EQUINE GASTRIC ULCER SYNDROME Part 2

Dr Kirstie Pickles BVMS MSc PhD CertEM(IntMed) DipECEIM MRCVS

Over the following weeks we will be looking in detail at stomach ulcers in the horse. Last week we reviewed the anatomy of the stomach, clinical signs and diagnosis of EGUS CATCH UP HERE. This week we are looking at equine squamous gastric disease (ESGD) in more detail.

Equine Squamous Gastric Disease (ESGD)

Squamous ulcers are the result of the squamous mucosa coming in contact with stomach acid. This region of the stomach (the upper region) is not designed to be in contact with acid, and as a result does not have a defence mechanism in place to protect against acid injury. Acid splashing up onto the squamous mucosa is more likely to happen when the horse moves faster than the walk and when the horse has an empty stomach. Squamous ulcers range from mild erosions to large bleeding craters and are graded 1-4 according to their severity (Figure 1).

Figure 1: Endoscopic views of the inside of a horse’s stomach showing the squamous (S) and glandular (G) areas of the stomach showing equine squamous gastric disease (ESGD). A: Grade 1 ESGD with thickened squamous mucosa showing a cobblestone, yellow appearance; B: Grade 2 ESGD showing focal small ulcerations; C: Grade 4 ESGD with large areas of ulcerated mucosa.

Treatment

As ESGD is caused by acid splashing onto the squamous mucosa, ESGD is very effectively treated by switching off acid production. Omeprazole is a proton pump inhibitor (often termed a ‘PPI’) available as a licenced oral paste or granules which switches off acid production. Unfortunately feed lowers absorption of this product so it is best given on an empty stomach (2-3h without food) and at least 30 minutes prior to being fed. Three to four weeks of omeprazole usually gives excellent healing of ESGD. Repeat gastroscopy is advised to ensure full healing before stopping treatment.

Management

Several risk factors have been recognised for the development of ESGD. These factors should be minimised in all horses but are particularly important to pay attention to for those horses with a previous history of ESGD. Without addressing these issues, ulcers are very likely to return.

  • Acid splash: Feeding 2L of forage or chaff 30 minutes before exercise will help to soak up some stomach acid and also form a fibrous mat within the stomach on top of this fluid thereby limiting acid splashing.
  • Time without forage: Time spent without access to forage increases the risk of squamous ulcers four-fold. Remember this includes time spent exercising/competing/travelling. Ensure constant access to forage where possible. For horses on restrictive diets forage can be soaked to reduce sugar content or even mixed with up to 25% straw which provides fibre but no nutritive value to the horse.
  • High starch meals: Avoid using starch as an energy source. Where more energy is required, select a “high oil feed”; these should be around 10% oil. Feeds should not contain more than 20% non-structural carbohydrates (NSC). NSC is the sum of the sugar and the starch in a feed. Guidelines recommend less than 1g/kg bodyweight of starch per meal and less than 2g/kg bodyweight per day. For a 500kg horse this would equate to a maximum of 500g starch per meal, which would mean no more than 2.5kg of a 20% NSC hard feed twice daily. Ideally this quantity of feed should be split between more than two meals.
  • Intense exercise: Moving at speeds faster than walk increases the risk of squamous ulcers. Explosive exercise, such as jumping or galloping result in very high abdominal pressures. High abdominal pressure pushes the stomach contents towards the vulnerable squamous epithelium, causing acid splash injuries. Explosive exercise should be reduced where possible. When such activities need to be performed, make sure a fibrous meal is fed 30 minutes prior to exercise.
  • Low dietary forage content: Forage (hay/ haylage or grass) should comprise a minimum of 75% of the diet. A horse of a healthy weight, should be fed around 2% of its bodyweight a day in dry matter (the weight of feed once the water is removed) per day. For a 500kg horse this would be 10kg of feed (dry matter). In general terms, most hays and hard feeds are 85-90% dry matter. This would mean feeding a minimum 8.5kg of forage plus a maximum 2.8kg hard feed. Where possible, the amount of hay should be maximised and the amount of hard feed should be minimised.
  • Lack of pasture turnout: The exact role of pasture turnout in the management of EGUS is not clear. Increasing turnout is recommended, but there are certain caveats. Turnout should not cause the horse unnecessary stress (e.g. avoid solitary turnout if the horse does not like this). It is not uncommon for some performance horses to dislike field turnout; standing sulking by the gate is not of benefit to these horses. They would do better in their stable eating hay. Poor quality grazing can act in the same way as food deprivation. If there is not a lot of grass in the field and the horse enjoys turnout, ensure there is additional hay/haylage provided.
  • Access to water: Restricted access to water while at pasture has been highlighted as a risk for ESGD and constant access to water should be implemented at all times. This is hard to do while travelling, which highlights again the increased risk transport poses. Some horses are particular about regional water differences and drink much less away from home. If this is the case, take water from home away to competition.

Additionally, supplements may be useful in ongoing management of ulcer-prone horses. Current research suggests that providing an antioxidant to address oxidative stress within the stomach, buffers/antacids to reduce stomach acidity, and a mucus stimulant are all sensible ingredients for a gastric supplement to contain. Some horses may require a gastric supplement on a long-term basis, whereas others may only need additional support around stressful events, such as travel and competition. Certain supplements can also be used alongside medical treatment.

NEXT WEEK: Equine glandular gastric disease.

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