EQUINE VETERINARY EDUCATION / AE / JANUARY 2017


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Review Article Nutritional management of gastric ulceration


F. M. Andrews†*, C. Larson‡ and P. Harris§ †Equine Health Studies Program, Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, USA; ‡Zinpro Corporation, Eden Prairie, Minnesota, USA; and §WALTHAM Centre for Pet Nutrition, Waltham-on-the-Wolds, Leicestershire, UK. *Corresponding author email: fandrews@lsu.edu


Keywords: horse; gastric ulcers; dietary management


Summary Gastric ulcers are common in horses and equine gastric ulcer syndrome describes ulcers in the distal oesophagus, nonglandular and glandular stomach as well as the proximal duodenum. Ulcers in the distal oesophagus and nonglandular region of the stomach are probably caused by hydrochloric acid, whereas ulcers in the glandular stomach and proximal duodenum are likely to be caused by a breakdown in the mucosal defence mechanisms. Regardless of the location of ulcers, initial treatment with pharmacological agents is necessary to suppress hydrochloric acid; however, nutrition and management changes are required to maintain ulcer healing and help prevent recurrence. In addition, many dietary supplements have been marketed to help maintain stomach health and some scientific data on their effects on gastric ulcer scores and gastric juice pH are presented.


Introduction


Ulcers found in the terminal oesophagus, proximal nonglandular (squamous) stomach, distal (glandular) stomach and proximal duodenum are collectively referred to as the equine gastric ulcer syndrome (EGUS) (Andrews et al. 1999a). All ages and breeds of horses are susceptible to EGUS and diet, as well as management, plays an important role in the formation and maintenance of ulcers (Nadeau et al. 2000, 2003a,b; Andrews et al. 2006; Lybbert et al. 2007; Luthersson et al. 2009). Pharmacological therapy and maintaining a gastric juice pH >4.0 form the foundation of any treatment. Diet and nutritional management, however, are more long-term solutions that might reduce the risk or help prevent recurrence and complications associated with chronic ulceration. Although complications, such as strictures, gastric and duodenal bleeding, and stomach rupture with resulting peritonitis, occur primarily in foals, they may uncommonly be seen in mature horses (Traub-Dagartz et al. 1985; Bezdekova and Hanak 2009; Bezdekova 2009; Camacho-Luna and Andrews 2015). This article focuses on nutritional and dietary factors important in the cause of squamous and glandular stomach ulcers of mature horses and how the horse’s diet can be managed to lessen ulcer severity and help prevent recurrence and chronic ulceration.


Anatomy and pathogenesis


Horses are predisposed to squamous gastric ulcers because of their compound stomach. Squamous ulcers occur in the proximal third of the stomach, predominantly near the margo


plicatus, which is lined by nonglandular stratified squamous epithelia. The squamous region of the equine stomach has an osmiophilic phospholipid surfactant-like layer that contributes to the mucosal barrier, but it lacks a significant mucus layer, has poor blood supply and has a variable ability to heal spontaneously once injured (Ethell et al. 2000; Bullimore et al. 2001). Spontaneous healing of squamous ulcers varied from 4 to 8% in untreated stall-confined horses maintained in race training, and from 9 to 33% in horses under field conditions and 33% of horses when they were moved from pasture to stalls (Andrews et al. 1999a,b; MacAllister et al. 1999; Woodward et al. 2014). In addition, in one study, when horses were housed in stalls and moved to pasture, spontaneous healing of lesions occurred in 6/11 horses (55%) and new lesions occurred in 5/12 horses (42%), during a 6-week pasture recovery period (McGowan et al. 2007). Thus, the actual spontaneous healing rate and formation of new squamous ulcers is variable. The distal two-thirds of the stomach consists of glandular


mucosa, which secretes a thick protective mucus and bicarbonate layer, as well as hydrochloric acid (HCl), pepsinogen (converted to pepsin at pH <4.0) and gastric lipase, which are all involved in digestion (although the importance of gastric lipase and pepsin is unknown) (Argenzio 1999; Murray 1999; Merritt and Julliand 2013). The glandular region is also where gastrin, histamine and somatostatin are synthesised. The glandular mucosa has an extensive capillary network and, as extrapolated from human studies, undergoes rapid restitution once injured (Silen 1987). It was once thought that ulcers in this region were infrequent; however, a recent review reported that glandular gastric ulcers varied in prevalence from 8 to 63% in certain populations of horses (Malmkvist et al. 2012; Sykes and Jokisalo 2015).


Squamous/nonglandular ulcers Horses are continuous, although variable, gastric HCl secretors and acid exposure is thought to be the primary cause of squamous ulcers (Campbell-Thompson and Merritt 1990; Murray and Schusser 1993; Widenhouse et al. 2002). Gastric acid secretion is stimulated by vagally released acetylcholine and gastrin working potentially through released histamine and is modulated by somatostatin in response to various factors including the size and nature of the meal as well as the intragastric pH (Merritt and Julliand 2013). A proximal-to-distal pH gradient exists in the fed equine stomach (Baker and Gerring 1993). The proximal stomach, just below the lower oesophageal sphincter, in fed horses showed a near neutral pH (7.0), whereas ventrally the ingesta


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