ISSN 2398-2977      

Stomach: gastric ulceration - foal


Synonym(s): GDU, Equine gastric ulceration syndrome (EGUS


  • Equine gastric ulcer syndrome (EGUS) is a multifactorial condition which can affect foals and horses   Stomach: gastric ulceration   of all ages. Foals may also develop associated ulceration of the esophagus or duodenum.
  • Causes: multifactorial but essentially due to acid insult to gastric mucosal surface.
  • Signs: assymptomatic or one or more of the following:
    • Bruxism.
    • Reduced appetite.
    • Weight loss.
    • Dullness.
    • Dorsal recumbency.
    • Ptylaism usually due to concurrent esophagitis.
    • Shock and death (if perforation occurs).
    • Diarrhea.
  • Diagnosis: clinical signs aid diagnosis but definitive diagnosis requires gastric endoscopy.
  • Treatment: anti-ulcer medication, removal of causative agents.
  • Prognosis: generally good depending on severity of lesions.



  • Complex etiology but basically ulcers occur when mucosal protective factors are overwhelmed by acid insult (mucosal aggressive factors).
  • Foals develop ability for gastric acidification at very early age and development of mucosal defence mechanisms parallels this.
  • Stomach has two different types of mucosal surface: 
    • Squamous epithelium over dorsal portion to greater curvature which has no secretory or absorptive function.
    • Glandular mucosa covering rest has both secretory and absorptive function.
    • Separated bymargo plicatus.
  • Aggressive factors include hydrochloric acid from parietal cells, pepsin (pepsinogen from chief cells is converted to pepsin which can be proteolytic against gastric mucosa), bile acids and organic acids from digestion of food material).
  • Acid secretion stimulated by histamine (main stimulus), vagal stimulation, gastrin and acetylcholine.
  • Protective factors include bicarbonate-rich mucus layer overlying the gastric glandular mucosa which buffers gastric acids, mucosal blood flow, high rate of replacement of damaged mucosal cells by cells in gastric pits, prostaglandins, especially PGE2, epidermal growth factor (stimulates growth of gastrointestinal mucosa) and gastroduodenal motility which facilitates removal of acidic contents from stomach and proximal duodenum.
  • Severe squamous mucosal ulceration is due mainly to excessive acid exposure as this area does not have the protective bicarbonate layer.
  • Glandular mucosal ulceration has more complex etiopathogenesis. Impairment of mucosal protective layer and/or mucosal blood supply, etc, allows H+ ions to enter deeper epithelial cells   →   their death.

Predisposing factors

  • Concurrent disease. 
  • When a foal is suckling milk gastric pH increases significantly.
  • When foal is unwell or recumbent and frequency of sucking decreases or ceases, gastric pH decreases.
  • Stress is implicated by extension from human situation due to potential effects on mucosal blood flow, etc.


  • Administration of NSAIDs   Therapeutics: anti-inflammatory drugs  has been shown to be associated with increased incidence and severity of gastric glandular and squamous ulceration. The mechanism of this association is considered to be interference with prostaglandin synthesis, especially PGE2 which inhibits gastric acid secretion.
  • Rotavirus   Rotavirus  infection also appears to be associated with higher incidence of ulceration. Rotavirus attacks intestinal villous cells and it is possible that some damage occurs to stomach which allows acid attack.
  • Conditions which delay gastric emptying.
  • Intensive medical treatment.


  • Most gastric ulcers in foals are located in the squamous mucosa.
  • In most foals, lesions in the squamous mucosa adjacent to themargo plicatusalong the greater curvature resolve without treatment.
  • In some foals, lesions may coalesce - squamous mucosal lesions which are moderate to severe may be associated with diarrhea   Diarrhea: neonate  .
  • Lesions in the glandular mucosa can develop rapidly and cause abdominal pain   Abdomen: pain - neonate  or loss of appetite.
  • Lesions are seen more commonly in the glandular mucosa in stressed foals.
  • Severe lesions associated with abdominal discomfort   Abdomen: pain - neonate  . 
  • Damage adjacent to pylorus or in proximal duodenum can result in obstruction to gastric outflow and increased exposure of gastric mucosa to acidic gastric fluid. 
  • Severe ulcer formation can result in blood and protein loss into GIT.
  • Deep duodenal lesions are at risk of perforation with development of fibrinous peritonitis, shock and death. If lesions do not perforate, scarring and stricture can follow causing colic symptoms.
  • Reflux esophagitis may result in ptyalism and can cause esophageal stricture.


  • Variable.
  • Spontaneous healing of asymptomatic ulcers can occur within 14 days.
  • Ulcers can form very quickly, within 24 h of acid insult to mucosa.
  • Mild signs can progress over hours or days to become severe even if treatment instigated as lesions are often severe before clinical signs apparent.
  • Lesions typically heal in 2-5 weeks.


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Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • O'Connor M S, Steiner J M, Roussel A J et al (2004) Evaluation of urine sucrose concentration for detection of gastric ulcers in horses. Am J Vet Res 65 (1), 31-39 PubMed.
  • Lewis S (2003) Gastric ulceration in an equine neonate. Can Vet J 44 (5), 420-421 PubMed.
  • Andrews F M, Reinemeyer C R, McCracken M D et al (2002) Comparison of endoscopic, necropsy and histology scoring of equine gastric ulcers. Equine Vet J 34 (5), 475-478 PubMed.
  • Murray M J (1999) Gastroduodenal ulceration in foals. Equine Vet Educ 11 (4), 199-207 VetMedResource.
  • Murray M J (1999) Pathophysiology of peptic disorders in foals and horses: a review. Equine Vet Suppl 29, 14-18 PubMed.
  • Borrow H A (1993) Duodenal perforations and gastric ulcers in foals. Vet Rec 132, 297-299 PubMed.
  • Furr M O, Murray M J & Ferguson D C (1992) The effects of stress on gastric ulceration, T3, T4, reverse T3 and cortisol in neonatal foals. Equine Vet J 24 (1), 37-40 PubMed.
  • Murray M J (1992) Aetiopathogenesis and treatment of peptic ulcer in the horse: a comparative review. Equine Vet J Suppl 13, 63-74 VetMedResource.
  • Murray M J, Murray C M, Sweeney H J et al (1990) Prevalence of gastric lesions in foals without signs of gastric disease: an endoscopic survey. Equine Vet J 22 (1), 6-8 PubMed.

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