30 May 2016
Emily Haggett summarises diagnosis and possible treatment and prevention options for equine stomach ulcers – a common problem for the performance horse industry.
Figure 3. Gastroscopy is the only reliable way to diagnose equine gastric ulcer syndrome.
Equine gastric ulcer syndrome (EGUS) is a major concern for the performance horse industry and a high prevalence exists in horses competing in a variety of disciplines.
This has implications not only for performance, but also equine welfare. Drug withdrawal times must also be considered when treating equine athletes.
This article summarises the pathophysiology, prevalence, performance implications and treatment strategies for EGUS.
The equine stomach consists of two distinct types of gastric mucosa – squamous and glandular. Therefore, diseases of the stomach can be split into two distinct syndromes – equine squamous gastric disease (ESGD) and equine glandular gastric disease (EGGD).
Regular squamous mucosa has relatively little exposure to acid due to the presence of a fibre mat in the stomach that helps buffer acid produced in the ventral portion. Ulceration of squamous mucosa occurs when there is increased contact with acid, in both a time and dose-dependent fashion. Hydrochloric acid and volatile fatty acids can both contribute to injury.
High-concentrate diets can lead to bacterial fermentation of sugars with increased production of volatile fatty acids and lactic acid, which can exacerbate injury to the squamous mucosa.
Exercise and training are major risk factors for squamous ulcer disease. Intra-abdominal pressure increases with exercise, which has the effect of pushing the ventral acid gastric contents to the squamous mucosa. This is potentiated when the stomach is empty prior to exercise. Increased severity of gastric ulceration is often seen with an increased duration or intensity of exercise.
Nutritional risk factors are also very important in the development of squamous ulceration. Full-time access to turnout or long stem forage is thought to be protective for squamous ulceration. However, evidence to support this is slightly inconclusive and it is possible other risk factors play a more important role in the development of ulceration.
Full-time pasture turnout is frequently not an option for many types of performance horses. Forage type is also important. Starvation or fasting is strongly associated with the development of ESGD and periods without food due to stress or travel play a major role in the development of ulceration.
Large amounts of high concentrate feed are also a major risk factor. A diet containing more than 2g/kg of body-weight per day has been shown to be associated with an increased prevalence of gastric ulceration. Similarly, feeding high concentrate feeds prior to forage or exercise has been shown to increase the risk of ESGD. Many performance horses have a high-energy requirement and this often creates management pressure to feed a high-concentrate diet.
Stress is often implicated in the development of ESGD. Studies have shown ulcers can be induced by management changes, such as long distance transport or moving to a training yard (McClure et al, 2005).
The pathophysiology of glandular ulceration is less understood. Exposure to acid is not a major trigger factor, as the glandular mucosa normally exists in an acid environment. Other factors thought to play a role include reduced mucosal blood flow, reduced local production of mucus or bicarbonate. However, the underlying mechanisms for these factors are not understood. Exercise may have a role in reducing mucosal blood flow.
NSAIDs are frequently implicated in the development of EGGD. This is related to their mechanism that reduces prostaglandin production, which is protective for normal mucosal blood flow. However, NSAID use is only a factor in the minority of horses with EGGD.
The role of bacteria in the syndrome is also unclear. Bacterial overgrowth or “gastritis” can be identified in many horses with EGGD, but it is unclear whether these represent primary pathogens or secondary invaders. No clear evidence exists to suggest a primary Helicobacter-like pathogen in the horse.
A high prevalence of EGUS exists in performance horses from many disciplines. Published studies suggest 80% to 100% of Thoroughbred racehorses in training have ESGD (Sykes et al, 2015a; Figure 1). The prevalence is similar in standardbred racehorses and in sports horses is thought to be around 30% to 50%, and up to 93% of endurance horses in full competition have ESGD.
Fewer studies evaluate the prevalence of EGGD (Sykes et al, 2015a). However, published studies suggest around 60% of Thoroughbred racehorses, 30% of endurance horses and 50% of sports horses have EGGD.
The clinical signs associated with EGUS are often vague. It is common for ulcers to be identified in horses without any external clinical signs of disease. Reported clinical signs include reduced appetite, weight loss, poor coat quality, behavioural change, bruxism, reduced performance and colic (Figure 2).
In the author’s experience, reduced appetite and weight loss are more likely to be associated with severe squamous ulceration and colic associated with severe glandular ulceration. Clinical signs, such as sensitivity over flanks or “girthiness”, are commonly reported for EGUS. However, published evidence to support these signs is lacking and the prevalence in horses presenting with only these symptoms is probably low.
The exact effect of EGUS on equine performance is not known. Many horses with severe gastric ulcers will still perform to a high level. Pain and discomfort from ulceration is suspected to be the major underlying factor for reduced performance. However, individual horse susceptibility is probably extremely important.
Treadmill studies have shown horses with ESGD have a reduced time to fatigue, stride length and maximal oxygen consumption compared to horses without ulcers (Nieto et al, 2009). The presence of ESGD has also been shown to be associated with decreased performance in Thoroughbred racehorses. However, it is important evaluation for gastric ulcers is undertaken in conjunction with investigations of other causes of poor performance, as many factors can play a role.
