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Basics ⬇

Outline

BASICS

Definition!!navigator!!

Areas of mucosal disruption in the nonglandular stratified squamous mucosa, margo plicatus, and glandular mucosa (fundus and pylorus) of the stomach.

Pathophysiology!!navigator!!

  • Gastric ulcers are caused by an imbalance between mucosal aggressive factors (HCl, pepsin, bile acids) and mucosal protective factors (mucosal blood flow, mucus–bicarbonate layer, mucosal PGE1 and motility)
  • Ulcers in the squamous mucosa are related to prolonged exposure to gastric acids. Delayed gastric emptying and recumbency can increase this exposure. Milk buffers gastric acid, so infrequent nursing may lead to increased acid exposure
  • Gastric ulcers may be related to desquamation of the squamous epithelium that occurs in 80% of normal foals up to 40 days of age
  • Endogenous corticosteroids and NSAID treatment can decrease mucosal blood flow, inhibit bicarbonate secretion, and stimulate gastric acid secretion by blocking prostaglandin synthesis
  • Glandular ulceration is considered the most clinically significant. The mucus–bicarbonate layer covers the surface of the glandular mucosa. Ulcers in this region are primarily due to disruption of blood flow and decreased secretion of mucus and bicarbonate. Septic shock and hypovolemia leading to hypoperfusion and reduced oxygen delivery may be involved in the pathogenesis of glandular mucosal injury
  • Foals may also have ulcers in the pylorus or proximal duodenum that can lead to squamous gastric and esophageal ulcers from delayed gastric emptying

Systems Affected!!navigator!!

Gastrointestinal

Incidence/Prevalence!!navigator!!

  • The reported prevalence in foals varies from 25% to 57%
  • Endoscopic surveys of normal foals 2–85 days of age revealed that 50% had squamous ulcers and 4–9% had glandular ulcers

Signalment!!navigator!!

No breed or sex predilection.

Signs!!navigator!!

General Comments

In foals, there appear to be 4 separate clinical syndromes:

  1. Silent (subclinical) ulcers are most common
    • Most commonly found in foals <4 months of age
    • Usually seen in foals with concurrent illness
    • Ulcers may heal spontaneously or may be found incidentally at necropsy
  2. Active (clinical) ulcers
    • Primarily in the squamous mucosa
    • Clinical signs include depression, anorexia, bruxism, ptyalism, dorsal recumbency, and colic
  3. Perforating ulcers with diffuse peritonitis are uncommon
    • Most frequent in the squamous mucosa
    • Clinical signs usually absent until just before rupture
    • Severity poorly predicted by endoscopic appearance
    • Once ruptured, foals show progressive evidence of endotoxemia and may have abdominal distention and colic
  4. Pyloric strictures associated with gastric outflow obstruction are uncommon
    • Bruxism, ptyalism, postprandial colic, aspiration pneumonia, dehydration, systemic hypochloremic alkalosis
    • Most common in foals 3–5 months of age

Historical Findings

Poor growth, rough haircoat, pot-bellied appearance, and history of prior illness, including diarrhea, colic, lethargy, or anorexia.

Physical Examination Findings

  • Depression and intermittent nursing are the most commonly observed clinical signs
  • Colic
  • Diarrhea
  • Bruxism and ptyalism

Causes!!navigator!!

  • Increased mucosal exposure to gastric acid
  • Mucosal blood flow disruption

Risk Factors!!navigator!!

  • Fasting, decreased gastric motility, and delayed gastric emptying may lead to squamous ulcers
  • Disruption of mucosal blood flow due to hypovolemia, shock, stress, and/or NSAID use may cause glandular ulcers

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis!!navigator!!

Any disorder resulting in signs of colic, e.g. small intestinal intussusception, small intestinal volvulus, pyloric stenosis, enterocolitis.

CBC/Biochemistry/Urinalysis!!navigator!!

  • Hematology values are usually normal but may reveal a stress leukogram
  • Anemia may be present with blood loss

Other Laboratory Tests!!navigator!!

