2. Plain thoracic radiographs usually reveal generalized esophageal dilation2 with or without evidence of aspiration pneumonia. Barium contrast esophagram may be required to detect subtle hypomotility and to rule out an obstructive lesion if plain radiographs are normal2. In some cases, fluoroscopic evaluation may be necessary to assess esophageal motility. Most cases of acquired megaesophagus are idiopathic in nature. Myasthenia gravis (focal or generalized) accounts for as many as 25% of cases of acquired megaesophagus1. Myasthenia gravis with megaesophagus can occur as a paraneoplastic syndrome secondary to thymoma. Thoracic radiographs must be closely evaluated for a mass in the region of the cranial mediastinum suggestive of thymoma. Hypothyroidism and hypoadrenocorticism (usually the atypical form) are infrequently associated with the development of megaesophagus. In addition to a complete blood count, serum biochemical profile and urinalysis, acetylcholine receptor antibody titres, total thyroid hormone concentration and ACTH-stimulation testing are recommended in all dogs with megaesophagus. If total thyroid hormone concentration is found to below the reference range, measurement of free T4 and thyroid stimulating hormone concentration are required to differentiate hypothyroidism from euthyroid sick syndrome. Other less common causes of megaesophagus include systemic lupus erythematosus, polymyositis/myopathy, dysautonomia and lead or organophosphate toxicosis. Animals with acquired megaesophagus secondary to an identifiable underlying condition should be treated for the specific disorder. All animals with megaesophagus should be offered small, frequent meals from an elevated or upright position to assist passage of food into the stomach1. A variety of food consistencies should be offered (kibble vs. canned food vs. gruel) to determine which the animal best tolerates1,2. The animal should be kept calm and quiet for a period approximately 30 minutes after eating during which time the owner may need to hold the animal in an elevated position (e.g. standing on hind legs). Malnourishment (due to an inability to keep food down), inability to administer oral medications or recurrent aspiration pneumonia are indications for gastrotomy tube placement1. Gastrotomy tube feeding may decrease but does not negate the risk of developing aspiration pneumonia. Antibiotics are only indicated for treatment of aspiration pneumonia1. Promotility drugs are of uncertain benefit. Metoclopramide and cisapride are smooth muscle prokinetic agents and as such have no effect on the striated muscle of the canine esophagus1. The anecdotal clinical improvement sometimes observed following treatment with these agents may be due to decreased GER secondary to improved stomach emptying. As such, treatment with metoclopramide (dogs or cats: 0.2-0.4 mg/kg PO q8hrs) or cisapride (cats: 0.1-0.5 mg/kg PO q8-12hrs, max 5mg total dose) may be useful. Additional treatment is as per esophagitis (described below). The prognosis for acquired idiopathic megaesophagus is guarded to poor1,2. Reasons for euthanasia include repeated episodes of aspiration pneumonia, inability to maintain proper nutrition or the irreversible nature of the disease1,2. The prognosis for dogs with megaesophagus secondary to myasthenia gravis is favourable with approximately 50% of dogs responding to treatment with acetylcholine esterase inhibitors and immunosuppression2.

Esophagitis

Inflammation of the esophageal mucosa may be caused by GER (most commonly), persistent vomiting, chemical injury (e.g. doxycycline in cats), trauma (e.g. esophageal foreign body, trichobezoar), neoplasia or primary infection (e.g. pythiosis)10. The esophagus is easily damaged by GER because, unlike the stomach, the esophagus does not have a mucus-bicarbonate barrier or protection from endogenous prostaglandins10. Esophageal inflammation alters esophageal motility and causes dysfunction of the LES, favouring regurgitation and GER, respectively. Clinical signs may be due directly to esophageal dysfunction or to secondary esophageal stricture10. Plain thoracic radiographs are usually normal or infrequently reveal segmental or diffuse esophageal dilation1. Barium contrast study may reveal an irregular esophageal mucosa with some retention of barium10. Strictly speaking, esophagitis is an endoscopic (erythema, friable tissue, bleeding, erosion) and histologic diagnosis, however most patients are diagnosed and treated based on clinical suspicion1, 10. Successful treatment of esophagitis requires elimination of the underlying cause and prevention of exposure to gastric acid, thereby allowing the inflamed mucosa to heal10. Treatment should include prokinetic agents, antacids and cytoprotective agents. Prokinetic agents such as metoclopramide (0.2-0.4 mg/kg PO q8hrs) and cisapride (0.25 mg/kg PO q8-12 hrs) decrease GER by promoting gastric emptying10,11 Inhibition of gastric acid secretion protects the esophageal mucosa by decreasing the acidity of the refluxed material. H2 receptor antagonists (famotidine 0.5 mg/kg IV or POq12 hours OR ranitidine 1-2 mg/kg IV, SQ or PO q12 hours) or H2 receptor blockers (omeprazole 1.0 mg/kg PO q24 hours OR pantoprazole 1 mg/kg q24 hours) are indicated. Sulcralfate suspension (0.5 to 1.0 g orally, three times a day) selectively binds to eroded mucosa and provides barrier protection against refluxed gastric contents. However, since the efficacy of sucralfate in the non-acidic environment of the esophagus is questionable, it should not be used as single agent therapy11. Animals should be fed frequent small meals of a soft and easily digestible diet. This may be a commercial canned diet or the animals kibble diet soaked in water. Animals having more severe esophagitis, especially those with anorexia, weight loss, or the inability to retain food, may require gastrostomy tube feeding.

References

Jergens AE. Diseases of the esophagus. In: Ettinger SJ, Feldman EC, eds. Textbook of Veterinary Internal Medicine. 7th ed. St. Louis: Saunders Elsevier; 2010:1487-1499.

Johnson BM, et al. Canine megaesophagus. In: Bonagura JD, Twedt DC, eds. Current Vaterinary Therapy XIV. St. Louis: Saunders Elsevier; 2009:486-492.

Buchanan JW. Tracheal signs and associated vascular anomalies in dogs with persistent right aortic arch. JVIM 2004; 18: 510-514.

Willard MD. Disorders of the oral cavity, pharynx and esophagus. In: Nelson RW, Couto CG, eds. Small Animal Internal Medicine. 4th ed. St. Louis Mosby Elsevier; 2009: 414-426.

Sale GSH and Williams JM. Results of Transthoracic Esophagotomy Retrieval of Esophageal Foreign Body Obstructions in Dogs: 14 Cases(2000-2004). JAAHA 2006;42:450-456.

Leib MS and Sartor LL. Esophageal foreign body obstruction caused by a dental chew treat in 31 dogs (2000-2006). JAVMA. 2008;232:1021–1025.

Bisset SA et al., Risk factors and outcome of bougienage for treatment of benign esophageal strictures in dogs and cats: 28 cases (1995-2004). JAVMA. 2009;235:844–850.

Fraune C, et al., Intralesional corticosteroid injection in addition to endoscopic balloon dilation in a dog with benign oesophageal strictures. JSAP. 2009; 50: 550-553.

Leib MS et al., Endoscopic balloon dilation of benign esophageal strictures in dogs and cats. JVIM 2001; 15: 547-552.

Willard MD and Carsten EW. Esophagitis. In: Bonagura JD, Twedt DC, eds. Current Vaterinary Therapy XIV. St. Louis: Saunders Elsevier; 2009: 482-486.

Han E. Diagnosis and management of reflux esophagitis. Clin Tech In Small Animal Practice 2003; 18(4): 231-238.