Equine gastric ulcer syndrome

Equine gastric ulcer syndrome (EGUS) is a common cause of colic and decreased performance in horses. Horses form ulcers in the mucosa of the stomach, leading to pain, decreased appetite, weight loss, and behavioral changes. Treatment generally involves reducing acid production of the stomach and dietary management. Unlike some animals, however, stomach rupture is rare, and the main goal of treating is to reduce pain and improve performance of animals used for showing or racing. Equine gastric ulcer syndrome (EGUS) is a common cause of colic and decreased performance in horses. Horses form ulcers in the mucosa of the stomach, leading to pain, decreased appetite, weight loss, and behavioral changes. Treatment generally involves reducing acid production of the stomach and dietary management. Unlike some animals, however, stomach rupture is rare, and the main goal of treating is to reduce pain and improve performance of animals used for showing or racing. The digestive system of the horse evolved for its grazing lifestyle, where it would almost constantly eat small amounts of roughage throughout the day. Unlike carnivores, who produce stomach acid during meals, horses constantly secrete acid to help digest this source of grass, leading up to 9 gallons produced per day. Unchecked, the stomach acid can lower the pH to levels that will damage the gastric mucosa, leading to ulcers. The stomach is divided into 2 main sections: a squamous region at the upper 1/3 of the stomach near the cardiac sphincter, and a lower glandular region. These 2 regions are separated by a band of tissue called the margo plicatus. The pH of the stomach contents varies by location. The most dorsal part of the stomach has the highest pH, usually close to 7, dropping to a pH of 3.0–6.0 near the margo plicatus, and reaching as low as 1.5–4.0 in the glandular regions. In foals, pH is uniform since all gastric contents are liquid, and pH rises for a around one hour after milk ingestion. The esophagus and dorsal stomach is made of stratified squamous epithelium, which is only weakly protected from the effects of hydrochloric acid, and those cells deeper in the layer of tissue transport hydrogen ions intracellularly, leading to death. This region is therefore especially vulnerable, and accounts for 80% of all gastric ulcers. The glandular portion produces hydrochloric acid and enzymes such as pepsinogen, as well as bicarbonate and mucus that helps prevent self-digestion. Mucosal blood flow is also an important factor in glandular epithelium health, since it provides oxygen and nutrients to the cells and helps to remove excess hydrogen ions. When a horse is on a diet high in roughage, the fibrous mat of chewed roughage provides a physical barrier and helps prevent splashing of acid up onto the squamous region of the stomach. Additionally, the horse's saliva is alkaline, and provides a chemical buffer that is produced during constant chewing and swallowing. Both the esophagus and duodenum are also at risk for ulceration. Esophageal ulceration is partially prevented by the tone of the cardia sphincter to prevent reflux, as well as by saliva, which both washes the esophagus and contains mucins that can help protect its surface. The duodenum is protected by its motility which removes HCl, glands in its surface that produce mucins, and products from the pancreas, including bicarbonate, to help neutralize the acidity. Most duodenal ulcers occur in foals, and there appears to be an association between duodenal ulcers and enteritis in these animals. Duodenal ulcers may result in inflammation of the duodenum so profound it blocks gastric emptying, which can cause severe gastric ulcers and occasionally esophageal ulcers. Often this must be treated with a gastrojejunostomy, which is a risky procedure. Horses used for competitive activities, such as showing or racing are at greatest risk of gastric ulceration, with up to 60% of show horses, 60–70% of endurance horses, 75% of event horses, and 80-90% of race horses having ulcers. These horses have stressful lives compared to non-competitive animals, which includes travel, frequent change of environment, and high workload. Additionally, their diet often consists of a higher proportion of grain relative to roughage, to account for their increased caloric requirements. Horses undergoing treatment for other medical problems, such as illness or lameness, are also at increased risk, due to the stress of the disease and because they are often confined and placed on long-term non-steroidal anti-inflammatory drugs (NSAIDs). Foals start secreting hydrochloric acid at two days of age. Nursing has been shown to increase pH, while gastric pH decreases in foals that are recumbent and not sucking regularly. Up to 50% of all foals and 90% of foals in the ICU have ulcers. This may be due to decreased feedings and recumbency. Ulcers in foals are often 'silent', producing no clinical signs, and usually occur in the squamous portion of the stomach in animals four months old and younger. Glandular ulcers in foals are thought to be caused by stress, and are often seen in foals four months old and younger that are also sick or debilitated. Clinical ulcers in foals primarily occur in animals < 270 days old, and are usually found on the squamous epithelium of the stomach. Pyloric or duodenal ulcers are rare, and most often seen in animals three to five months of age. Ulcers in these regions are usually asymptomatic, but can cause stricture, leading to gastric outflow obstruction. Perforation secondary to ulcers, although rare, can occur both in the stomach and the duodenum, producing peritonitis. Rupture can not be predicted by ulcer severity as seen on endoscopic examination, and clinical signs are often not present until just prior to the event.