Equine Gastric Ulcer Syndrome

James Wallace BVMS GP CertEP CertEM (Int Med) MRCVS CertEP RCVS Advanced Practitioner Internal Medicine Equine Veterinary Surgeon

Physiotherapists are often the first point of contact for a client concerned with poor ridden behaviour and performance. It is often necessary to rule out nonorthopaedic problems before embarking on treatment. Equine gastric ulcer syndrome (EGUS), is one such common cause of poor performance, bad ridden behaviour, weight loss, and colic (Sykes & Jokisalo, 2014). As with all poor performance issues, teamwork, and liaison between different professions (physiotherapists, nutritionists, farriers, and veterinarians) is essential for a successful outcome. EGUS is a broad group of inter-related conditions, which have different causal factors and management regimes. In this article we will summarise what EGUS is, and how you can identify it.

Figure 1: Evolution of the horse

Horses have evolved over the last 50 million years from a mainly herbivorous omnivore, with a similar diet to modern pigs, to the modern horse on a forage based diet. The digestive system of the modern horse is configured to digest poor quality grass based diets, which are low in soluble carbohydrates (starch and fructan), and high in structural carbohydrate (cellulose and hemi-cellulose). Horses are well adapted to living in an arid climate with sparse grassland with high mineral contents such as the steppes middle Asia and themid-west of the USA; in conditions which would not allow other herbivores such as cattle and sheep to thrive (Mihlbachler et al., 2011).

Figure 2: Diagram of equine gastric anatomy

The stomach is highly acidic (pH<1.4), and is split into 3 main portions (Sykes et al., 2015). The squamous portion (1) is an extension of the oesophageal lining and is a food storage vat. It has poor defence against acid exposure but has high stretch ability. If exposed to acid and bile from the gastric juices, it will oxidise and form squamous ulcers or EGSD (Figure 3). In a wild horse this is unlikely because the stomach would likely be full of fibre, which naturally floats on the gastric juice pool, and slowly makes its way down into the pylorus and further on into the digestive system. The glandular portion (2) is an acid secreting mucous membrane. This has good defences against acid, assuming there is no disruption to normal blood flow and hormone balances.Equine gastric glandular disease (EGGD) is not well understood, but can be erosions, ulcers, or thickened and inflamed membrane (Figure 4). The pylorus (3) has the same coating as the glandular portion, but is the barrier between the stomach and the small intestine. In addition, it acts as a pump and the trigger for normal intestinal propulsion of the food,measuring its sugar, fibre, and protein content; adjusting the digestive cycle using hormones and changes in the intestinal smooth muscle contraction. A more serious condition, delayed gastric emptying/gastric dilation can also be linked to ulceration, and is a cause of severe poor ridden behaviour (Bezdekova et al., 2020). There is no current link between the organism which can cause ulceration in humans (H. pylori) and horses.

Figure 3: Squamous ulceration

Figure 4: Glandular and pyloric disease

Initially, gastric ulcers were thought to predominately occur in highly stressed horses, or those under metabolic stress such as race horses and intensively stabled event horses. Recent work suggests the incidence in the general equine population of 45% increasing markedly with excessive exercise, cereal based diets, and stabling. In unpublished work by the author and other internists, there is a tentative link between obese horses with equine metabolic syndrome and EGGD. There is also emerging evidence of refractory EGGD and dietary allergens detected by serum IgE well testing (Wallace, 2021).

Horses with EGUS can show a wide variety of signs from weight loss, soft stools, teeth grinding, not finishing feed, colic, difficulty girthing, and poor ridden behaviour (Sykes & Jokisalo, 2014). Often they are uncomfortable on deep palpation of the left epigastric area, or application

of a tight surcingle. In addition some horse will have ventral abdominal spasm and pain in the L1-3lumbar area. Other tests such as faecal occult blood and saliva testing are of little or no diagnostic value (Wallace, 2017).

Investigation is relatively straightforward with gastroscopy now a routine outpatient procedure in most veterinary practices. It is well tolerated by horses, requiring only light sedation in most cases.

