Stress ulcer prophylaxis

GUIDELINES FOR APPROPRIATE STRESS ULCER PROPHYLAXIS
The following information, derived from the ASHP guidelines, can be used as a screening tool to determine appropriateness of prophylaxis. Medical Intensive Care Unit patients
ONE OR MORE OF THE FOLLOWING RISK FACTORS • Likely to require mechanical ventilation for > 48 hours • Non-intentional coagulapathy, i.e. not on warfarin, heparin, or other anticoagulants resulting in an INR > 1.5, platelets < 50,000 or therapeutic aPTT Medical Intensive Care Unit patients
TWO OR MORE OF THE FOLLOWING RISK FACTORS • History of gastric ulceration or bleeding within the last 12 months PTA • Head injury with Glascow Coma Score (GCS) < 10 • Multiple trauma with an injury severity score > 16 • Hepatic failure or renal failure (serum creatinine > 5.7 mg/dL) Stress Ulcer Prophylaxis
Stress ulcers are superficial inflammatory lesions of the gastric mucosa caused by abnormally elevated physiological demands on the body. Studies have reported evidence of mucosal damage within 24 hours of admittance in 75-100% of intensive care unit (ICU) patients. This damage can be associated with a significant bleeding risk and therefore, certain patients require prophylaxis. The most current guidelines for stress ulcer prophylaxis (SUP), written by the American Society of Health-System Pharmacists (ASHP) in 1999, include recommendations for ICU patients only. Prophylaxis is not recommended for medical or surgical patients who are not in the ICU. However, data has shown that inappropriate use of acid-suppressive therapy (AST) in general medicine units has been as high as 71%. The use of AST has been linked to an increased risk of serious infections such as pneumonia and Clostridium difficile associated disease along with elevated risk of fractures. Inappropriate use also increases drug costs for hospitals and patients. For these reasons, it is important to determine the patient populations in which stress ulcer prophylaxis is appropriate.
Clinical Pearls:

 To prevent 1 case of clinically important GI bleeding, you need to treat 60 ICU pts1
 To prevent one case of overt GI bleeding, you need to treat 18 ICU pts prophylactically1
 One add’l case of nosocomial pneumonia will occur for every 25 ICU pts treated with H2RA1
 Outpatient treatment with PPI has a 2.9-fold higher incidence of community-acquired C. difficile.
 H2RAs have a 2-fold higher incidence2 risk associated with inpatient C. difficile.  Corticosteroid use alone is not a risk factor for stress ulcers1,2,3  Coagulopathies must be intrinsic-not resulting from treatment with warfarin or heparin, etc.3  Most data uses H2RA, antacids, or sucralfate in studies, very little data on use of PPIs  Most patients will not meet criteria for stress ulcer prophylaxis
 Trials only in ICU patients; there is NO DATA IN MEDICAL PATIENTS
References
1.
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J Crit Care 2009; Hussain S, Stefan M, Visintainer P, Rothberg M. Why Do Physicians Prescribe Stress Ulcer Prophylaxis to General Medicine Patients? Southern Medical Journal 2010; 103 (11): 1103-10. Qadeer MA, Richter JE, Brotman DJ. Hospital-Acquired Gastrointestinal Bleeding Outside the Critical Care Unit. Risk Factors, Role of Acid Suppression, and Endoscopy Findings. J Hosp Med 2006; 1 (1):13-20. Sesler JM. Stress-related Mucosal Disease in the Intensive Care Unit. An Update on Prophylaxis. AACN Advanced Critical Care 2007; 18 (2): 119–128. Singh H, Houy TL, Singh N, Sekhon S. Gastrointestinal Prophylaxis in Critically Ill Patients. Crit Care Nurs Q 2008; 31 (4): 291–301. Anon. ASHP Therapeutic Guidelines on Stress Ulcer Prophylaxis. Am J Health-Syst Pharm. 1999; 56:347-79 Quenot JP, Thiery N, BarbarS. When should stress ulcer prophylaxis be used in the ICU? Current Opinion in Critical Care 2009,15:139–143. Allen ME, Kopp BJ, Erstad BL. 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Use of gastric acid-suppressive agents and the risk of community-acquired Clostridium difficile-associated diseas Muto C, Pokrywka M, Shutt K, et al. A large outbreak of Clostridium difficile-associated disease with an unexpected proportion of deaths and colectomies at a teaching hospital following increased fluoroquinolone us Pepin J, Saheb N, Coulombe MA, et al. Emergence of fluoroquinolones as the predominant risk factor for Clostridium difficile-associated diarrhea: a cohort study during an epidemic in Quebec Shah S, Lewis A, Leopold D, et al. Gastric acid suppression does not promote clostridial diarrhoea in the elderly Dial S, Delaney JA, Schneider V, Suissa S. Proton pump inhibitor use and risk of community-acquired Clostridium difficile-associated disease defined by prescription for oral vancomycin therapy Dial S, Kezouh A, Dascal A, et al. Patterns of antibiotic use and risk of hospital admission because of Clostridium difficile infecti Loo VG, Poirier L, Miller MA, et al. 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Source: http://www.nch.org/physicians/scan/2012/july/documents/SUP_Synopsis.pdf

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