Gastric ulcer disease is common in foals and horses and the term Equine Gastric Ulcer Syndrome (EGUS) has been used to describe this disease because of its multifactorial and complicated nature. Prevalence (disease in the population) estimates have been reported to range from 25% to 50% in foals and 60% to 90% in adult horses, depending on age, performance, and evaluated populations. Gastric ulcers have been identified in all regions of the equine stomach and two age related clinical syndromes have been described, one in foals (< 9 months of age) and the other in yearlings and adult horses (> 9 months of age). Although the pathogenesis of ulcers is similar in foals and horses, the syndromes frequently have different inciting causes and may produce different clinical signs. A presumptive diagnosis of these clinical syndromes relies on recognition of clinical signs, while a definitive diagnosis is based on endoscopic examination of the stomach. The purpose of these proceedings is to review the functional anatomy of the equine stomach that predisposes it to gastric ulceration and describe the clinical syndromes in foals and horses that make up EGUS. It is hoped that through and better understanding of EGUS that early recognition of clinical signs can result in prompt treatment, thus reducing secondary complications, such as pyloric stricture (narrowing of the opening between the stomach and small intestine), bleeding, or gastric rupture.
Anatomy of the Equine Stomach
The equine stomach is divided into two distinct anatomic regions, the esophageal or non-glandular region and the glandular region. The esophageal region or squamous mucosa covers approximately one-third of the equine stomach, is void of glands, and is covered by stratified squamous epithelium similar to the esophagus. The glandular region covers the remaining two-thirds of the stomach and contains glands that secrete hydrochloric acid, pepsin, bicarbonate, and mucus. A sharp demarcation or margo plicatus (cuticular ridge) separates the squamous mucosa from the glandular mucosa. Gastric ulcers in foals (less than 50 days of age) are commonly located in the non-glandular region of the stomach adjacent to the margo plicatus along the greater curvature. However, foals with a concurrent medical disorder or being given non-steroidal anti-inflammatory drugs (NSAIDs) may have gastric ulcers located in the glandular region of the stomach. Foals may also have ulcers in the pylorus or proximal duodenum, which may lead to gastric and esophageal ulcer, secondary to delayed gastric emptying.
Gastric ulcers in yearlings and adult horses are commonly located in the non-glandular region of the stomach along the lesser and greater curvature at the margo plicatus. If the ulcers become more severe they may extend more dorsally into the squamous fundus. In yearling and adult horses, ulceration of the glandular region of the stomach and proximal duodenum are less prevalent than ulcers in the squamous mucosa.
The horse stomach continuously secretes variable amounts of hydrochloric acid throughout the day and night and secretion of acid occurs without the presence of feed material. Foals secrete gastric acid as early as 2-days-of-age and pH of gastric fluid has been reported to range from less than 1.0 to 7.0. This low gastric pH may be related to plasma gastrin concentrations, as values in foals are similar to those in adult horses. Low gastric pH and high plasma gastrin concentration may predispose foals to EGUS.
The adult horses, the stomach secretes approximately 1.5 liters of acid rich gastric juice hourly and pH of gastric contents ranges from 1.5 to 7.0, depending on region measured. A near neutral pH can be found in the dorsal portion of the esophageal region (saccus cecus) near the lower esophageal sphincter, whereas, more acidic pHs can be found near the margo plicatus (3.0-6.0) and in the glandular region near the pylorus (1.5-4.0). Gastric emptying of a liquid meal occurs in approximately 30 minutes, whereas complete gastric emptying of hay occurs in 24 hours.
