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My four-year-old Quarter Horse mare died of a ruptured stomach due to perforating gastric ulcers. While I suspect the stress of a 20-hour haul in hot weather caused the ulcerations, the vet who performed the necropsy suggested the ulcers had been brewing awhile, even mentioning her low weight as a sign (she had a drawn or tucked-up appearance). After discussing my mare’s diet and management, she said ulceration might have been due to “meal feeding.” I should have asked what she meant by that, but I was upset at the time. I fed her two or three thin flakes of local-sourced grass hay with a coffee can of all-purpose grain twice a day (5 a.m. and 4:30 p.m.). She was pretty demanding at feeding time, kicking walls and tossing her head, but I chalked up that to being a mare and being in a stall for most of the day. Could “meal feeding” cause chronic gastric ulceration that led to stomach rupture? Could ulcers, in turn, cause her weird mealtime behavior? I feel like a lot of horse owners feed as I do, two big meals a day. I just want to avoid any management missteps in the future.

Answer

“Meal feeding” is simply the provision of feedstuffs in large meals rather than ad libitum, which is a Latin phrase meaning “as much of or as often as desired.” Horsemen frequently feed forage ad libitum because the practice closely mimics the evolutionary behavior of horses, which involved continuous consumption of high-fiber, low-starch feedstuffs. One benefit of ad libitum forage intake is that it allows the gastrointestinal tract to churn slowly and steadily, thus keeping the tract primed for continual processing and holding pH levels in normal ranges in delicate organs, such as the stomach and hindgut. Due to its energy density and because it’s intended to augment a forage-based diet, concentrates (or grains) are fed in meals, usually no larger than 5 lb (2.2 kg).

The science is clear on meal feeding: fasting induces ulcers. In a study conducted nearly 30 years ago, researchers found that pH drops quickly to 2 or below if feed is withheld for several hours.1 The pH scales runs from 0 to 14, with 0 most acidic, 7 neutral, and 14 most basic. A pH of 2, therefore, is considered acidic, much like that of lemon juice. To add to that point, in an earlier study, horses fed timothy hay ad libitum for 24 hours, gastric pH was significantly higher (3.1) when compared to fasted horses (1.5).2 The pH of the horse’s stomach runs the gamut between about 1 and 6, so even in the best of circumstances, the stomach is an acidic environment. Withholding feed for several hours each day is therefore a risk factor for gastric ulcers.

Based on the amount of hay you fed (“two or three thin flakes” twice each day), it is possible that your mare had little or nothing to eat for several hours of the day.

Weight loss or inability to maintain reasonable body condition is a sign of gastric ulcers. While some horses will lose weight because of inappetence, weight loss may also be indicative of increased metabolic rate due to chronic, low-grade pain. In horses whose gastric ulcers were addressed with an appropriate course of omeprazole and follow-up preventive supplements, weight gain and maintenance of desired body condition can usually be achieved.

Behavioral changes are common in horses with gastric ulcers. Aside from being hungry, feeding-time behavior often shifts because horses may recognize that eating temporarily alleviates discomfort associated with gastric lesions. Horses with free-choice access to hay seem to have fewer negative behaviors associated with feeding time than horses that are meal-fed hay and feed. Finally, horses have an innate desire to chew, which is why horses that endure forage deprivation for hours will sometimes resort to wood-chewing or other vices.

Stall confinement can bring about ulcers. In one study, ulcers formed within seven days of taking horses from pasture to stall confinement, despite free-choice hay and no training stressors.3

Gastric rupture accounts for only 1-8% of all fatal colic cases, and severe ulceration with perforation is an established cause of rupture. In one study, when a cause for gastric rupture could be definitively identified at necropsy, perforated ulcers were responsible for 13% of deaths.4

Multiple factors may play into the development of gastric ulcers. To avoid a similar situation, consider these management strategies:

  • Identify a hay that complements the energy demands of the horse. For some horses, hay supplies all of the calories required for maintenance of optimal body weight, which for most show horses would be a body condition score of 5 or 6. If hay meets energy requirements, make sure to top off the diet with an appropriate ration balancer to be sure all protein, vitamin, and mineral needs are met. In choosing hay, consider an alfalfa-blend, as the calcium content in legumes like alfalfa help buffer gastric acid.
  • Arrange for free-choice access to the forage.
  • If a horse requires a concentrate to meet energy demands, choose one that best fits the horse’s energy needs and then feed accordingly, being sure to not overfeed. A feed that contains vegetable oil may help reduce the risk of ulcers.5
  • Provide turnout for the horse. As mentioned above, stalled horses have an increased occurrence of gastric ulcers. Turnout has the added benefit of helping to stave off colic.
  • Give ad libitum access to clean, fresh water, both in the stall and during turnout.
  • Maintain ulcer-prone horses on a research-proven antiulcer supplement, especially if a horse is given a nonsteroidal anti-inflammatory drug such as phenylbutazone or flunixin meglumine.
  • Seek the advice of a veterinarian knowledgeable in gastric ulcers.

 1Murray, M.J. 1992. Aetiopathogenesis and treatment of peptic ulcer in the horse: A comparative review. Equine Veterinary Journal Supplement 7:68-72.

 2Murray, M.J., and G.F. Schusser. 1989. Application of gastric pH-metry in horses: Measurement of 24-hour gastric acid pH in horses fed, fasted, and treated with ranitidine. Journal of Veterinary Internal Medicine 6:133.

 3Murray, M.J., and E.S. Eichorn. 1996. Effects of intermittent feed deprivation, intermittent feed deprivation with ranitidine administration, and stall confinement with ad libitum access to hay on gastric ulceration in horses. American Journal of Veterinary Research 57:1599-1603.

 4Winfield, L.S., and J.E. Dechant. 2015. Primary gastric rupture in 47 horses (1995-2011)Canadian Veterinary Journal 56:953–958.

 5Cargile, J.L., J.A. Burrow, I. Kim, et al. 2004. Effect of dietary corn oil supplementation on equine gastric fluid, sodium, and prostaglandin E2 content before and during pentagastrin infusion. Journal of Veterinary Internal Medicine 18:545-549.

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