1
Diseases of the Stomach

The stomach is rarely affected by diseases that require surgery and is more likely to become involved secondary to obstructions in other parts of the gastrointestinal tract. However, some primary diseases of the stomach can cause colic, and can be difficult to distinguish from surgical lesions in other sites.

Gastric Mucosal Diseases

These are the most common types of gastric diseases in horses and typically respond to medical treatment. However, many can be presented as colic and need to be distinguished from other diseases that display such signs. Duodenitis/proximal jejunitis (DPJ) probably has a component of gastritis but is covered in Chapter 2 because of small intestinal involvement.

Gastric Ulcers

Gastric ulceration is the most common disease of the equine stomach.1-3 Equine Gastric Ulcer Syndrome (EGUS) is an early grouping of diseases characterized by ulcers in the terminal esophagus, nonglandular or squamous portion of the stomach, the glandular portion of the stomach, and proximal duodenum (Figure 1.1).4 Reported prevalence of ulcers in mature horses varies from 17% in a population of Swedish horses at necropsy, 82-91% in a racehorse population, 71% in Thoroughbred broodmares at pasture,5 58% in show horses,6-11 and 53% in pleasure horses not in active training.12 A prevalence of 91% recorded in horses in race training can increase to 100% in those horses actively racing.6,13,14 The prevalence of gastric ulcers in foals is 25-50%.15 Within the syndrome of EGUS, two different disease entities are currently recognized (Figure 1.1): equine squamous gastric disease (ESGD) and equine glandular gastric disease (EGGD).1,3,16 This distinction is based on different locations, rates of prevalence, risk factors, and responses to treatments.16 Compared with a prevalence of 50-93% for ESGD, a prevalence of EGGD ranges from 8% to 63%.10,16

Pathophysiology

Although typically regarded as a single-compartment organ, the stomach can be divided into the fundus dorsally, the body in the mid-third, and then the pyloric antrum in the most distal third.1 The dorsal third is covered with thick cornified, stratified squamous epithelium that is nonglandular and continuous with esophageal mucosa (Figure 1.2). The remainder of the stomach is covered with glandular mucosa (Figure 1.2).17 The glandular portion contains mucous neck cells, chief cells (produce pepsinogen), parietal or oxyntic cells (produce HCl), and enterochromaffin-like cells (ECL; produce histamine).18 The lining of the most distal part or antrum is arranged in prominent folds and has the largest concentration of gastrin-producing cells or G-cells (stimulate acid production).18 Secretion of HCl by the glandular part of the stomach and the resulting acidity (and pepsin activation) are considered the dominant causes of gastric ulcers, with little if any contribution from short-chain fatty acids, lactic acid, and duodenal bile salts.3 The associated injury to tight junctions could increase paracellular permeability and allow acid to diffuse into the intercellular space and induce cell damage.19 Unlike human gastric ulcers, a bacterial cause (e.g. Helicobacter pylori) has not been identified in horses.20-22

The concentration of acid in gastric fluid is determined by the rate of its secretion, neutralization with exogenous or endogenous buffers, dilution and neutralization with salivary secretions and food, and loss through the pylorus.23 Horses secrete HCl almost continuously,24 and gastric pH is likely to be lowest during periods when horses are not eating and gastric acid is not buffered by breakdown products of food.3 Contents of the nonglandular region have a pH of approximately 5.4, compared with a pH of approximately 2.6 in pyloric contents,25 which suggests poor mixing between these segments. However, this is not a consistent finding, and variation is considerable during interdigestive periods.25 Feeding reduces gastric pH from near neutrality to about 2.5 over an eight-hour period with some dependence on the type of feed and feeding regimen.19 Withholding food from horses decreases gastric pH rapidly and exposes the nonglandular mucosa to acid.26 Intermittent feeding can increase severity of nonglandular ulcers and provides a useful model to produce these lesions.27 More recent evidence suggests that the pH in the proximal part of the stomach can follow a circadian rhythm, with a significant decrease from 01.00 to 09.00?hours compared with 13.00 to 20.00?hours.28 In the glandular (distal) part of the stomach, pH remains stable throughout the day.28,29

Figure 1.1 Equine squamous gastric disease (ESGD) and equine glandular gastric disease (EGGD) to left and bottom of necropsy image.

