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Equine gastric ulcer syndrome (EGUS) is a common cause of colic and decreased performance in horses. Horses form ulcers in the mucosa of the stomach, leading to pain, decreased appetite, weight loss, and behavioral changes. Treatment generally involves reducing acid production of the stomach and dietary management.
Gastroscopy, or endoscopic evaluation of the stomach, is useful in chronic cases of colic suspected to be caused by gastric ulcers, gastric impactions, and gastric masses. [42] A 3-meter scope is required to visualize the stomach of most horses, and the horse must be fasted prior to scoping.
Ileus is a cause of colic in horses due to functional obstruction of the intestines. It is most commonly seen in horses postoperatively, especially following colic surgery. [ 9 ] Horses experiencing ileus are at risk for gastric rupture due to rapid reflux build-up, and require intense medical management with frequent nasogastric intubation. [ 9 ]
Extension of the ulcer through the lining of the digestive tract results in spillage of the stomach or intestinal contents into the abdominal cavity, leading to an acute chemical peritonitis. [13] [14] Helicobacter pylori infection and overuse of non-steroidal anti-inflammatory drugs [15] [16] may contribute to formation of peptic ulcers.
Based on evidence from people with other health problems crystalloid and colloids are believed to be equivalent for peptic ulcer bleeding. [15] In people with a confirmed peptic ulcer, proton pump inhibitors do not reduce death rates, later bleeding events, or need for surgery. [18] They may decrease signs of bleeding at endoscopy however. [18]
Skin lesions probably due to Habronema Horse recovering from skin lesions probably due to Habronema, after treatment with ivermectin. For most horses, the lesions will resolve by the end of summer. Topical or systemic treatment with Ivermectin is effective against Habronemiasis. Ivermectin or moxidectin can eliminate nematodes in the stomach.
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Gastric ulcers may develop; it is unclear if they are the causes or the consequences. Intestinal metaplasia typically begins in response to chronic mucosal injury in the antrum and may extend to the body. Gastric mucosa cells change to resemble intestinal mucosa and may even assume absorptive characteristics.