Gastric Ulcers / EGUS

Equine Gastric Ulcer Syndrome, commonly known as EGUS, represents one of the most prevalent and clinically significant conditions affecting domestic horses. This syndrome encompasses ulceration of the stomach lining and is now recognized to include two distinct disease entities based on anatomical location within the stomach. Equine Squamous Gastric Disease affects the upper, non-glandular portion of the stomach lined by squamous epithelium, while Equine Glandular Gastric Disease involves the lower, acid-producing glandular region. Understanding this distinction is critical because these two conditions have different underlying causes, risk factors, and responses to treatment.

The prevalence of gastric ulcers in horses is remarkably high, with studies documenting ulceration in sixty to ninety percent of racehorses in active training and fifty to seventy percent of other performance horses. Even pleasure horses and those in light work show ulcer rates of approximately thirty to fifty percent. Foals are particularly susceptible, with ulcers documented in up to fifty percent of foals during the first few months of life. These statistics demonstrate that gastric ulceration is not simply a disease of high-level competition horses but affects equines across all disciplines and management systems.

The impact of gastric ulcers on equine health and performance ranges from subtle behavioral changes to severe clinical disease. Affected horses may show decreased appetite, poor body condition, changes in attitude or willingness to work, and various colic symptoms. Performance horses often demonstrate reduced competitive ability, reluctance during training, and behavioral issues that owners may not initially connect to gastrointestinal disease. Economic impacts include decreased performance, training time lost to illness, and the substantial costs of diagnosis and treatment.

Gastric ulcers in horses are highly treatable when properly diagnosed and managed. Proton pump inhibitors, particularly omeprazole, effectively heal squamous ulceration in most cases when combined with appropriate management changes. Glandular ulcers may be more challenging to resolve and often require longer treatment duration. Prevention through management modifications can significantly reduce ulcer development and recurrence. Early recognition of symptoms and prompt treatment prevent progression to more severe disease and chronic problems that become increasingly difficult to resolve.

The primary cause of squamous gastric ulceration relates to the acid environment of the equine stomach and the vulnerability of the non-glandular squamous epithelium to acid damage. The horse stomach produces hydrochloric acid continuously, not just in response to feeding as in some other species. The lower glandular region of the stomach secretes this acid but is protected by mucus and bicarbonate secretion. The upper squamous region lacks these protective mechanisms and is normally protected by the buffering effect of saliva and feed material. When horses go extended periods without eating, or when acid splashes onto the squamous region during exercise, ulceration develops.

Genetic or breed predisposition to gastric ulcers is documented primarily as a function of how different breeds are typically managed rather than inherent genetic susceptibility. Thoroughbreds show extremely high ulcer prevalence because they are commonly managed in intensive training programs with feeding practices that predispose to ulceration. Standardbreds, Warmbloods, and other performance breeds similarly show elevated rates when in active training and competition. Breed differences likely reflect management rather than genetics, though some individual horses may be more susceptible to ulceration than others.

Environmental and management factors play critical roles in gastric ulcer development. Stall confinement limits continuous grazing behavior and extends intervals between meals. High-grain, low-forage diets reduce saliva production and stomach buffering. Intense exercise, particularly at speed, causes the stomach to compress, splashing acid onto the unprotected squamous region. Stress from training, competition, travel, or social isolation contributes to ulcer development. Water restriction and non-steroidal anti-inflammatory drug use, common in performance settings, further increase risk.

Risk factors for equine gastric ulcers include age, use, nutrition, and individual susceptibility. Foals in their first weeks of life are highly susceptible due to high gastric acid output relative to stomach size. Horses in active training face dramatically increased risk compared to those at pasture. Feeding schedules that result in extended fasting periods, particularly overnight, allow prolonged acid exposure. Stressful events including transport, competition, changes in herd dynamics, or illness precipitate ulcer development or worsening.

The pathophysiology of squamous gastric ulceration involves direct acid injury to epithelium lacking protective mechanisms. When gastric pH drops below four, the squamous mucosa is damaged. Volatile fatty acids produced by fermentation of grain in the stomach penetrate epithelial cells in acidic environments, causing cellular damage. Bile acids that reflux from the duodenum contribute to injury. The result is progressive erosion of the squamous lining, ranging from mild superficial damage to deep ulceration that may bleed or perforate. Glandular ulceration involves different mechanisms including impaired mucosal blood flow, reduced mucus production, and possible bacterial involvement, explaining why it responds differently to treatment.

