Gastric Ulcers in Horses: Signs, Causes, and Treatment (EGUS Guide)

Gastric ulcers are wildly common in horses. That's not an exaggeration. Studies consistently show prevalence rates between 60-90% in performance horses, and even pasture-kept horses aren't immune. The numbers are staggering when you actually sit with them. Your horse probably has some degree of gastric ulceration right now, or has had it at some point. That's not meant to alarm you. It's meant to get you paying attention, because ulcers are treatable, preventable, and far better managed when caught early rather than allowed to fester.

Two Stomachs in One: Why Horses Are Built for Ulcers

The equine stomach is surprisingly small, holding only about 8-15 liters in an average-sized horse. For an animal that weighs half a ton, that's remarkably compact. But the real story is how it's divided.

A distinct boundary called the margo plicatus separates the stomach into two fundamentally different regions. Above this line sits the squamous mucosa: pale, thin, and completely unprotected. It looks almost like the lining of your esophagus, because developmentally, that's exactly what it is. Below the line lies the glandular mucosa: darker, thicker, and equipped with mucus-producing cells, bicarbonate secretion, and robust blood flow designed to withstand constant acid exposure.

Here's the catch. Horses produce hydrochloric acid continuously, 24 hours a day, regardless of whether food is present. In a wild or feral horse grazing 16-18 hours daily, the constant flow of saliva (which contains bicarbonate) and the physical presence of fibrous feed buffer that acid effectively. The squamous region stays relatively protected because the fibrous mat of forage floats on top of gastric fluid, keeping acid in the lower glandular zone where it belongs.

Domestication broke this system. Meal feeding, long gaps between hay, stall confinement, grain-heavy diets, and the physical demands of training all conspire against the horse's gastric lining. When the stomach empties, acid splashes freely onto unprotected squamous tissue. That's when ulcers start forming.

Squamous vs. Glandular: Different Problems, Different Solutions

This distinction matters enormously and it's something that older ulcer research glossed over. The equine veterinary community now formally separates EGUS into two subcategories:

Equine Squamous Gastric Disease (ESGD) affects the upper, unprotected portion of the stomach. The mechanism is straightforward acid injury. Acid contacts tissue that has no defense against it, and erosion follows. Risk factors include intermittent feeding, high-grain diets, intense exercise (which increases abdominal pressure and pushes acid upward), and transport stress.

Equine Glandular Gastric Disease (EGGD) involves the lower, gland-lined region. This tissue normally handles acid just fine, so when ulcers develop here, the problem isn't excess acid. It's breakdown of the protective mechanisms: reduced mucus production, impaired blood flow, or disruption of the mucosal barrier. NSAID use (phenylbutazone, flunixin) is a well-documented risk factor, as these drugs inhibit prostaglandins that maintain glandular mucosal defenses.

Why does this matter practically? Because omeprazole (the frontline treatment) works by suppressing acid production. That's extremely effective for squamous ulcers, where acid is the direct culprit. For glandular ulcers, acid suppression alone often isn't enough. The protective barrier itself needs support, which is where sucralfate and other strategies come in.

Recognizing the Signs

Horses can't tell you their stomach hurts. They show you, often subtly, and often in ways that get attributed to training issues, attitude, or just being "that horse." Learning to recognize ulcer-associated behaviors can save months of frustration and prevent progression to severe disease.

Common behavioral signs include:

• Poor appetite or picky eating, especially reluctance to finish grain
• Weight loss or difficulty maintaining condition despite adequate calories
• Girthiness: flinching, pinning ears, or biting when the girth is tightened
• Attitude changes under saddle, particularly resistance, sourness, or reluctance to go forward
• Dull coat that doesn't respond to nutritional adjustments
• Mild recurring colic episodes, especially after eating
• Grinding teeth (bruxism)
• Excessive salivation
• Preferring hay over grain, or vice versa

None of these signs are specific to ulcers. Every single one has other possible explanations. That's what makes this frustrating. A girthy horse might have ulcers, or might have a poorly fitted saddle, or might have learned that dramatic behavior during tacking up gets a response. Context matters. When multiple signs cluster together, especially in a horse with risk factors for ulcers, investigation is warranted.

One pattern worth highlighting: horses that seem uncomfortable when their stomach is empty but settle after eating. If your horse is cranky in the morning before hay but fine an hour later, acid exposure on an empty stomach could be the issue.

Gastroscopy: The Only Real Answer

Blood tests can't diagnose ulcers. Fecal tests can't diagnose ulcers. Behavioral assessments suggest them but don't confirm them. The only definitive diagnostic tool is gastroscopy: passing a three-meter endoscope through the nostril, down the esophagus, and into the stomach to directly visualize the mucosa.

The horse needs to be fasted for 12-16 hours (water withheld for 4-6 hours) to ensure the stomach is empty enough for adequate visualization. Light sedation keeps the horse comfortable. The procedure takes about 15-20 minutes and provides immediate, visual answers.

Ulcers are graded on a 0-4 scale:

• Grade 0: Intact epithelium, no lesions
• Grade 1: Intact mucosa with areas of reddening (hyperemia) or hyperkeratosis
• Grade 2: Small, single or multifocal ulceration
• Grade 3: Large single or extensive multifocal ulceration
• Grade 4: Extensive ulceration with areas of deep ulceration

Grading the squamous and glandular regions separately is current best practice, since treatment differs. A horse might have Grade 3 squamous ulcers with Grade 0 glandular tissue, or vice versa, or any combination.

Cost varies by region but typically runs $250-$500. When you consider the expense of treating empirically (guessing), potentially treating the wrong problem, or missing an unrelated condition entirely, scoping often saves money in the long run.

Risk Factors: What Pushes Horses Toward Ulcers

Understanding risk factors helps with both prevention and understanding why a particular horse developed problems.

