Equine Gastric Ulcer Syndrome (EGUS)
Affecting up to 60% of show horses and 90% of racehorses, EGUS is a primary cause of behavioral resistance, weight loss, and poor performance. This clinical guide breaks down squamous vs. glandular pathology, gastroscopy, and evidence-based treatment.
1. Gastric Anatomy & The Two Distinct Ulcer Diseases
The horse possesses a relatively small, single-chambered stomach (holding 8 to 15 liters) designed for continuous trickle-feeding over 16 to 18 hours per day. Unlike humans who secrete stomach acid primarily in response to food consumption, the equine stomach continuously produces hydrochloric acid 24 hours a day (up to 30 liters daily), regardless of whether food is present.
The equine stomach is divided into two histologically distinct regions separated by a jagged anatomical boundary line called the margo plicatus:
Equine Squamous Gastric Disease (ESGD)
Occurs in the upper, non-glandular third of the stomach. The squamous epithelium is composed of stratified cells similar to the esophagus, possessing zero mucus or bicarbonate glands. Ulcers here are caused by mechanical acid exposure—when an empty stomach allows raw hydrochloric acid and bile salts to splash upward onto the unprotected squamous lining during exercise.
Equine Glandular Gastric Disease (EGGD)
Occurs in the lower two-thirds of the stomach and pylorus. The glandular mucosa is designed to produce acid and is normally shielded by a thick phospholipid and mucus-bicarbonate barrier. Ulcers here represent a breakdown of mucosal defenses, frequently triggered by chronic physiological stress, immune suppression, or NSAID therapy (Bute/Banamine).
2. Clinical Recognition & Definitive 3-Meter Gastroscopy
Clinical manifestations of EGUS are frequently insidious and misdiagnosed as behavioral defiance. Key warning signs include:
- "Girthiness" or Cinch Sensitivity: Biting, pinning ears, kicking out, or stomping when the girth is tightened.
- Changes in Eating Behavior: Backing away from concentrate grain meals after a few mouthfuls, eating slowly, or consuming hay before grain.
- Sub-Clinical Performance Decline: Reluctance to go forward off the rider’s leg, unwillingness to collect or jump, and hollowed-back posture.
- Chronic Mild Colic: Low-grade discomfort, flehmen response, or yawning repeatedly after feeding.
The only definitive diagnostic standard is a 3-meter flexible video endoscope. Following a 12-to-16-hour feed fast, the veterinarian passes the endoscope through the ventral nasal meatus, down the esophagus, and into the stomach. Squamous ulcers are graded on an established clinical scale:
3. Evidence-Based Pharmacology & Nutritional Buffering Strategies
Successful ulcer resolution requires a dual approach combining pharmaceutical acid suppression with management modifications:
The FDA-approved cornerstone therapy (GastroGard) dosed at 4.0 mg/kg once daily for 28 consecutive days. Irreversibly binds to H+/K+ ATPase pumps in gastric parietal cells, shutting down acid production. Must be given on an empty stomach 30 to 60 minutes before morning feed. Followed by a preventative maintenance dose (1.0 mg/kg/day) during travel and competition.
Essential for glandular lesions (EGGD). Formulates a protective sticky polymer paste over active ulcer craters in an acidic environment, adhering to exposed protein exudates and stimulating local prostaglandin production. Must be spaced at least 60–90 minutes away from omeprazole to prevent drug binding interference.
Feeding 1 to 2 flakes of high-quality alfalfa hay 30 minutes before exercise creates a dense physical "fiber mat" floating atop the stomach liquid, physically blocking acid splash onto the squamous epithelium during trot and canter work. Furthermore, alfalfa’s natural high calcium and crude protein content acts as a chemical antacid buffer.
Frequently Asked Questions: Equine Gastric Ulcer Syndrome
What is the anatomical difference between Squamous (ESGD) and Glandular (EGGD) ulcers?
The equine stomach is divided by the margo plicatus. The upper squamous region has no glandular secretion and lacks a protective mucus-bicarbonate barrier, making it vulnerable to acid splash during exercise. The lower glandular region produces hydrochloric acid and possesses a natural mucosal lining; ulcers here represent a failure of mucosal defense mechanisms rather than simple acid overload.
What is the only definitive method to diagnose equine gastric ulcers?
A 3-meter flexible video gastroscopy is the sole definitive diagnostic method. Blood tests, fecal occult blood tests, and ultrasound cannot visualize or grade gastric ulcers. Gastroscopy is performed after a 12-to-16-hour feed fast to allow complete visual inspection of the squamous mucosa, margo plicatus, glandular mucosa, and pylorus.
Why is alfalfa hay recommended for horses prone to gastric ulceration?
Alfalfa hay contains significantly higher concentrations of calcium and crude protein than grass hay. Calcium and magnesium act as natural chemical buffers, neutralizing hydrochloric acid in the stomach lumen and raising gastric pH for up to 4 to 6 hours after consumption.
What is the standard pharmacological treatment protocol for ESGD?
The FDA-approved gold standard is buffered oral omeprazole (GastroGard) administered at 4.0 mg/kg once daily for 28 consecutive days, given on an empty stomach at least 30 to 60 minutes before the morning meal, followed by a repeat gastroscopy or a tapered preventative dose (1.0 mg/kg).
Why does phenylbutazone (Bute) or Banamine usage increase ulcer risk?
Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenase (COX-1 and COX-2) enzymes, which decreases the production of protective prostaglandins. Prostaglandins maintain gastric mucosal blood flow and stimulate mucus and bicarbonate secretion; their suppression leads directly to glandular ulceration.