Gastroesophageal Reflux

Chapter 122

Gastroesophageal Reflux

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.

Historical and Clinical Signs

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.

Care should be taken to evaluate the respiratory system, because pulmonary manifestations of GERD potentially may include aspiration pneumonia, chronic bronchitis, and interstitial pulmonary fibrosis. Concerning this aspect, idiopathic pulmonary fibrosis is seen nearly exclusively in older West Highland white terriers, a breed that is also notoriously famous for lodged esophageal foreign bodies. Chronic intermittent microaspiration of gastric acid secondary to primary esophageal motility problem could be the causative event in this breed.


Although historical and clinical findings may be suggestive of esophagitis, results of routine laboratory testing are usually normal. Survey thoracic radiographs are seldom diagnostic for esophagitis, but compatible findings may be mild esophageal dilations or fluid accumulation in the distal esophagus. However, foreign bodies, hiatal hernias, esophageal dilation, ring anomalies, or masses could be detected, and a pathologic lung pattern may reflect aspiration injury to the lungs. Mediastinal or pleural air or liquid accumulation may indicate esophageal perforation. If a perforation is considered likely, an iodinated contrast medium should be used instead of barium. A contrast esophagram is an inexpensive, readily available, and noninvasive test that is most useful in demonstrating stenotic narrowing of the esophagus. No veterinary study has evaluated the ability of barium esophagram to detect esophagitis. However, mucosal irregularities and a prolonged retention of the contrast medium can be seen with moderate to severe inflammation, whereas mild esophagitis most likely will be missed. The benefit of fluoroscopic swallow studies is assessing the esophageal motility during the whole swallow with less chance to miss the moment when the contrast medium passes a narrow point, as could be the case with static images. It is important to perform wet swallows with liquid contrast medium and dry swallows with a barium-food mixed bolus, because liquids sometimes can pass a partial stricture, whereas a food bolus may be retained.

With the exception of detecting strictures, these procedures cannot diagnose GER. Hiatal hernias may be seen during fluoroscopic contrast studies of the LES area by applying pressure on the cranial abdomen. In health the gastroesophageal junction should lie caudal to the hiatus, and no stomach or other viscera should lie cranial to the gastroesophageal junction. However, it can still be difficult to assess the clinical significance of small sliding hiatal hernias.

Endoscopic examination is the most sensitive method to diagnose esophagitis, although reliable diagnostic endoscopic criteria and grading schemes for severity of esophagitis have not been established in small animals. No descriptive endoscopic work larger than case reports has been published on canine or feline esophagitis. Early signs of esophagitis are erythema and edema, but these findings are nonspecific and depend on the quality of endoscopic equipment. More reliable signs include increased vascularity because enlarged capillaries develop in response to acid near the mucosal surface. Mucosal striations with visible submucosal vascularity may be seen in the distal third of the esophagus. Another common sign is increased granularity; the mucosal surface appears rough and puckered. Findings compatible with severe esophagitis are areas of exudative pseudomembranes and ulcerative mucosa. In contrast to people, linear mucosal breaks (erosions) with a sharp demarcation line from adjacent normal mucosa uncommonly are seen. Although typical for reflux esophagitis, circular inflammation just above the LES should not be confused with the squamocolumnar junction (demarcation line between the squamous esophageal lining and the columnar gastric lining), which can appear sharply delineated in cats and dogs with reddened gastric mucosa. This is especially the case with esophageal overinsufflation.

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.

All aforementioned diagnostics may aid in the diagnosis of esophagitis but still fail to detect GER. Approaches other than endoscopy are needed. In humans, catheter-free esophageal pH monitoring has become the gold standard for diagnosing GERD. This technique provides information on distal esophageal acid exposure and also is able to assess symptoms associated with acid reflux episodes. A widely used system in humans is the Bravo system. It includes a small capsule (26 mm × 5.5 mm × 6.5 mm) containing an antimony pH electrode with internal reference, miniaturized electronics with radiofrequency transmitter and battery, a capsule delivery system, as well as an external receiver to monitor intraesophageal pH. The capsule is positioned approximately 3 cm above the LES and attached (i.e., pierced) to the mucosa. Once released from the delivery system, pH data are recorded by a receiver attached to the dog’s harness. Owners are instructed to maintain a logbook to record all events presumed to be related to GER. Our experience with the Bravo Capsule pH test indicates that this technique can be used safely in patients from 5 kg to 50 kg bodyweight, and all dogs tolerate the measurements well. Our preliminary results contradict the previous hypothesis that minute amounts of acid could damage severely the canine esophagus. In healthy dogs with normal upper gastrointestinal endoscopy, the number of refluxes (defined as esophageal pH <4) and the duration of long refluxes (>5 min) vary considerably over the course of 96 hours. Although single reflux episodes lasting as long as 20 minutes rarely can be recorded, the overall fraction time pH less than 4 remains low and usually ranges between 0 and 3.2% (median 0.3%). These numbers actually are lower than the established norm in humans. First results in dogs with clinical signs commonly attributed to reflux esophagitis are surprising, because clinically relevant reflux episodes could not be demonstrated in the majority of suspected dogs and a temporal relationship between presenting signs observed by owners and reflux episodes lacked overall agreement. Because this is an ongoing study, more dogs must be evaluated before definitive conclusions can be made. Current disadvantages of the system are the high cost and need of upper endoscopy for accurate placement.

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Jul 18, 2016 | Posted by in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Gastroesophageal Reflux
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