Chapter 122 Esophagitis denotes a localized or diffuse inflammation of the esophageal mucosa. It generally is thought to result from a caustic (e.g., acid, alkali, bile salts) or chemical (e.g., drug-induced) injury that starts at the luminal surface and progresses to the deeper layers of the tissue. In people, gastroesophageal reflux disease (GERD) results from a failure of the normal antireflux barrier to protect against frequent and abnormal amounts of gastroesophageal reflux (GER). Although GER is not a disease, but a normal physiologic process occurring multiple times a day, GERD is regarded as a multifactorial process usually producing symptoms of heartburn and acid regurgitation. The most frequent mechanism for reflux is thought to result from lower esophageal sphincter (LES) incompetence. However, esophageal inflammation also may cause esophageal hypomotility and LES weakness by impairing the excitatory cholinergic pathways to the LES. In cats, these changes have been shown to be reversible with healing of the esophagus (Zhang et al, 2005). GER occurs spontaneously in healthy dogs and is not associated with exercise, positioning of the animal, or sleeping. GER also has been evaluated in anesthetized patients and is affected by positioning of the animal during anesthesia and the type of surgical procedure. It has been reported that intraabdominal procedures have a higher risk for GER, and the duration of preoperative fasting and choice of preanesthetic drugs influence the incidence of GER during anesthesia (Galatos and Raptopoulos, 1995). No information exists on quantification of intraoperative GER and the risk for subsequent esophageal inflammation. Hiatal hernias may predispose to GER in dogs and cats because of the altered functional anatomy of the gastroesophageal pressure barrier (losing the intrinsic support of the crural diaphragm) and impaired esophageal acid clearance. Reflux esophagitis resulting from upper airway obstruction can become a problem in brachycephalic dogs (Lecoindre and Richard, 2004; Poncet et al, 2005), but non–breed-specific upper airway obstruction may cause GER. The supposed pathomechanism is the negative intrathoracic pressure generated by increased inspiratory effort. In veterinary medicine GERD secondary to a primary LES abnormality is poorly understood. Diagnosing GERD based on history and observed symptoms, as it often is done in human medicine, is not applicable. Esophagitis secondary to presumed GER has been reported in cats (Gualtieri and Olivero, 2006; Han et al, 2003); however, the diagnosis was based on a combination of presumably typical historical and clinical signs, as well as radiographic, endoscopic, or histopathologic findings without actual demonstration of acidic esophageal pH. At present it is not clear if GERD also represents a relevant problem in small animals. More common scenarios for increased esophageal acid exposure in dogs and cats are lodged foreign bodies, frequent vomiting, malpositioned esophageal feeding tubes, potentially aggressive gastric factors such as gastric volume, and duodenal contents associated with delayed gastric emptying. In chronic esophagitis cases, histologic changes comparable with Barrett’s esophagus (replacement of the normal squamous epithelium of the distal esophagus with metaplastic columnar epithelium) rarely can be found. Animals with mild esophagitis may show no clinical signs, whereas animals with severe esophagitis can show reduced appetite, anorexia, odynophagia or dysphagia, ptyalism, coughing, and regurgitation. Clinical signs noted by the author include retching, gagging, repeated swallowing motions, smacking, discomfort at night (or bedtime), and refusal to eat despite apparent interest in food. Although it would appear plausible that severity of clinical signs depends on the extent and depth of esophageal lesions, they do not always correlate and may vary greatly. Hoarseness, stridor or change of phonation, and dyspnea suggest injury to the epiglottis, larynx, and upper airway (Lux et al, 2012). Onset of anesthesia-associated reflux esophagitis varies from days to weeks after a causative anesthetic event. On physical examination, patients may have evidence of halitosis and laryngeal signs with redness, hyperemia, and edema of the vocal folds and arytenoids. However, the majority of patients have normal physical examinations. It could be argued that esophagoscopy without biopsy is insufficient to rule out esophagitis, as are cases with grossly normal appearing mucosa on endoscopy and necropsy, but histopathologic evidence of esophagitis has been reported (Dodds et al, 1970; Han et al, 2003). This is in accordance with findings in humans, in which endoscopic results in patients with GERD vary from no visible mucosal damage to esophagitis, peptic strictures, or Barrett’s esophagus (a metaplastic change of normal squamous epithelium to columnar epithelium associated with chronic acid exposure). Because of the composition of the esophageal mucosa with its tough stratified squamous epithelium, it is difficult to obtain adequate esophageal biopsies; however, adequate endoscopic biopsy specimens from the lower canine esophagus showing the stratified squamous epithelium with basal cell layer, as well as the lamina propria with papillae, can be obtained by experienced endoscopists (Münster et al, 2012). The endoscopic examination always should include a full gastric inspection with special attention to the cardia and pylorus; this excludes underlying abnormality, such as obstructive lesions or radiolucent foreign bodies, and confirms that the esophagitis is a primary problem.
Gastroesophageal Reflux
Historical and Clinical Signs
Diagnosis
Gastroesophageal Reflux
Only gold members can continue reading. Log In or Register a > to continue