INTRODUCTION
Gastric ulcers are common in horses but have been rarely diagnosed until recently.  It has “escaped” the clinician’s finding leading to treatment for the abdominal crises as a whole but not specifically to the cause, gastric ulcers.  This is because gastric ulcers can weaken the whole gastro intestinal tract, as in man and create many and diverse manifestations such as lower bowel crisis or weight loss, inappetance, low grade colic, etc.

The clinical emphasis had been primarily focused on foals until description of the syndrome in adults were documented.  Compromise to athletic training and performance were recognized in conjunction with gastric ulcers and endoscopic surveys of horses in training yielded high percentage of gastric ulceration.  This clinical syndrome has caused loss of income and reduced performance in horses.

FACTORS CAUSING GASTRIC ULCERATIONS
The actual cause of gastric ulceration has not been properly determined but it has been noted that gastric ulcers could have been induced with corticosteroid medications, non-steroidal anti-inflammatory (mainly oral route) stress related diseases.  Rotavirus and fungal infections in foals have also been implicated.

Also feeding and environment factors have been found to result in development of gastric ulcers.Parasites such as Habronema and Draschia species are the major cause of gastric ulceration throughout the world.  A survey of stomachs from 280 horses killed at an abattoir in Australia revealed 72% with Habronema ulceration.

CLINICAL SYMPTOMS
Clinical symptoms consist of silent ulcers, clinical ulcers, pyloric strictures and spontaneous perforations of gastro-duodenal ulcers.  Silent ulcers are usually non clinical and documented by gastro endoscopy or autopsy findings. 

Clinical ulcers are shown by various symptoms like low grade colic, curling of lips, salivation, bruixism, tearing from eyes, intermittent pawing, dorsal recumbency, diarrhoea and weight loss as well as poor performance.  In adult horses the clinical signs appear while eating especially after finishing the feed.

Sometimes these horses may display a thrifty hair coat, eat slowly, exhibit grinding of teeth, excessive sweating in the paddock and display distress and colic after racing.  Surveys in America showed that horses entering training had less incidences of gastric ulcers.  However, as training progressed 90% of the horses developed gastroduodenal ulcers.  At the same time sporting horses  had a lesser incidence of about 50% – 60% .

DIAGNOSIS
Physical examination and blood analysis would not help to provide adequate diagnosis of sub-clinical gastric ulcerations.  The clinical signs of salivation, bruixism and refluxing can seldom be confused with other clinical entities.  In the case of perforation, ultra sound finding or free abdominal fluid with abdominal tap consistent with faecal contamination usually lead to a grave prognosis.

Gastro endoscopy is the definite method for the diagnosis of ulcers. Endoscopes with a diameter of 9 mm thickness and 120 cm in length can be used in foals. Horses require endoscope of at least 200 cm to 300 cm with a diameter of 9 – 11 mm.  The horse should be fasted for 8 – 10 hrs to eliminate food substances in the stomach and to allow proper visualization of the stomach.

In the author’s experience in the field, diagnosis is often made by stomach tube drenching with a concentrated low volume salt drench on an empty stomach.  Colic often develops within 2 to 3 mins to up to 20 mins.  Often the colic attack is violent and will disappear with drenching with 6 L of water or in most cases it can be relieved without treatment in approximately 20 to 40 mins.

TREATMENT
Treatment for gastric ulcers depends on individual clinician’s preference, endoscopy, history and clinical findings.  The use of antacids, buffers, bismuth-subsalicylate, aluminium hydroxide may be palliative but their effectiveness in treatment and prevention are anecdotal.

Hystamine-type 2(H₂) antagonists consist of cimetidine (Tagamet) at 8 – 10 mg/kg p.o. TID or 4.4 mg/kg intra muscular (I/M) or intravenous (I/V) BID to TID; ranitidine 4.4 mg/kg p.o. BID to TID or 1.4 mg/kg IM or IV BID; or famotidine 1 – 2 mg/kg p.o. BID or 0.4 mg/kg IV BID.  More complete and varied dosages can be obtained from specific references.

Omeprazol, a hydrogen proton pump inhibitor, has been proven to be the most effective treatment for both squamous and mucosal ulceration of the stomach and duodenum.  An initial dose, for approximately 28 days, of 2.0mg/kg per oz once a day reverting to 1.0mg/kg per oz once a day.

CONCLUSION
Gastric ulceration in the horse has been present without being diagnosed for a long time.  It is only recently that this condition has been proven to be a real entity and has been responsible for many other disorders.  Diagnosis required utilization of expensive specialized equipments.  It can be said that gastric ulcers have been a cause of wastage and non performance in the horse.  Specific treatments for this condition are now on the market.

REFERENCES
Anon. (1997).  Rural Industries Research and Development Corporation, Ulceration Of The Stomach In Horses – Important Influences Of Environment, Equine Research News Issue 1/97.
Byars, T. D. (1995).  Gastric Ulceration in Horse, Proceedings of the 17^th Bain Fallon Memorial Lectures
Madigan, J. E. (1992).  Gastroduodenal ulcers, Proceedings of the 14^th Bain Fallon Memorial Lectures