Equine Gastric Ulcer Syndrome is well known amongst equine veterinarians.
By Dr Michael Robinson
Aetiology
EGUS is best regarded as two separate entities: Equine Squamous Gastric Disease (ESGD) and Equine Glandular Gastric Disease (EGGD)1.
The two conditions may occur either independently or concurrently in the same horse. The presence or absence of one cannot be used as a predictor for the presence of absence of the other1.
ESGD is very common (between 11-95% depending on discipline and management)1,2. The causes of ESGD are well documented and it is known to be highly responsive to routine treatment with proton-pump inhibitors, such as omeprazole1.
EGGD is becoming more widely recognised (between 16-65% depending on discipline and management)1,2 as more veterinarians seek out the pyloric region of the stomach on routine gastrocopies. Visualisation of this region may be technically challenging but is an essential part of a full gastroscopy (Figure 1). The specific causes of EGGD are multifactorial and largely speculative, although prolonged courses of high dose NSAID’s are one recognised cause. EGGD tends to be somewhat recalcitrant to treatment with longer term treatment and follow up required.
The clinical signs of gastric ulcers include:
• failure to thrive • weight loss • poor coat quality • behavoural changes • inappetence • mild colic.
In addition, gastric ulcers have the potential to have a significant impact on the horse’s ability to perform at its optimum level irrespective of discipline3,4. Horses with EGUS are known to have a shorter stride length, a decrease in maximum oxygen uptake and to fatigue sooner.
Discontinuous/intermittent feeding remains the most common cause of ESGD, as the horse is biologically a continuous grazer and gastric acid secretor.
“Unused” free acid in the stomach readily splashes onto the squamous mucosa, especially during exercise, causing “acid burn” (Figure 2). This occurs even during walking exercise.
The most common site for gastric ulcers to occur is along the lesser curvature2, which is the lowest point of the squamous mucosa and therefore most susceptible to acid splashing.
To avoid false negative results, the lesser curvature should always be visualised on gastroscopy. This may involve inflating the stomach with air to lift the lesser curvature up out of the gastric fluid.
In addition to the lesser curvature, a routine gastroscopy should also include visualisation of the pyloric region.
Gastric glandular disease and gastric squamous disease may exist independently or coexist in the same horse.
Remember that ponies with Equine Metabolic Syndrome (EMS) on restricted diets are prime candidates to develop EGUS and may benefit from ulcer prevention treatment.
Treatment
It is strongly recommended that all horses be gastroscoped prior to commencing a treatment course and again on completion to assess the effectiveness of any treatment and establish whether a revised treatment/management plan is required.
Once present, ulcers rarely heal by themselves (<10%). Putting a horse out to pasture without treating its ulcers may not result in resolution.
Omeprazole based products remain the most effective treatment for gastric ulceration in the horse. Omeprazole is a proton-pump inhibitor which acts on the gastric parietal cells via the systemic circulation, blocking acid secretion in a dose-dependent manner. Effective dosing and absorption of omeprazole is therefore essential for it to work.
The absorption of omeprazole is greatly reduced by the presence of food in the stomach (especially hay). All omeprazole products should be administered on a relatively empty stomach. Where horses are being fed, the omeprazole should be administered a minimum of 20 min, and preferably 60 min, prior to feeding.
There is a large body of research work and clinical experience showing that the buffered omeprazole paste formulation 370 mg/g given at a dose of 4mg/kg (eg Ulcershield) is the most efficacious, safe and practical once daily treatment. Long term treatment is also known to be safe.
Omeprazole is also available as an enteric-coated microsphere paste (eg Gastropell Daily or Gastropell Forte). Chewing of the microsphere coating may destroy the enteric coating which protects the omeprazole from degradation by gastric acid.
The published maintenance/prevention dose of buffered omeprazole (1mg/kg) is likely to be ineffective in horses subjected to strenuous exercise, frequent competition or high levels of stress.
In these horses prevention of ulcers may require ongoing treatment with either the full treatment dose of buffered omeprazole (4mg/kg) or at least 2mg/kg. The lower maintenance dose of omeprazole may be adequate in preventing ulcers in horses exercised at low intensity or in low stress scenarios.
Two longer term published studies have shown that omeprazole does not significantly affect calcium absorption and bone density in the horse.