Fecal or gastric occult blood may suggest bleeding ulcers; these tests are neither sensitive nor specific.

Imaging!!navigator!!

  • Abdominal radiographs may help rule out other causes of colic
  • Barium contrast radiographs should be taken in foals with suspected gastric outflow obstruction
  • Abdominal ultrasonography should be performed to evaluate intestinal wall thickness and to evaluate for ileus and peritoneal effusion

Other Diagnostic Procedures!!navigator!!

  • Gastroscopy or gastroduodenoscopy will definitively confirm the diagnosis. Use a 1 m long endoscope with a maximal outer diameter of 9 mm
  • Nuclear scintigraphy, acetaminophen (paracetamol) absorption, and postconsumption [13C]-octanoic acid blood or breath testing can be used to diagnose delayed gastric emptying

Pathologic Findings!!navigator!!

NSAID toxicity produces ulcers in the glandular and nonglandular stomach. Ulcer size is highly variable, ranging from 2 mm to >2 cm in diameter. Larger ulcers may be 1–2 mm in depth and surrounded by hyperemia.

Treatment ⬆ ⬇

Outline

TREATMENT

Aims!!navigator!!

  • Suppression or neutralization of gastric acid
  • Supportive therapy
  • Foals with mild to moderate gastric ulcers should respond to treatment within 24–48 h

Appropriate Health Care!!navigator!!

  • Patients with gastric ulcers can be treated in the field
  • Hospitalization is recommended for foals with dehydration or electrolyte imbalance, peritonitis, signs of sepsis, esophageal reflux, or uncontrolled pain

Nursing Care!!navigator!!

In severely compromised critically ill foals, supportive care (including fluid therapy and inotropic support) is needed to maintain perfusion.

Activity!!navigator!!

Normal

Diet!!navigator!!

  • Normal diet in cases without reflux
  • In case of reflux, parenteral nutrition is sometimes necessary

Client Education!!navigator!!

Avoid use of NSAIDs without veterinary supervision.

Surgical Considerations!!navigator!!

  • Foals with severe gastroduodenal ulcer disease can develop duodenal strictures. If medical therapy is unsuccessful, then surgical correction is necessary
  • Surgical techniques include pyloroplasty or bypass techniques

Medications ⬆ ⬇

Outline

MEDICATIONS

Drug(s) of Choice!!navigator!!

Histamine H2 Receptor Antagonists

Suppress HCl secretion by binding and competitively inhibiting the histamine H2 receptor on parietal cells:

  • Cimetidine—6–20 mg/kg PO every 6–8 h or 6.6 mg/kg IV every 6 h
  • Ranitidine—6.6 mg/kg PO every 8 h or 1.5–2 mg/kg IV every 6–8 h
  • Famotidine—2–3 mg/kg PO every 12 h

Proton Pump Inhibitors

  • Block secretion of H+ by parietal cell membrane H+/K+-ATPase pump (proton pump)
  • Acid secretion is effectively suppressed for up to 27 h
  • Omeprazole—4.0 mg/kg PO every 24 h for treatment of gastric ulcers; 1.0–2.0 mg/kg PO every 24 h for prophylaxis

Antacids

  • Aluminum hydroxide, magnesium hydroxide, and calcium carbonate (200–250 mL PO every 6 h)
  • Can be used to ameliorate clinical signs or to prevent recurrence; efficacy not determined

Sucralfate

  • Adheres to ulcerated mucosa, forms a proteinaceous barrier, and stimulates PGE1 synthesis and mucus secretion
  • Efficacy in treatment of squamous mucosal lesions has not been determined
  • Best used as an adjunct in addition to H2 antagonists or proton pump inhibitors
  • Dose is 10–20 mg/kg PO TID or QID
  • Do not administer at the same time as other oral medications (may inhibit absorption of other drugs)

Prostaglandin Analogs

  • Misoprostol (Cytotec™)—1–4 μg/kg PO every 12–24 h
  • Synthetic PGE1 analog
  • PGE1 inhibits HCl and gastrin secretion; increases gastric mucus formation and mucosal blood flow
  • May aid in the treatment/prevention of gastric ulcers induced by NSAIDs

Prokinetics

  • May be administered to foals with duodenal ulcers, with gastroesophageal reflux, and when delayed gastric emptying without a physical obstruction is suspected
  • Bethanechol—0.02 mg/kg SC every 6–8 h; cholinergic agonist that increases the rate of gastric emptying in horses

Contraindications!!navigator!!