Early warning signs of gastric ulcers in horses are often subtle and easily overlooked or attributed to other causes. Many horses with significant ulceration show no obvious clinical signs, making gastroscopic examination the only reliable way to confirm the condition. When symptoms do occur, decreased appetite is often the first indication, with horses becoming selective in their eating, leaving grain while eating hay, or showing reduced enthusiasm for meals. Mild changes in attitude, including increased irritability or decreased willingness to work, may precede more obvious signs. Owners who know their horses well are most likely to recognize these subtle early changes.

Common symptoms of equine gastric ulcers include various signs of abdominal discomfort and changes in condition. Horses may show mild, recurrent colic episodes, particularly in relation to feeding or exercise. Weight loss or poor body condition despite adequate nutrition suggests impaired digestive function. Rough, dull hair coat indicates nutritional compromise even when horses maintain weight. Changes in manure consistency, including loose stool or diarrhea, occur in some affected horses. Excessive salivation or wood chewing may indicate gastric discomfort.

Behavioral changes associated with gastric ulcers can significantly impact training and performance. Horses may become girthy, showing discomfort when the girth is tightened or objecting to saddling. Resistance during work, including reluctance to go forward, bucking, bolting, or refusing jumps, may reflect gastric pain. Changes in attitude ranging from depression and withdrawal to irritability and aggression develop in some horses. Performance decline is common, with horses unable to maintain their previous competitive level. These behavioral issues often resolve with ulcer treatment, confirming the diagnosis retrospectively.

Physical signs of gastric ulcers include those visible on examination and those detected during exercise. Poor body condition with prominent ribs and hip bones develops when ulcers interfere with appetite and digestion. Some horses show sensitivity on abdominal palpation, flinching or moving away when pressure is applied to the abdomen. During exercise, affected horses may grind their teeth, swish their tails excessively, or show other signs of discomfort. Severe cases may show signs of colic during or after exercise when acid exposure is greatest.

Symptom progression in untreated gastric ulcers typically involves gradual worsening of clinical signs as ulceration becomes more extensive and severe. Horses that initially show only subtle performance issues may develop obvious colic episodes, significant weight loss, and marked behavioral changes. Some horses develop severe, deep ulcers that bleed, causing anemia in extreme cases. The most dangerous progression involves ulcer perforation, though this is rare compared to the high prevalence of the condition.

Emergency symptoms requiring immediate veterinary care include signs of severe colic that may indicate ulcer complications. While most gastric ulcers do not require emergency treatment, horses showing uncontrollable pain, signs of internal bleeding such as dark tarry stool or pale mucous membranes, or evidence of systemic illness including fever and depression should receive immediate veterinary evaluation. Foals with gastric ulcers may deteriorate rapidly and require emergency intervention more frequently than adult horses.

Physical examination of horses with suspected gastric ulcers typically reveals nonspecific findings that suggest but cannot confirm the diagnosis. Body condition assessment may show weight loss or failure to maintain appropriate weight despite adequate feeding. Abdominal auscultation is usually normal, distinguishing ulcer-related colic from conditions causing decreased gut sounds. Heart rate and other vital parameters are typically normal in stable ulcer cases. The physical examination primarily serves to rule out other conditions and assess overall health status.

The definitive diagnostic test for gastric ulcers is gastroscopy, the visual examination of the stomach using a video endoscope passed through the nostril, down the esophagus, and into the stomach. This procedure requires a three-meter endoscope to reach the equine stomach and is performed under standing sedation following twelve to eighteen hours of feed withholding to ensure an empty stomach. Gastroscopy allows direct visualization of both squamous and glandular regions, identification of ulcer location and severity, and grading according to established scoring systems. The procedure also evaluates the esophagus and pylorus for concurrent abnormalities.

