Ventriculus (Gaster)
The equine stomach is relatively small (8-15 liters capacity, approximately 8-10% of the total gastrointestinal tract volume), reflecting the horse's evolutionary adaptation as a continuous grazer rather than a meal feeder. It is divided by the margo plicatus into a proximal non-glandular (squamous) region and a distal glandular region. Gastric acid is secreted continuously, even when the horse is not eating, which is why prolonged fasting predisposes to squamous ulceration. The powerful cardiac sphincter and the oblique angle of esophageal entry prevent vomiting, meaning the stomach can rupture before contents can be expelled retrograde.
Gastric ulcers (especially squamous) are common in performance horses and horses that are fasted or stressed. Diagnosis uses endoscopy. Treatment includes management changes and medications that reduce acid. Gastric rupture is a life-threatening emergency.
## Overview Equine gastric ulcer syndrome (EGUS) encompasses ulceration of the squamous (upper) and glandular (lower) stomach lining. It is extremely common in performance horses. Risk factors includ
## Overview Gastric rupture is a catastrophic tear of the stomach wall, usually from severe distension (impaction, outflow obstruction, or grain overload). Horses often show acute severe colic follow
## Overview Gastric impaction is accumulation of solid feed material in the stomach that fails to empty normally. It causes chronic or intermittent low-grade colic, reduced appetite, and weight loss.
## Overview Gastric squamous cell carcinoma is the most common stomach tumor in horses. It arises in the squamous (non-glandular) region and is highly metastatic. Clinical signs are nonspecific: prog
## Overview Pyloric stenosis is narrowing of the outflow from the stomach to the duodenum. It may be congenital in foals or acquired in adults from chronic ulceration or neoplasia. Horses show chroni
Free access to forage helps buffer gastric acid. Signs of colic or poor appetite should be evaluated. Prolonged fasting increases ulcer risk.
## Overview Equine gastric ulcer syndrome (EGUS) encompasses ulceration of the squamous (upper) and glandular (lower) stomach lining. It is extremely common in performance horses. Risk factors include high-grain diets, intermittent feeding, stress, and intense training. Many horses show subtle or no outward signs. ## Causes Acid exposure of unprotected squamous mucosa, plus impaired glandular defenses. Management and stress factors predominate. ## Diagnosis Gastroscopy is required for definitive diagnosis and grading. ## Treatment Omeprazole is the primary acid-suppressing medication. Management changes (forage availability, reduced grain, stress reduction) are essential for healing and prevention. ## Recovery and Prognosis Good with appropriate medication and management. Recurrence is common if risk factors persist. ## Prevention Maximize forage, minimize grain boluses, and reduce stressors. Low-dose omeprazole can be used preventively in high-risk horses. Signs include: poor appetite; poor body condition; recurrent mild colic; girthiness; behavioral changes; teeth grinding; many horses are asymptomatic
## Overview Gastric rupture is a catastrophic tear of the stomach wall, usually from severe distension (impaction, outflow obstruction, or grain overload). Horses often show acute severe colic followed by sudden apparent improvement as the stomach decompresses into the abdomen, then rapid shock and death from peritonitis. ## Causes Over-distension from impaction, grain engorgement, or ileus. ## Diagnosis Clinical progression from severe pain to sudden quietness with cardiovascular collapse. Abdominocentesis yields feed-contaminated fluid. Most cases are confirmed at necropsy. ## Treatment None effective once rupture has occurred. Euthanasia is indicated. Prevention of rupture by relieving gastric distension is the only intervention. ## Recovery and Prognosis Fatal. ## Prevention Prompt treatment of colic and gastric distension; secure grain storage. Signs include: acute severe colic followed by sudden quietness; rapid cardiovascular collapse; peritonitis; death within hours
## Overview Gastric impaction is accumulation of solid feed material in the stomach that fails to empty normally. It causes chronic or intermittent low-grade colic, reduced appetite, and weight loss. Reflux may be minimal because the material is too solid to siphon. Friesians appear predisposed. ## Causes Poor gastric motility, ingestion of poorly digestible material, dental disease, or underlying pyloric or duodenal obstruction. ## Diagnosis Gastroscopy showing a large mass of impacted feed, and ultrasound demonstrating an enlarged stomach. Response to treatment supports the diagnosis. ## Treatment Repeated gastric lavage. Administration of cola via nasogastric tube has been associated with improved resolution and survival in recent studies. Address any underlying motility or outflow problem. Surgery is rarely indicated. ## Recovery and Prognosis Historically poor, but recent data show better survival (over 50 percent overall, higher with cola treatment). Chronic cases can recur. ## Prevention Appropriate forage, dental care, and management of predisposed breeds. Signs include: chronic low-grade colic; anorexia; weight loss; large stomach on ultrasound; minimal nasogastric reflux
## Overview Gastric squamous cell carcinoma is the most common stomach tumor in horses. It arises in the squamous (non-glandular) region and is highly metastatic. Clinical signs are nonspecific: progressive weight loss, low-grade colic, intermittent fever, anemia, and low protein. Gastroscopy reveals an irregular ulcerated mass. ## Causes Unknown. Equine papillomavirus type 2 has been identified in some lesions. ## Diagnosis Gastroscopy with biopsy. Abdominal ultrasound may show metastasis or effusion. Bloodwork often shows anemia and hypoproteinemia. ## Treatment No effective treatment. Palliative care only. Most horses are euthanized once diagnosed. ## Recovery and Prognosis Grave. Metastasis is common at diagnosis. ## Prevention None. Signs include: progressive weight loss; chronic low-grade colic; intermittent fever; anemia; hypoproteinemia; ulcerated mass on gastroscopy
## Overview Pyloric stenosis is narrowing of the outflow from the stomach to the duodenum. It may be congenital in foals or acquired in adults from chronic ulceration or neoplasia. Horses show chronic colic after eating, teeth grinding, excessive salivation, gastric distension, and large volumes of reflux. ## Causes Congenital malformation, scarring from ulcers, or tumor. ## Diagnosis Gastroscopy showing a narrowed pylorus, and large-volume reflux. ## Treatment Surgical bypass (gastrojejunostomy) in selected cases. Medical management of underlying ulceration. Prognosis is guarded. ## Recovery and Prognosis Guarded. Congenital cases in foals and severe acquired stenosis have limited options. ## Prevention Management of gastric ulceration may reduce acquired cases. Signs include: chronic colic after eating; teeth grinding; excessive salivation; gastric distension; large-volume nasogastric reflux
Gastric ulcers (especially squamous) are common in performance horses and horses that are fasted or stressed. Diagnosis uses endoscopy. Treatment includes management changes and medications that reduce acid. Gastric rupture is a life-threatening emergency.
Free access to forage helps buffer gastric acid. Signs of colic or poor appetite should be evaluated. Prolonged fasting increases ulcer risk.
See the Stomach on our interactive 3D horse model. Open 3D Model