Prokinetics should not be used if mechanical obstruction is suspected.

Precautions!!navigator!!

  • Side effects of prostaglandin analog use may include abdominal pain, diarrhea, bloating, and cramping
  • Bethanechol—adverse effects include diarrhea, inappetence, salivation, and colic

Possible Interactions!!navigator!!

  • Cimetidine may inhibit hepatic microsomal enzyme systems and thereby reduce metabolism, prolong half-lives, and increase serum levels of some drugs, e.g. metronidazole
  • Do not use bethanechol concomitantly with other cholinergic or anticholinesterase agents

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

Patient Monitoring!!navigator!!

  • Recheck gastroscopy 14–28 days after initiating treatment
  • If gastroscopy is unavailable, the efficacy of treatment can be based on clinical signs
  • Signs of colic or diarrhea that result from gastric ulcers usually resolve within 48 h. Appetite, body condition, and attitude improve within 1–3 weeks

Prevention/Avoidance!!navigator!!

  • Prophylactic antiulcer therapy is routinely administered in critically ill foals. Some critically ill foals have a predominantly alkaline gastric pH profile, and because gastric acidity may be protective against bacterial translocation in neonates the need for prophylactic ulcer therapy is controversial (this practice has been associated with diarrhea in neonatal foals)
  • Avoid unnecessary NSAID use in foals

Possible Complications!!navigator!!

  • Pyloric stricture
  • Acute hemorrhage
  • Gastric, duodenal rupture, and peritonitis

Expected Course and Prognosis!!navigator!!

  • Outcome is variable
  • Foals with gastric ulcers that respond favorably to therapy for a primary problem have a good prognosis. Ulcers may heal in 2–3 weeks
  • Foals with duodenal ulcers have a guarded prognosis due to potential for duodenal stricture, fibrosis, and gastric outflow obstruction
  • Foals with perforating ulcers have a grave prognosis
  • Mortality from gastric ulceration has been reported to range from 7.1% to 16.2% in foals

Miscellaneous ⬆ ⬇

Outline

MISCELLANEOUS

Associated Conditions!!navigator!!

  • Septicemia
  • Neonatal maladjustment syndrome

Age-Related Factors!!navigator!!

Frequently seen in neonatal foals with other comorbidities

Synonyms!!navigator!!

  • Gastroduodenal ulcer syndrome
  • Peptic ulcers

Abbreviations!!navigator!!

  • NSAID = nonsteroidal anti-inflammatory drug
  • PGE1 = prostaglandin E1

Suggested Reading ⬆ ⬇

Elfenbein JR, Sanchez LC. Prevalence of gastric and duodenal ulceration in 691 nonsurviving foals (1995–2006). Equine Vet J Suppl 2012;41:76–79.

Furr M, Cohen ND, Axon JE, et al. Treatment with histamine-type 2 receptor antagonists and omeprazole increase the risk of diarrhea in neonatal foals treated in intensive care units. Equine Vet J Suppl 2012;41:80–86.

Magdesian G. Gastrointestinal problems in the neonatal foal. In: Paradis MR, ed. Equine Neonatal Medicine: A Case-Based Approach. Philadelphia, PA: Saunders, 2006:208.

Ryan CA, Sanchez LC. Nondiarrheal disorders of the gastrointestinal tract in neonatal foals. Vet Clin North Am Equine Pract 2005;21:313–332.

Author(s) ⬆

Author: Teresa A. Burns

Consulting Editor: Margaret C. Mudge

Acknowledgment: The author and editor acknowledge the prior contribution of Sandra C. Valdez-Almada.