Advanced diagnostics beyond gastroscopy are rarely necessary but may be indicated in specific situations. Blood work may reveal anemia in cases of chronic bleeding ulcers or elevated fibrinogen indicating inflammation. Fecal occult blood testing can detect gastrointestinal bleeding but lacks specificity for gastric versus intestinal sources. Transabdominal ultrasound cannot visualize stomach ulcers but may identify other conditions causing similar symptoms. In cases where gastroscopy is unavailable, response to empirical treatment with omeprazole may support a presumptive diagnosis.

Differential diagnosis of conditions mimicking gastric ulcers is extensive, as the nonspecific symptoms of ulceration overlap with many other equine health problems. Dental abnormalities cause poor condition and eating difficulties. Parasitism contributes to weight loss and poor coat quality. Other gastrointestinal conditions including hindgut ulceration, inflammatory bowel disease, and sand accumulation produce similar clinical signs. Musculoskeletal pain may cause performance issues and behavioral changes mistaken for ulcer-related problems. Thorough evaluation including gastroscopy allows accurate diagnosis and appropriate treatment.

Treatment of equine gastric ulcers centers on acid suppression to allow mucosal healing, with omeprazole as the primary therapeutic agent. Omeprazole is a proton pump inhibitor that blocks gastric acid secretion at its source, raising stomach pH and creating an environment conducive to epithelial healing. The standard treatment dose is four milligrams per kilogram body weight administered orally once daily. For a typical five-hundred-kilogram horse, this equates to approximately two grams daily. Treatment continues for a minimum of twenty-eight days for squamous ulcers, with longer courses often necessary for glandular disease.

Medical management options beyond omeprazole include other acid-suppressing medications and mucosal protectants. Histamine-2 receptor antagonists such as ranitidine and famotidine represent alternatives to omeprazole but are generally less effective for squamous ulceration. Sucralfate, which forms a protective coating over ulcerated mucosa, may benefit glandular ulcers and is often used in combination with omeprazole for this indication. Misoprostol, a synthetic prostaglandin, is sometimes prescribed for refractory glandular ulcers due to its mucosal protective effects.

Management changes are essential components of ulcer treatment and often determine long-term success. Increasing forage intake and providing continuous access to hay or pasture maintains stomach buffering throughout the day. Reducing grain and concentrated feed portions decreases volatile fatty acid production in the stomach. Feeding small meals frequently rather than large meals twice daily reduces fasting intervals. Adding alfalfa hay, which has natural buffering properties due to its calcium and protein content, provides additional protection.

Supportive care during ulcer treatment addresses concurrent issues and supports overall health. Horses with significant weight loss may require increased caloric intake through digestible fat sources rather than additional grain. Reducing training intensity during treatment allows healing without the stress of intense exercise. Minimizing use of non-steroidal anti-inflammatory drugs eliminates their contribution to gastric damage. Addressing stress through environmental modifications, social contact, and turnout supports healing.

Follow-up gastroscopy is recommended after completing treatment to confirm ulcer healing. Approximately seventy to eighty percent of squamous ulcers heal with standard omeprazole treatment, though recheck endoscopy often reveals some residual changes. Glandular ulcers may require extended treatment and have lower healing rates with standard protocols. Ulcers that do not respond to initial treatment may require dose adjustments, medication changes, or investigation for complicating factors.

Treatment decisions for gastric ulcers depend on severity, type, economic considerations, and planned use of the horse. Mild squamous ulcers may respond to management changes alone or shortened treatment courses. Severe or glandular ulcers require full treatment duration and often longer. Performance horses continuing in work may need ongoing prevention protocols. The cost of omeprazole treatment is substantial, though generic formulations have improved affordability. Alternative approaches using dietary management alone are less reliable but may be appropriate for mild cases or economic constraints.

Recovery timeline for equine gastric ulcers depends on ulcer type, severity, and treatment compliance. Squamous ulcers typically show clinical improvement within one to two weeks of initiating omeprazole treatment, though complete healing requires the full twenty-eight-day treatment course. Glandular ulcers generally require longer treatment, often six to eight weeks or more, and may not heal completely despite appropriate therapy. Return to normal appetite, attitude, and performance usually parallels clinical improvement and provides evidence of treatment response.

