Esophagitis

Etiology

Esophagitis is an acute or chronic inflammatory disorder of the esophageal mucosa that occasionally involves the underlying submucosa and muscularis. It most often results from chemical injury from swallowed substances, esophageal foreign bodies, or gastro-esophageal reflux. The esophageal mucosa has several important barrier mechanisms to withstand caustic substances, including stratified squamous epithelium with tight intracellular junctions, mucus gel, and surface bicarbonate ions. Disruption of these barrier mechanisms results in inflammation, erosion, and/or ulceration of the underlying structures (Eastwood et al., 1975; Biancani et al. 1984; Geisinger et al., 1990; Han et al, 2003). Clinical signs are related to the type of chemical injury, the severity of inflammation, and the involvement of structures underlying the esophageal mucosa, e.g., the muscularis (Cassidy et al., 1992). Esophagitis may occur at any age, however, young animals with congenital esophageal hiatal hernia may be at increased risk for reflux esophagitis (Callan et al., 1993; Pratschke et al., 2001). Cats appear to be particularly susceptible to doxycycline-associated esophagitis and oesophageal stricture (Melendez et al., 1998; Graham et al., 2000; Westfall et al., 2001). Anaesthesia, poor patient preparation, and poor patient positioning during anaesthesia places other animals at risk for gastro-esophageal reflux and esophagitis (Pearson et al., 1978a; Galatos et al., 1995a, 1995b).

Treatment

Animals with mild esophagitis may be managed on an out-patient basis. Oral food intake should be withheld for 2-3 days in cases of mild esophagitis. Animals with more severe esophagitis (e.g., complete anorexia, dehydration, aspiration pneumonia) may require hospitalization. Food and water should be withheld in such cases, and animals may need additional nutritional maintenance either by enteral or total parenteral nutrition. Oral sucralfate suspensions (0.5-1.0 grams p/o, tid) are the most important and specific therapy for esophagitis (Clark et al., 1987; Katz et al., 1988). Sucralfate suspensions are more therapeutic than intact sucralfate tablets because the liquid suspension will bind more readily to an erosive or ulcerative site. Gastric acid secretory inhibitors (e.g., cimetidine 5-10 mg/kg p/o or i/v, tid-qid; ranitidine 1.0-2.0 mg/kg p/o or i/v, bid-tid; famotidine 0.1-0.5/mg/kg p/o or i/v bid; omeprazole 0.7 mg/kg p/o, sid) might be useful in suspected cases of gastro-esophageal reflux. Broad spectrum antibiotics should be used in animals with aspiration pneumonia or severe esophagitis.

Esophageal Stricture

Etiology

Esophageal stricture is an abnormal narrowing of the esophageal lumen. The most important etiologies of stricture are chemical injury from swallowed substances, esophageal foreign bodies, esophageal surgery, and intraluminal or extraluminal mass lesions (neoplasia or abscesses). Anesthesia, poor patient preparation, and poor patient positioning during anesthesia place some animals at risk for gastro-esophageal reflux, esophagitis, and subsequent stricture formation (Pearson et al., 1978a; Leib et al., 2001; Adamama-Moraitou et al., 2002). Cats appear to be particularly susceptible to doxycycline-associated esophagitis and esophageal stricture (Melendez et al., 1998; Graham et al., 2000; Westfall et al., 2001). Fibrosis and mass compression are the most important pathogenetic mechanisms involved in stricture formation.

Treatment

Oral feedings should be withheld in cases of severe stricture. In such cases, a temporary gastrostomy tube may be placed at the time of esophageal dilation as a means of providing continuous nutritional support. Liquid meals should be used when re-instituting oral feedings. Animals may be discharged from the hospital after adequate rehydration, dilation of the affected esophageal segment, nutritional intervention, and appropriate therapy for aspiration pneumonia. Esophageal strictures are best managed with mechanical dilation. Dilation may be achieved with balloon dilation catheters or bougienage tubes (Burk et al., 1987; Harai et al., 1995; Leib et al., 2001). Balloon dilations are safer and more effective in applying radial forces to expand the stricture site. A greater risk of perforation is associated with the use of bougienage tubes due to shearing forces applied by the instrument. Multiple re-dilations at 1- to 2-week intervals may be necessary until the stricture is resolved (Willard et al., 1994; Melendez et al., 1998; Leib et al, 2001; Adamama-Moraitou et al., 2002). Esophageal dilation is best performed with direct observation at the time of endoscopy, but it could be performed with videofluoroscopy.