Ranitidine is also registered for the treatment of gastric ulcers. Omeprazole is known to be 10x more effective than ranitidine in blocking gastric acid secretion. In addition, ranitidine needs to be given twice, and preferably three times, daily.
Although specific bacteria have not been identified in the aetiology of EGUS, long term treatment with oral antibiotics has been advocated in the treatment of chronic, recalcitrant cases of both ESGD and EGGD by specialists in this field. Presumably chronic ulcer beds can become secondarily infected delaying ulcer resolution.
Esomeprazole is the S-enantiomer of omeprazole (a chiral mix of equal parts of R- and S-). The advantage of esomeprazole in humans remains equivocal. It is not currently known if horses process the R- and Senantiomers differently and any advantages this drug may have over omeprazole have not been established.
Beware non-APVMA approved omeprazole products. They are a recognised cause of “treatment failures”. The pH and solubility of the formulation is critical for the protection and absorption of the omeprazole. These products are seldom formulated correctly nor carry the necessary quality control guarantees.
Beware unsubstantiated claims on nutraceuticals and other supplements. It is advisable to gastroscope horses before commencing a course of treatment with these products and again on completion. Our experience with over 7000 facilitated gastroscopies shows that these products seldom meet their label claims.
Prevention/Management
It is important to keep the time of administration of omeprazole consistent from day-to-day. Ideally omeprazole would be administered first thing in the morning when gastric fluid pH is at its most acidic.
Ideally omeprazole paste should also be administered at least 60 minutes prior to exercise. During exercise the increase in intra-abdominal pressure and reduction in gastric volume is known to cause excessive gastric acid splashing on the vulnerable squamous mucosa.
Horses should always receive a small amount of feed (including roughage) prior to exercise. This feed “balls up” in the stomach effectively acting as a fibre sponge to absorb the free acid and reduce gastric fluid splashing (Figure 5).
Reducing the amount of fermentable starch (ie grain) in the diet will reduce the overall acid burden in the stomach. To meet the horse’s caloric requirements, grain can be replaced by oils. Oils high in Omega-3’s are preferred and should be introduced at a rate of 50mL bid each week until a total of 200mL twice daily is reached.
Measuring gastric pH at the time of gastroscopy is a useful tool for monitoring treatment efficacy, administration compliance and determining causes of perceived treatment failures.
GLANDULAR/PYLORIC LESIONS (EGGD)
• It is essential to attempt to visualise the pylorus in all gastroscopies.
• Glandular/pyloric lesions are usually inflammatory in nature with only the severe cases demonstrating true ulceration.
• Pyloric lesions are more common than glandular lesions and will be detected in approximately 50% of gastroscopies.
• Clinical signs of glandular disease are similar to those of squamous disease. Behavioural changes are the most commonly reported sign.
• Horses that are worked ≥ 5 days per week are tenfold more likely to develop EGGD.
• EGGD lesions tend to be chronic, recalcitrant and difficult to treat. • Long-term treatment (8-12 weeks) is usually required for resolution.
• Treatment recommendations include Omeprazole buffered paste (4mg/kg sd) AND Sucralfate (20mg/kg bd-qd) and/or Misoprostol (2-5μg/kg bd/td) and/or Oral antibiotics
• As sucralfate may inhibit the absorption of omeprazole, it should be administered at least 60 minutes after the omeprazole. It may be administered in the feed or by syringe.
• It is recommended to soften all feeds by soaking or wetting prior to feeding in horses with EGGD.
• It is essential to perform follow up gastroscopies on all horses with EGGD to monitor the efficacy of any treatments.
References:
1. European College of Equine Internal Medicine Consensus Statement—Equine Gastric Ulcer Syndrome in Adult Horses. Sykes, B.W., Hewetson, M., Hepburn, R.J., Luthersson, N. and Tamzali, Y. 2015 Journal of Veterinary Internal Medicine, 29(5), pp.1288-1299. 2. Data on file, Randlab Gastroscoping Service Data 2014-2019. 3. Poor performance associated with Equine Gastric Ulceration Syndrome in four Thoroughbred racehorses. Franklin, S.H., Brazil, T.J. and Allen, K.J., 2008. Equine Veterinary Education, 20(3), pp.119-124. 4. Effect of gastric ulceration on physiologic responses to exercise in horses. Nieto JE, Snyder JR, Vatistas NJ, Jones JH. Am J Vet Res 2009;70:787–795.
