In association with Mark Andrews, BVM&S CertEP MRCVS, of Equine Science Update we are pleased to provide the latest Equine Veterinary Information Gastric Ulcers Equine Gastric Ulcers Equine gastric ulcer syndrome (EGUS) is the most common disorder of the equine stomach. It affects over 90% of racehorses in training and nearly 60% of other sport horses. (1) No specific cause has been determined, but various factors are thought to play a part, including stabling, ingestion of concentrate foods, intensive exercise and transport. Normal anatomy of the stomach Horses are well adapted to eating little and often. They have a relatively small stomach, holding between 8 and 15 litres. The inside surface of the stomach can be divided into two parts according to the different types of cells that make up the lining (mucosa). The non-glandular part of the stomach is pale pink; the glandular mucosa is darker in colour. The upper ( non-glandular) part is covered with layers of cells ("stratified squamous epithelium" ). In the adult horse it is usually up to 20 cells thick, although it can be thinner in foals. The outer layers are hardened (cornified) and form a mechanical protective barrier. This part of the stomach has no absorptive or secretory functions. The lower (glandular ) part is similar to the stomach of other single-stomached animals. The glandular mucosa contains numerous gastric glands which secrete hydrochloric acid . The acid helps in the breakdown of food, providing ideal conditions for the digestive enzymes to work. The gastric glands also secrete pepsinogen. It is activated by the acid conditions, becoming pepsin, the major enzyme involved in protein digestion. There are also cells that secrete a bicarbonate-rich mucus which protects the mucosa from the acidity of the gastric fluid. Chemical messengers known as prostaglandins help to maintain the blood supply to the epithelium and increase mucus secretion from the gastric glandular mucosa How do ulcers form? Ulcers in the non-glandular part of the stomach form when excessive hydrochloric acid and pepsin in gastric secretions overwhelm the protective mechanisms of the gastric mucosa. The secretion of acid from the gastric glands is stimulated by the vagus nerve, and also by gastrin, a hormone released in response to feeding. Although the amount of acid increases when the horse is eating, secretion continues all the time. Normally the acidity of the stomach contents is buffered by saliva. However, saliva is only produced in significant amounts when the horse is eating. So horses that are grazing most of the time have a constant flow of saliva to neutralise the stomach acid. The high grain, low roughage diet of horses in training is thought by many to contribute to the development of gastric ulcers. Grain requires less chewing and so stimulates less saliva. It is also more potent at stimulating acid production than is hay. If a horse is deprived of food for only a couple of hours the stomach contents will rapidly become more acidic (pH2 or lower).Ulcers can appear within 24-48 hours if the horse is prevented from eating. Others (2) have suggested that a mechanical effect of exercise keeps the stomach acid in contact with the non-glandular mucosa for longer). They suggest that an increase in pressure in the abdomen during intense exercise compresses the stomach, pushing the acidic contents up onto the non-glandular part of the stomach. According to their theory, horses that spend more time training, have acid in contact with the non-glandular part of the stomach for longer, causing more ulcers. ulcers of the glandular mucosa are commonly caused by overdose/ area common side effect of NSAID treatment. What factors increase the risk of gastric ulcers? Various factors are known to increase the risk of gastric ulcers: intense physical activity. During physical exertion the blood is diverted from the intestines to the skeletal muscles and skin. Gastric acid secretion increases during hard work As mentioned above, (2) exercise tends to push the acidic stomach contents up onto the non-glandular mucosa. diet. Grain and pelleted rations promote higher levels of gastrin in the blood than does hay and so stimulate more acid production.. Eating hay stimulates twice as much saliva production as does eating grain. stress and illness may cause ulcers by restricting the blood flow to the mucosa drug-induced. Non-steroidal anti-inflammatory drugs (NSAID`s - such as phenylbutazone) are thought to exert their effects on the gastric mucosa by inhibiting prostaglandin synthesis, leading to restriction of the blood supply to the glandular mucosa. What are the signs of gastric ulcers? Adult horses with gastric ulcers often show no signs. However, they may show non-specific signs such as: weight loss, reduced appetite, poor physical condition, dullness, colic, diarrhoea, poor performance, or change in behaviour. Often the degree of ulceration doesn't relate to the severity of the signs. A horse with mild ulceration may show marked clinical effects; whereas those with extensive ulceration may not appear ill. Foals usually show more obvious signs of pain. Diarrhoea is the most common sign, other signs include excess salivation, grinding their teeth ( bruxism ) and colic. Ulcers and crib-biting Recent work suggests a relationship between gastric ulcers and some stereotypies (previously referred to as vices ). Crib-biting and wind-sucking may be attempts by the horse to stimulate saliva production to neutralise stomach acid. Professor Christine Nicol and her colleagues have been investigating the relationship between crib-biting and gastric ulceration in foals. They looked at what effect feeding an antacid diet had on both crib-biting behaviour and gastric ulceration. (5) They found that crib-biting foals had more signs of gastric ulceration than did foals that did not crib-bite. Foals that were fed an antacid diet for 14 weeks showed a significant improvement in the condition of the stomach. Although most foals showed a reduction in crib-biting behaviour over the duration of the trial, the reduction was most marked in the foals on the antacid diet. Eleven of twelve foals on the antacid diet showed either an improvement or no change in the gastric ulceration score - (ie they had fewer ulcers at the end of the study.) In contrast, only three foals on the base diet improved or did not change, and