Ulcers in Horses

Equine gastric ulcers represent one of the most prevalent health problems affecting horses today, with extensive research documenting that the majority of performance horses have some degree of gastric ulceration even though many show no obvious clinical signs. The widespread nature of the problem reflects the gap between natural equine digestive physiology, which evolved for continuous grazing of forage, and the modern management practices that keep horses in stalls with scheduled feeding patterns. Understanding ulcers and their complex etiology allows horse owners to recognize potential problems, implement prevention strategies, and seek appropriate treatment when ulceration develops.

Gastric ulcers occur when the horse's stomach lining becomes damaged, creating erosions or deeper ulcerations through the protective mucus layer into the underlying tissue. The stomach normally produces acid continuously, even when empty, creating a harsh chemical environment that the stomach lining must withstand. When protective mechanisms fail or acid production exceeds the stomach's ability to protect itself, ulcers develop. The protective lining usually can withstand this acidic environment, but numerous factors can disrupt this delicate balance.

Colonic ulcers, less commonly discussed but increasingly recognized as a significant health problem, occur in the colon through inflammatory processes that damage the protective colon lining. Right dorsal colitis, an inflammatory condition affecting the colon, is sometimes associated with intensive training or NSAID use. The precise mechanisms of colonic ulcer development are less well understood than gastric ulcer mechanisms, but management approaches overlap substantially with gastric ulcer treatment.

The impact of ulcers extends beyond visible illness, with subclinical ulceration affecting appetite, digestive efficiency, and performance in ways that owners may not initially recognize as ulcer-related. Some affected horses show only subtle behavioral changes or minor performance decrements that owners attribute to training issues, temperament problems, or other causes. The silent nature of many ulcer cases makes recognition challenging but also emphasizes the importance of preventive approaches.

This guide provides comprehensive information about the physiology of ulcer development, causes and risk factors that predispose horses to ulceration, clinical signs of gastric and colonic ulcers, diagnostic approaches, and both treatment and prevention strategies. You will learn why horses are so susceptible to ulcers given modern management practices, recognize signs that may indicate your horse has ulcers, and understand the approaches that address both the immediate problem and the factors that created it. Armed with knowledge about equine ulcers, you can make informed decisions about your horse's health.

Gastric ulcers develop from a combination of excessive stomach acid production and failure of protective mechanisms that normally prevent acid from damaging the stomach lining. The stomach continuously produces acid for digestive purposes and for its antimicrobial effects, with acid production continuing even when the stomach is empty. This constant acid production is normal and necessary, but it becomes problematic when the stomach lacks protective buffering from food material or when protective mechanisms are compromised.

Natural feeding patterns in wild horses involve nearly continuous grazing of forage throughout the day and night, maintaining relatively constant stomach fill with forage that buffers acid. Modern horse management practices involve scheduled feeding with large meals twice or three times daily, creating periods of several hours when the stomach is empty but acid continues being secreted. These periods of empty stomach with continued acid production create the acidic environment that damages the stomach lining.

The type of feed consumed influences ulcer risk substantially, with high-grain, low-forage diets associated with increased ulcer incidence. Grain is processed and moved through the stomach relatively rapidly, creating longer empty stomach periods compared to forage. Diets with inadequate forage fail to stimulate sufficient saliva production, which naturally buffers stomach acid. The quality of forage also influences buffering capacity, with excellent-quality legume hay providing superior buffering to poor-quality grass hay.

Stress represents a major risk factor for ulcer development, with horses subjected to significant stress showing elevated cortisol and other stress hormones that increase stomach acid production and decrease protective mechanisms. Competition stress, transportation, management changes, social disruption, and environmental changes all create stress that increases ulcer risk. High-intensity exercise itself creates a stress response that increases acid production. Horses with anxious temperaments or those sensitive to environmental changes show higher predisposition.

Intensive training and competition create multiple simultaneous risk factors for ulcer development. The physical stress of intense training increases acid production. The stress of competition elevates cortisol. Transportation associated with competition creates both physical and psychological stress. Performance schedules may involve feeding schedule changes, fasting before competition, or dietary modifications that increase ulcer risk. Racing and endurance horses show particularly high ulcer prevalence due to these combined factors.

Medication use, particularly NSAIDs including phenylbutazone commonly used for pain management, directly damages the stomach's protective lining and predisposes to ulcer development. The risk increases with higher doses and longer duration of treatment. Chronic NSAID use is a common cause of gastric ulcers in horses receiving medication for lameness, arthritis, or other pain conditions. Some horses show ulcer development even with short-term NSAID use at standard doses.

Fasting or fasting before exercise directly causes ulcer risk by eliminating stomach buffering while acid continues production. This practice is sometimes recommended by riders or trainers but increases ulcer risk substantially. Even brief periods without forage increase empty stomach time and acid exposure. Fasting should be avoided as an ulcer prevention strategy, contrary to some traditional training philosophies.

