Gastric Ulcers in Horses: A Comprehensive Guide to EGUS

What Are Gastric Ulcers?

Gastric ulcers in horses, formally termed Equine Gastric Ulcer Syndrome (EGUS), represent erosions or lesions in the lining of the stomach caused by damage to the protective mucosal layer. These painful sores develop when the delicate balance between protective factors (mucus production, bicarbonate secretion, adequate blood flow) and aggressive factors (gastric acid, bile acids, digestive enzymes) is disrupted, allowing stomach acid to damage the underlying tissue.

Unlike humans who typically develop ulcers from bacterial infection (Helicobacter pylori) or NSAID use, equine gastric ulcers primarily result from management practices and physiological factors unique to horses. The equine stomach’s anatomy, horses’ natural feeding behaviors, and the demands placed on modern performance horses create conditions where gastric ulcers have become alarmingly common—affecting an estimated 60-90% of adult performance horsesand significant percentages of horses across all disciplines and management systems.

The equine stomach consists of two distinct regions with different characteristics:

Squamous (non-glandular) region: The upper portion of the stomach, comprising approximately 50% of the stomach’s surface area. This region lacks protective glands and is lined with squamous epithelium similar to the esophagus. It has minimal natural protection against acid and is highly vulnerable to acid damage. Most equine gastric ulcers occur in this region, particularly along the margo plicatus—the border between the squamous and glandular regions.

Glandular region: The lower portion of the stomach, lined with specialized cells that produce gastric acid, enzymes, and protective mucus. This region has natural defenses against acid but can still develop ulcers, though less commonly than the squamous region.

Understanding this anatomical distinction is critical because Equine Gastric Ulcer Syndrome is now recognized as encompassing two somewhat distinct conditions:

Equine Squamous Gastric Disease (ESGD): Ulceration of the non-glandular squamous region
Equine Glandular Gastric Disease (EGGD): Ulceration of the glandular region

These conditions have different causes, risk factors, and treatment responses, though both are commonly referred to under the umbrella term EGUS.

Gastric ulcers cause significant pain and discomfort, affecting horses’ well-being, behavior, and performance. Left untreated, ulcers can lead to serious complications including life-threatening gastric rupture (though this is rare). The good news is that gastric ulcers are both highly treatable and largely preventable through appropriate management modifications and medical therapy when necessary.

This comprehensive guide examines the causes, risk factors, clinical signs, diagnosis, treatment, prevention, and long-term management of equine gastric ulcers, providing horse owners with the knowledge needed to recognize, address, and prevent this prevalent condition.

Anatomy and Physiology of the Equine Stomach

To understand why horses develop gastric ulcers, we must first examine the unique characteristics of the equine digestive system.

Stomach Structure and Function

The equine stomach is relatively small compared to the horse’s overall body size and digestive tract length—typically holding only 8-15 liters (2-4 gallons), representing about 10% of total digestive tract capacity. This small stomach size reflects horses’ evolution as trickle feeders—animals designed to consume small amounts of forage nearly continuously throughout the day.

The stomach is divided into the squamous and glandular regions by the margo plicatus:

Squamous region characteristics:

Thin, delicate epithelial lining
No mucus-producing cells
No acid-secreting cells
Minimal buffering capacity
Highly susceptible to acid damage
Located in the upper portion where acid can splash during movement

Glandular region characteristics:

Thick protective mucus layer
Bicarbonate secretion neutralizing acid at mucosal surface
Rich blood supply supporting mucosal health
Prostaglandin production supporting protective mechanisms
Better equipped to handle acidic environment

Gastric Acid Production

Unlike many species that produce acid only during meals, horses produce gastric acid continuously—approximately 24 hours per day—at a rate of about 1.5 liters per hour. This constant acid production evolved to handle the nearly continuous intake of forage in natural grazing conditions.

Acid production serves essential digestive functions:

Initiating protein digestion
Activating pepsinogen to pepsin (protein-digesting enzyme)
Killing ingested bacteria
Facilitating mineral absorption

However, this continuous acid production becomes problematic when horses aren’t eating regularly, as there’s no food to buffer the acid, leaving the stomach vulnerable to self-digestion.

