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Chapter 12. Stress Ulcer Prophylaxis

Rebecca L. Attridge

  • Stress ulcer → superficial lesion of mucosal layer of the stomach after traumatic event; can develop into deeper lesion with significant gastroduodenal bleeding (may occur within 1st 24h of ICU admission)
  • Etiology: ↓ mucosal blood flow → ischemia → acid hypersecretion; due to excessive gastrin stimulation of parietal cells & alteration of normal protective mechanisms (epithelial turnover in gastric mucosa & change in mucus & bicarbonate secretion)
  • Frequency of clinically important bleeding: 1–5%

Figure 12-1.
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Etiology of stress ulcers. (Adapted from Stollman N, Metz DC: Pathophysiology and prophylaxis of stress ulcer in intensive care unit patients, J Crit Care 2005 Mar;20(1):35.)

Table 12-1 Risk Factors for Stress Ulcers (N Engl J Med 1994;330:337)
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Table 12-1 Risk Factors for Stress Ulcers (N Engl J Med 1994;330:337)

Respiratory failure (defined by mechanical ventilation >48h)*

Coagulopathy (INR >1.5 or platelets <50)*

General (medical, surgical, respiratory) ICU populations

Head injury (GCS ≤10) or inability to obey commands

Thermal injury >35% BSA

Hypotension

Severe sepsis

Partial hepatectomy

Hepatic or renal transplantation

Multiple trauma with injury severity score of ≥16

Spinal cord injury

Hepatic failure

History of gastric ulceration or bleeding during year before admission

Presence of at least 2 of the following: sepsis, ICU stay >1wk, occult or overt bleeding for ≥6d, corticosteroid therapy

(>250mg hydrocortisone or equivalent daily)

IMPORTANT NOTES:

Risk of bleeding in the absence of these risk factors: <0.1%

Risk of bleeding increases with ↑ number of risk factors present

*Independent risk factor for bleeding.

Treatment Goal: prevent clinically significant bleeding (hemodynamic compromise or need for blood transfusion)

Pharmacological Treatment

(Am J Health-Syst Pharm 1999;56:347)

  • H2-receptor antagonists (H2RA): famotidine, ranitidine, nizatidine, cimetidine
    • MOA: inhibits gastric acid secretion by antagonizing the histamine-2 receptor on parietal cells; may have immunomodulatory effects
    • Dose-limiting side effects: CNS toxicity (confusion, agitation, seizures); thrombocytopenia; ↑ rate of VAP (↓ risk vs PPIs); ↑ risk of C. difficile diarrhea (↓ risk vs PPIs; JAMA 2005;294:2989)
    • Monitoring: renal dose adjustment; may develop tolerance with prolonged use
    • Drug/drug interactions: cimetidine not recommended due to CYP450 interactions
  • Proton pump inhibitors (PPI): esomeprazole, lansoprazole, omeprazole, pantoprazole, rabeprazole
    • MOA: inhibition of proton pump in parietal cell, the final step in gastric acid production
    • Dose-limiting side effects: thrombocytopenia, ↑ risk of C. difficile diarrhea, ↑ rate of VAP & CAP
    • Drug/drug interactions: ↓ effectiveness of clopidogrel; ↓ atazanavir concentrations
  • Sucralfate
    • MOA: becomes polar at acidic pH & binds to granulation tissue of ulcer to form a protective layer on gastric mucosa; also stimulates prostaglandin production & modulates pepsin & mucus activity, arachidonic acid metabolism, bicarbonate secretion, & tissue growth & repair; does not ↑ gastric pH
    • Dose-limiting side effects: ↑ serum aluminum concentrations in elderly, renal insufficiency; may contribute to esophageal & GI bezoar ...

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