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Basics ⬇

Outline

BASICS

Definition!!navigator!!

Gastric ulcers are defects in the gastric mucosa that extend into the muscularis mucosa. Erosions are less severe and do not extend into the muscularis mucosa. Ulcers and/or erosions in the glandular mucosa of the stomach are referred to as EGGD. Lesions affecting the squamous portion of the equine stomach are referred to as ESGD.

Pathophysiology!!navigator!!

  • The proximal third of the equine stomach or nonglandular region is covered by stratified squamous epithelium and has no mucous or bicarbonate layer to protect it against acid-induced injury
  • Primary ESGD is common in horses in training and racing, probably because of an increased exposure of the nonglandular region to acidic gastric contents during exercise. It is also possible that diets high in fermentable carbohydrates cause production of short-chain fatty acids by resident bacteria acting synergistically with HCl in destruction of the squamous epithelium
  • Secondary ESGD develops in animals with delayed gastric emptying due to gastric ulceration, pyloric stenosis, equine dysautonomia, ileus, gastric impaction, and/or idiopathic recurrent colic
  • EGGD is thought to occur when the imbalance between aggressive and protective factors causes back-diffusion of HCl. The aggressive factors are primarily HCl and pepsin with their acidic and proteolytic properties. Protective factors include the gastric mucosal barrier (mucus, sodium bicarbonate), prostaglandins, mucosal blood flow, and mucosal restitution
  • NSAIDs cause EGGD by topical irritation given PO or parenterally, by inhibiting the biosynthesis of gastric prostaglandins. GI damage is dose dependent. NSAIDs more selective for COX-2 than COX-1 are less likely to cause GI mucosa damage
  • Stress-induced gastric ulcerations in patients that are critically ill or under extreme physiologic stress probably develop as a result of reduced splanchnic blood flow

Systems Affected!!navigator!!

GI

EGUS has been adopted in reference to a number of specifically unique problems that describe erosive and ulcerative diseases of the stomach.

Respiratory

Foals with gastroesophageal reflux may develop aspiration pneumonia.

Hepatobiliary

Ascending cholangitis is possible with duodenal ulceration.

Incidence/Prevalence!!navigator!!

  • The reported prevalence in foals is 25–50%
  • Depending on breed and/or the level of work, the prevalence of ESGD is 11–100%, and the prevalence of EGGD is 16–64%

Signalment!!navigator!!

Breed Predilections

No sex, age, or breed predilections.

Signs!!navigator!!

General Comments

Asymptomatic in many animals. Signs may vary with the age group and are not specific for the condition.

Historical Findings

  • Poor appetite
  • Decrease in performance
  • Weight loss
  • Low-grade colic or abdominal discomfort (rare—depends on the severity of the ulceration)
  • Poor performance

Physical Examination Findings

  • Foals—often asymptomatic. Clinical signs include poor appetite, inappetence, intermittent nursing (may nurse for short period and then act mildly uncomfortable), episodes of mild colic, diarrhea, pot-bellied appearance, bruxism, salivation, and dorsal recumbency. Salivation and bruxism are usually indicative of severe glandular or duodenal ulcers with concurrent gastroesophageal reflux and delayed gastric emptying
  • Adults—often asymptomatic. Clinical signs include poor appetite, inappetence, poor body condition, rough haircoat, low-grade colic, behavior change, weight loss, and poor performance

Causes!!navigator!!

Multifactorial. Helicobacter species or any other bacteria are currently not considered as an etiological factor.

Risk Factors!!navigator!!

  • Significant illness
  • Intense training
  • Halter breaking, confining and handling of young horses
  • Administration of NSAIDs
  • Hospitalization
  • High-grain, low-roughage diet
  • Fasting
  • Water deprivation

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

A definitive diagnosis can only be reached with gastroscopy. Although a tentative diagnosis can be made based on clinical signs and response to therapy, the initiation of treatment without prior gastroscopy is not recommended.

Differential Diagnosis!!navigator!!

The clinical signs and physical examination findings with gastric ulcers are not pathognomonic and can be associated with many other conditions. EGUS often occurs secondary to other diseases.

CBC/Biochemistry/Urinalysis!!navigator!!

There are no changes associated with EGUS. Anemia and hypoproteinemia are uncommon and, when present, other causes should be pursued.

Other Laboratory Tests!!navigator!!

Fecal occult blood tests are often negative because colonic microflora digest hemoglobin.

Imaging!!navigator!!

Although, in foals, positive contrast studies might outline gastric ulcers, abdominal radiography is not a reliable diagnostic tool.

Other Diagnostic Procedures!!navigator!!

Gastroscopic examination is the most effective diagnostic procedure. For foals, a ≤10 mm diameter, 1 m endoscope is adequate. In adult horses, a 2–3 m gastroscope is necessary. Fasting is necessary to ensure gastric emptying for adequate visualization. Young foals require minimum fasting. However, older foals and adults eating roughage require a fasting period of 8–18 h.

Treatment ⬆ ⬇

Outline

TREATMENT

Appropriate Health Care!!navigator!!

Treat as outpatient if stable and underlying conditions causing EGUS have been corrected.

Nursing Care!!navigator!!

N/A

Activity!!navigator!!

Decrease level of intense training if possible.

Diet!!navigator!!

Turn out to pasture if practical.

Client Education!!navigator!!

  • Decrease intensity of training
  • Allow as much pasture time as possible
  • Minimize NSAID administration
  • Minimize periods of fasting
  • Ulcers will likely recur when intense training is resumed

Surgical Considerations!!navigator!!

Foals with chronic gastric outflow disease caused by stricture of the pylorus or duodenum after ulcer healing may require gastrojejunostomy.

