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Equine Gastric Ulceration

Equine gastric ulcer syndrome is a disease complex in horses that is associated with damage to the lining of the oesophagus, stomach and duodenum. Clinical signs are often non-specific and include lack of appetite, weight loss/poor body condition, acute and recurrent colic, loose feces, poor performance and changes in attitude. The non-specific nature of the clinical signs associated with gastric ulceration often leads owners and veterinarians to suspect gastric ulceration as a cause of poor condition and poor performance in horses.

So, why are horses so susceptible to gastric ulcers? The anatomy and physiology of the equine stomach gives us some clues. The equine stomach is divided into two parts, a squamous part (closest to the oesophagus) and a glandular part (closest to the duodenum). Most gastric ulcers occur in the squamous part of the stomach where there are very few defence mechanisms against increased gastric acidity. Gastric acidity is determined by the acidity of the stomach contents, which are a mixture of salivary, gastric, duodenal, biliary and pancreatic secretions.

Saliva plays an important role in decreasing the acidity of the stomach contents and it is thought that low roughage diets may decrease the production of saliva and increase the acidity of the stomach. The horse is also a continuous secretor of gastric acid. This means that acid secretion occurs even without the presence of feed material in the stomach. When horses are stabled for long periods of time and have no access to pasture, they spend less time eating, even when provided with feed ad libitum. It is likely that this decreases the amount of saliva produced and increases the acidity within the stomach.

High grain diets can also play a role in gastric ulceration. Many grains contain high concentrations of fermentable carbohydrates that are converted by bacteria in the stomach to volatile fatty acids. Volatile fatty acids can cause cellular swelling, inflammation and result in gastric ulceration. Concentrations of volatile fatty acids in the stomach are highest 2-6 hours after feeding and decrease as food moves out of the stomach. However, the negative effects of volatile fatty acids can be reduced by feeding grain in conjunction with lucerne hay. Lucerne hay is high in protein and calcium which both help to decrease gastric acidity for up to 6 hours after ingestion.

Other risk factors for gastric ulceration include stress, transport, intermittent feeding, non- steroidal anti-inflammatory drugs, intense exercise and racing. Indeed, one study showed that up to 90% of racehorses in training develop gastric ulcers by the time they have been in work three months! In comparison, the prevalence of gastric ulcers in show and riding school horses is lower with one study demonstrating 23/62 (37%) of these types of horses having endoscopic evidence of lesions. The prevalence of lesions in show horses wasshown in another study to increase to 13/23 (56%) after three consecutive days of travel and competition.

In many horses, a presumptive diagnosis of ulcers is often based on clinical signs. Due to the number of studies demonstrating a high prevalence of gastric ulceration in racehorses, preventative therapy for gastric ulcers in racehorses is easily justified and often recommended by our practice. In show, pleasure and performance horses our recommendations often vary on a case by case basis.

Definitive diagnosis of equine gastric ulcers is based upon endoscopic examination of the stomach with a 3m gastroendoscope. At the present time, our practice refers cases to the University of Melbourne Equine Hospital at Werribee for gastroscopy. It is necessary to withhold food for 6-12 hours before the examination. The horse is sedated, twitched and the gastroscope is passed up the nostril, down the oesophagus and into the stomach. The stomach is insufflated with air to allow visualisation of the entire lining. Any lesions are then assessed based on their location and severity and a treatment plan is formulated bearing this information in mind.

The two main drugs we use to treat equine gastric ulcers are histamine H2 receptor antagonists and proton pump inhibitors.

Histamine H2 Receptor Antagonists

These drugs act primarily to inhibit gastric acid secretion. They act in a dose dependent manner and need to be administered at least twice daily. Ranitidine (Ulcerguard) is the most potent H2 receptor antagonist available for use in horses. Studies published in the veterinary literature have been able to demonstrate the prevention of ulcers in adult horses with ranitidine administration. However, there does not appear to be convincing evidence to support ranitidine as an effective treatment for existing gastric ulceration. In light of this, our practice prefers to use ranitidine for prevention, rather than treatment of gastric ulcers.

Proton Pump Inhibitors

These drugs are potent and highly specific inhibitors of gastric acid secretion. They act to inhibit an enzyme that is necessary for the last step in the acid secretory pathway. Omeprazole (Gastrozol) is the proton pump inhibitor available for use in horses. Omeprazole has prolonged antisecretory effects and this allows for once daily dosing. A recent study has shown that treatment with omeprazole at 4mg/kg once daily for 28 days results in a significant improvement in the appearance of gastric ulcers in 92% of treated horses. Other studes have shown that after the initial course of omeprazole, a lower daily dose of omeprazole can be used to prevent the recurrence of ulcers in most horses in training. Our practice routinely uses omeprazole for the treatment of equine gastric ulcers.

Kilde: tevs.com.au