Natural Protective Mechanisms

In the glandular region, multiple protective factors normally prevent ulceration:

Mucus-bicarbonate layer: A thick gel-like layer coating the glandular mucosa, creating a physical barrier and neutralizing acid at the tissue surface

Prostaglandins: These compounds stimulate mucus and bicarbonate production, maintain mucosal blood flow, and promote cell turnover and repair

Epithelial cell regeneration: Rapid turnover of surface cells replaces damaged cells

Adequate blood flow: Delivers oxygen and nutrients supporting tissue health and removes damaging substances

In the squamous region, protection is minimal and relies primarily on:

Saliva: Horses produce large volumes of saliva (10-12 liters daily) during chewing, which contains bicarbonate that helps buffer stomach acid. However, horses only produce saliva when chewing—unlike humans who produce saliva continuously

Physical barrier: The mucus layer and squamous cells themselves provide limited protection

Gravity: In grazing horses with heads down, the squamous region sits above the acid pool, reducing exposure

Causes and Risk Factors for Gastric Ulcers

Gastric ulcers develop when aggressive factors overwhelm protective mechanisms. Multiple risk factors contribute to this imbalance:

Diet and Feeding Management

Dietary factors represent the most significant modifiable risk factors for EGUS:

Infrequent Feeding and Extended Fasting

Intermittent feeding patterns—offering meals 2-3 times daily with long intervals between feedings—create prolonged periods when the stomach is empty or nearly empty. Without food to:

Buffer stomach acid
Stimulate saliva production
Provide a physical barrier protecting the squamous region

The acidic environment damages the unprotected squamous mucosa.

Overnight fasting particularly increases risk. If horses finish their evening hay by midnight but don’t eat again until morning feeding (8-12 hours later), acid continuously bathes vulnerable tissue without buffering.

Research demonstrates that even 4 hours without food significantly increases squamous acid exposure and ulcer risk.

High-Grain/Concentrate Diets

Grain-based feeds contribute to ulcer development through multiple mechanisms:

Rapid fermentation: Grains ferment in the stomach, producing volatile fatty acids (VFAs) including acetic, propionic, and butyric acids. These VFAs:

Directly damage squamous epithelium
Increase acidity beyond gastric acid alone
Penetrate and injure squamous cells

Reduced chewing time: Concentrated feeds require minimal chewing compared to forage, resulting in:

Less saliva production and reduced acid buffering
Faster consumption leaving longer non-eating periods
Less physical fill buffering acid

Increased gastric acidity: High-starch diets may increase gastric acid secretion

Delayed gastric emptying: Some studies suggest high-starch meals empty more slowly, prolonging acid exposure

Insufficient Forage

Forage (hay, pasture) provides critical protection:

Physical buffering: Forage creates a “fiber mat” in the stomach that:

Absorbs and buffers acid
Provides a physical barrier protecting squamous mucosa
Slows acid movement reducing “splashing” on squamous region

Saliva production: Long-stem forage requires extensive chewing, producing copious saliva (buffering acid)

Continuous intake: Free-choice hay approximates natural grazing patterns

Low starch content: Unlike grain, forage doesn’t produce problematic VFAs

Horses receiving less than 1-1.5% of body weight in forage daily face dramatically increased ulcer risk.

Alfalfa vs. Grass Hay

Alfalfa hay may provide superior ulcer protection compared to grass hays:

Higher protein and calcium content provides better buffering capacity
May stimulate greater saliva production
Creates better protective mat in stomach

However, alfalfa alone isn’t sufficient—management and other factors remain critical.

Exercise and Training Intensity

Strenuous exercise significantly increases gastric ulcer risk:

Increased Intra-Abdominal Pressure

During intense exercise (particularly galloping, jumping):

Abdominal contractions increase pressure in the stomach
Acid splashes upward onto the squamous region
The squamous mucosa experiences repeated acid exposure

Studies using endoscopy show visible acid splash marks in the squamous region of exercised horses.

Reduced Gastric Blood Flow

Exercise redistributes blood flow from the gastrointestinal tract to working muscles:

Reduced mucosal blood flow compromises protective mechanisms
Impairs mucus and bicarbonate production
Slows healing of existing damage

Increased Acid Production

Some evidence suggests intense exercise may stimulate gastric acid secretion.

