Gastric ulcers in racehorses – what trainers should know
/Article by Dr Michael Hewetson
Why are gastric ulcers so important in racehorses?
Gastric ulcers are very prevalent in racehorses, with between 52% and 93% of horses in active training affected. This is significant, because gastric ulcers can impact both the horse's performance and its overall health and welfare, which in turn can have financial and competitive implications for their owners, trainers, and the racing industry as a whole.
Gastric ulcers can affect a horse's performance by causing abdominal discomfort and reduced appetite. This can lead to changes in stride length and decreased energy levels that may impact their racing performance. Horses with gastric ulcers may also exhibit changes in behaviour, such as nervousness, aggression, or reluctance to train or race, which again, can affect their overall performance and temperament. If left untreated, gastric ulcers can lead to more serious health concerns such as colic, potentially requiring costly medical intervention and downtime for the horse. But most importantly, gastric ulcers are a welfare issue for the Thoroughbred racing industry, and with growing public scrutiny on the industry, ensuring the well-being of racehorses is a priority, and addressing gastric ulcers promptly should be considered part of responsible horse management. This requires a close working relationship with your vet, who will be able to give you expert advice about diagnosis, treatment, and management of this frustrating disease.
Understanding gastric ulcers
FIGURE 1
Equine gastric ulcer syndrome (EGUS) is a general term used to describe erosions and ulcers of the horse’s stomach and is similar to the term peptic ulcer disease in people. Unlike people however, the horse is unique in that the stomach lining (mucosa) is divided into an upper squamous and a lower glandular portion (figure 1); and it is important to realise that there are differences between these two regions with respect to how these lesions develop, their prevalence, associated risk factors and response to treatment. Therefore, when referring to EGUS, your vet may use the terms Equine Squamous Gastric Disease (ESGD) and Equine Glandular Gastric Disease (EGGD) to clearly distinguish the anatomical region of the stomach affected.
FIGURE 2
There does not appear to be a clear relationship between the presence of squamous disease and glandular disease, and the fact that both conditions may occur concurrently in the same horse does not indicate that they are associated. In the case of squamous disease, the cause of the ulcers is well understood, with a variety of managemental risk factors (e.g. increase in exercise intensity, low roughage/high starch diet, stall confinement) contributing to an increase in the exposure of the squamous mucosa to acid. The squamous mucosa is not normally exposed to acid. As such it is inherently susceptible to acid injury, and with prolonged acid exposure, ulcers may develop (figure 2).
FIGURE 3
In contrast to squamous disease, the cause of glandular disease is poorly understood. The glandular mucosa is fundamentally different from the squamous mucosa in that it is exposed to a highly acidic environment under normal physiological conditions. As such, it is only when there is a breakdown of the normal defence mechanisms that protect the glandular mucosa from acidic gastric contents that glandular disease occurs. While ulcers are most commonly seen with squamous disease, horses with glandular disease rarely present with ulcers. Rather, the lesions are more consistent with an erosive inflammatory gastritis and can vary widely in their appearance (figure 3). There is a now evidence to suggest that stress, both psychological (e.g. multiple riders or caretakers; confinement; stress associated with transport and competition) and physiological (e.g. increases in the total amount and frequency of exercise without adequate rest periods) may increase the risk of glandular disease in horses. This may be due to a variety of mechanisms including a reduction in the mucus coating and blood supply to the glandular mucosa; both of which compromise the gastric barrier, resulting in acid injury.
The prevalence of gastric ulcers appears to vary with age, use, stage of training, as well as the region of the stomach affected. The prevalence of squamous disease is consistently highest in performance horses, with 52-93% of Thoroughbred racehorses found to be affected. The prevalence of glandular disease is less well reported, however up to 47% of Thoroughbred racehorses may be affected.
Why are racehorses so susceptible to gastric ulcers?
It is most likely because of their unique management when compared to most other horse populations; and the intensity of exercise that is inherent of racing competition. For example, it has been shown that the risk of squamous disease increases with an increase in the intensity of exercise and the duration of time at work. Strenuous exercise causes an increase in intra abdominal pressure associated with contraction of the abdominal muscles1. This results in compression of the stomach, and exposure of the sensitive squamous mucosa to acidic gastric content (acid splash). Strenuous exercise has also been shown to cause an increase in a hormone called gastrin, which stimulates acid production in the stomach.