Treatment for EGUS differs from which areas of the stomach are affected, and the severity of disease. In all cases dietary modification is essential, with increased fibre intake being key. In addition adding in oil (rapeseed and fish oils), to each feed increases poly-unsaturated fatty acids, which can act as anti-inflammatory eicosanoid precursors in the stomach, and have a beneficial effect on blood flow. Feeding a calcium-rich chaff (such as alfalfa) before riding acts as fibre trap for acid,and is especially useful in EGSD. Modifying exercise to reduce high intensity work, but increasing slow gait fitness is also beneficial (Luthersson et al., 2019; Sutton, 2014). Pasture turnout is not as protective as initially thought, and many horses can develop ulcers at grass if other predisposing factors are present (Sutton, 2014, Sykes et al., 2014, Wallace 2017).

Pharmacological management of EGUS relies on the use of ant-acid drugs (Sutton, 2014), proton pump inhibitors such as omeprazole / esomeprazole (which are particularly effective in EGSD), or the use of protectants such as sucralfate, which acts as a biofilm protecting areas of ulceration and encouraging healing (as used for EGGD). In some cases there additional medication may be required such as misoprostol (a synthetic prostaglandin) or prednisolone (a corticosteroid). In all cases, changes to diet and medication may need to be given over the working life of the horse (Lutherson et al., 2019).

Early identification of EGUS can lead to more successful treatment outcomes. As such, as a medical professional, if you suspect gastric disease, liaising with the clients veterinarian to perform a gastroscopy will allow this condition to be ruled out as a cause of poor performance.

Bezdekova, B., Wohlsein, P., & Venner, M. (2020). Chronic severe pyloric lesions in horses: 47 cases. Equine Veterinary Journal. https://doi.org/10.1111/evj.13157

Luthersson, N., Bolger, C., Fores, P., Barfoot, C., Nelson, S., Parkin, T., & Harris, P. (2019). Effect of Changing Diet on Gastric Ulceration in Exercising Horses and Ponies After Cessation of Omeprazole Treatment. Journal of

Mihlbachler, M. C., Rivals, F., Solounias, N., & Semprebon, G. M. (2011). Dietary change and evolution of horses in North America. Science. https://doi.org/10.1126/ science.1196166

Sutton, D. (2014). Equine gastric ulceration syndrome: Treatment and prevention. In Veterinary Record. https:// doi.org/10.1136/vr.g4613

Sykes, B. W., & Jokisalo, J. M. (2014). Rethinking equine gastric ulcer syndrome: Part 1 - Terminology, clinical signs and diagnosis. In Equine Veterinary Education. https://doi.org/10.1111/eve.12236

Sykes, B. W., Mcgowan, C. M., & Mills, P. C. (2015). Placement of an indwelling percutaneous gastrotomy (PEG) tube for the measurement of intra-gastric pH in two horses. Equine Veterinary Education. https://doi.org/10.1111/eve.12395

Wallace, JDG (2017). Equine Gastric Disease- a review. Proceedings of the Scottish Vet Fair – 2017.

Wallace JDG (2021). Weight loss in Horses. Proceedings ofVets4NHS Congress-2021

Physiotherapy for Cranial Cruciate Disease

Pain management post op

• Heat • Cryotherapy • Transcutaneous electrical nerve stimulation • Class 3B laser • Gentle weight bearing exercises to encourage healing and reduce swelling • Neuromuscular electrical stimulation to recruit hypotrophied muscles • Maintain range of movement • Gait re-education • Manual therapy to reduce compensatory muscle soreness • Proprioceptive stimulation e.g. kinesiotape to facilitate muscle contraction • Hydrotherapy

Research

Berte et al (2012) found no instability was caused and lameness was improved 90 days post CCLR stabilised with lateral suture stabilisation (UWTM walking started at week 2). Full extension whilst weight bearing improves static quadriceps ef.ciency & helps reduce the risk of patella luxation (Lafaver et al 2007). Risk of complication CCLR post op increased without physio (Lafaver et al 2007). Monk et al (2006) found that 6/52 after TPLO, the physical rehabilitation group had signi.cantly larger thigh circumference and range of movement than the home exercise group.