Medications ⬆ ⬇

Outline

MEDICATIONS

Drug(s) of Choice!!navigator!!

  • PPIs (omeprazole) significantly decrease gastric acid secretion by specifically inhibiting the activity of proton pumps in the canalicular membrane of gastric parietal cells. Omeprazole is administered 1–4 mg/kg PO once daily for at least 28 days. Omeprazole has a time- and dose-related effect on healing of gastric ulcers. Higher doses result in more rapid and complete healing, whereas lower doses are appropriate for prevention of EGUS. Omeprazole requires 3–5 days of treatment for maximum antisecretory effect to occur. Control gastroscopy should be performed before the discontinuation of treatment
  • Histamine H2 receptor antagonists (cimetidine, ranitidine, and famotidine) inhibit gastric acid secretion by blocking the effect of histamine on the parietal cells. These compounds rapidly inhibit secretion after oral or IV administration. However, the effect is short-lived and they must be administered at least every 6–8 h. Cimetidine is administered at 20–25 mg/kg PO or at 4–6 mg/kg IV body weight every 6–8 h. Ranitidine is administered at 6–8 mg/kg PO or 1.5–2.0 mg/kg IV every 6–8 h
  • The use of mucosal protectants, especially in foals, is warranted. Sucralfate is administered at 10–20 mg/kg PO every 6–8 h and 20–40 mg/kg PO every 8 h in foals and adults, respectively. Sucralfate is less likely to be effective in the treatment of ESGD but could possibly be effective in EGGD
  • Antimicrobial therapy is presently not recommended as a routine therapy for EGUS

Contraindications!!navigator!!

Use NSAIDs with caution. These compounds may increase the severity of EGUS and prevent mucosal healing.

Precautions!!navigator!!

Clinical signs of gastric ulcers usually diminish quickly with appropriate therapy. If signs or condition worsen while on appropriate treatment, pursue a concurrent disease.

Possible Interactions!!navigator!!

Cimetidine and, to a lesser extent, omeprazole are hepatic cytochrome P450 inhibitors and might slow the metabolism of concurrently administered compounds that require this enzyme for metabolism and elimination. Treatment with PPIs and/or sucralfate may also have a negative impact on other medications.

Alternative Drugs!!navigator!!

Antacid Compounds

Antacid compounds buffer gastric acid. Their effect is short lived (≤2 h). Bismuth subsalicylate paste is given at 1000 mg/45 kg (100 lb); application via the nasogastric tube is recommended.

Nutraceuticals

Nutraceuticals alone or together with antacids are currently being investigated for prevention of EGUS.

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

Patient Monitoring!!navigator!!

Clinical Signs

  • Diminished appetite
  • Interrupted nursing
  • Teeth grinding
  • Mild to moderate colic—if colic is more than low grade or persists for >24–48 h, an alternate diagnosis should be pursued

Prevention/Avoidance!!navigator!!

Susceptible horses may require prophylactic treatment with omeprazole or H2 receptor antagonists during periods of intense training/racing. Horses with access to pasture have fewer gastric ulcers than horses in confinement. Avoid chronic administration of NSAIDs and minimize periods of fasting.

Possible Complications!!navigator!!

Pyloric or duodenal stricture in foals. Gastric or duodenal perforation, with severe hemorrhage, is rare.

Expected Course and Prognosis!!navigator!!

The prognosis is generally good for uncomplicated cases. However, recurrence is frequent when intense training is resumed. Foals that develop pyloric or duodenal strictures and require surgical intervention have a guarded prognosis.

Miscellaneous ⬆ ⬇

Outline

MISCELLANEOUS

Associated Conditions!!navigator!!

Any disease process has the potential to cause secondary gastric ulceration.

Age-Related Factors!!navigator!!

Foals have a higher incidence of glandular mucosal and duodenal ulcers.

Zoonotic Potential!!navigator!!

N/A

Pregnancy/Fertility/Breeding!!navigator!!

There are inadequate data on the use of histamine H2 receptor antagonists or omeprazole in pregnant mares. However, clinical cases of gastric ulcers in pregnant mares have been treated successfully with these compounds with no apparent adverse effects on the mare or the fetus.

Synonyms!!navigator!!

N/A

Abbreviations!!navigator!!

  • COX = cyclooxygenase
  • EGGD = equine glandular gastric disease
  • EGUS = equine gastric ulcer syndrome
  • ESGD = equine squamous gastric disease
  • NSAID = nonsteroidal anti-inflammatory drug
  • PPI = proton pump inhibitor

Suggested Reading ⬆ ⬇

Hunt RH, Camilleri M, Crowe SE, et al. The stomach in health and disease. Gut 2015;64:1650–1668.

Martineau H, Thompson H, Taylor D. Pathology of gastritis and gastric ulceration in the horse. Part 1: range of lesions present in 21 mature individuals. Equine Vet J 2009;41:638–644.

Martineau H, Thompson H, Taylor D. Pathology of gastritis and gastric ulceration in the horse. Part 2: a scoring system. Equine Vet J 2009;41:646–651.

Sykes BW, Hewetson M, Hepburn RJ, et al. European College of Equine Internal Medicine consensus statement—equine gastric ulcer syndrome in adult horses. J Vet Intern Med 2015;29:1288–1299.

Sykes BW, Underwood C, Greer R, et al. The effects of dose and diet on the pharmacodynamics of omeprazole in the horse. Equine Vet J 2016;49(4):525-531.

Author(s) ⬆

Author: Modest Vengust

Consulting Editors: Henry Stämpfli and Olimpo Oliver-Espinosa