Studies have shown that gastric ulcer disease is a common problem in foals and adult horses. Prevalence estimates range from 25% to 51% of foals and 60% to 90% of adults. There are several types of gastric ulcer disease in horses, depending upon the specific part of the stomach that is involved and the particular causes involved. To simplify, all of these various types of gastric ulcer disease have been grouped together under a single label, Equine Gastric Ulcer Syndrome or EGUS.
Causes of Egus
The horse’s stomach can be divided anatomically into two parts, the upper non-glandular part that connects to the esophagus and the lower glandular part that empties into the small intestine. Gastric acids, important in the breakdown of food, are produced in the glandular part of the stomach. Foals begin secreting high levels of gastric acid by the time they are 2-days old. Adults secrete approximately 1.5 liters of gastric juice hourly.
The lining of the non-glandular stomach is similar to the lining of the esophagus and, like the esophagus, lacks mechanisms that protect it from acid. This region of the stomach is not normally very acidic. Ulcers in this area are caused by prolonged exposure to abnormally high levels of acid. Many factors can lead these high levels of acid. Here are some examples:
• Feed deprivation has been found to be a cause of ulcers in the non-glandular part of the stomach. Hay and roughage stimulate large amounts of saliva production. Saliva is high in bicarbonate, which buffers stomach acids. Studies have shown that horses with continued access to hay have a lower incidence of ulcers.
• In foals, milk may have a buffering effect on stomach acid. Weak or sick newborn foals nurse less often than normal, so they get less of this buffering effect. Less frequent nursing also results in slower emptying of the stomach into the small intestine, allowing acids to build up in the stomach.
• The stress of vigorous exercise slows down stomach emptying into the small intestine, allowing acid to build up in the stomach.
• During vigorous exercise, abdominal pressure is increased. This has the effect of forcing very acidic stomach juices from the lower glandular stomach up into non-glandular area of the stomach.
• High grain diets are rich in fermentable carbohydrates. Bacteria in the digestive system of the horse ferment these carbohydrates, resulting in byproducts called volatile fatty acids (VFA’s). VFA’s can penetrate lining of the non-glandular stomach, causing cell damage and ulceration.
As mentioned above, the lower glandular stomach normally has a very high acid content. Here, the lining of the stomach produces mucus and bicarbonate to protect itself from the highly acid environment that is necessary for proper digestion. Chemical messengers called prostaglandins present in the cells of the stomach lining regulate the production of this protective mucus and bicarbonate. Problems that interfere with this process lead to ulcers in this part of the stomach. Here are some examples:
• Non-steroidal anti-inflammatory drugs (NSAIDS) such as Phenylbutazone (“Bute”) and Flunixamine (“Banamine”) are commonly used in horses for a multitude of reasons. The anti-inflammatory effect that these drugs have is through their ability to block prostaglandin production. Unfortunately, they also block prostaglandins in the stomach lining that produce the protective mucus and bicarbonate. Prolonged use and high dosages of NSAIDS can result in ulcers. Foals are particularly sensitive to this side effect since they have very high levels of acids already and the lining of their stomachs are much thinner.
• Stress from its many causes (disease, confinement, strenuous exercise, etc.) results in the body producing higher levels of their own “endogenous” corticosteroids such as cortisol. Corticosteroids have a similar blocking effect on prostaglandin production that NSAIDS do. In this way, stress leads to a breakdown of the protective mechanisms in the glandular stomach, resulting in ulcers.
• Illness can sometimes result in reduced blood flow to the glandular stomach. Like any tissue, the cells of the glandular stomach that produce the protective substances depend on adequate blood supply. In this way, illness can lead to ulcers, especially in foals.
Diagnosis of Egus
Diagnosis of gastric ulcers in horses is based upon clinical signs, endoscopic examination, and response to treatment. Endoscopic examination is the only method of definitely confirming the diagnosis of EGUS. Unfortunately, the specialized equipment required for this procedure is generally only available veterinary teaching hospitals or larger referral centers.
Clinical signs of gastric ulcers in yearlings and older horses are rather non-specific. Poor performance, poor appetite, listlessness, rough hair coat, repeated episodes of mild colic, lying down excessively, poor body condition, pot-bellied body profile and weight loss are examples of the type of vague signs found with EGUS. Response to therapy helps confirm the diagnosis.
In foals, the most distinctive sign of EGUS is teeth grinding or “bruxism.” Other signs include reduced nursing, intermittent colic, lying down excessively, rolling up onto their back, excessive salivation & drooling, diarrhea, pot-bellied appearance and rough hair coats.
Treatment of Egus
To sum up the discussion thus far, there are two broad categories of EGUS. First, those that occur in the non-glandular stomach due to prolonged exposure to stomach acids. The other group occurs in the glandular stomach due a breakdown in the normal protective mechanisms. Within each category, there were a number of inciting causes listed. The common link between the two groups is that it is stomach acid that generates the destructive action on the stomach lining. Not surprising then, one of the main methods for treatment of EGUS is to reduce production of stomach acids. There is only one medication that has obtained FDA approval by conducting the clinical trials necessary to prove efficacy for the treatment of EGUS. The medication is called Gastroguard (from the pharmaceutical Merial). The active ingredient is omeprazole, an “H2-Blocker” which blocks the production of gastric acid and is used in the treatment of human ulcers also. Treatment is continued for 28 days. Blocking the production of gastric acid over this time period allows the ulcer to heal. Merial has another product called Ulcerguard, which is the only FDA-approved medication for the prevention of EGUS. It also contains omperazole but at half the level of Gastroguard.
Other H2-Blockers have been used for treating EGUS but they have not undergone the FDA approval process (e.g. ranitidine and cimetadine). Antacids such as Maalox have been used but studies to establish their efficacy are lacking. Some studies have shown that the effect that these antacids have on stomach acid is short-lived, not allowing enough time for the ulcer to heal.
Sucralfate is another medication used to treat gastric ulcers. It is indicated for the ulcers that occur in the glandular stomach. It binds to the damaged stomach lining and promotes the protective mechanisms that shield the lining from the acids in the stomach. Efficacy of sucralfate in the treatment of EGUS has not been thoroughly evaluated.
Feed schedules, feed program, training program, turnout schedule and the use of NSAIDS have all been implicated as issues in the development of gastric ulcers. Careful review of these horse management issues is important to identify problem areas and make appropriate changes when possible.
Copyright © 2009 The NW Horse Source, LLC
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