Equine Gastric Ulceration Study Guide

Overview and Clinical Importance

Equine Gastric Ulcer Syndrome (EGUS) is an umbrella term describing erosive and ulcerative diseases of the equine stomach. EGUS is one of the most common gastrointestinal disorders in horses, with prevalence rates reaching 80-100% in Thoroughbred racehorses in active training. Understanding the distinction between Equine Squamous Gastric Disease (ESGD) and Equine Glandular Gastric Disease (EGGD) is critical for the NAVLE, as these represent distinct disease entities with different pathophysiology, risk factors, and treatment responses.

The horse stomach is uniquely susceptible to ulceration due to continuous acid secretion regardless of feeding status, a relatively small stomach capacity (8-16 liters), and the presence of an unprotected squamous mucosal region in the proximal third of the stomach.

Gastric Anatomy and EGUS Terminology

Equine Stomach Anatomy

The equine stomach is a J-shaped, relatively small organ (capacity 8-16 liters) located primarily on the left side of the abdomen. It is divided into two distinct mucosal regions separated by the margo plicatus, a distinct ridge that marks the junction between the squamous and glandular mucosa.

Gastric Regions and Characteristics

EGUS Terminology (ECEIM Consensus 2015)

Prevalence and Risk Factors

Prevalence by Discipline

Risk Factors for ESGD

All risk factors for ESGD share a common trait: they increase exposure of the squamous mucosa to acid.

• Intense exercise: Increased intra-abdominal pressure during gaits faster than a walk pushes acidic gastric contents against squamous mucosa ("acid splash")
• High-concentrate diets: Starch intake greater than 2 g/kg BW/day doubles risk; fermentation produces VFAs that synergize with HCl
• Intermittent feeding/fasting: Greater than 6 hours between meals increases risk; continuous acid secretion without buffering
• Straw as sole forage: Low buffering capacity; inadequate saliva production
• Limited water access: Horses without paddock water access 2.5x more likely to develop EGUS
• Stall confinement: Reduced grazing time and social contact
• Transportation stress: Ulcers can develop within hours of transport

Risk Factors for EGGD

EGGD pathophysiology is less understood; believed to result from breakdown of normal mucosal defense mechanisms.

• Exercise frequency: Greater than or equal to 5-6 days per week increases risk
• Stress/cortisol: Horses with elevated ACTH responses have higher EGGD prevalence
• Warmblood breed: May have increased predisposition (limited evidence)
• Lack of experience: Less experienced competition horses may be more susceptible (stress-related)
• NSAIDs: Potential contributor at high doses (greater than 50% above label dose); role at clinical doses unclear

Pathophysiology

ESGD Pathophysiology

The pathophysiology of ESGD is well understood and follows the principle: "No acid, no ulcer." The squamous mucosa lacks protective mechanisms and is susceptible to damage from:

• Hydrochloric acid (HCl): Primary damaging agent; damages outer cell barrier, followed by diffusion into stratum spinosum
• Volatile fatty acids (VFAs): Acetic, butyric, propionic acids from bacterial fermentation of concentrates; synergize with HCl
• Bile acids: From duodenal reflux; synergize with HCl
• Pepsin: Proteolytic enzyme active at low pH

Exercise-Induced "Acid Splash" Mechanism

During exercise at gaits faster than a walk, increased intra-abdominal pressure compresses the stomach, forcing acidic contents from the ventral glandular region upward against the unprotected dorsal squamous mucosa. The severity of ESGD correlates with exercise intensity, duration, and frequency.

EGGD Pathophysiology

Unlike ESGD, the glandular mucosa is normally exposed to highly acidic contents (pH 1-3) and is protected by multiple defense mechanisms:

• Mucus-bicarbonate barrier
• Prostaglandin-mediated mucosal blood flow
• Rapid epithelial cell turnover
• Tight junctions between epithelial cells

EGGD results from breakdown of these defense mechanisms, rather than excessive acid exposure. The exact cause of barrier breakdown in horses is unclear, but stress, inflammation, and altered mucosal blood flow are suspected contributors. Unlike in humans, Helicobacter pylori has NOT been definitively established as a causative agent in horses.

Clinical Signs

Important: Clinical signs of EGUS are nonspecific and many horses with severe ulceration are asymptomatic ("silent ulcers"). Clinical signs do NOT reliably predict the presence, severity, or location of gastric ulcers.

Exam Focus: Girthiness and diarrhea are commonly attributed to gastric ulcers but are more likely indicative of HINDGUT disorders (colonic ulceration, right dorsal colitis). The stomach is located too cranially to be affected by girth pressure, and diarrhea requires colonic involvement.

Diagnosis

Gastroscopy (Gold Standard)

Gastroscopy is the ONLY reliable method for definitive diagnosis of EGUS. A 3-meter endoscope is required to visualize the entire stomach, including the pylorus and proximal duodenum.

Gastroscopy Protocol

• Fasting: 12-16 hours (food); 2-3 hours (water)
• Sedation: Xylazine or detomidine with or without butorphanol
• Equipment: 3-meter video endoscope
• Complete examination: Must visualize squamous mucosa, margo plicatus, glandular fundus, antrum, pylorus, and proximal duodenum

EGUS Council Grading System for ESGD

EGGD Grading: A hierarchical grading system is NOT recommended for EGGD. Instead, describe lesions by:

• Anatomical location: Cardia, fundus, antrum, or pylorus
• Distribution: Focal, multifocal, or diffuse
• Appearance: Hyperemic, hemorrhagic, fibrinosuppurative, ulcerated
• Mucosal contour: Depressed, flat, raised, or nodular

Treatment

ESGD Treatment

The cornerstone of ESGD treatment is acid suppression with omeprazole, a proton pump inhibitor (PPI) that irreversibly inhibits the H+/K+-ATPase proton pump in gastric parietal cells.

EGGD Treatment

EGGD responds POORLY to omeprazole monotherapy (only 25% healing vs 78% for ESGD). Combination therapy with mucosal protectants is recommended.

Prevention and Management Strategies

Nutritional Management

• Continuous forage access: Minimum 1.5 kg dry matter per 100 kg bodyweight daily; grass pasture ideal
• Frequent feeding: 4-6 small meals/day; never more than 6 hours between meals
• Limit concentrates: Less than 2 g/kg bodyweight starch per day; less than 1 g/kg per meal
• Include alfalfa: Higher protein and calcium content buffers gastric acid; feed 30 minutes before exercise
• Avoid straw as sole forage: Low buffering capacity; can include up to 0.25 kg/100 kg BW with other forage
• Continuous water access: Essential; intermittent access increases risk 2.5-fold

Environmental and Training Management

• Maximize pasture turnout; provide social contact with other horses
• Feed hay or small meal before exercise (buffers against acid splash)
• Consider prophylactic omeprazole (1-2 mg/kg) during high-risk periods (competition, transport)
• Minimize NSAID use; if necessary, use lowest effective dose for shortest duration
• Reduce training intensity if clinical signs develop