Gastric ulcers (equine gastric ulcer syndrome [EGUS]) are common in horses and foals. This syndrome is most closely associated with horses involved in performance disciplines; changes in housing or social interaction; and illness. Prevalence in unmedicated racehorses in active training is at least 90% while that in non-racing performance disciplines exceeds 60%. Neonatal foals are at significant risk for development of perforating peptic ulcers until they are several weeks old because their gastric mucosa is not developed to full thickness at birth. Although spontaneous healing of peptic ulcer lesions has been noted, if the horse is maintained in the circumstances inciting EGUS, the lesions are unlikely to heal without medical intervention.
EGUS describes a spectrum of inflammatory and disruptive mucosal pathophysiology affecting tissues of the distal esophagus, stomach and entrance into the duodenum. Endoscopic surveys indicate that ~90% of these lesions are found in the nonglandular squamous mucosa of the stomach, especially on the lesser curvature just proximal to the margo plicatus. However, significant portions of the squamous mucosa along the greater curvature and up into the fundus may also be involved, along with lesions in the antrum or pylorus. Duodenal ulceration in adult horses and foals is considered part of EGUS and, hence, a peptic (acid-induced) disorder. Duodenal ulceration, perforation, and stricture can occur, and it is not known whether these problems develop solely as a result of enteritis (duodenitis) or whether peptic factors have a role. However, once a stricture occurs, gastric and esophageal ulcers are often present and severe, secondary to delayed gastric emptying.
Ulcers in the nonglandular squamous mucosa are associated with repeated direct insult from ultra-low pH fluid normally found in the glandular region of the stomach. Pressure increases inside the abdomen (associated with exercise) collapsing the stomach and forcing the acid gastric contents upward. The more fluid (and highly acidic) contents of the lower stomach come in contact with the nonglandular squamous mucosa, causing inflammation and, potentially, erosions to varying degrees.
The causes of ulcers in the glandular mucosa of the stomach are less well defined. Use of nonselective NSAID are known to reduce blood flow to the GI tract, causing decreased production of the muco-bicarbonate matrix by the gastric glandular mucosa and resulting in ulceration. This is not a consistent finding, however. Additionally, attempts have been made to isolate and/or correlate evidence of Helicobacter spp organisms from the stomach of horses with and without gastritis and ulcers. Results of these studies have been equivocal or negative, and the role for this organism in glandular equine gastric ulcers has not been determined.
Most foals with gastric ulcers do not exhibit clinical signs. Clinical signs become apparent when the ulceration is widespread or severe. The classic clinical signs for gastric ulcers in foals include diarrhea, bruxism, poor nursing, dorsal recumbency, and ptyalism. These signs are vague and not specific for gastric ulcers. In fact, ptyalism is a sign of esophagitis, which in most foals is secondary to gastric outflow obstruction and gastroesophageal reflux. Other causes, including esophageal obstruction and Candida infection, should be considered. Importantly, when a foal exhibits clinical signs, the ulcers are severe and should be diagnosed and treated immediately. Sudden gastric perforation without prior signs occurs sporadically in foals.
Adult horses with ulcers display nonspecific signs, including abdominal discomfort (colic), poor appetite, mild weight loss, poor body condition, and attitude changes. Horses with severe abdominal pain or colic may have gastric ulcers, but they are unlikely to be the primary cause of the abdominal pain. No strong correlation between the extent of ulceration and the severity of clinical signs has been observed.
Complications related to gastric ulcers are most frequent and severe in foals and include perforation, delayed gastric emptying, gastroesophageal reflux and esophagitis, and megaesophagus secondary to chronic gastroesophageal reflux. Ulcers in the proximal duodenum or at the pylorus can cause fibrosis and stricture. Duodenal and pyloric stricture can lead to delayed gastric emptying in foals and adult horses. In rare cases, severe gastric ulceration causes fibrosis and contracture of the stomach.
Neither clinical signs nor clinicopathologic laboratory tests are specific for gastric ulcers, and an abnormality in a laboratory test does not preclude the possibility that another disorder may be present. Gastric ulcers can develop secondary to stress due to problems in many organ systems or as a result of hospitalization or stall confinement. Endoscopy and visualization of the ulcers in an empty stomach is the only definitive method of diagnosis. Endoscopes with light sources that can be varied in wavelength may be used to more easily visualize inflammatory stages of this disease prior to breaching of the epithelium by outright ulceration. A presumptive diagnosis can be reasonably made from significant reduction in clinical signs following several days of treatment with a medication known to be effective in raising gastric pH and allowing healing of gastric mucosa.
Suppression of gastric acidity and maintenance of a pH between 4 and 5 are the primary treatment objectives. Studies have examined the use of surface coating agents, antacids, with histamine type-2 receptor antagonists (ranitidine and cimetidine), and the proton pump inhibitor omeprazole in a carrier designed to aid passage through the acid stomach into the small intestine for absorption. Of these, omeprazole in the gastric pass-through formulation has been the only medication shown to consistently allow gastric ulcers to heal in horses that continue their normal training. It is the only medication approved by the FDA for treatment (4 mg/kg, PO, sid) or prevention (1 mg/kg, PO, sid) of gastric ulcers in horses. Sucralfate binds to the gastric glandular mucosa and may promote healing there, although studies using sucralfate have not shown it to be efficacious in the treatment of gastric ulcers in horses or foals. Thus, its use in horses is questionable. Antacids have yet to be proved effective in either healing or preventing gastric ulcers. They must be administered in relatively high volumes every 2 hr to neutralize stomach acid. Ranitidine (6.6 mg/kg, PO, tid) has been shown to be effective in healing gastric ulcers when horses were removed from training. Studies have not shown cimetidine to be effective.
Last full review/revision March 2012 by Frank M. Andrews