Equine Gastric Ulcers
The term ‘ulcers’ refers to a break or erosion in the lining of the esophagus, stomach or small intestines. The depth of the erosion determines the severity of the ulcer. Equine
Stomach ulcers are more common and occur primarily in the non-glandular (squamous) area of the stomach. Less commonly, ulcers occur in the glandular area of the stomach. In studies on horse populations, stomach ulcers are very common with up to 90% of Standardbred and Thoroughbred horses in race training affected. The clinical signs of ulcers are not noticeable in most horses. Of those horses clinically affected, the signs may include poor athletic performance, weight loss, and colic. Horses may also have an unthrifty appearance and mild diarrhea. In foals, teeth grinding (a sign of pain) and excessive salivation are common. Ulcers also occur in the first part of the small intestine (duodenum) and in the esophagus.
Ulcers are caused by a variety of factors, including:
- diet and feeding management – including meal feeding, feeding high levels of concentrates, feed deprivation and types of feed (timothy versus alfalfa).
- the stress of training and the stress of disease.
- medications such as corticosteroids.
- bile acid reflux.
This is quite different than with ulcers in man where the bacterium Helicobacter pylori is now thought to be important in the pathogenesis of 90% of duodenal ulcers and about 70% of gastric ulcers (1).
Food enters the stomach via the esophagus, leaves through the opening called the pylorus and passes into the first portion of the small intestine (duodenum). The stomach contains both squamous and glandular portions.
Diet and feeding management may play a major role in inducing ulcers in horses. By nature, horses are grazing animals, spending much of their day feeding. The grazing horse has a constant flow of saliva and passage of grass into the stomach, buffering stomach acid (2). Most horses graze pasture during the year. However, there are many horses, e.g., racehorses and high-level event horses, that are managed as meal-eaters rather than being allowed to feed or graze continuously. They receive dry hay and concentrates year-round, or for the majority of the year, in a meal rather than eating continuously as in grazing. (Concentrates are mixtures of grain, crushed or whole, along with vitamins and minerals combined in various forms or textures (e.g., sweet-feed, pelletted feed) to compliment the nutrients found in the hay.)
The feeding of high volumes of concentrates in itself increases the production of volatile fatty acids. This, combined with meal-feeding, results in sudden drops in gastric pH and damage to cells in the stomach and intestine.Measurements of gastric pH revealed that acidity (< pH 2.0) was greatest in horses deprived of food (3). An alternating regimen of feed deprivation for 24 hours followed by free choice hay for 24 hours resulted in erosions and ulceration of gastric mucosa with as little as 48 hours of cumulative food deprivation (3). This is important to remember; horses that are anorectic (not eating) or partially anorectic because of an underlying medical condition can develop erosions and ulcers in their gastric squamous mucosa within one to two days. When horses were fedtimothy grass hay, gastric pH measurements were often greater than pH 6 (3). The feeding of alfalfa hay and grain resulted in a higher gastric pH than feeding grass hay. This may be due to the constituents of alfalfa but further research is needed in the area of the effect of forage type on gastric pH (3). The stress of training regimen on the animal causes the increased release of corticosteroids and subsequent decrease in blood flow to the stomach lining. This interferes with the natural protective mechanisms and results in more damage from stomach acids.