Medical therapies aimed at treating the inflammatory component of this lesion (esophagitis) are best used as adjunctive therapy to mechanical dilation.

Hiatal Hernia

Etiology

Two types of hiatal hernia have been recognized in the dog and cat: 1) sliding hiatal hernia, in which the abdominal segment of the esophagus and parts of the stomach are displaced cranially through the esophageal hiatus, and 2) para-esophageal hiatal hernia, in which the abdominal segment of the esophagus and caudal esophageal sphincter remain in a fixed position but a portion of the stomach herniates into the mediastinum alongside the thoracic esophagus. Sliding hiatal hernia is the most common form and may occur as a congenital or acquired lesion in the dog and cat.

Congenital sliding hiatal herniae have been reported in the Chinese Shar-pei, Chow, English bulldog, and French bulldog breeds. The hernia results from incomplete fusion of the diaphragm during early embryonic development. Affected animals develop clinical signs shortly after weaning (Callan et al., 1993).

Acquired hiatal hernia may occur in any breed of dog or cat. The pathogenesis of acquired hiatal hernia is incompletely understood, but may result from chronic increases in intra-abdominal pressure with chronic vomiting disorders, or from chronic increases in negative intra-thoracic pressure in animals with intermittent airway obstruction, e.g., laryngeal paralysis (Washabau, 2000).

Treatment

A sliding hiatal hernia is not always associated with clinical signs, particularly the acquired form of the disease. When animals develop clinical signs, medical therapy should be attempted first. Medical therapy is similar to that for gastro-esophageal reflux and should be directed at reducing gastric acid secretion (e.g., H₂ receptor antagonism, H⁺, K⁺ ATPase inhibition), restoring the health of the esophageal mucosa (e.g., sucralfate), and increasing the tone of the caudal esophageal sphincter (e.g., metoclopramide or erythromycin). Many acquired sliding hiatal hernias will respond to conservative medical therapy (Lorinson and Bright, 1998), although laryngeal surgery (e.g., partial laryngectomy or lateralization of the vocal folds) should be considered if laryngeal paralysis has contributed to the pathogenesis of the hernia. Congenital hiatal herniae often require surgical correction. Diaphragmatic crural apposition, esophagopexy, and gastropexy are usually sufficient to restore normal hiatus anatomy (Prymak et al., 1989). Fundoplication procedures may be performed but are generally not necessary (Prymak et al., 1989; Cox et al., 2000).

Esophageal Neoplasia

Etiology

Esophageal cancer accounts for less than 0.5 per cent of all cancers in the dog and cat (Ridgway and Suter, 1979; Head et al., 2002). Tumours of the esophagus may be of primary esophageal, peri-esophageal, or metastatic origin. The most common primary esophageal tumours in the dog are osteosarcomas and fibrosarcomas, particularly in areas of Spirocerca lupi endemicity. Spirocercal esophageal granulomas may undergo metaplastic or neoplastic transformation to fibrosarcomas and osteogenic sarcomas (Fox et al., 1988; Harrus, 1996; Berry, 2000). Squamous cell carcinoma is the most common primary esophageal tumour in the cat. Less commonly reported primary esophageal tumours of the dog and cat include leiomyo(sarco)mas, scirrhous carcinomas, and adenocarcinomas (Frost et al., 2003). Metastatic lesions appear to be the most common esophageal tumours in dogs and cats and include thyroid, pulmonary, and gastric carcinomas (Swann and Holt, 2002). Tumors of the peri-esophageal structures (lymph node, thyroid, thymus, and heart base) cause local esophageal invasion and/or direct mechanical obstruction of the esophagus.

Treatment

Chemotherapy, surgical resection, and radiation therapy are conventionally accepted methods for the treatment of malignant esophageal neoplasia (Head et al., 2002). Radiation therapy may be complicated by acute or chronic injury to adjacent mediastinal structures (Gillette et al., 1992; Gillette et al., 1998), while surgical resections are complicated by inadequate surgical exposure, lengthy resections, tension on the anastomosis, and poor healing properties of the thoracic esophagus. Photodynamic and cryotherapy have been studied under physiologic circumstances (Panjehpour et al., 2002; Pasricha et al., 1999), but have not yet been applied in clinical patients. Recent developments with bioresorbable collagen or extracellular matrix scaffolds may help to facilitate repair following esophageal resection (Yamamoto et al., 1999; Badylak et al., 2000; Kovacs et al., 2001). Lymphosarcoma may be treated in some cases with chemo- or immunotherapy. Benign esophageal neoplasia, e.g., leiomyoma, generally have a favorable prognosis following surgical resection.