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Equine Squamous Gastric Disease

Equine Squamous Gastric Disease (ESGD) refers to lesions specifically affecting the squamous portion of the equine stomach, the upper third above the margo plicatus. ESGD can be the primary problem or, less frequently, can be a secondary problem resulting from obstructed gastric outflow and the subsequent backflow of acids.

ESGD typically occurs when the mucosal lining of the squamous region has been compromised, such as by bacteria or parasites and/or resulting from or exacerbated by increased exposure to highly acidic gastric contents. The squamous mucosa has limited defense against constantly secreted gastric acids and is therefore easily susceptible to damage.

Horses in their natural state or kept under pasture conditions are at limited risk for ESGD, as saliva produced by constant chewing and the steady trickle of roughage into the stomach buffers the acids. When the equine stomach is kept full, a feed bolus the size of a basketball absorbs gastric acids and prevents splashing on the unprotected squamous mucosa. Modern horsekeeping methods and usage, however, create mechanisms that work against this natural protection and thus management is largely responsible for inducing ESGD.

Presentation and Symptoms of ESGD

In some studies, Equine Squamous Gastric Disease incidence and severity correlates directly with increased level of activity, such as in racehorses and other performance horses in rigorous training. However, other research has also shown ESGD indiscriminately afflicts horses in heavy work and at rest, across disciplines, and used in performance, leisure, or even retired at pasture. While incidence and severity is typically lower in non-working horses at pasture, grade 3 and 4 ulceration has still been found to occur. Incidence across multiple reports averages around 70% for performance horses ranging from race to endurance, show, and western performance.

Risk of ESGD increases with any changes in normal feeding and behavior, as well as with grain-based feeds, limiting forage, restricting turnout, intermittent feeding, rigorous exercise, travel, and competition.

Symptomatic horses may display:

  • loss of appetite,
  • difficulty maintaining weight or weight loss,
  • changes in hair coat,
  • poor behavior,
  • underperformance,
  • stereotypies such as cribbing, weaving, or wood chewing.

In particular, commencement of training and the resulting management changes, diets high in concentrates and low in roughage, and exercise can result in the develop of ulceration in as little as seven days.

Note that pain on girthing, flank sensitivity, and diarrhea have oft been misattributed to gastric ulceration, when they are more likely indicative of hindgut disorders. It’s also critical to remember that clinical experience among practitioners shows many horses to be asymptomatic even in the face of severe gastric ulceration, and their symptoms are more readily overlooked.

Differential Diagnosis of Equine Squamous Gastric Disease

Gastroscopy continues to be the only reliable method for the differential diagnosis of gastric ulceration in horses. A complete and thorough examination of the stomach is essential to confirm the presence of squamous ulceration and grade it accordingly. It’s critical to also examine the glandular region of the stomach for ulceration there, as the causative factors and treatment response vary for EGGD. Keep in mind that the presence or absence of gastric ulceration does not rule out an accompanying hindgut pathology.

GradeSquamous MucosaGlandular Mucosa
0The epithelium is intact and there is no appearance of hyperkeratosis (yellow appearance to the mucosa)The epithelium is intact and there is no hyperemia (reddening) of the mucosa
1The mucosa is intact, but there are areas of hyperkeratosisThe mucosa is intact, but there are areas of hyperemia
2Small single, or multifocal lesionsSmall single, or multifocal lesions
3Large single, or multifocal lesions, or extensive superficial lesionsLarge single, or multifocal lesions, or extensive superficial lesions
4Extensive lesions with areas of apparent deep ulcerationExtensive lesions with areas of apparent deep ulceration

Treatment for Equine Squamous Gastric Disease

Because management methods are the primary causative factor in ESGD, improving care practices is essential to the complete remission of squamous ulceration in horses. In order for short-term healing to occur, though, it is typically necessary to suppress acid production and create an environment conducive for healing.

Omeprazole remains the “gold standard” pharmaceutical therapy for the treatment of squamous gastric ulceration in horses. Omeprazole suppresses production of gastric acids, thereby removing the ongoing insult to damaged mucosa and allowing the tissue to heal. It also alleviates discomfort, encouraging the horse to regain normal appetite for forage which helps restore the pH of the stomach.

However, acid suppression should be considered a short-term solution. Because omeprazole therapy does not resolve the causative factors in ESGD and acid suppression may reduce digestion contributing to hindgut dysfunction, additional therapies must be considered. For instance, an independent study has shown one nutritional digestive aid supplement to be more effective than omeprazole on the long-term healing of gastric ulceration.

Removing the horse from work temporarily is advised whenever possible. Additionally, reducing concentrates, increasing forage, feeding smaller meals more often, and increasing turnout time are helpful for near-term healing and critical for long-term health.

Other treatment options are less effective than omeprazole but have been shown to have some positive effect:

  • Ranitidine – an H2 receptor antagonist, shown to effectively suppress gastric acidity. This is an option when omeprazole is not available or is cost prohibitive. Studies show the effects are less than those of omeprazole.
  • Cimetidine – also an H2 receptor antagonist with comparatively low performance in studies.
  • Antacids – effective for short-term symptom control only, as a dose works for just two hours or less while equine gastric acid production is constant.
  • Mucosal protectants – pectin-lecithin complexes for example, provide a physical barrier between mucosa and acid, so may be useful as a preventative and perhaps to aid in healing.

Alternate, nutritional approaches may be equally, if not more effective in the treatment of gastric ulceration long-term. Recent studies have shown that a dietary supplement may be just as effective in treating gastric ulcers as the omeprazole.

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