European College of Equine Internal Medicine Consensus Statement - Equine Gastric Ulcer Syndrome in Adult Horses

The term Equine Gastric Ulcer Syndrome (EGUS) was first used in 1999 to describe gastric ulceration in horses. It is an all encompassing term to describe erosive and ulcerative diseases of the equine stomach lining. The equine stomach consists of two distinct regions; the squamous mucosa at the top and the glandular mucosa at the bottom. Both regions can be effected by ulceration. The disease process and treatment varies according to the location of gastric ulcers and so the terms Equine Squamous Gastric Disease (ESGD) and Equine Glandular Gastric Disease (EGGD) are used to more accurately describe the condition.

The highest prevalence of squamous ulceration (ESGD) occurs in thoroughbred racehorses with 37% of horses out of training and 66-93% of horses in training being effected. 

Horses that are rarely competed and are predominantly used in their home environment have the lowest prevalence of ESGD at 11%.

Epidemiological studies reveal that Thoroughbreds are predisposed to Equine Squamous Gastric Disease and that intensity and duration of exercise outweigh any age or sex predispositions.

There are surprisingly few large scale epidemiological studies that have investigated other risk factors for equine gastric ulcer syndrome. Of those available, significant associations have been shown between

  • individual trainer,
  • a metropolitan yard location (horses trained in an urban are were 3.9 times more likely to have gastric ulcers)
  • lack of direct contact with other horses
  • solid barriers between horses instead of bars
  • talk radio instead of music.
  • feeding straw
  • lack of access to water

Nutritional Risk Factors:

Although pasture turnout is considered to reduce the risk of equine gastric ulcer syndrome, the scientific evidence supporting this belief is conflicting, suggesting that pasture turnout on its own might not affect gastric pH per se. Similarly, while free access to fibrous feed or frequent forage feeding is widely considered to reduce the risk of gastric ulceration, in the presence of other risk factors the protective impact of feeding roughage might not be as great as previously believed.

Excessive grain intake, intermittent access to water and intermittent fasting  are all associated with increased risk of equine gastric ulcer syndrome.

Increased grain intake has been associated  with an increased risk of Equine Squamous Gastric Disease in animals working at various levels of intensity in a number of studies. There is a marked increase in ulceration when non exercising animals are stabled and fed grain at 1% of body weight an hour before hay is fed. Similarily, exceeding 2 g/kg of bodyweight of starch intake per day is associated with an approximate 2-fold increase in the likelihood of  the severity of Equine Squamous Gastric Disease. (Equine Squamous Gastric Disease developed in all horses within 14 days of their removal from pasture, stabling and entering a simulated training regimen whilst being fed a 6kg concentrate feed per day).

Intermittent access to water increases the risk of Equine Gastric Ulcer Syndrome (EGUS). It has been shown that horses without access to water in their paddocks are more than 2.5 times more likely to have EGUS compared to horse with free water access in their paddocks.

Fasting is also a well described risk factor for ESGD and intermittent starvation causes and increases the severity of Equine Squamous Gastric Disease.

Clinical Signs:

Reported clinical signs include poor appetite or picky eating, poor body condition, bruxism, behavioural changes (including a nervous or aggressive disposition) acute or recurrent colic and poor performance. There is little statistical evidence linking diarrhoea and poor coat condition to Equine Gastric Ulcer Syndrome. 

The potential for Equine Gastric Ulcer Syndrome to cause poor performance is of particular importance yet to date there have been few studies to investigate the potential relationship between poor performance and Equine Gastric Ulcer Syndrome. It has been porposed that poor performance may be a direct consequence of gastric pain. Human athletes with gastric ulcers and reflux report that the intensity of the pain associated with such conditions increases in line with the intensity of their training. Additionaly, such athletes reach levels of exhaustion more easily compared to athletes without reflux. Untreated horses with Equine Squamous Gastric Disease subjected to an incremental treadmill study exhibited reduced time to fatigue, lower maximal oxygen uptake and reduced stride length. The authors of this particular study postulated that abdominal pain was affecting stride length and ventilation.


The committee consider that gastroscopy is the only reliable method for definitively identifying gastric ulceration in a live horse.  There is no reliable relationship between Equine Squamous Gastric Disease and Equine Glandular Gastric Disease, and so the presence or absence of one cannot be used as a predictor for the presence or absence of the other. This necessitates a thorough examination of the entire (fasted) stomach. There are currently no reliable blood tests (haematological or biochemical) or faecal tests available to aid the diagnosis of gastric ulcers.

