For more than 50 years, ulceration of the equine stomach has been recognized as a very prevalent disease condition. First described in foal stomachs in 1964, it is known to be responsible for poor performance and illness in horses with many different job descriptions, all ages and sexes, from retired “pasture-pals” to highly successful competition horses. It can be root cause for poor hair coats, poor appetite, unthriftiness, fever, weight loss and colic. Estimates of its prevalence range from 55-100% of all horses regardless of their job description. When grading ulcers on a scale of 1 to 4, where 1 is mild and 4 is severe, those in the 1-2 range are less likely to cause clinical diseases than those in the 3-4 range.3 That being said, each horse is an individual and could be mildly affected by the less severe levels of ulceration.
The root cause of the ulceration is the normal secretion of acid by the stomach lining cells. The acid is hydrochloric acid or HCl. In concentrations greater than 25% it is called Muriatic Acid. HCl is an acid that has many industrial applications including “pickling” steel or jewelry. Pickling is the application of acid to the surface of the metal to chemically clean the surface making it possible to metallurgically bond something to the surface, as in galvanizing screws, bolts and fence posts. Other uses are in the production of PVC (pipes and coatings), Iron Chloride (for water and sewage treatment plants), calcium chloride (road treatment salt), household cleaner (toilet bowl and tile cleaners), and illicit drugs (cocaine).2
Not unique to the equine stomach, HCl is produced in the stomach of all mammals. The roughage diet of the horse, release of saliva, and other mechanisms, dilutes and buffers the HCL from an approximate pH of 2 down to about pH of 7 when it exits the stomach into the duodenum (beginning of the small intestine). The duodenum further buffers the HCl by stimulating the liver to release alkaline bile through the release of cholecystokinin, and, stimulating the pancreas to release bicarbonate by releasing secretin. The horse, being grazing animal, almost always has a large bolus of roughage in its stomach. When in athletic training the horse may have more concentrate feed in its stomach than roughage. The concentrates are less effective in neutralizing the stomach acid. Additionally, concentrates ferment, creating volatile fatty acids, which are also ulcerogenic. When circumstances develop and persist that allow for the production of stomach acid without the buffering effects of roughage, the stomach lining cells begin to die and erode, exposing the submucosal tissue which is far less tolerant of the low, acidic pH.
The Equine stomach is unique in that there are two distinct regions known as the squamous region and the glandular region. The squamous region is the top 1/3rd of the stomach and the glandular portion is the bottom 2/3rds. The bottom, glandular part secretes HCl, mucous and bicarbonate and is relatively less prone to ulceration because of the protective nature of the lining cells and the buffering by the mucous and bicarbonate. But the upper squamous region is not so protected and buffered and as such has a lower or acidic pH and much higher incidence of ulceration. But ulcers can occur in both regions as well as in the esophagus just before the stomach and in the duodenum just behind the stomach.
Risk factors involved in the development of ulcers include intense training programs, stall confinement, relative high concentrate low roughage diets, and over-population of horses in pasture or paddock environments (e.g., large groups of brood mares in a small space). Interestingly, there is no association with age or sex, EGUS is equally distributed through all populations of horses. Nonsteroidal anti-inflammatory medications (NSAID) like phenylbutazone and flunixin (Banamine®), known to cause ulcers in other species, may also be ulcerogenic in horses. The ulcer mechanism of ketoprofen and firocoxib has been shown to cause fewer ulcers in other species and may also be safer in horses. The ulcerations caused by this class of drugs (NSAIDs) has been shown to be very significant in the large colon of horses and can be life threatening.
The most accurate means of diagnosis of EGUS is by gastroscopic exam to directly visualize the esophageal, gastric and duodenal lining to identify ulcers. Other indirect diagnostic methods described include fecal occult blood testing (FOBT) – but fecal blood can more comely from many common intestinal parasites, thereby decreasing the specificity and accuracy of this test; sucrose permeability tests and serum alpha1-antitrypsin detection. There are no hematologic or biochemical markers which can be used to diagnose EGUS.1
Treatment is aimed at reducing risk factors, protecting the stomach lining from the acid and suppressing acid production. Over-the –counter antacids can be symptom modifying but prescription medications that stop the production of acid are the most effective. Prescription medications that can protect the lining cells and the submucosa are also very effective. Ulcer healing is promoted by antacid therapy. Proton pump inhibitors (omeprazole)
offer a better option than H2 antagonists (ranitidine, cimetidine – must be administered 4-6 times daily to be effective) in stomach ulceration treatment. Omeprozole can be used once daily and its antiulcer effectiveness is long acting. Omeprazole (Gastrogard®) (4 mg/kg of body weight orally every 24 hours) inhibits gastric secretion in horses and it was proven to be effective in EGUS treatment and prevention. It is difficult to recommend the duration of pharmacologic treatment. Gastric ulcerations (similarly to skin wounds) in horses are individual. Endoscopic examination is recommended after two weeks of omeprazole treatment to evaluate ulcer healing.1 Coating and binding agents such as sucralfate and bismuth subsalycylate can promote ulcer healing in the equine stomach. Sucralfate is the hydroxyl aluminum salt of sucrose octasulfate and in the stomach environment is converted to a sticky mass covering the mucosal lesions. Sucralfate is widely used in neonate foals where antacid therapy can lead to increased risk of nosocomial infections.1 The use of synthetic prostaglandin 1 (PGE 1) analog and somatostatin analog were studied in connection with EGUS (misoprostol). Prostaglandins would be most indicated in horses with NSAIDs administration or under stressful conditions. The cost limits their use in horses and it is contraindicated in pregnant and nursing mares because of its effect on the female reproductive tract [can cause abortion].1
Discuss EGUS with your veterinarian and determine the best diagnostic testing, treatment plan and preventative protocol for your horse.
-References:
1) Equine Gastric Ulcer Syndrome (EGUS), Proceedings of the 13th International
Congress of the World Equine Veterinary Association, WEVA, October 3 - 5, 2013
Budapest, Hungary, Barbora Bezdekova, University of Veterinary and Pharmaceutical Sciences, Faculty of Veterinary Medicine, Equine Clinic, Brno, Czech Republic.
2) Hydrochloric Acid - Wikipedia 2015
3) Rethinking equine gastric ulcer syndrome: Part 2 – Equine squamous gastric ulcer syndrome (ESGUS), B.W. Sykes, et al, Equine Veterinary Education, American Edition, May 2015.
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