Age and life stage affect ulcer risk, with foals showing particularly high ulcer incidence during weaning and early training periods. The stress of separation, dietary changes during weaning, and introduction to training all create risk factors in young horses. Performance careers beginning in young animals subjected to intensive training show high ulcer rates. Senior horses may show increased ulcer risk from reduced ability to buffer stomach acid or from concurrent illness.

Subclinical ulcers in many horses produce no obvious signs, allowing significant ulceration to exist unrecognized. Many performance horses with diagnosed ulcers showed no clinical signs before diagnosis, demonstrating the subtle nature of many cases. This reality emphasizes that absence of obvious signs does not indicate absence of ulceration, particularly in performance horses at risk.

Appetite changes represent one of the most common clinical signs, with affected horses showing decreased appetite, selectivity about what they eat, or refusal of certain foods. Some horses show reluctance to eat shortly after feeding begins, suggesting stomach discomfort from feeding. Others show decreased appetite progressively throughout the day. Some horses show abnormal eating patterns such as eating very slowly or dropping feed repeatedly while chewing.

Behavior and attitude changes may appear subtle or dramatic depending on ulcer severity. Irritability, aggression, or unusual behavioral patterns sometimes develop secondary to stomach discomfort. Some horses become difficult to handle, touchy about grooming in certain areas, or show changes in temperament without obvious cause. These behavioral changes are frequently misinterpreted as training issues or temperament problems when they represent pain-related responses.

Performance decrements including reduced exercise tolerance, reluctance to work, or inability to maintain previous fitness levels can result from ulcer-related discomfort. Jumping horses may show jumping refusals or reduced jumping enthusiasm. Racing horses show dropped claims or slower times. Dressage horses show reduced collection or forward movement. Endurance horses show reduced distance capacity. Competition horses show inability to place or win at previous levels.

Colic-like abdominal pain appears with severe gastric ulcers or more commonly with colonic ulcers, with affected horses showing obvious discomfort, rolling behavior, or apparent abdominal pain. Low-grade recurrent colic without apparent cause should raise suspicion of underlying ulceration. Some horses show periodic episodes of pain that resolve spontaneously, making the pattern difficult to recognize without careful observation.

Digestive inefficiency manifesting as weight loss or failure to maintain weight despite adequate feed intake occurs with significant ulceration. Horses fail to gain weight even when fed apparently adequate amounts. Some horses show poor hair coat quality or general unthriftiness from impaired feed utilization. The efficiency of weight gain decreases despite apparently adequate or even increased feed intake.

Water intake changes sometimes accompany ulceration, with some horses drinking excessively while others show decreased intake. Excessive drinking may represent attempts to dilute stomach acid. Drinking preferences may change, with horses showing preference for certain water sources over others or preferring cold water over warm water.

Fecal changes including soft stool or occasional diarrhea sometimes appear with colonic ulcers or severe gastric disease, though many horses with significant gastric ulcers show completely normal fecal character. Occult blood in feces can indicate ulceration though this is not easily detected without specific testing. Most gastric ulcer cases show normal fecal appearance despite significant ulceration.

Gastroscopic examination remains the definitive diagnostic method, allowing direct visualization of the stomach lining and identification of ulcer location, severity, and extent. The scope passes through the nose into the stomach, requiring sedation and proper equipment. Video documentation allows baseline establishment and comparison with follow-up examinations. Gastroscopy provides definitive diagnosis and guides treatment decisions about intensity and duration of therapy. However, the procedure requires specialized equipment and expertise, limiting accessibility for many horse owners.

Clinical diagnosis without gastroscopy relies on history, signs, and response to empiric treatment. Horses showing compatible signs including appetite loss, behavior changes, or performance decrements in the context of known ulcer risk factors are presumed to have ulcers and are treated accordingly. If clinical improvement occurs with treatment, presumptive diagnosis of gastric ulcers is supported.

Colonic ulcer diagnosis is more challenging, as gastroscopy cannot visualize the colon. Endoscopy of the colon (colonoscopy) can be performed in some cases but is less commonly available than gastroscopy. Most colonic ulcer diagnosis is presumptive based on clinical signs and response to treatment. Blood work showing elevated inflammatory markers or other abnormalities may support suspicion of colonic disease.

Treatment of gastric ulcers involves acid suppression with medications, typically omeprazole, combined with dietary modification and stress reduction. Proton pump inhibitors like omeprazole reduce acid production substantially, allowing the stomach lining to repair itself. Treatment typically extends four to six weeks, though some cases require longer therapy. Most horses show substantial improvement within two to three weeks with appropriate treatment.

Dietary management is critical to successful treatment, with increased forage, reduced grain, and increased feeding frequency all supporting healing. Unlimited hay or frequent hay meals maintain stomach buffering. Grain should be minimized or eliminated during treatment to reduce acid stimulation. High-quality hay, particularly legume-based hay, provides superior buffering capacity.

