By Nora Grenager, VMD, DACVIM
Equine gastric ulcer syndrome (EGUS) is prevalent in our equine population and can be a cause of a huge variety of clinical signs ranging from suboptimal performance and behavioral issues to poor appetite and mild colic. It has been estimated that 50 to 100 percent of adult horses have gastric ulcers depending on level of work and management practices.
Unlike in humans, a horse’s stomach continuously secretes gastric acid because horses were designed to graze throughout the day. The equine stomach is divided into two parts — a smaller upper squamous portion (about one third) and a larger lower glandular portion (about two thirds) — separated by a raised border of tissue called the “margo plicatus.” The upper squamous portion is like a continuation of the esophagus; the lower glandular portion is where acid is produced.
EGUS occurs when there is an imbalance between gastric acid secretion and the stomach’s normal protective mechanisms.
Types of Gastric Ulcers
There are two syndromes of EGUS that have different predisposing factors, signs,
and treatments — gastric ulceration in the squamous portion and gastric ulceration in the glandular portion. The glandular portion of the stomach secretes acid and other compounds. It has intrinsic protective mechanisms to deal with acid and is accustomed to acid exposure. Ulceration in this portion is likely due to both an increased acid exposure as well as a decrease in its protective mechanisms. Gastric ulcers in the squamous portion is likely due to the fact that this region is not accustomed to, nor equipped for, acid exposure.
The majority of gastric ulcers in the squamous portion of the stomach occur along the margo plicatus, which is closest to the glandular acid-producing portion.
Factors that likely predispose horses to glandular ulceration include stress and administration of nonsteroidal anti-inflammatory drugs, called “NSAIDs,” such as phenylbutazone (Bute™), flunixin meglumine (Banamine™), and less commonly firocoxib (Equioxx™). Stress decreases the stomach’s natural protective mechanisms. NSAIDs also decrease the stomach’s natural protective mechanisms, more often with high doses or long duration of treatment.
Factors that predispose horses to squamous ulceration include infrequent feedings, high concentrate diets, and intensive training. Stress and NSAID administration can augment these processes in this region as well. Feed deprivation or infrequent feeding has been found to cause gastric ulcers because when the stomach is small and contracted the squamous portion of the stomach is exposed to acid. The byproducts from fermentation of high concentrate diets can also cause acid injury of the squamous portion. Consuming hay and the salivation that accompanies eating (because saliva contains natural buffers) help to buffer stomach acid. Intense exercise potentially increases intra-abdominal pressure and delays gastric emptying time, which increases the exposure of the squamous portion to acid.
Many instances of gastric ulceration probably go unrecognized. Interestingly, the severity of a horse’s clinical signs does not correlate with the degree of gastric ulceration. Horses with EGUS may have poor or picky appetite, weight loss, rough hair coat, poor performance, poor body condition, sore back, “girthy” behavior, or changes in attitude (the horse may seem “grumpy”). A horse with EGUS can present with excessive teeth grinding or excessive salivation, mild recurrent colic or even a more severe acute colic episode, though this is uncommon.
Suspicion of EGUS may be based on history and clinical signs, but evaluation of the stomach with an endoscope (a procedure called “gastroscopy”) is the only way to confirm the presence, type, and severity of EGUS. This procedure can be performed at the barn or at a referral veterinary facility. The procedure is usually done in the morning after an overnight fast (the horse must be fasted for a minimum of 12 hours prior to gastroscopy so that the stomach is empty for evaluation). The horse is typically sedated and the endoscope is passed through the nostril down the esophagus into the stomach. The presence, severity, chronicity, and type of gastric ulceration is determined. Unfortunately, there is no blood or fecal test available that can accurately diagnose EGUS.
Several types of drugs are available and commonly used to treat EGUS, and it depends on whether ulceration is present in the squamous, glandular, or both parts of the stomach. Treatment duration usually lasts 4–8 weeks. The gold standard treatment for squamous ulceration is omeprazole (Gastrogard™), a proton-pump inhibitor drug that directly blocks acid secretion. It is formulated as a flavored oral paste given once daily and has been proven to most effectively cure gastric ulceration. Ideally this is given on an empty stomach, 30–60 minutes prior to feeding (so usually first thing in the morning or just before lunch). Antacids (such as aluminum or magnesium hydroxide and calcium carbonate) can help relieve immediate clinical signs, but do not effectively treat the ulceration. Antacids also have a short duration of effect and need to be administered orally every 2–3 hours so they are not convenient for long-term treatment.
The typical treatments for glandular gastric ulceration include sucralfate and misoprostol, sometimes along with Gastrogard™. Sucralfate coats ulcerated areas and stimulates the GI tract’s own local protective mechanisms. It is sometimes used alone, or in conjunction with Gastrogard™ for mild to moderate cases of glandular ulceration. Misoprostol is used for moderate to severe glandular ulceration (usually in conjunction with sucralfate +/- Gastrogard™). It increases the body’s own protective mechanisms against glandular ulceration. It cannot be used in pregnant mares and it can occasionally cause transient cramping at the start of administration.
Therapy is typically tapered off rather than stopped cold turkey. We usually recommend repeat gastroscopy at the end of the treatment interval to assess the response to treatment. Most cases of squamous ulceration respond well to appropriate treatment, but glandular ulceration is less predictable. Some cases respond well to one month of treatment, while others require longer; unfortunately, it is difficult to predict into which category a horse will fall.
Last but certainly not least, it is widely believed that EGUS does not occur in a vacuum. There is typically something else driving the condition — be it musculoskeletal pain, other GI pain, stress, or feed changes. It is very important to try to home in on any other potential causes to maximize the efficacy of your treatment and prevent recurrence.
Gastrogard™ given at a quarter dose once daily (called Ulcergard™ — available over the counter) is effective at preventing the formation of gastric ulcers. This is often recommended around times of stress or NSAID administration in horses at risk for EGUS. Corn oil added to the feed has also been shown to help increase gastric pH (i.e., decrease the amount of acid), although some horses can become “hot” with corn oil supplementation. It has been shown that supplements containing pectin and lecithin can help prevent EGUS, and mineral-rich calcified marine algae helps prevent squamous ulceration.
Most importantly, prevention of EGUS involves recognition of situations that may predispose a horse to gastric ulceration. Horses on high doses of NSAIDs or long-term treatment with NSAIDs are theoretically at higher risk for EGUS. Horses in training or who are fed high concentrate meals without access to roughage are at an increased risk. Performance horses are not the only horses at risk for EGUS, as severe ulceration has been diagnosed in recreational and retired horses in seemingly calm environments. It is important to keep EGUS in mind if a horse is being exposed to potential stresses, particularly those horses that have had EGUS in the past.
Recognition of clinical signs with appropriate diagnosis and treatment of EGUS improves attitude, performance, and quality of life for our horses.