Equine Gastric Ulcer Syndrome

Note.  The term EGUS includes both equine glandular gastric disease (EGGD) which relates to disease of the glandular area of the stomach, and equine squamous gastric disease (ESGD) which refers to disease of the squamous part of the stomach

Gastric Ulcers are very common in domesticated horses of all types affecting from 25%-50% of foals and 60%-90% of adult horses depending on age and performance. Ulcers, which are wounds in the stomach lining, are categorized into two types based on their position in the stomach. The stomach itself is divided into two distinct regions, the oesophageal, non-glandular or squamous region and the glandular region. The two parts are divided by a distinct demarcation line, the margo plicatus with the upper squamous part covering 1/3rd, and the lower glandular part 2/3rds of the total area. The margo plicatus is a common site of ulceration.

Although the structure and appearance of the ulcers is the same the precipitating causes may differ between foals <9month age and yearlings and adult horses. Diagnosis is based on clinical signs and examination of the stomach by means of a flexible fibre optic endoscope. The small intestine adjacent to the stomach (duodenum) may also be ulcerated as may the oesophagus and are included in EGUS. The squamous area is the most commonly affected but the glandular area may also be involved.

Mechanisms: the stomach contains strong acids, principally Hydrochloric acid secreted by glandular cells but also other organic acids and bile acids, plus the enzyme pepsin. Countering the damaging effect of the acids is bicarbonate buffer and the natural protective mucus layer lining the stomach. When the balance between these opposing sides is disturbed, acid attacks the lining causing ulceration. In the squamous part ulceration is probably related to the exposure time to acid and enzyme attack. In the glandular part, which is better protected by mucosal mucus and bicarbonate secretions, the mechanism may be different involving disruption to the blood supply and reduction in secretion of those protective factors, permitting acid attack on the lining cells. In humans and dogs stomach ulcers have a strong correlation with the presence of the bacterium Helicobacter pylori but whilst some Helicobacter species have been found in horses, they do not seem to be related to EGUS.

Causes: In foals, intermittent fasting or infrequent feeding and recumbency have been shown to lower gastric pH. Milk may have a buffering effect on gastric acid so lack of it increases the risk of acid attack, whilst recumbency is associated with reduced nursing and that position may result in more contact between the squamous area and gastric juice. Treatment with N.S.A.I.D.’s is strongly correlated with glandular region gastric ulcers in foals. These drugs work by inhibiting the synthesis of prostaglandins which in turn decreases blood flow to the mucosa, suppresses the normal production of bicarbonate buffer by the stomach, and increases acid production.

In adult horses, intermittent fasting (2 meals per day) as well as mechanical factors in performance horses have been implicated. Gastric motility and emptying time may be impacted by both exercise and the type of diet routinely fed to performance horses, and racehorses in particular. Horses with continual access to hay tend to have less acidity. Saliva contains bicarbonate buffer so higher saliva production which happens when horses chew roughages, acts to buffer stomach acid. High starch diets are strongly correlated with EGUS. Hard exercise may inhibit gastric emptying and be another reason why racehorses have such a high incidence. Stress, e.g., from competition away from the home environment, may be a contributing or triggering factor.

Signs of EGUS. In foals repeated episodes of colic, especially after suckling, lying on their back, teeth grinding, interrupted nursing due to stomach discomfort, poor appetite, diarrhoea, and excessive salivation, and failure to thrive. In adults and yearlings, failure to clean up their feed, poor appetite, reluctance to exercise, dullness, poor body condition, weight loss, rough hair coat, girthing issues, low grade colic, teeth grinding / yawning (signs of low- grade Abdominal pain). None of these signs are specific to EGUS and a positive diagnosis should not be presumed without endoscopic examination of the stomach. Efforts are underway to develop alternatives such as a blood test for EGUS but have not yet come to fruition.

Treatment. The treatment of choice and the one registered for use for EGUS treatment in Australia is Omeprazole given for 28 days initially then at a half dose as a preventative. It works by blocking the production of hydrochloric acid by the stomach. A recent study on Esomeprazole (Nexium) shows promise for that as an alternative but requires further research to confirm suitability in horses and as yet is unlicensed for equine use (as of September 2021).

Other products such as sucralfate which coats ulcers, and some fermented soy extracts may have some merit in reducing recurrence following omeprazole treatment. Ranitidine is prescription only product which suppresses acid production but is less popular than Omeprazole because it requires tree times daily dosing. Lucerne hay helps by provision of some additional buffering activity, more than cereal or grass hay. The more hours in the day the horse has access to forage feeds the better. Grain meals should be fed preferably on a ‘’little and often’’ basis so far as practicable.

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