Several factors associated with management have also been shown to increase the risk of squamous disease, many of which are imposed on racehorses at the commencement of training or during racing competition. These include a high starch/low roughage diet, intermittent fasting, stall confinement, transport, intermittent access to water and administration of hypertonic solutions of electrolytes. In fact, exposure to a combination of a high starch diet, stall confinement and strenuous exercise has been shown to induce ulcers in as little as 7 days; and intermittent fasting is so effective at inducing ulcers that it is used as a model for squamous disease in experimental studies. Thoroughbred racehorses are also exposed to many of the risk factors for glandular disease, most notably, multiple riders or caretakers; confinement; and stress associated with transport and competition.
How do you know if your horse has gastric ulcers and how might they affect performance?
A variety of clinical signs may suggest that a horse has gastric ulcers, however there is currently very little evidence to support a direct association between any of these signs and the presence or absence of ulcers seen on gastroscopy. This is likely because most of the clinical signs are non-specific and are often very subjective. This is complicated further by the fact that horses with gastric ulcers may not demonstrate clinical signs and if they do, the signs do not necessarily correlate with the severity of the lesions seen on gastroscopy. Clinical signs suggestive of gastric ulcers should therefore always be interpreted with caution, and most importantly, gastroscopy should always be performed to confirm the disease (figure 4).
In racehorses, gastric ulcers have been associated with poor appetite, poor body condition, changes in behaviour (including an aggressive or nervous attitude), post prandial colic, stereotypic behaviour and resentment of girthing. Any one of these clinical signs can potentially have an indirect effect on performance (for example, through reduced appetite or interruption in training), but the big question is if gastric ulcers themselves, in the absence of other clinical signs, have an effect on performance. Despite the fact that it is a well entrenched ’fact’ amongst trainers that gastric ulcers have a direct effect on poor performance or reluctance to train, there is surprisingly little evidence in the literature to back this up. This may be in part due to the difficulties in excluding the many confounding factors that might influence poor performance (e.g. lameness, respiratory disease etc.).
The mechanism by which gastric ulcers may affect performance has not been identified but is likely to be related to epigastric pain. In people, epigastric pain is defined as pain localised to an area below the sternum and above the umbilicus and is common in athletes with gastro-oesophageal reflux disease (GERD). Acid reflux onto the sensitive squamous mucosa of the oesophagus during exercise causes a “burning sensation” that gets worse with increasing exercise intensity and has been shown to affect performance. Horses with squamous gastric disease have similar lesions to those causing GERD in human athletes, and the problem is likely to be exacerbated by the fact that the squamous mucosa extends from the oesophagus into the upper one-third of the stomach and is not protected by an oesophageal sphincter. Interestingly, a recent study in human athletes suggested that GERD may be associated with increased abdominal pressure during exercise, a mechanism that I have already alluded to in the equine athlete. How exactly epigastric pain impacts on athletic performance in the horse is a matter of ongoing speculation. One theory is that it may affect stride length. It has been shown that horses with gastric ulcers have a reduced stride length when galloping, likely due to abdominal discomfort. Stride length and lung ventilation are mechanically coupled in the galloping horse, and therefore, reduced stride length will result in decreased oxygen uptake, thus limiting aerobic capacity during peak exercise.
How are gastric ulcers treated and what can you do to prevent them?
Let’s turn our attention now to the treatment of gastric ulcers. Because there is currently little evidence to suggest an association between clinical signs and the presence or severity of gastric ulcers, treatment should always be based on gastroscopic evidence of ulcers. Some trainers may still choose to commence treatment based entirely on clinic signs without gastroscopy and assess for a clinical response. I would caution against this approach, as it can be costly if the horse does not have ulcers, and gastroscopy is still going to be necessary to conclusively rule out gastric ulcers if clinical improvement is not seen with treatment.
Treatment of gastric ulcers will vary depending upon the severity and the location of the ulcers and your vet will be able to give you advice on the best approach. In most cases treatment consists of management and dietary modification in conjunction with the use of proton pump inhibitors which suppress acid production. Oral omeprazole is the drug of choice and is currently the only licensed drug for the treatment and prevention of gastric ulcers in horses in the UK and Ireland.