Causes of Clinical Syndromes of Gastric Ulceration in Foals and Horses
Equine Gastric Ulcer Syndrome in foals and horses results from a disequilibrium between mucosal aggressive factors (hydrochloric acid, pepsin, bile acids) and mucosal protective factors (mucus, bicarbonate). Since mucosal protective factors are more developed in the glandular mucosa of the equine stomach when compared to the squamous mucosa, different causative mechanisms may lead to ulceration in these regions. Ulcers in the squamous mucosa are primarily due to prolonged exposure to hydrochloric acid, pepsin, or bile acids. Ulcers occurring in this region are similar to Gastroesophageal Reflux Disease Syndrome (GERDS) in humans, since this region lacks well-developed intrinsic mucosal protective factors, similar to the esophagus. The severity of squamous ulcers is probably related to length of time of acid exposure. The squamous mucosa near the margo plicatus is constantly exposed to these acids and this region is where gastric ulcers are frequently found in foals and horses. Ulcers in the glandular mucosa are primarily due to disruption of blood flow and decreased mucus and bicarbonate secretion, which results in back diffusion of hydrogen ions and damage to the underlying submucosa. Inhibition of prostaglandins may play a major role in the pathogenesis of gastric ulcers in the glandular region of the equine stomach.
In contrast to the increases in aerobic enzymes, there are few changes in the activities of anaerobic enzymes in response to most routine training programs. Only when training involves short-term, intense bursts of exercise will it result in an increase in the activities of glycolytic enzymes needed for anaerobic energy production.
Causes of Gastric Ulceration of the Squamous Mucosa in Foals and Horses
Gastric ulceration in the squamous mucosa is directly related to the degree and severity of gastric acid exposure. Several factors have been implicated in causing ulceration and these include, fasting, gastric acid clearance (gastric motility and emptying), aggressiveness of the gastric juice (acid, pepsin, bile acids) and the process of desquamation. Fasting is an important factor in causing ulcers in the squamous mucosa in foals and adult horses. In foals, infrequent or interrupted feeding and recumbency has been shown lead to lower gastric fluid pH in foals. These findings suggest that milk may have a buffering effect on gastric acid and recumbency may increase exposure of the squamous mucosa to acid. Low gastric pH from interrupted or infrequent nursing may play a role in the cause of squamous ulceration in foals.
Feed deprivation has been shown to cause ulcers in the squamous mucosa of horses, which is due to repeated exposure of the squamous mucosa to high acidity. In yearling and adult horses, hay and saliva (rich in sodium bicarbonate), may help buffer gastric hydrochloric acid. The timing of feeding and the type of roughage source may contribute to gastric ulceration in yearling and adult horses. In a one study, horses fed hay continuously had higher median 24-hour gastric juice pH (3.1), when compared to horses that were fasted (1.6). In another study, horses fed alfalfa hay had significantly higher gastric juice pH and lower gastric ulcer scores, when compared to horses fed bromegrass hay. High protein (21%) and calcium concentration in the alfalfa hay was thought to provide buffering of stomach acid up to 6 hours after feeding. Also, high roughage diets stimulate production of bicarbonate rich saliva, which may contribute buffering of gastric acid.
In adult horses, the prevalence of gastric ulcers is high in the performance horse and may be due to prolonged exposure of acid to the squamous mucosa. The mechanical aspects of exercise and the abdominal pressure may be sufficient to provide prolonged exposure of the non-glandular mucosa to aggressive factors. Furthermore, especially in racehorses that perform at near maximal levels, exercise may have an inhibitory effect on gastric emptying. Decreased gastric and esophageal motility and delayed gastric emptying have been implicated in the cause of GERDS in humans during exercise and may lead to gastric ulceration in the performance horses, especially the racehorse.
Other organic acid may act synergistically with hydrochloric acid to play a role in the pathogenesis of gastric ulcer disease in horses. Recently, volatile fatty acids (VFAs), fermentation byproducts of carbohydrates, were found to induce acid injury to the gastroesophageal (squamous) mucosa of pigs. The VFAs are highly lipid soluble and easily penetrate the squamous mucosa of the stomach at low gastric pH. In their undissociated form, VFAs readily enter squamous epithelial cells causing acidification, cell swelling, inflammation and ulceration. Since the proximal one-third of the horse's stomach is covered by squamous epithelium, similar to the pig, VFAs may play a role in EGUS pathogenesis, since horses are fed high concentrate diets. In a previous report, VFAs were found to be present in the stomach of horses in significant enough quantities to lead to acid injury. Since performance horses are fed diets that are high in fermentable carbohydrates, VFAs, generated by resident bacteria, may cause acid injury and ulceration in the squamous mucosa.