Prevalence in Performance Horses

The relationship between exercise and ulcers is clear from prevalence data:

Racehorses: 80-100% have gastric ulcers
Endurance horses: 70-93% affected
Show horses: 60-70% affected
Pleasure horses: 40-60% affected
Pasture horses: 30-50% affected

Stress and Psychological Factors

Stress increases ulcer risk through multiple pathways:

Physiological stress responses:

Increased cortisol and other stress hormones
Altered gastrointestinal motility
Changes in blood flow distribution
Potential increases in acid secretion

Sources of stress:

Training demands and performance pressure
Transport: Particularly long-distance or frequent hauling
Confinement: Stall housing vs. natural turnout
Social stress: Isolation, incompatible herd mates, unstable social structures
Environmental changes: Moving to new facilities, schedule disruptions
Competition: Show environments, racing

Behavioral indicators of stress (weaving, cribbing, stall walking) often correlate with higher ulcer prevalence, though it’s unclear if stress causes ulcers or ulcer pain causes behavioral changes.

Medication Use

Non-steroidal anti-inflammatory drugs (NSAIDs):

NSAIDs like phenylbutazone (bute), flunixin meglumine (Banamine), and firocoxib (Equioxx) are commonly used to manage pain and inflammation in horses. While generally safe when used appropriately, NSAIDs can contribute to gastric ulcers, particularly glandular ulcers (EGGD).

Mechanism: NSAIDs inhibit cyclooxygenase (COX) enzymes, reducing prostaglandin production. Prostaglandins are critical for:

Mucus secretion
Bicarbonate production
Maintaining mucosal blood flow
Promoting epithelial cell turnover

Reduced prostaglandins compromise these protective mechanisms, increasing ulcer risk.

Risk factors for NSAID-induced ulcers:

High doses or prolonged use
Concurrent use of multiple NSAIDs
Administration on empty stomach
Dehydration or concurrent illness
Pre-existing gastric disease

COX-selective NSAIDs (like firocoxib) that preferentially inhibit COX-2 over COX-1 may have reduced gastrointestinal side effects, though risk still exists.

Individual Susceptibility Factors

Some horses appear more vulnerable to ulcers:

Age:

Foals can develop ulcers (different presentation than adults)
Young horses in training face high risk
Adult prevalence relatively stable across ages

Sex: Some studies suggest males may have higher prevalence than females, though findings are inconsistent

Breed: No clear breed predisposition, though Thoroughbreds show very high prevalence (likely reflecting training intensity rather than genetic susceptibility)

Temperament: Anxious or high-strung horses may be more susceptible

Previous ulcer history: Horses with past ulcers face higher recurrence risk

Clinical Signs and Symptoms

Gastric ulcers produce variable clinical presentations ranging from subtle to severe. No single sign is pathognomonic (uniquely diagnostic), and many horses with significant ulcers show minimal obvious symptoms.

Common Clinical Signs

Poor Appetite and Eating Behavior Changes

Decreased appetite: Reluctance to eat, leaving feed, slow eating
Selective eating: Preferring certain feeds, avoiding grain
Interrupted eating: Starting to eat then walking away repeatedly
“Picky” eating: Horses that were previously good eaters becoming finicky
Eating dirt or bedding: Abnormal ingestive behaviors (though this also occurs for other reasons)

Mechanism: Eating causes gastric distension and acid production, both potentially painful with ulcers present. Horses may subconsciously avoid eating to avoid discomfort.

Weight Loss and Poor Body Condition

Gradual weight loss despite adequate feed availability
Poor hair coat quality
Decreased muscle development or muscle loss
Inability to maintain condition despite increased feed

Mechanism: Reduced feed intake combined with potential malabsorption and metabolic effects of chronic pain and inflammation lead to weight loss.

Behavioral Changes

Attitude changes: Depression, dullness, reduced interest in surroundings
Irritability or aggression: Particularly when girthing, mounting, or during grooming
Decreased performance: Reluctance to work, reduced effort, unwillingness to extend
Resistance to training: Previously willing horses becoming difficult
Stereotypies: Cribbing, weaving, stall walking (though causality unclear—do ulcers cause these behaviors or do stressed horses prone to stereotypies also get ulcers?)

Colic or Abdominal Discomfort

Recurrent mild colic episodes: Vague abdominal discomfort
Lying down more than normal
Stretching out as if to urinate (abdominal stretching)
Looking at flanks
Teeth grinding (bruxism)
Excessive yawning

Presentation: Unlike typical colic, ulcer-related discomfort is often chronic or recurring rather than acute and severe.

