Equine gastric ulcer syndrome

Because of its multiple causes and complex nature, the term syndrome of equine gastric ulcer (EGUS) has been used to describe gastric ulcer disease in horses. It is quite common, with a prevalence ranging from 25% to 50% in foals and 60% to 90% in adult horses.
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STOMACH Anatomy and Physiology
The horse stomach is divided into two distinct regions: the esophagus or NO glandular region and the glandular region.
The region is covered by esophageal squamous mucosa and covers approximately one third of the entire stomach. Glandular region covers the remaining two thirds of the stomach and contains glands that secrete hydrochloric acid, pepsin, bicarbonate and mucus.
The horse’s stomach secretes hydrochloric acid (HCl) continuously around 1.5 liters of gastric juice per hour regardless of the presence or absence of food. Colts tend to maintain a particularly high level of acidity (low pH) within the gastric fluid; This environment has been implicated as a predisposing factor for the development of EGUS.
healthy stomach
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Gastric emptying of a liquid meal usually occurs within 30 minutes, while the gastric emptying of a meal forage (hay) requires about 24 hours.
Syndrome equine gastric ulcer occurs as a result of an imbalance between aggressive factors mucosal (HCl, pepsin, bile acids, organic acids) and protective factors mucosal (mucus, bicarbonate).
ulcerated stomach
Glandular mucosa ulceration is usually due to interruption of blood flow and a secondary decrease in mucus secretion and bicarbonate (which are factors mucosal protection).
Of course, excessive exposure to aggressive factors (as a result of decreased gastric / esophageal motility, delayed gastric emptying, recumbent, etc.) can also result in glandular ulceration.
Inhibition of prostaglandins (PGs) may also play a role in the pathogenesis of ulceration glandular. PGs help maintain the integrity of the mucosa stimulating repair and prevent mucosal damage.
nonsteroidal antiinflammatory drugs (NSAIDs) block prostaglandin synthesis (PGE2 mainly, I and A) and have been associated with glandular ulceration, especially in foals.
Stress has also been associated with the development of glandular ulcers, presumably through excessive release of endogenous corticosteroids, which also inhibits prostaglandin synthesis.
The volatile fatty acids (VFA) have been associated with gastroesophageal acid to mucosal injury in horses. AGVs are generated by resident bacteria during fermentation of carbohydrates. Many competition horses are fed diets high in fermentable carbohydrates (eg cereals), being at increased risk of gastric ulceration.
An abnormal history and clinical presentation are the first indications of the possible existence of gastric ulcers.
Clinical signs in older horses include:
Loss of appetitehorse vet
Lethargy (clumsiness)
Changes in attitudes
Decreased performance
Reluctance to train
The poor conditionhorse vet
rough hair
Excessive recumbent (lying)
Mild (low grade) colic
Bruxism (teeth grinding)
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Suge diagnosis is based on clinical signs, videoendoscopic findings, and / or response to empirical treatment.
Although suspected EGUS often derives from the presence of typical symptoms, definitive diagnosis is rarely performed based on clinical signs alone. A definitive diagnosis can only be made by EGUS. In fact, it was the development of this technology that dramatically increases the awareness of veterinary gastric ulcers in horses.
Response to empiric treatmenthorse vet
It should be noted that the lack of definitive endoscopic abnormalities not confirm the absence of gastric ulceration. Indeed, a false negative endoscopic evaluation is not uncommon. They will be observed only large lesions (macroscopic), smaller lesions can escape visual detection (microscopic).
In these cases, a positive response to empiric therapy is often considered diagnostic. In many cases of equine gastric ulcer, suppression of clinical signs occurred under treatment endoscopically normal individuals.
A number of strategies have been used for the treatment and prevention of gastric ulcers in horses and foals.
The success of therapy is aimed at:
Minimizing Risk factors (such as drugs or stress). The elimination of risk factors is quite obvious.
Drugs that have been shown to promote the formation of ulcers should be used with caution. Nonsteroidal antiinflammatory drugs (NSAIDs) such as Bute, Banamine, Ketofen, etc.) are often used to relieve clinical signs (ie, inflammation and pain) in arthritis associated with horses. However, repeated use can lead to gastric ulceration and renal dysfunction and liver.
PROTECTION stomach lining. This strategy involves the use of food and / or drug mucosal protective function, they are designed to “shield” of the stomach lining.
A diet rich in fiber (as hay) has been shown to stimulate the production of saliva rich bicarbonate in older horses. Saliva rich in bicarbonate serves as an effective protector in the stomach.horse vet
Alfalf hay, which is high in protein and calcium, appears to have an extra-powerful buffering effect in the stomach. Horses fed alfalfa hay have less acidity and presenting lower than those fed other types of hay horses gastric ulcer. The damping effect of alfalfa hay can last up to 5 hours after feeding.
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Moreover, horses continuously fed hay have less heartburn (ie, a higher pH) compared to those fed intermittently or fasted for a period of time. For this reason, usually using slow feeds hay for horses with gastric ulcer is recommended. Small mesh nets hay provide continuous access to hay
The most common drug that is currently used to coat the stomach lining is Sucralfate (Carafate), which is only effective for lining glandular stomach and duodenum, where ulcers are less likely to occur. Although this treatment strategy has proven useful in many cases EGUS, it is not considered appropriate when used as the sole treatment.
INHIBITION acid secretion in the stomach. Inhibition of gastric acid secretion is the mainstay of treatment of gastric ulcers in horses.
There are 3 categories of acid suppressants:
1_ANTIACIDOS simply absorb everything that is acid in the stomach. They are the least expensive form of acid suppressant. On the other hand, they are also less effective. Antacids should be administered in large and frequent doses to provide any benefit. Therefore, antacids not considered suitable therapy when used alone.
2_Histamina type 2 receptor (H2) antagonists are designed to block acid secretion by the stomach lining. This form of treatment has been available and used successfully for years.
Cimetidine (Tagamet) and ranitidine (Zantac) have historically been the most used, and both effectively inhibit gastric acid secretion in horses. Usually a period of 3 weeks treatment is required to ensure complete cure.
Two other H2 antagonists on the market for use in humans are famotidine (Pepsid®) and Nizatidine (Axid®). Not yet been established effective doses for horses.
3_Inhibidores proton pump also block secretion of acid by the stomach lining.
Omeprazole is a proton-pump inhibitor that is labeled for both treatment EGUS (GastroGard or generic) and preventing recurrence. Omeprazole is the only FDA approved drug for use in horses. Besides being the most effective drug, it is also the most expensive.
Therapeutic treatment involves oral omeprazole administration once daily. preventive therapy requires only a quarter of the dose of treatment.
Recent research suggests that Aloe Vera juice may also possibly comparable to omeprazole potent anti-ulcer effects. Although nothing has been published, the initial results are promising. Aloe Vera juice is much less expensive and is readily available.
Most vets do not have the same degree of confidence in Aloe Vera juice as omeprazole regarding treatment of gastric ulcer. However, all Aloe Vera juice days is a potential option if the cost is prohibitive omeprazole. Manage we recommend 1/4 cup Aloe Vera juice (with food) twice daily as needed.

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