Stress reduction through consistent management, minimal transportation, and social stability supports healing. Some horses benefit from temporary reduction in training or competition during acute treatment phases. Turnout and herd interaction when possible reduces stress from confinement and social isolation.

H2 blockers including ranitidine provide supplemental acid reduction, sometimes combined with proton pump inhibitors for more aggressive acid suppression in severe cases. Antacids provide buffering but require frequent administration for continuous coverage. Sucralfate provides some protective coating of the ulcer bed, though its benefit as primary treatment is limited.

Monitoring treatment response involves observation of appetite improvement, attitude changes, performance improvements, and absence of new concerning signs. Most horses show significant improvement within one to two weeks if response is adequate. Continued appetite loss or slow improvement after two weeks warrants treatment modification or investigation for alternative causes of persistent signs.

Colonic ulcer treatment is less standardized, with management modifications often providing primary benefit. Some horses respond to systemic anti-inflammatory therapy, reduced training intensity, and dietary modifications. Ongoing research continues to clarify optimal colonic ulcer management approaches.

Active treatment typically spans four to six weeks, with medication administration being consistent and daily. During this period, horses require careful management to support healing alongside medication therapy. Forage should be optimized with unlimited or nearly unlimited hay access. Grain should be minimized or eliminated. Feeding should occur at frequent intervals to maintain stomach buffering.

Activity during acute treatment should be reduced from previous levels, with light exercise and turnout typically not interfering with healing. Complete stall confinement is rarely necessary and may actually impede healing through stress and mental stagnation. Gradual return to normal activity occurs as ulcers heal, with full return to previous activity levels achieved as healing completes.

Nutrition during treatment should support healing without overloading the recovering GI tract. Consistent forage-based diet provides optimal nutrition. Minimal supplementation is typically necessary. Some horses benefit from addition of micronutrients supporting tissue healing, though the evidence for specific supplementation is limited.

Monitoring during the treatment course includes tracking appetite, attitude, performance, and elimination patterns. Rapid appetite improvement within days typically indicates good treatment response. Continued appetite loss after one to two weeks suggests inadequate medication response or possible alternative causes of persistent signs. Any development of new concerning signs should be reported to the veterinarian.

Post-treatment monitoring continues after the prescribed treatment course ends, with ongoing attention to appetite, attitude, and performance. Some horses show persistence of mild signs even after standard treatment completion, potentially indicating incomplete healing or beginning recurrence. Return of concerning signs warrants prompt veterinary reassessment.

Return to full activity should occur gradually, with progression determined by the horse's response. Most horses return to normal training by four to six weeks after treatment initiation. Full return to competition typically occurs by eight to twelve weeks as healing completes. Return should be progressive rather than abrupt, with gradual increases in training intensity and duration.

Long-term management focuses on preventing recurrence through implementation of dietary and management modifications learned during treatment. Horses that return to management patterns that created initial ulcers frequently experience recurrence. The investment in continued prevention-focused management extends the interval between treatment episodes and reduces long-term recurrence risk.

Prevention of initial ulcer development and recurrence after treatment relies on addressing the factors that create ulcer risk. Dietary management is the foundation of all prevention strategies, with maximum forage intake representing the single most important intervention. Unlimited hay access or multiple daily hay feedings maintain stomach buffering and reduce empty stomach time. Minimizing grain and concentrates reduces acid stimulation and maintains appropriate digestion time.

Feeding management involving frequent small meals rather than large meals approximates more natural feeding patterns. Complete elimination of scheduled fasting prevents creation of extended empty stomach periods. Some horses benefit from soaking hay to improve palatability and digestibility. Addition of water to feed increases moisture content and supports hydration.

Stress management through consistent routines, minimal unnecessary transportation, and stable social environments supports prevention. Allowing turnout and herd interaction provides social enrichment and more natural movement patterns. Minimizing environmental changes and maintaining consistent handling reduces stress-related acid production.

Exercise management involves balancing adequate training with appropriate rest recovery. Avoiding sudden increases in training intensity prevents stress overload. Fasting before exercise should be absolutely avoided. Allowing adequate recovery time between intense training sessions supports overall digestive health.

Medication considerations include minimizing NSAID use when possible. When NSAIDs are necessary, concurrent preventive medication with omeprazole protects against ulcer development. Using lowest effective NSAID doses for shortest possible duration reduces ulcer risk.

Prognosis for complete ulcer healing with appropriate treatment is good, with the majority of horses showing substantial healing by six weeks and complete healing by eight to twelve weeks. Performance improvement generally correlates with healing progression, with most horses returning to previous performance levels.

Long-term prognosis depends on the horse's inherent predisposition and the owner's commitment to ongoing prevention. Horses with intense predisposition returning to stressful management frequently experience recurrence. Those maintained on optimized preventive management may remain ulcer-free long-term. The cost-benefit analysis of prevention clearly favors ongoing preventive management over repeated treatment cycles.