Diarrhea or Loose Manure

Some horses develop chronic loose stools or diarrhea
Mechanism incompletely understood; may relate to altered motility or inflammatory mediators

Poor Performance

In performance horses, ulcers commonly manifest as:

Reduced speed or stamina
Difficulty with collection or engagement
Unwillingness to jump or refusal
Changes in gait quality
Resistance to bit or contact
Bucking or rearing during work

Subtle presentation: Performance decrements may be gradual, attributed to training issues, soundness problems, or behavioral problems rather than gastric ulcers.

Signs Specific to Foals

Foals with gastric ulcers show distinct presentations:

Intermittent colic (often after nursing)
Diarrhea
Poor nursing or milk consumption
Bruxism (teeth grinding)
Salivation (ptyalism)
Dorsal recumbency (lying on back)—characteristic of foal ulcers
Poor growth rates

Gastric ulcers in foals can be severe, including duodenal ulcers that may perforate, causing life-threatening peritonitis.

Important Considerations

No pathognomonic signs: None of the above signs is specific to gastric ulcers—many other conditions produce similar symptoms.

Variable presentation: Some horses with severe ulcers show minimal signs, while others with modest ulceration demonstrate significant symptoms.

Individual variation: Pain tolerance and manifestation vary among horses.

Multiple concurrent problems: Horses often have ulcers alongside other health or management issues, complicating clinical picture.

Definitive diagnosis requires gastroscopy: Clinical signs alone cannot confirm or rule out gastric ulcers.

Diagnosis of Gastric Ulcers

While clinical suspicion based on signs and risk factors guides initial assessment, definitive diagnosis requires gastroscopy—direct visualization of the stomach using an endoscope.

Gastroscopy (Endoscopy)

Gastroscopy is the gold standard diagnostic method for EGUS.

Procedure

Preparation:

Horses must be fasted for 12-18 hours (no feed) to ensure the stomach is empty for adequate visualization
Water typically withheld for 2-4 hours before procedure
Sedation administered for safety and cooperation

Endoscopic examination:

A flexible endoscope (a long tube with camera and light source) is passed through the horse’s nostril
The endoscope advances down the esophagus into the stomach
The stomach is insufflated (inflated with air) to expand the stomach walls for visualization
The veterinarian systematically examines all regions of the stomach
Video or still images are captured documenting findings

Duration: Typically 15-30 minutes

Location: Can be performed in the field or at veterinary hospitals (requires specialized equipment)

What Gastroscopy Reveals

The examiner assesses:

Squamous region:

Presence, location, and severity of ulceration
Appearance of mucosa (normal pink-white vs. reddened, damaged)
Evidence of healing (granulation tissue, epithelialization)

Margo plicatus: The border region most commonly affected

Glandular region:

More difficult to assess thoroughly (folds obscure some areas)
Ulceration, erosions, thickening
Excessive redness or inflammation

Esophagus and pylorus: Sometimes examined as well

Ulcer Grading

A standardized grading system assesses ulcer severity:

Squamous ulcers (0-4 scale):

Grade 0: Intact epithelium, no lesions
Grade 1: Mucosal hyperkeratosis (thickening) and/or reddening
Grade 2: Small single or multifocal lesions
Grade 3: Large single or multifocal lesions, or extensive superficial lesions
Grade 4: Extensive lesions with areas of deep ulceration

Glandular ulcers (0-4 scale):

Grade 0: Normal appearance
Grade 1: Hyperemia (redness) and/or petechiae (pinpoint hemorrhages)
Grade 2: Focal mucosal defects (small ulcers)
Grade 3: Multifocal mucosal defects
Grade 4: Extensive areas of ulceration

Clinical significance: Ulcer grade doesn’t always correlate with symptom severity—some horses with Grade 4 ulcers show minimal signs, while others with Grade 2 lesions exhibit significant symptoms.