Reliable diagnosis can only be made by gastroscopy (Figure 3) examination. This simple procedure can be rapidly performed in a lightly sedated horse. A minimum period of 8 hours to 12 hours of fasting is needed prior to examination.
Gastroscopy allows full evaluation of both the squamous and glandular mucosa, including an assessment of ulcer grade, location and severity. A score should be given using the Equine Gastric Ulcer Council system (Table 1; Figures 4 and 5). The use of this is not validated for glandular lesions and a European College of Equine Internal Medicine consensus statement has recommended a description based on epithelial appearance (hyperaemic, haemorrhagic, fibrinosuppurative and ulcerated) and mucosal contour (depressed, flat and raised).
Proxy tests, such as measurement of faecal albumin or haemoglobin, are not reliable predictors of EGUS.
Treatment of EGUS must be tailored to the type of ulceration and the individual horse. Medication should be used to treat active lesions and management practices should be used to prevent recurrence. This is not possible in all cases and, for some horses, maintenance therapy may be necessary. Withdrawal times should be considered when using medication.
Omeprazole is a proton pump inhibitor that suppresses acid production. It is generally considered as the first line of treatment for ESGD. The formulation of the product is essential for its efficacy and must be administered in a formulation that allows the product to avoid acid degradation in the stomach and be absorbed in the small intestine.
An original product was patented for the treatment of the syndrome and, since the patent’s expiration, a wider range of commercial preparations have become available. These products are backed by less scientific data, but are thought to be effective.
Original studies suggested a dose of 4mg/kg orally once daily for the treatment of ESGD (Sykes et al, 2015a). Omeprazole is a highly effective drug and this dosing regime reliably results in about 75% ulcer resolution. Studies have suggested a lower dose of 1mg/kg orally once daily may be equally effective (Sykes et al, 2015b). Whichever dose is used, it is important follow-up gastroscopy examination, usually after three weeks to four weeks of treatment, is used to ensure treatment efficacy.
The administration of omeprazole is allowed under Fédération Equestre Internationale (FEI) rules, but a 72-hour drug withdrawal time is recommended by the British Horseracing Authority when given at 1mg/kg once daily for 28 days.
Histamine receptor antagonists, such as cimetidine and ranitidine, can also be used to suppress acid production. However, they are less effective than omeprazole.
Treatment for EGGD is more controversial. Treatment with omeprazole at 4mg/kg as a sole therapy is reported to only resolve 25% of glandular lesions. Sucralfate can also be used to treat EGGD at a dose of 12mg/kg to 20mg/kg orally, two times to four times daily. This medication is thought to adhere to ulcerated mucosa and encourage prostaglandin secretion, mucosal blood flow and bicarbonate production. The European College of Equine Internal Medicine (ECEIM) consensus statement recommends a combination of omeprazole and sucralfate as a first line EGGD therapy. This medication has no reported withdrawal time and is not on the FEI prohibited substance list.
Resolution of EGGD usually takes longer than the resolution of squamous ulcer disease and treatment for six weeks to eight weeks is commonly required. The use of antimicrobials, such as trimethoprim sulfadiazine, has been proposed to treat any bacterial component of EGGD. However, clinical evidence to support its use is lacking. Antimicrobials should, therefore, not be used as first line therapy.
Misoprostol is a prostaglandin analogue proposed for the treatment of EGGD with the aim of improving mucosal blood flow. This medication can be used at a dose of 2mcg/kg to 5mcg/kg orally two times or three times daily. More evidence is needed to evaluate whether this medication is more or less effective than a combination of omeprazole and sucralfate.
Nutritional management is essential in the prevention of ulceration. Pasture turnout should be considered, if feasible.
Frequent access to high-quality forage should be provided as an alternative. A minimum of 1.5% of bodyweight in hay should be provided daily in frequent meals to try to maximise time spent eating. Concentrate feeds should be fed to the minimal volume required to maintain energy intake. They should be split into frequent small feeds to minimise the volume of acid and volatile fatty acids produced. High starch feeds should be replaced with feeds designed to release energy more slowly.
Concentrate feeds with a higher fat content can be used to provide additional energy. In addition, supplementation with vegetable oil – 100ml to 400ml split between meals on a daily basis – may help treat or prevent EGGD.
Avoiding exercise prior to feeding is essential in the prevention of ESGD. Provision of forage or a small amount of alfalfa prior to exercise should help buffer acid stomach contents and reduce splash injury.
Prevention of stress is difficult, but changes in routine and management should be minimised as much as possible. For example, avoiding changes in pasture companions/adjacent stable companions can be helpful. The individual horse’s personality needs to be considered when planning travel to and from competitions to try to minimise disruptions to normal routine.
A wide variety of supplements marketed to prevent EGUS are available. Some evidence suggests products containing a combination of pectin-lecithin complexes, antacids and Saccharomyces cerevisiae may help in prevention, but further research is required. A sea buckthorn extract has also been shown in one model to help prevent EGGD. However, good dietary management should be considered the mainstay of prevention.
If risk factors cannot be controlled, ongoing treatment with omeprazole at 1mg/kg daily dose may need to be considered to prevent ulcers in specific individuals.
EGUS is a common problem in performance horses. Identification and treatment of affected horses is important to improve welfare and maximise performance potential.
Medication can be used to treat active lesions, but prevention should focus on good management and nutrition.