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In 1772 John Hunter first associated head injury with “gastromalacia.” Rokitansky (1841) later suggested hyperacidity as a potential mechanism. Harvey Cushing made the case for the ulcer now bearing his name in the 1932 Balfour lecture in Toronto. The original work resulting in the now widely adopted practice of GI stress ulcer prophylaxis was in patients with respiratory failure, hypotension, and sepsis. However recent studies suggest clinically significant hemorrhage from stress ulceration in the critical care setting is extremely uncommon (<1%). Furthermore, clinical trials on which the current recommendations are based were performed in the 1980s and early 1990s when it was common to keep ICU patients nil-per-os and when the early initiation of enteral nutrition was uncommon. It has been suggested that patients receiving enteral alimentation have a lower incidence of stress ulceration than unfed patients. Enteral nutrition has been shown to be as efficacious as pharmacologic stress ulcer prophylaxis in mechanically ventilated patients. Several studies suggest a trend in efficacy of GI hemorrhage prophylaxis being directly proportional to rate of nosocomial pneumonia. This most likely relates to increased colonization of UGI tracts with pathogenic organisms at higher gastric pH. Cook et al (1996) is one of the most widely cited studies for the use of ranitidine in SUP. Although there were13 fewer gastrointestinal hemorrhages compared to sucralfate, the ranitidine group had 15 more ventilator associated pneumonias. The study has been subsequently criticized for suggesting efficacy, but not controlling for potential harm due to lack of a placebo arm. A growing body of data now suggest significant risks of acid suppressing therapies including hospital acquired pneumonia, Clostridium difficile infection and drug-drug interactions. Potential for drug-drug interactions specific to NeuroICU patients include clopidogrel and many first generation antiepileptic medications. Current data suggest a lack of efficacy and possible harm in ICU patients receiving combination of enteral feedings and GI prophylaxis. Identification of an optimum sub-group of ICU patients who may benefit from SUP relevant to well-established risks is key. B) Application to NeuroICU patient population: Prospective trials of critically ill neurosurgical patients support the notion of rarity of and GI hemorrhage and raise doubts of any efficacy of acid suppressing therapy. Limited neurosurgical literature suggests increased prevalence of stress ulcers in patients with Glascow Coma Score < 10. Limited high quality data exist to support the current widely held practice of SUP with corticosteroid use. Chronic corticosteroid use is generally considered a risk factor for GI ulcers. Studies in the neurosurgical literature have found stress ulcer formation occurred irrespective of steroid use. The use of steroids concurrently with NSAIDs does enhance the risk of ulcer and complications, likely via impaired healing of NSAID-induced ulcers.
Suggested Guideline:

Patients who should receive stress ulcer prophylaxis:
1. All NeuroICU patients who are NPO and mechanically ventilated should receive stress ulcer prophylaxis with either H2 receptor antagonist or proton pump inhibitor. 2. NeuroICU patients expected to be on chronic steroids (>10 days)* 3. NeuroICU patients with GCS < 10 (all disease categories including but not limited to TBI, craniotomy, SAH, tumor, refractory ICP elevation of any etiology). 4. Any patient with known active gastritis, known Upper GI ulcer, or known prior Upper GI 5. Any patient receiving combination of NSAID’s and Corticosteroids (an unlikely event for Patients who should not receive stress ulcer prophylaxis: 1) Patients receiving enteral nutrition (Per NGT, GT or PO) within 48hours of admission, who do not meet the above criteria. 2) Brief periods of NPO status. (i.e. < 12 hours for procedure). 3) Short course post operative steroids should not be provided GI prophylaxis.* *For patients experiencing the common side effect of high dose steroids (dyspepsia, reflux), symptomatic relief may be achieved with any agent including calcium carbonate (tums), sucralfate, H2 blocker, PPI. Duration of the treatment should not exceed duration of corticosteroid use. Suggested agents for use: Ranitidine is superior to sucralfate for prevention of GI hemorrhage. There is insufficient evidence to recommend H2 blockers versus proton pump inhibitors. Some data suggest higher rates of C. difficile infection with PPI’s. 1 Hastings PR, Skillman JJ, Bushnell LS, et al. Antacid titration in the prevention of acute gastrointestinal bleeding: A controlled, randomized trial in 100 critically ill patients. N Engl J Med 1978; 298:1041–1045 2 Pingleton SK, Hadzima SK: Enteral alimentation and gastrointestinal bleeding in mechanicallyventilated patients. Crit Care Med 1983; 11:13–16. 3 Faisy C, Guerot E, Diehl JL, et al: Clinically significant gastrointestinal bleeding in critically ill patients with and without stressulcer prophylaxis. Intensive Care Med 2003; 29:1306–1313 4 Messori A, Trippoli S, Vaiani M, Gorini M, Corrado A. Bleeding and pneumonia in intensive care patients given ranitidine and sucralfate for prevention of stress ulcer: meta-analysis of randomised controlled trials. BMJ 2000; 321: 1103–6. -- Summary: ranitidine-treated patients had significantly increased rates of pneumonia as compared with sucralfate. 5 Cook DJ, Reeve BK, Guyatt GH, et al. Stress ulcer prophylaxis in critically ill patients. Resolving discordant meta-analyses. JAMA 1996; 275: 308–14. 6 , . Stress ulcer prophylaxis in the new millennium: a systematic review and meta-analysis. 2010 Nov;38(11):2222-8. 7 , stinal bleeding after craniotomy: a retrospective review of 5185(4):384-7. 8 steroids and peptic ulcer: meta-analysis of adverse events during steroid therap 1994 Dec;236(6):619-32.

Source: http://www.mghneuroicu.org/pdf/Stress%20ulcer%20prophylaxis.pdf

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