Figure 1.2 Anatomy of the interior of the stomach of the horse, displaying the sites relevant to gastric ulceration.

In ESGD, ulcers develop along the margo plicatus (Figure 1.3), especially along the lesser curvature of the stomach,10 a predilection site attributed to the absence of critical protective mucous and HCO3 - secretion on the surface of these cells.4 Galloping could increase the risk of damage to this site through abdominal compression, which would force acidic contents dorsally into the poorly protected nonglandular portion of the stomach.30 By comparison, the distal portion of the stomach is lined by glandular mucosa with extensive protective mechanisms from mucous and HCO3 - secretions.4 Most of these glandular mucosal ulcers (EGGD) are labeled as erosions on histological examination2 and might be capable of repair through rapid restitution of damaged epithelial layers, even in the absence of any pharmacologic intervention.4

Figure 1.3 Extensive ESGD extending along the margo plicatus at the lesser curvature of the stomach in a horse with depression, inappetence, and colic.

Gastric Ulcers and NSAIDs

Gastric mucosal injury by nonsteroidal antiinflammatory drugs (NSAIDs) has been documented in horses31-33 and has been attributed to reduced mucus and HCO3 - production, decreased mucosal blood flow, neutrophil plugging of capillaries, and impaired healing.34 The role of prostaglandins in phenylbutazone (PBZ) ulcers is unclear.35-37 In adults and foals, PBZ has a greater ulcerogenic effect in the glandular mucosa and even the pyloric region than in the nonglandular mucosa,33,35,36 whereas the nonglandular mucosa seems more susceptible to flunixin meglumine (FM) ulcers.32 In a study on horses at necropsy, no difference was found between rate of gastric ulceration in horses treated with NSAIDs and those without.10 This underscores the complex nature of gastric ulceration in horses and the many potential factors involved in any one case.

Because of the potential role of COX-2 in mucosal repair, COX-2 selective and nonselective NSAIDs could interfere with healing of gastric ulcers.38 Both selective (firocoxib) and nonselective NSAIDs (PBZ) can induce gastric ulcers in both glandular and squamous portions but with greater severity in the glandular mucosa in horses treated with PBZ.39 However, there is some controversy about the role of NSAIDs in the development of EGGD,20 and PBZ can induce these ulcers in horses and ponies without decreasing basal glandular concentration of prostaglandin E2.37 Relevant to the more severe forms of colic, lipopolysaccharide (LPS) infusion can significantly increase the mean pH of gastric contents and decrease gastric concentration of H+ and acid output compared with saline infusion.40 These findings would suggest a protective effect from LPS against gastric mucosal injury that is mediated through over-expression of inducible COX-enhanced release of mucosal prostaglandin E2.40

Risk Factors

The prevalence of ESGUS appears related to the intensity of exercise, which could explain the higher prevalence in Thoroughbred and Standardbred racehorses,3,10 especially those actively racing and training.9,13 Competing endurance horses also have a high prevalence (93%).3 Although race training and racing could be risk factors for ESGD, EGGD does not appear to be associated with work intensity and duration in the same manner,20 and ESGD is not limited to high-performance horses.3 In a study on Thoroughbred broodmares at pasture, a 71% prevalence of gastric ulcers was recorded, mostly ESGD with a median score of 3.0/4.0, with no effect from pregnancy.5 The role of stress from a severe GI or orthopedic disease in inducing gastric ulcers is difficult to assess,15,23,41 although stress could increase the risk of EGGD.2,3,16 In horses treated with abdominal pain, those with proximal enteritis had a higher prevalence of gastric ulceration than horses that had colic surgery.42

Intermittent feeding programs seem to put horses at greater risk of gastric...