Post-treatment care involves transitioning from therapeutic doses to prevention protocols while implementing management changes that reduce recurrence risk. Omeprazole dose may be reduced gradually rather than stopped abruptly to prevent acid rebound. Implementing permanent management changes including increased forage access, reduced grain feeding, and stress minimization supports maintained healing. Horses returning to training should do so gradually, with monitoring for any return of symptoms.

Prognosis factors for gastric ulcer recovery include initial ulcer severity, adherence to treatment protocols, ability to implement management changes, and the horse's ongoing use and environment. Horses that can transition to pasture-based management with minimal stress have excellent long-term prognoses. Performance horses continuing in intensive training face higher recurrence rates regardless of treatment success. Individual variation in ulcer susceptibility means some horses require ongoing prevention while others remain healthy with standard management.

Long-term outlook for horses with gastric ulcers is generally favorable when appropriate treatment and management are implemented. Many horses return to their previous level of performance once ulcers heal. Recurrence is common, particularly in horses remaining in environments and management systems that contributed to initial ulcer development. Prevention protocols using lower-dose omeprazole or other strategies may be necessary for horses with repeated episodes. Understanding that gastric ulcers represent a management-related condition allows realistic planning for ongoing prevention.

Management practices form the foundation of gastric ulcer prevention in horses. Maximizing forage intake provides continuous buffering of gastric acid and stimulates saliva production. Horses should have access to hay or pasture as much as possible, ideally with no more than four to six hours between forage availability. Slow-feed hay nets extend eating time and reduce periods of gastric acid exposure. Providing forage before exercise helps buffer the acid that will splash onto squamous mucosa during work. These fundamental practices significantly reduce ulcer development in horses at any level of work.

Nutritional prevention strategies extend beyond forage access to overall diet composition. Reducing concentrate and grain feeding decreases volatile fatty acid production that contributes to squamous damage. Choosing feeds with higher fiber and lower starch content provides necessary calories with less ulcer risk. Adding alfalfa hay to the diet provides natural buffering from its high calcium and protein content. Supplementing with dietary oils provides calories without gastric irritation. Avoiding extended periods without feed access prevents the acid accumulation that initiates ulceration.

Exercise and conditioning considerations acknowledge the role of physical activity in ulcer development while recognizing that horses can work and compete with reduced risk through appropriate management. Providing forage within thirty minutes before exercise helps buffer stomach acid during work. Warming up gradually before intense exercise allows adaptation. Cooling down properly after work and offering hay soon afterward restores normal stomach function. Recognizing that intense, prolonged exercise carries the highest risk allows appropriate management of competition horses.

Environmental factors in ulcer prevention include social structure, housing, and stress management. Horses are social animals that experience stress from isolation, and providing companionship reduces ulcer risk. Turnout allows natural behavior including movement and grazing that supports digestive health. Minimizing stressful experiences including frequent transport, competition pressure, and unstable social groups reduces ulcer incidence. Consistent routines and calm handling create environments that support gastric health.

Preventive medication may be appropriate for horses at high risk of ulcer development or recurrence. Omeprazole at reduced doses, typically one to two milligrams per kilogram daily, prevents ulcer development during high-risk periods. This approach is common during competitions, transport, or other stressful events. Alternative prevention strategies including various supplements and management protocols have varying evidence of efficacy. Working with veterinarians to develop individualized prevention plans based on each horse's risk factors and management constraints provides the best outcomes.

Daily management for horses prone to gastric ulcers emphasizes consistent feeding practices and stress minimization. Forage should be provided multiple times daily with minimal fasting periods, ideally not exceeding four to six hours between access. Feeding hay before grain allows buffering before the more rapidly fermented concentrate reaches the stomach. Using slow-feed hay nets or multiple small hay portions extends eating time and maintains stomach buffering. Water should always be available, as hydration supports normal digestive function. Observing eating behavior and appetite daily allows early detection of any changes suggesting ulcer recurrence.

Housing and turnout considerations for ulcer-prone horses favor environments allowing natural behavior. Pasture turnout provides continuous grazing that represents ideal acid management. When stall housing is necessary, providing constant hay access mimics grazing behavior. Social housing allowing contact with other horses reduces stress-related ulcer risk. Stall environments should minimize stressors including excessive noise, traffic, or unpredictable events. Maintaining consistent routines for feeding, turnout, and handling reduces anxiety that contributes to ulceration.