Feeding patterns top the list. Long periods without forage allow gastric acid to accumulate and attack squamous tissue. Horses fed twice daily with nothing in between are at higher risk than those with continuous hay access. High-starch diets (grain) stimulate gastrin release, which increases acid production, and ferment in the stomach to produce volatile fatty acids that compound squamous damage.

Stall confinement correlates with higher ulcer rates compared to pasture turnout. The reasons are multifactorial: restricted forage access, reduced movement (which affects gastric motility), and psychological stress.

Exercise intensity matters. During strenuous exercise, increased abdominal pressure pushes acidic gastric contents up against the squamous mucosa. Racehorses and upper-level sport horses show the highest prevalence rates.

NSAID use particularly affects the glandular region. Bute and banamine are staples of equine practice, but chronic or high-dose use damages the prostaglandin-mediated defenses that protect glandular tissue. Short courses at standard doses carry lower risk than prolonged daily use.

Stress, while hard to quantify, clearly plays a role. Transport, competition, social disruption, and changes in routine all correlate with ulcer development or worsening. The equine digestive system evolved for a predictable, low-stress existence. Modern management often provides the opposite.

Treatment: What Actually Works

Omeprazole: The Foundation

Omeprazole is a proton pump inhibitor that suppresses gastric acid secretion. It's the gold standard for squamous ulcer treatment, and the evidence behind it is robust.

Treatment dose: 4 mg/kg once daily for 28 days (GastroGard, the FDA-approved formulation). This heals the majority of squamous ulcers.

Prevention dose: 1 mg/kg once daily (UlcerGard, same drug, lower concentration, available over the counter). Used during periods of known risk: travel, competition, stall rest.

Generic omeprazole products exist at lower price points, and compounded formulations are cheaper still. Here's the issue: bioavailability varies significantly between products. GastroGard uses a proprietary buffered formulation designed to survive the acidic stomach environment. Many compounded products degrade before reaching the small intestine where absorption occurs. If you're treating confirmed Grade 3-4 ulcers, the branded product is worth the investment. For prevention or mild cases, discuss options with your vet.

Omeprazole should be given on an empty stomach, ideally 30-60 minutes before the morning feeding. This maximizes the drug's contact with actively secreting proton pumps.

Glandular Ulcer Treatment

Glandular ulcers respond less predictably to omeprazole alone. Current best practice combines omeprazole with sucralfate, a mucosal protectant that forms a physical barrier over ulcerated tissue. Sucralfate is typically dosed at 12-20 mg/kg two to three times daily.

Treatment duration for glandular ulcers is often longer: 8-12 weeks rather than the standard 4 weeks for squamous disease. Follow-up gastroscopy is strongly recommended, as glandular ulcers are more prone to incomplete healing and recurrence.

Misoprostol, a prostaglandin analog, has been used for refractory glandular ulcers but carries risks (potential for causing diarrhea and contraindicated in pregnant mares) and is generally reserved for cases that don't respond to first-line treatment.

Management Changes: The Part People Skip

Here's the thing about ulcer treatment that nobody wants to hear: without management changes, ulcers come back. You can run a full course of GastroGard, scope clean, put the horse back into the exact same routine, and have ulcers again within weeks. The medication treats the lesions. Management prevents recurrence.

Evidence-backed management strategies:

• Maximize forage access. Free-choice hay or pasture turnout keeps saliva flowing and maintains a fibrous buffer in the stomach. If free-choice isn't feasible, slow-feeder nets extend consumption time significantly
• Reduce starch intake. Replace grain calories with fat (vegetable oil, rice bran, stabilized flax) and fermentable fiber (beet pulp, hay cubes). Keep individual grain meals under 2 grams of starch per kilogram of body weight
• Feed hay before exercise. A small amount of alfalfa (which has natural buffering capacity due to its calcium and protein content) 30 minutes before riding creates a physical buffer against acid splash during work
• Increase turnout. More time on pasture correlates with lower ulcer prevalence across multiple studies
• Minimize NSAID use. When anti-inflammatories are necessary, use the lowest effective dose for the shortest duration. Consider COX-2 selective options (firocoxib) which carry lower gastrointestinal risk
• Provide social contact. Isolation is stressful. Visual and physical contact with other horses helps

Alfalfa deserves special mention. Research from Texas A&M demonstrated that alfalfa hay and alfalfa-grain diets produced higher gastric pH compared to grass hay diets. The calcium and protein in alfalfa buffer gastric acid effectively. Feeding a flake of alfalfa before work or as part of the diet is one of the simplest, most cost-effective ulcer prevention strategies available.

The Supplement Question

The equine supplement market is flooded with ulcer products. Antacids, coating agents, herbal blends, probiotics. Do any of them work?

Some have limited evidence supporting their use as adjuncts: pectin-lecithin complexes, sea buckthorn berry extract, and certain probiotic strains have shown modest effects in small studies. None approach the efficacy of omeprazole for treating existing ulcers. They may have a role in maintenance, but they shouldn't replace veterinary treatment for confirmed disease.

Calcium carbonate (Tums) and other antacids provide extremely short-lived acid neutralization, maybe 30-60 minutes at best. For a condition driven by 24-hour acid production, that's a band-aid on a broken pipe.

If you want to explore the anatomy of the equine stomach in detail and see exactly where these ulcers develop relative to surrounding structures, the visual context makes the clinical picture much clearer.

Frequently Asked Questions

Sources

• European College of Equine Internal Medicine - EGUS Consensus Statement
• Texas A&M University College of Veterinary Medicine - Equine Gastric Ulcer Research
• American Association of Equine Practitioners - AAEP Ulcer Guidelines
• University of Liverpool Equine Hospital - Glandular Ulcer Research