Where gastric ulcers are are identified on gastroscopy, it is important that these lesions are properly graded such that a response to treatment can be quantified. It is important to note that some patients will not show resolution of clinical signs until complete healing of lesions has occurred. This further highlights the importance of repeat gastroscopy in the management of equine gastric ulcer disease. Treatment trials (i.e. assessing response to treatment in the absence of diagnostic testing) are common where gastroscopy is not available. However, given the cost of treatment, the importance of distinguishing between squamous and glandular disease, the need for ongoing monitoring and the fact that the failure of a horse to respond to treatment does not rule out gastric disease, the initiation of treatment without gastroscopy is not recommended.


A variety of management factors contribute to the development of Equine Squamous Gastric Disease. All of these factors share the common trait that they increase the exposure of the squamous mucosa of the stomach to acid. Excessive exposure of the squamous mucosa to stomach acid occurs when the acidic gastric content is pushed upwards by the increased intra-abdominal pressure associated with gaits faster than a walk.

In contrast, the pathophysiology of Equine Glandular Gastric Disease is poorly understood but is believed to result from a breakdown of the normal defence mechanisms that protect the mucosa from the acidic gastric contents. In humans non steroidal anti-inflammatory drugs (NSAIDs) and Helicobacter pylori are implicated. In horses, bacteria appears to play only a minimal role as acid suppressants are quite effective even where bacteria are present and NSAIDs (e.g. phenylbutazone and meloxicam) at therapeutic levels have failed to induce Equine Glandular Gastric Disease even when administered for 15 consecutive days.

Treatment of Equine Gastric Ulcer Syndrome (EGUS):

Acid suppression is considered the cornerstone of gastric ulcer management. Omeperazole remains the drug of choice in the treatment of EGUS.  It acts to irreversibly impair the secretion of acid, with new acid secreting units needing to be made by the body before acid production can resume.

Omeperazole is administered via the mouth and a variety of  factors including formulation, dose rate and duration of treatment influence treatment outcomes. The omeperazole needs to be in a protected formulation to prevent degradation in the the acidic stomach. Enteric coated granule formulations like Gastrozol and buffered formulations like GastroGard have similar efficacy and bioavailability and  are currently used at 4mg/kg once daily. Regardless of formulation or dose used only  70-80% of Equine Squamous Gastric Disease lesions will heal within a 28 day period and so repeat gastroscopy is recommended before cessation of treatment to ensure complete healing has occurred.

Ranitidine could also be considered at 6mg/kg where omeperazole is not available or has been shown to be innefective.

Until recently treatment recommendation for equine gastric ulcer syndrome had not differentiated between glandular and squamous disease. However, in recent studies only 25% of glandular lesions (EGGD) had healed within 28-35 days of omeperazole treatment compared to 78% of squamous lesions (ESGD). More work needs to be done to look at adjunctive therapies and duration of intra day acid suppression. The authors therefor recommended the addition of an additional drug, sucralfate at 12mg/kg given orally twice daily. The two drugs may need to be given concurrently for 8 weeks.


  • In addition to the management of risk factors as outlined above omeperazole in either the enteric coated or buffered formulation is used at 1mg/kg for the prevention of EGUS.
  • Continuous access to good quality grass pasture, free choice for at least 4-6 meals/day of hay when the horse is stabled. Horse should receive a minimum of 1.5kg of (DM)/100kg bodyweight per day.
  • Overweight horse and ponies should receive a minimum amount of high quality forage (1.5kg of DM/100kg bodyweight per day) that is mature and has a low energy content. If low energy forage is not available then a mixture of high quality hay and straw divided into a minimum of 4 feedings  can be substituted. Straw should not be the only forage provided but can be safely included in the ration at 0.25kg (DM)/100kg of bodyweight.
  • Horses should be fed grain and concentrates as sparingly as possible
  • The diet should not exceed 2g/kg bodyweight of starch per meal
  • Concentrate meals should not be fed less than 6 hours apart.
  • Water should be provided continuously
  • An increased risk of ESGD has been shown with electrolyte pastes and  hypertonic solutions given PO (by mouth) so electrolytes should be mixed in with the feed or given in lower doses in water.