four grew worse. They found that foals that showed the greatest improvement in ulceration score also tended to show the most reduction in crib-biting. Daniel Mills and Clare MacLeod showed that feeding adult horses an antacid diet led to a reduction in cribbing activity after just one week. Further reductions in cribbing occurred when the antacid diet was fed for another five weeks. They also found that neither age, nor the duration of the cribbing behaviour prior to being fed the antacid diet, affected the effectiveness of the treatment. (6) How do we diagnose gastric ulcers? Endoscopic examination of the stomach is used to reach a definitive diagnosis. A long (2-3metre) endoscope is required to inspect the inside of the stomach. The examination is best done after starving the horse for 12-14 hours. Schemes for grading the severity of ulcers have been developed. For example the Equine Gastric Ulcer Syndrome (EGUS) Council recommends the following system: Grade 0: The epithelium is intact and there is no hyperaemia of hyperkeratosis - normal. Grade 1: the mucosa is intact but there are areas of reddening and hyperkeratosis (thickening) Grade2: Small, single or multiple ulcers present Grade3: Large, single or multiple ulcers or extensive superficial lesions. Grade4: Extensive, deep ulcers Bleeding is not considered to be a helpful sign in grading ulcers because some small ulcers may bleed while large deep ulcers may not. However, much debate exists regarding the accuracy of these grading systems. One study carried out in America (3) found that endoscopic examination underestimated the severity of the ulceration. Many vets do not have access to endoscopes that are long enough to examine horse`s stomachs. Researchers have been investigating other methods for identifying gastric ulcers. One technique that might prove useful as a screening test is to measure the absorption of sucrose across the stomach wall. Normally sucrose is not absorbed in the stomach and is rapidly broken down to fructose and glucose when it reaches the small intestine. However, it can be absorbed across the stomach wall when ulcers are present. The sucrose is then excreted the urine. Researchers have been investigating whether the measurement of sucrose in the urine after oral dosing can be used as a screening test for gastric ulceration. (4) If endoscopy is not available, a course of empirical therapy that produces an improvement is strong supporting evidence Treatment stop training. The simplest treatment is pasture grazing. In many cases that is not a practical solution for the type of horses that suffer from EGUS. However in one study , untreated ulcers did not heal spontaneously and tended to get worse while the horses continued in training (7) Conversely, one study showed spontaneous improvement even if no antacid treatment was given provided the horses were taken out of training.(8) avoid stress such as box confinement long transportation. antacids. These buffer (neutralise) the gastric acids. They usually consist of mixtures of magnesium hydroxide and aluminium hydroxide. They only have a short lived effect. There is some doubt whether horses can be treated often enough to have a significant effect on gastric acidity under practical conditions. sucralfate. This is the aluminium hydroxide salt of sucrose. It forms a sticky gel in acid conditions ( pH less than 4), attaches to ulcerated tissue and remains there for six hours or more. Because it requires acid conditions, it will probably not be effective if given at the same time as antacid medication. Sucralfate has not been shown to be effective in treating ulcers of the non-glandular mucosa. It may, however, stimulate mucus production and increase prostaglandin production from the glandular mucosa. So it may be more effective for treating ulcers of the glandular mucosa. Histamine H2 receptor antagonists. These are used for treatment of gastric ulcers in humans (eg cimetidine, ranitidine). They block acid secretion by blocking the action of histamine on the H2 receptor of the parietal cell which stimulates acid secretion. There is evidence that they reduce acid production, but their effect on ulcer healing is less certain Acid pump inhibitors. These block the action of the final step in the acid secreting pathway. Omeprazole is currently available in USA and should be licensed in the UK by the end of 2003. Recent studies show that a dose of 4mg/kg is most effective, resulting in healing in 77% and improvement in 92%. It exerts its maximum effect on acid secretion in 3-5 days. Ulcers may take 2 - 4 weeks to heal although horses often feel more comfortable within a few days of starting treatment. References Field survey of the prevalence of gastric ulcers in Thoroughbred racehorses and on response to treatment of affected horses with omeprazole paste. JH Johnson, N Vatistas, L Castro, T Fischer, FS Pipers, D Maye. Equine Vet Educ (2001) 13, (4) 221-224. Is the cause of training-related squamous gastric ulceration primarily a mechanical phenomenon?M Lorenzo-Figueras, JA Burrow, GD Lester, AM Merrit. Proc Seventh Int Colic Research Symp (2002) 80 Inability of endoscopic examination to predict gastric ulcer severity in horses. FM Andrews Proc Seventh Int Equine Colic Research Symposium (2002) 83. M O`Connor, A Roussel, J Steiner, J Meddings, N Cohen. Sucrose permeability as a marker for equine gastric ulceration. Proc 7th Equine Colic Research Symposium (2002) p84. Study of crib biting and gastric inflammation and ulceration in young horses. CJ Nicol, HPD Davidson, PA Harris, AJ Waters, AD Wilson. Vet Rec (2002) 151, 658 - 662. Mills DS, MacLeod CA. The response of crib-biting and windsucking in horses to dietary supplementation with an antacid mixture. Ippologia (2002)13, (2) 33 - 41 Murray MJ, Schusser GF, Pipers FS, Gross SJ. Factors associated with gastric lesions in thoroughbred racehorses. Equine Vet J (1996) 28, 368-74. Murray MJ, Haven ML, Eichorn ES, Zhang D, Eagleson J, Hickey GJ. Effects of omeprazole on healing of naturally-occurring gastric ulcers in thoroughbred racehorses. Equine Vet J (1997) 29, 425-429 PRODUCT TRIAL FOR ULCERS We have been asked to trial a new product called "EXTREME". If we go ahead - we are awaiting confirmation of exactly what is in it - our findings will be posted on the Bulletin Board in due course. Helpful Navigation to: Noticeboard Vet Clinic Horsetalk