Horses on pasture, and exercised lightly, typically have normal stomachs, where horses kept in box stalls and trained intensively have a high incidence of gastric ulcers. (50-91% in racing and show horses, depending on the reference). Many studies also confirm that progressive training is correlated with worsening of lesions. 

The equine stomach is small in capacity (8-15 litres) compared to the rest of the gastrointestinal system, and favours consumption of small meals regularly. Horses are, by nature, continual grazers which take in food for up to 16-18 hours per day in nature. When horses are deprived of food, even for short periods, gastric pH levels typically reach levels less than 2 (highly acidic).

Access to hay or roughage can rapidly return gastric pH levels to about 6, largely because of neutralisation of gastric acid by salivary bicarbonate, plus absorption of some stomach acid by the hay or roughage meal.

Many trials show that gastric erosions, and sometimes bleeding, are seen after as little as 48 hours cumulative feed deprivation, with gastric ulcers consistently seen after 96 hours. Imposed feed deprivation (such as in management of digestive upsets or colic, before surgery, long distance transport) can rapidly ulcerate gastric squamous mucosa. Even changing horses from a pasture environment to stall confinement with free choice hay can result in erosion of squamous mucosa in susceptible horses. 

Feeding grain, pelleted feed, high concentrate rations is associated with significantly greater gastric acidity after feeding than is seen with hay or roughage. 

The equine stomach secretes acid, even when food is not available. The predominant factor in damage to gastric mucosa is hydrochloric acid, as most regions of the mucosa of the oesophagus, dorsal stomach and duodenum have no real protection from acid injury.  Protection of the gastric mucosa relies primarily on limiting exposure to acidic gastric secretions.

Foals already secrete acid from 2 days of age. The pH of gastric fluid can thus vary between pH 1-7. Adult horses produce about 1.5 litres of stomach fluid per hour. This fluid is predominantly hydrochloric acid, and extreme irritant to the gastric mucosal lining. In general terms, a nearly neutral pH is measured in the dorsal stomach (squamous epithelium), while more acid pH levels are measured close to the Margo Plicatus - the common site of EGUS lesions. 

Saliva is only produced when a horse eats. If eating can be regular, with no long periods of food deprivation, then the highly alkaline saliva will assist significantly in maintaining a healthy gastric pH. 

The stomach empties in about 30 minutes after a liquid meal, but takes up to 24 hours to empty completely after a hay / roughage meal. If a stomach can be encouraged to hold food material for longer periods then acid levels will be maintained at levels closer to neutral pH, thus reducing the incidence of EGUS lesions. 

Factors that may influence gastric acidity and squamous mucosal damage from acidity include issues such as, the eating behaviour of the horse (grazing versus feeding high grain diets), natural constituents of pasture grasses, prepared hays or different feeds (concentrations of soluble carbohydrates vary, and time taken to eat a meal will vary depending on components. If a grain meal is eaten it clears the stomach much more rapidly than roughage, hence leaving the stomach exposed to excessive acid for longer than from, say, a hay meal).

Exercise and training influence gastric injury - the prevalence of EGUS lesions in racehorses in training is 70-90%, and it is well documented that increasing training activity is associated with severity of gastric lesions. There are inter-related effects of feed components, feeding management and eating behaviour, as well as the effects of exercise, and the effects of daily management practices which all contribute to EGUS. 

In foals, nursing is associated with an increase in pH, and gastric pH becomes highly acid when foals remain recumbent and do not suckle for more than 2 hours. 

The administration of non-steroidal anti-inflammatory drugs (NSAID’s) is a well known cause of ulceration of gastric glandular and squamous epithelium in both foals and horses. Injury in this instance results from impairment of blood flow to the gastric mucosa.

Clinical signs in horses with EGUS can include; acute and recurrent colic, poor body condition, partial anorexia or intermittent feeding behaviour, poor performance and attitude changes. Ulcers may occur secondary to other disease states, such as diarrhoea. 

Prevention of EGUS

Eliminate as many negative factors as possible. Fresh food (roughage), available day and night is highly important in all horses, especially when in box stalls. If feeding grain and concentrates, keep the hay or roughage levels as high as possible.

Training must be gradually staged to reduce stress on inexperienced horses.

Recurrent fasting, even while travelling or at strange venues, must be avoided.

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