Jubb, Kennedy & Palmer's Pathology of Domestic Animals - E-Book: Volume 2 (eBook)

Anomalies, epithelial metaplasia, and similar lesions

The mucosa of the distal portion of the feline esophagus normally has a herringbone pattern of superficial folds. Hypertrophy of the smooth muscle of the distal esophagus, most commonly the inner smooth circular layer, occurs in horses. It is usually found incidentally at autopsy, although some cases also have concurrent terminal ileal muscular hypertrophy. The lesion is considered idiopathic, but potential factors in the pathogenesis include autonomic imbalances or defects in the smooth muscle pacemaker cells normally found at these sites.

Congenital anomalies of the esophagus are very rarely recorded in domestic animals, and their interpretation as such can be difficult because similar defects may develop as sequelae of esophageal trauma or inflammation.

Congenital duplication cysts of the esophagus have been reported in horses and dogs. Esophageal cysts are classified as duplication by 3 essential criteria. The cyst must (1) be located within the esophageal wall, (2) be lined by columnar, squamous, cuboidal, ciliated, or pseudostratified epithelium, and (3) have a double muscle layer in the wall. Esophageal duplication cysts may be clinically silent; however, they manifest as space-occupying lesions if they fill with cellular debris and secretion. Potential complications are associated with compression of adjacent structures or cyst rupture.

Rare segmental aplasia of the proximal esophagus may be apparent in the neonate. A short blind pouch communicates with the pharynx, and a thin fibrous band connects it to the distal patent esophagus that follows a normal course to the stomach. Esophageal atresia and congenital esophagorespiratory communications result from anomalies occurring when the respiratory primordium buds from the embryonic foregut.

Esophagorespiratory fistulae without esophageal atresia are also rare in animals. Esophageal fistula formation is likely acquired following foreign body perforation of the esophagus; however, in calves and dogs, some are likely congenital. Short fibrous bands with a narrow epithelial-lined lumen connecting an esophagus of normal diameter with the trachea or bronchus are reported, as are small apertures connecting the lining of esophageal diverticula with the respiratory tree. The lining of such defects changes from stratified squamous to columnar respiratory epithelium in the fistula or wall of the diverticulum. Gastric distention by air in calves, and pneumonia resulting from aspiration, have been associated with esophagorespiratory fistulae.

Esophageal diverticula are irregular outpouchings or herniations of the esophageal mucosa through a defect in the esophageal tunica muscularis. They communicate with the esophagus by variously sized, often slit-like apertures. Most are probably acquired, and they occur most often in the lower cervical esophagus near the thoracic inlet and the distal thoracic esophagus just cranial to the diaphragm. Increased intraluminal pressure associated with foreign bodies, obstruction or stenosis are potential causes of pulsion diverticula, in which the mucosa is forced out through the distended or ruptured muscularis. Such diverticula may be large spherical structures with a narrow neck and are most common in the horse and dog. The rare traction diverticulum is the result of contraction of a paraesophageal fibrous adhesion, following perforation and inflammation, drawing with it a pouch of esophageal mucosa that is usually small and inconsequential. In contrast to pulsion diverticula, which have a layer of epithelium lining the inner aspect of a wall of fibrous connective tissue, traction diverticula have a wall comprised of all layers of the esophagus. Ingesta and foreign bodies may accumulate in diverticula, causing gradual enlargement with the potential for local esophagitis, ulceration, and perforation or formation of a fistula.

Other rare anomalies of the esophageal mucosa include epithelial inclusion cysts and distal esophageal papillae in cattle resembling those of the rumen, and gastric heterotopia.

Hyperkeratosis and hyperplasia of the esophageal epithelium may be signs of vitamin A deficiency or chlorinated naphthalene toxicity, which has been described in herbivores. This is accompanied by squamous metaplasia of mucous glands and ducts of the esophagus and throughout the body. Mild hyperkeratosis may be difficult to assess in herbivores because some degree of keratinization is normal and anorexia or failure to swallow results in loss of the abrasive effect of food passage leading to accumulation of keratinized squames. Parakeratosis and epithelial hyperplasia is indicative of response to epithelial injury (see later section on Esophagitis). In the distal esophagus of pigs, this lesion is often observed concomitant with ulceration of the pars esophagea of the stomach. Esophageal parakeratosis can also occur in pigs with cutaneous parakeratosis caused by zinc deficiency.

Esophagitis

Erosive and ulcerative esophagitis is a common finding associated with viral diseases causing similar lesions in the oropharynx or reticulorumen, including bovine viral diarrhea, rinderpest, bovine papular stomatitis, infectious bovine rhinotracheitis, and feline calicivirus. Epithelial proliferation or granulation tissue during healing of ulcers may result in raised opaque areas at the lesion margin or surface, respectively.

Caustic or irritant chemicals, ionizing radiation, electrochemical reactions (batteries), or heat may cause mucosal injury, the severity of which depends on the nature of the insult and duration of exposure. Mild acute insult may result in reddening of the mucosa. More severe insult results in liquefactive necrosis associated with alkalis, and coagulative necrosis associated with exposure to acids and toxins (paraquat, oak toxicosis) and may result in deep esophageal ulceration and sloughing of the mucosa.

Superficial epithelial damage heals uneventfully, though repeated insult may cause irregular epithelial hyperplasia. Ulcerated mucosa heals by granulation, and raised islands of surviving proliferative epithelium may be observed on the surface. The inflammatory reaction in ulceration frequently involves tunica muscularis and adventitia. Fibrosis and scarring may cause stricture or stenosis, if the original defect involved a significant portion of the esophageal circumference.

Reflux esophagitis occurs because of a loss of functional integrity of the lower esophageal sphincter associated with airway occlusion and increased intra-abdominal pressure, the pharmacologic effects of preanesthetic agents, or abnormality of the hiatus. Esophagitis is due to the action of gastric acid, pepsin, and probably regurgitated bile salts and pancreatic enzymes, on the esophageal mucosa. Reflux esophagitis is most common in dogs and cats as a sequel to surgery involving general anesthesia, although it may follow chronic gastric regurgitation or vomition for any cause (Fig. 1-22). In swine and horses, it may be associated with ulceration of the squamous portion of the stomach. In dogs, it can be associated with hiatus herniation. A high prevalence of apparent gastroesophageal reflux disease in the distal esophagus of premature calves was demonstrated by endoscopy; however, the pathogenesis remains unclear.

Stratified squamous epithelium appears more susceptible to the corrosive effects of gastric secretion than other types of mucosa in the lower gastrointestinal tract. Relatively short duration of exposure to refluxed gastric content is required to induce epithelial damage characterized by hyperemia, linear erosions, ulcers, or superficial...