Causes of Glandular Ulcers in Foals and Horses
Glandular gastric ulcers occur most frequently in foals, but can occur in adult horses. The cause of glandular gastric ulcers is most likely due to decreased blood flow and decreased mucus and bicarbonate secretion. Decreased prostaglandin synthesis (primarily PGE2, I and A) has been implicated in the cause of glandular gastric ulcers in foals, since non-steroidal anti-inflammatory drugs (NSAIDs) administration caused gastric ulcers in foals. Blocking prostaglandin synthesis causes deceased mucosal blood flow, stimulates gastric acid secretion, and inhibits bicarbonate secretion by the glandular mucosa. Prostaglandins may also help maintain the integrity of the squamous and glandular mucosa by stimulating production of surface-active protective phospholipid, stimulating mucosal repair, and preventing cell swelling by stimulating sodium transport. Furthermore, stress of parturition in foals and stress of training and confinement in horses, may also lead to excess release of endogenous corticosteroid, which can inhibit prostaglandin synthesis. A decrease in prostaglandins leads to a breakdown in mucosal protective factors and may be the primary cause of glandular gastric ulcers in foals and horses.
Clinical Syndromes of Gastric Ulceration in Foals
Equine Gastric Ulcer Syndrome in foals occurs from 2 day to 9 months of age. Four distinct clinical syndromes have been described in foals and include silent (subclinical) ulcers, active (clinical) ulcers, perforating ulcers with diffuse peritonitis, and pyloric strictures from healing ulcers, with may produce gastric outflow obstruction.
Clinically in-apparent or "silent" gastric ulceration occurs in foals and is probably the most common syndrome. Foals with "silent" ulcers show no apparent clinical signs. Ulcerations are usually found in the squamous mucosa along the greater curvature adjacent to the Margo Plicatus, but can be found in the glandular mucosa. "Silent" squamous ulcers are commonly seen in foals less than 4 months of age, where as "silent" glandular ulcers are usually seen in similar aged foals with a concurrent medical problem. Glandular gastric ulcers are thought to be stress induced. Silent ulcers may resolve without treatment and are found as an incidental finding at necropsy, however they can produce clinical signs that may be life threatening.
Clinical ulcers, ulcers producing clinical signs, usually occur in foals less than or equal to 270 days of age. These ulcers occur primarily in the non-glandular squamous mucosa along the greater or lesser curvature adjacent to the margo plicatus or in the glandular mucosa. When gastric ulcers in non-clinical foals become larger, more duffuse, and coalesce clinical signs are precipitated. Diarrhea and poor appetite are the most frequent clinical signs observed in these foals, however poor growth, rough hair coat, potbellied appearance, bruxism, dorsal recumbency, excessive salivation, interrupted nursing, and colic may also be seen in these foals. In advance cases, foals may be sensitive to abdominal palpation just caudal to the xyphoid process and exhibit severe signs of colic and tend to roll and to lie in dorsal recumbency. The later signs are most likely associated with gastric distention and gastroesophageal reflux.
Perforating gastric ulcers are an infrequent occurrence in foals. These ulcers can occur in the squamous mucosa and glandular mucosa of the stomach or in the duodenum and the severity cannot be predicted by their endoscopic appearance. Perforating ulcers occur most frequently in the squamous mucosa and may lead to diffuse peritonitis, which is almost always fatal. Frequently, clinical signs in these foals are absent until just prior to rupture. Once gastric rupture has occurred, initially foals show profound depression, a wide base stance and later show tachycardia, abdominal distention, colic, prolonged capillary refill time, cyanotic mucus membranes, and acute death. A severe metabolic acidosis may be seen in foals with septic peritonitis. Early detection of foals with clinical signs suggestive of gastric ulcers is essential and surgical correction in some cases decreases mortality. In some cases, prophylactic treatment in the high-risk foal can prevent gastric rupture.