Advantages of Gastroscopy

Definitive diagnosis: Directly visualizes ulcers
Severity assessment: Quantifies extent of damage
Differentiates ESGD from EGGD: Determines which region is affected
Monitors treatment response: Follow-up scoping assesses healing
Identifies other problems: May reveal masses, foreign bodies, other pathology

Limitations and Considerations

Cost: $300-600+ depending on location and facility
Requires specialized equipment: Not all practitioners have portable endoscopes
Requires fasting: May be challenging in some management situations
Sedation risks: Generally minimal but present
Doesn’t assess the entire stomach equally: Some glandular areas difficult to visualize

Presumptive Diagnosis and Therapeutic Trials

Given gastroscopy’s cost and availability limitations, many veterinarians and owners pursue presumptive diagnosis and treatment trials:

Approach:

Horse presents with clinical signs consistent with ulcers
Risk factors are present (e.g., performance horse on high-grain diet)
Other likely causes ruled out through physical exam and potentially other diagnostics
Therapeutic trial: Administer anti-ulcer medication (omeprazole) for 28 days
Monitor response: If symptoms resolve, presumptive ulcer diagnosis is supported

Advantages:

Less expensive than gastroscopy
Practical for horses where gastroscopy isn’t accessible
May be reasonable approach when ulcers are highly likely

Disadvantages:

No confirmation of diagnosis
Cannot assess severity or monitor healing
May miss other conditions mimicking ulcer signs
If treatment fails, cause remains unknown requiring further investigation

Best practice: While therapeutic trials are common and often reasonable, gastroscopy provides more definitive information and is preferable when accessible and affordable, particularly for horses not responding to treatment or those with atypical presentations.

Treatment of Gastric Ulcers

Treating gastric ulcers involves medical therapy to promote healing combined with management modifications addressing underlying causes.

Medical Treatment

Omeprazole: The Gold Standard

Omeprazole is a proton pump inhibitor (PPI) that suppresses gastric acid production, enabling ulcer healing.

Mechanism of action: Omeprazole irreversibly binds to and inactivates the hydrogen-potassium ATPase enzyme system (the “proton pump”) in parietal cells (acid-producing cells) in the glandular stomach, dramatically reducing acid secretion by 80-90%.

Formulations:

GastroGard® (FDA-approved product):

Omeprazole paste: 2.28 grams omeprazole per tube
Dosed at 4 mg/kg once daily
Treatment course: 28 days minimum for healing
Demonstrated efficacy in controlled trials
Somewhat expensive ($30-40+ per day for average 500 kg horse)

Compounded omeprazole:

Powdered omeprazole from compounding pharmacies
Significantly less expensive ($5-15 per day)
Controversy: Studies show variable bioavailability and efficacy
Formulation quality varies among compounding pharmacies
Some products demonstrate poor acid suppression

Generic omeprazole paste products: Recently available as GastroGard’s exclusivity expired; efficacy being evaluated

UlcerGard® (omeprazole for prevention):

Lower dose (1.84 grams per tube = 1 mg/kg)
FDA-approved for ulcer prevention during stressful periods
Can be used preventively during competition, transport, training

Administration:

Given orally, typically as paste or powder mixed with small amount of feed or water
Best absorbed on empty stomach (30-60 minutes before feeding)
Once-daily dosing

Efficacy:

Squamous ulcers: Excellent—studies show 70-85% healing rate after 28 days
Glandular ulcers: Less responsive—healing rates approximately 25-50% after 28 days

Treatment duration:

Initial treatment: Minimum 28 days (most products labeled for this duration)
Severe ulcers: May require 60-90 days
Glandular ulcers: Often require longer treatment (60-90 days)
Follow-up gastroscopy: Recommended to confirm healing before discontinuing treatment

Side effects: Generally minimal

Well-tolerated by most horses
Rare reports of loose stools or colic
Theoretical concerns about long-term acid suppression (impaired calcium absorption, altered gut microbiome) but clinical significance unclear

Alternative and Adjunctive Medications

Ranitidine and cimetidine (H2-receptor antagonists):

Older acid-suppressing drugs that reduce acid secretion by blocking histamine receptors
Less effective than omeprazole for equine gastric ulcers
Require frequent dosing (2-4 times daily)
Used occasionally when omeprazole unavailable or cost-prohibitive
Not recommended as first-line treatment

Sucralfate:

Forms a protective coating over ulcerated areas
Theoretically beneficial, particularly for glandular ulcers
Limited evidence of efficacy in horses
Requires dosing 3-4 times daily on empty stomach (impractical)
Occasionally used as adjunct therapy for severe or refractory glandular ulcers

Misoprostol:

Synthetic prostaglandin analog
May enhance mucosal protective mechanisms
Some evidence for treating glandular ulcers
Expensive, requires frequent dosing
Side effects include diarrhea, colic
Not routinely used but occasionally tried for refractory glandular disease

Antacids (calcium carbonate, aluminum/magnesium hydroxide):

Neutralize stomach acid
Provide very brief benefit (30-60 minutes)
Not sufficient as sole treatment
May provide temporary symptomatic relief

Pectin-lecithin products:

Marketed for “coating” the stomach
Limited scientific evidence of efficacy
May provide some benefit as dietary supplements

Glutamine and other nutraceuticals:

Amino acids theoretically supporting mucosal healing
Limited evidence in horses
May have supportive role

Management Modifications: Essential for Success

Medical treatment alone is insufficient—addressing underlying causes through management changes is critical for healing, preventing recurrence, and maintaining long-term gastric health.

Dietary Management

Maximize forage intake:

Provide free-choice grass hay whenever possible (minimum 1.5-2% body weight daily)
Alfalfa hay: Consider adding alfalfa (excellent buffering capacity)
Small meals frequently: If free-choice hay not possible, feed at least 4-6 times daily

Reduce or eliminate grain:

Minimize concentrate feeds, especially high-starch feeds
Switch to low-starch/high-fat alternatives when supplemental calories needed
Feed concentrate after forage (never on empty stomach)
Divide concentrates into small, frequent meals

Avoid fasting:

Never skip meals or go more than 4-6 hours without eating
Provide hay before transport or competition
Consider slow-feed hay nets that extend eating time

Pre-exercise feeding:

Provide small amount of alfalfa hay (1-2 flakes) 30-60 minutes before exercise
Creates protective fiber mat buffering acid during work

Adjust feeding for individual horses:

Monitor body condition and adjust feeding accordingly
Some horses maintain weight easily on forage alone; others need supplementation

Exercise and Training Modifications

Gradual conditioning:

Build fitness progressively rather than sudden intense work
Allow adequate recovery time

Pre-exercise feeding: As noted above, strategic pre-work feeding

Reduce training intensity if possible:

During treatment, reduce work demands when feasible
Particularly important for horses with severe ulcers

Modify exercise timing:

Consider adjusting schedule to allow eating before work

Stress Reduction

Turnout and socialization:

Maximize turnout time in compatible groups
Reduce stall confinement
Provide social interaction

Environmental enrichment:

Toys, mirrors, or other entertainment
Reduce boredom and frustration

Consistent routines:

Maintain predictable schedules
Minimize unnecessary changes

Transport management:

Reduce frequency/duration when possible
Provide hay during transport
Consider preventive omeprazole before stressful events

Medication Review

NSAID management:

Use NSAIDs only when necessary
Select lowest effective dose
Shortest treatment duration possible
Consider COX-2 selective options (firocoxib)
Always provide free-choice hay when using NSAIDs
Consider concurrent omeprazole during prolonged NSAID use

Treatment Monitoring

Clinical monitoring:

Track appetite, attitude, body condition
Monitor performance changes
Note resolution of behavioral signs

Follow-up gastroscopy:

Ideal to confirm healing before discontinuing treatment
Recommended after 28-60 days depending on initial severity
Particularly important for horses with glandular ulcers (which heal more slowly)
Allows adjustment of treatment if inadequate healing

Discontinuation:

Don’t abruptly stop omeprazole after long-term use
Some advocate gradual tapering (though not clearly proven necessary)
Ensure management changes are in place before stopping medication

Prevention of Gastric Ulcers

Prevention is far superior to treatment in both welfare and economic terms. Implementing management practices that reduce ulcer risk should be standard practice for all horses.

Dietary Prevention Strategies

Forage-based diet:

Feed minimum 1.5-2% body weight in forage daily
Free-choice hay ideal
Use slow-feed nets extending eating time

Strategic alfalfa inclusion:

Mix alfalfa with grass hay or feed alfalfa before grain/work
Excellent buffering properties

Minimize grain/concentrates:

Only supplement when forage insufficient for caloric needs
Use low-starch, high-fiber alternatives
Small, frequent meals rather than large infrequent ones

Avoid prolonged fasting:

Never more than 4-6 hours without feed access
Particularly important overnight

Appropriate feeding sequence:

Always feed forage before concentrates
Provide hay before exercise

Exercise and Training Management

Progressive conditioning:

Build fitness gradually
Adequate rest and recovery

Pre-exercise feeding:

Strategic hay feeding before work

Training intensity:

Match work demands to horse’s fitness and capacity
Allow recovery time

Stress Management

Maximize turnout:

As much pasture/paddock time as feasible
Compatible social groups

Minimize confinement stress:

Largest possible stalls with visual contact
Environmental enrichment

Consistent management:

Predictable routines
Minimize unnecessary disruptions

Careful transport practices:

Reduce frequency/duration when possible
Provide hay during transport

Preventive Medication

UlcerGard® (omeprazole 1 mg/kg):

FDA-approved for prevention during stressful periods
Consider during:
- Competition/show season
- Intensive training periods
- Travel
- Transition periods (moving barns, weaning, etc.)

Cost-benefit analysis:

Daily prevention expensive ($15-25+ per day)
May be cost-effective for high-risk horses during specific high-risk periods
Not typically recommended as indefinite preventive for all horses

Management changes preferable to chronic medication when possible

Monitoring and Early Detection

Regular observation:

Monitor appetite, attitude, body condition
Note any behavioral changes or performance issues

Periodic assessment:

Consider gastroscopy for high-risk horses even without obvious signs
Performance horses might benefit from annual screening

Prompt investigation:

Don’t ignore subtle signs
Early treatment easier and more successful than addressing chronic severe ulcers

Special Considerations

Glandular Ulcers: A Therapeutic Challenge

Equine Glandular Gastric Disease (EGGD) proves more challenging than squamous disease:

Poorer response to omeprazole:

Healing rates only 25-50% vs. 70-85% for squamous ulcers
May require longer treatment duration (60-90 days or more)
Often recurs despite treatment

Less understood pathophysiology:

Causes not as clear as for squamous disease
May involve inflammation more than simple acid damage
Possible role of bile acids, bacteria, or other factors

Treatment approaches:

Extended omeprazole: 60-90+ days at full dose
Sucralfate: Sometimes added (limited evidence)
Misoprostol: Occasionally tried for refractory cases
Management changes: Still essential though benefit less documented
Experimental approaches: Antibiotics (if bacterial involvement suspected), anti-inflammatory drugs, dietary modifications

Research ongoing: Better understanding and treatments for EGGD needed

Ulcers in Foals

Foal gastric ulcers differ from adult disease:

Risk factors:

Stress (weaning, transport, illness)
NSAID administration
Diarrhea or other illness
Prematurity

Presentation:

Often more severe than adults
Can include duodenal ulcers (small intestine)
Risk of perforation causing fatal peritonitis

Treatment:

Omeprazole: 4 mg/kg once daily (same dose as adults)
Sucralfate: Often used concurrently
Treatment duration: 28 days minimum
Aggressive supportive care if systemically ill

Prevention:

Minimize stress
Cautious NSAID use
Prompt treatment of illness

Recurrent or Refractory Ulcers

Some horses experience treatment failure or rapid recurrence:

Reasons for poor response:

Glandular ulcers: Inherently more difficult to treat
Inadequate treatment duration: Stopping treatment prematurely
Compounded omeprazole: Poor quality or bioavailability
Continued risk factors: Management not adequately modified
Unrecognized concurrent problems: Right dorsal colitis, other GI disease
Severe or long-standing ulcers: Extensive damage requiring longer healing

Management:

Confirm diagnosis: Repeat gastroscopy to assess healing and differentiate squamous vs. glandular
Extend treatment duration: 60-90 days or longer
Switch to brand-name omeprazole: If using compounded product
Increase dose: Some horses may need higher doses (though not typically recommended)
Add adjunct therapies: Sucralfate, misoprostol, dietary modifications
Aggressive management changes: Comprehensive review of all risk factors
Consider other diagnoses: Rule out alternative or concurrent conditions

Chronic Maintenance Therapy

Some horses require long-term or indefinite omeprazole:

Indications:

Rapid recurrence despite optimal management
Horses in unavoidably high-risk situations (racehorses, high-level competitors)
Chronic NSAID use for other conditions

Approaches:

Continuous therapy: Daily omeprazole indefinitely
Pulsed therapy: Periodic treatment courses
Reduced-dose maintenance: Lower than treatment dose (e.g., UlcerGard dose)