Administering oral omeprazole on an empty stomach can improve the bioavailability of the drug. This can be achieved practically by administering it first thing in the morning at least 1 hour prior to feeding. This ensures the stomach will be empty as horses eat very little during the night even if they have access to forage.
The duration of treatment will depend on the location of the lesions, with squamous disease tending to heal faster than glandular disease. In most cases, your vet will prescribe oral omeprazole for 3-4 weeks and then the requirement for additional medication will be determined following a repeat gastroscopy. In the case of glandular disease, oral omeprazole is often combined with sucralfate, which adheres to the damaged mucosa, providing a physical barrier while also stimulating mucus secretion, both of which reduce potential exposure to acid. Omeprazole is a controlled drug, and therefore needs to be withdrawn prior to competition. The BHA published detection time for oral omeprazole is ≤ 48hrs, so withdrawal of the drug 3-5 days before competition would be prudent. There is, however, some concern that the requirement for withdrawal times might influence the efficacy of oral omeprazole treatment in racehorses. Many vets report reoccurrence of squamous disease following discontinuation of treatment with omeprazole, often within as little as 3 days, and this was demonstrated in a recent study comparing withholding periods for oral omeprazole treatments in racing Thoroughbreds6. The authors reported a squamous disease prevalence of 83% in horses after a “2 clear days'' recommended withholding period for oral omeprazole, which was an increase from 25% of horses with squamous disease before the recommended withholding period, and they theorised that ‘rebound acid secretion’ may be implicated. This phenomenon occurs following the discontinuation of proton pump inhibitor drugs such as oral omeprazole, and is linked to a loss of negative feedback from gastric acid during treatment that causes an increased secretion of the hormone gastrin that can persist for up to 2-4 days after the last dose of omeprazole has been administered. This results in a short period of increased gastric acid production when treatment is stopped. Whilst nothing can currently be done about the required withdrawal periods during racing, strict management practices should be implemented for the 2-4 days following cessation of omeprazole treatment to mitigate against development of squamous gastric disease. This could include ensuring provision of adequate roughage during this time, avoiding fasting or withholding water, and perhaps limiting exercise or transport if possible.
Additional management and dietary adaptations which may help prevent gastric ulcers and can be implemented longer term in a racing yard include free choice access to roughage (and if not, ensuring that roughage is provided at intervals of no more than 4-6 hours); turn out into a paddock with good quality grazing where possible; a low starch/high fat diet (or alternatively, smaller concentrate meals more frequently); reduction/avoidance of any potential stressors; and provision of regular rest days. Where possible, training schedules should be adjusted so that they occur later in the day when enough roughage has been consumed to ensure that there is a mat of roughage in the stomach to buffer acid in the upper squamous portion and to reduce acid splash during exercise. Alternatively, a handful of palatable chaff should be fed 20 minutes prior to exercise.
Numerous supplements are marketed for prevention of gastric ulcers, however there is currently very limited evidence to support their use.
References
Lorenzo-Figueras M, Merritt AM. Effects of exercise on gastric volume and pH in the proximal portion of the stomach of horses. Am J Vet Res. 2002;63(11):1481–1487.
Vatistas NJ, Sifferman RL, Holste J, et al. Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl. 1999;29:40–44.
Murray MJ, Eichorn ES. 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. Am J Vet Res. 1996;57(11):1599–1603.
Herregods TV, van Hoeij FB, Oors JM, Bredenoord AJ, Smout AJ. Effect of running on gastroesophageal reflux and reflux mechanisms. Am J Gastroenterol. 2016;111(7):940–946. doi:10.1038/ajg.2016.122
Nieto JE, Snyder JR, Vatistas NJ, Jones JH. Effect of gastric ulceration on physiologic responses to exercise in horses. Am J Vet Res. 2009;70(6):787–795.
Shan R, Steel CM, Sykes B. The Impact of Two Recommended Withholding Periods for Omeprazole and the Use of a Nutraceutical Supplement on Recurrence of Equine Gastric Ulcer Syndrome in Thoroughbred Racehorses. Animals. 2023; 13(11):1823.
Clark B, Steel C, Vokes J, Shan JR, Gedye K, Lovett A, Sykes BW. Evaluation of the effects of medium-term (57-day) omeprazole administration and of omeprazole discontinuation on serum gastrin and serum chromogranin A concentrations in the horse. J Vet Intern Med. 2023 Jul-Aug;37(4):1537-1543.