Pyloric or duodenal ulcers are rare in foals but when healed can produce stricture and gastric outflow obstruction. Ulcers in the pylorus and duodenum occur in foals from 2 days to 1 year of age, but are most often seen in foals 3 to 5 months of age. No clinical signs may be seen in foals with pyloric or duodenal ulcers, but if clinical signs develop they are usually associated with a gastric outflow obstruction. Typical signs of gastric outflow obstruction include drooling of milk, bruxism, post-prandial colic, excess salivation, scant feces, and low volume diarrhea. These foals may have gastroesophageal reflux, cholangitis, severe gastric ulceration, erosive esophagitis, and aspiration pneumonia. In severe cases, duodenal strictures and outflow obstruction may be associated with dehydration and a systemic hypochloremic metabolic alkalosis.
Clinical Syndromes of Gastric Ulceration in Yearlings and Adult Horses
Clinical syndromes of gastric ulceration in yearling and adult horses are less well recognized than the clinical syndromes in foals, but may be more economically important. Two distinct clinical syndromes are recognized in yearling and adult horses and they include "silent" or non-clinical ulcers and clinical ulcers. However, duodenal ulcers, duodenal stricture, erosive esophagitis, and gastric rupture occur infrequently. In both of these syndromes, gastric ulcers occur primarily in the squamous mucosa adjacent to the margo plicatus along the greater and lesser curvatures. Glandular ulcers are less frequently in yearling and adult horses, when compared to foals, and are usually associated with administration of NSAIDs. Mild multifocal gastric ulcers in the squamous mucosa are usually seen in yearlings and two-year-olds in training without apparent clinical consequent. However, in two surveys of over two hundred young horses (6 months to 1.5 years of age), non-glandular ulcers were seen in 90% of these horses. These young horses were handled daily, halter-broken, and housed in box stalls. Very few of these horses had clinical signs of gastric ulceration, although the ulcers were severe in some of the horses. Frequently, gastric ulcers in this age group are not associated with clinical signs, but when these horses are put into training or stressed by concurrent disease or given NSAIDs, gastric ulcers become diffuse and involve the deeper tissue layers, which can lead to clinical signs. Clinical signs in horses with EGUS include acute and recurrent colic, poor body condition, partial anorexia, poor appetite, poor performance, and attitude changes. Typically, diarrhea is not a common clinical sign in horses with gastric ulcers. However, ulcers can occur secondary to disorders that cause diarrhea. Gastric ulcers are consistently more severe in horses with clinical signs when compared to horses not showing clinical signs. Gastric ulcers can be the primary cause of colic or may be secondary to other problems in the gastrointestinal tract. Often there is no correlation between gastric ulcer severity as viewed through an endoscope and clinical signs seen in these horses.
Equine Gastric Ulcers Syndromes represent a major health problem in foals, yearlings, and adult horses. Many foals and horses show subtle nonspecific clinical signs of gastric ulceration that may be overlooked during clinical examination. Recognizing the clinical syndromes and causes of EGUS in foals, yearlings, and horses is paramount, so that early treatment can be prescribed and secondary complications minimized.
About the Author
Dr. Frank Andrews is a Professor and Section Chief of Large Animal Medicine at the University of Tennessee, College of Veterinary Medicine. He has worked extensively in the area of gastric ulcers for 11 years. Dr. Andrews research interests include gastric physiology and secretion, dietary effects on the horse's stomach, and treatments to heal gastric ulcers.
This information was presented at, and appears in the Proceedings of, the 2001 Alberta Horse Breeders and Owners Conference.
This information is maintained by of the Horse Industry Section of Alberta Agriculture in conjunction with Sylvia Schneider at Pondside Web Productions.
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