Exercise modifications for horses with gastric ulcers balance the demands of their use with practices that reduce ulcer risk. Always feeding hay before exercise helps protect the squamous mucosa during work. Warming up adequately before intense exercise and cooling down properly afterward supports normal stomach function. Recognizing that intense speed work carries the highest ulcer risk allows appropriate management of exercise intensity. Reducing training demands during active ulcer treatment allows healing, with gradual return to full work as symptoms resolve.

Monitoring and ongoing care for horses with gastric ulcer history includes observation for symptom recurrence and periodic veterinary assessment. Owners should watch for decreased appetite, behavioral changes, poor condition, or colic signs that might indicate ulcer recurrence. Periodic gastroscopy may be warranted for horses with repeated problems or those in high-risk situations. Working with veterinarians to adjust prevention strategies based on individual response optimizes management. Maintaining records of symptoms, treatments, and responses helps identify patterns and effective interventions.

Quality of life and use considerations for horses with gastric ulcers acknowledge that many horses perform and compete successfully with appropriate management. Most horses with ulcer history return to their intended use once healed and appropriately managed. Some horses require ongoing prevention protocols including medication during high-risk periods. Career decisions should consider whether management changes necessary for ulcer control are compatible with competitive goals. For most horses, combining reasonable management modifications with targeted prevention during high-risk times allows full athletic careers.

Thoroughbreds demonstrate the highest documented prevalence of gastric ulcers among horse breeds, with studies showing ulceration in eighty to ninety percent of horses in active race training. This extreme prevalence reflects the intensive management practices typical of Thoroughbred racing rather than inherent breed susceptibility. Racehorses in training experience multiple risk factors simultaneously including stall confinement, high-grain diets, intense exercise, travel, and performance pressure. Thoroughbreds managed as pleasure horses or broodmares show dramatically lower ulcer rates, supporting the role of management over genetics.

Other performance breeds including Standardbreds, Warmbloods, and sport horses show elevated ulcer prevalence when in active training and competition. These breeds experience similar management factors to Thoroughbreds, though often to lesser degrees. Show horses, event horses, and other competitive athletes face ulcer risk proportional to their training intensity and competitive schedules. Quarter Horses and other stock breeds in performance disciplines including cutting, reining, and barrel racing also show significant ulcer rates when in intensive programs.

Breed-specific recommendations for gastric ulcer prevention focus on management appropriate to each breed's typical use rather than genetic considerations. Thoroughbreds and other racehorses in active training should receive proactive prevention during racing campaigns. Sport horses should have management optimized around competition schedules. Pleasure horses of any breed benefit from management practices that support gastric health regardless of current ulcer status. No genetic testing is relevant for gastric ulcer risk, and breeding decisions need not consider ulcer history as this represents an environmental rather than inherited condition.

Equine gastric ulcers commonly co-occur with hindgut conditions including right dorsal colitis and colonic ulceration. The same management factors that predispose to gastric ulcers, particularly non-steroidal anti-inflammatory drug use and high-grain diets, contribute to large intestinal damage. Horses showing symptoms of gastric ulcers may have concurrent hindgut disease requiring additional diagnostic evaluation and treatment. The combination of foregut and hindgut pathology can produce more severe clinical signs than either alone.

Conditions with symptoms similar to gastric ulcers require consideration in differential diagnosis. Other causes of poor performance include musculoskeletal pain, respiratory disease, and cardiac conditions. Poor body condition may result from dental disease, parasitism, or other digestive disorders. Behavioral issues attributed to ulcers may reflect training problems, pain from other sources, or temperament issues. Thorough evaluation including gastroscopy, dental examination, and other diagnostics as indicated allows accurate diagnosis and appropriate treatment.

Potential complications of gastric ulcers, while generally uncommon given the high prevalence of the condition, include severe consequences in extreme cases. Gastric perforation is rare but can occur with deep ulcers, resulting in fatal peritonitis. Chronic bleeding ulcers may cause anemia requiring treatment. Pyloric stricture from chronic ulceration can cause gastric outflow obstruction. Severe ulcer disease may contribute to chronic poor condition and ongoing performance issues despite treatment. These complications reinforce the importance of diagnosis and treatment before ulcers become severe.