Considerations:

Expensive
Unknown long-term effects of chronic acid suppression
Should attempt to address underlying factors rather than indefinite medication when possible

Economic Impact of Gastric Ulcers

Gastric ulcers create substantial economic costs for the equine industry:

Direct Costs

Diagnosis:

Gastroscopy: $300-600+

Treatment:

Brand-name omeprazole: $800-1200+ for 28-day course
Compounded omeprazole: $150-450 for 28 days
Longer treatment courses or recurrent ulcers: Thousands of dollars annually

Follow-up care:

Repeat gastroscopy
Extended treatment
Supportive therapies

Indirect Costs

Lost performance:

Reduced competitive success
Training delays
Career shortening

Lost sales value:

Horses with ulcer history may have reduced market value
Prospective buyers concerned about recurrence

Management expenses:

Premium forage and feeds
Additional labor for frequent feeding
Modified housing/turnout arrangements

Industry-wide impact:

Estimated hundreds of millions of dollars annually
Affects all sectors: racing, showing, pleasure horses

Research and Future Directions

Ongoing research continues improving understanding and management:

Current Research Focus

Glandular ulcers:

Understanding pathophysiology
Developing effective treatments
Identifying risk factors

Alternative treatments:

Novel acid-suppressing medications
Anti-inflammatory approaches
Mucosal protective agents
Probiotics and prebiotics

Prevention strategies:

Optimal dietary formulations
Feed additives and supplements
Management practice optimization

Genetic susceptibility:

Individual variation in ulcer risk
Potential for identifying high-risk horses

Microbiome research:

Role of gastric bacteria
Effects of acid suppression on microbial populations
Potential probiotic interventions

Promising Developments

New medications: Alternative PPIs, different drug classes

Nutraceuticals: Products supporting mucosal health

Diagnostic tools: Less invasive diagnostic methods

Precision management: Individualized risk assessment and prevention strategies

Conclusion

Equine Gastric Ulcer Syndrome (EGUS) represents one of the most prevalent health issues affecting horses, with staggeringly high incidence rates particularly among performance horses. These painful erosions of the stomach lining develop when the delicate balance between protective and aggressive factors is disrupted—primarily through management practices that conflict with horses’ evolutionary design as continuous trickle feeders.

Squamous ulcers (ESGD) result primarily from intermittent feeding, high-grain/low-forage diets, intense exercise, and stress—all common features of modern horse management. Glandular ulcers (EGGD) are less well understood but appear related to stress, NSAID use, and possibly other factors, presenting more challenging treatment dilemmas.

Clinical signs are variable and non-specific, ranging from poor appetite and weight loss to behavioral changes, recurrent colic, and reduced performance. Definitive diagnosis requires gastroscopy—direct visualization of the stomach—though therapeutic trials are common when endoscopy isn’t accessible.

Treatment combines medical therapy, primarily omeprazole (a highly effective proton pump inhibitor for squamous ulcers, less effective for glandular disease), with essential management modifications addressing underlying causes. Dietary changes maximizing forage intake while reducing grain, minimizing fasting periods, reducing training intensity and stress, and judicious NSAID use form the foundation of effective management.

Prevention through appropriate feeding practices (forage-based diets, frequent small meals, avoiding prolonged fasting), stress reduction (maximizing turnout, minimizing confinement), and appropriate training management proves far superior to treating established disease. While preventive medication has a role during unavoidably high-risk periods, management modifications should form the primary prevention strategy.

The economic burden of EGUS is substantial, encompassing diagnostic and treatment costs, lost performance, and reduced quality of life. However, the welfare impact—the suffering horses endure from painful ulceration—represents the more compelling motivation for prevention and treatment.

Looking forward, continued research improving our understanding of glandular disease, developing better treatments, identifying genetic risk factors, and optimizing prevention strategies will enhance our ability to protect horses from this prevalent condition. In the meantime, horse owners, trainers, and veterinarians must recognize that modern management practices create ulcer risk and that protecting gastric health requires conscious, proactive efforts to provide more natural feeding patterns and management conditions compatible with equine digestive physiology.

By understanding gastric ulcers—their causes, recognition, treatment, and prevention—and implementing evidence-based management practices, we can dramatically reduce the prevalence and impact of EGUS, improving welfare, performance, and quality of life for horses across all disciplines and management systems.