A Retrospective Analysis of the Epidemiology and Outcomes of Gastrointestinal Bleeding With Respect to the Use of Non-steroidal Anti-inflammatory Drugs: 157

Introduction: The association of non-steroidal anti-inflammatory drugs (NSAIDs) with gastrointestinal bleeding (GIB) has been a well-studied correlation. The mechanism of toxicity has been clearly defined and is known to result from the inhibition cyclo-oxgenase and prostaglandin synthesis, as have the risk factors that predispose to GIB. We retrospectively studied 336 consecutive patients presenting to the emergency room with GIB and separated them based on NSAID use. The aim of the study was to improve our understanding as to how NSAID use may have a changing role in the epidemiology of GIB. Methods: Retrospective analysis of 336 consecutive patients admitted to the University of Massachusetts Medical Center Emergency Department between 2011 and 2012. Two cohorts were identified of patients who were taking NSAIDS at admission or not. Analysis of medical records was performed identically for both cohorts. Information obtained from analysis includes initial laboratory values, patient characteristics, and final diagnosis. Results: Of the 336 patients, a significantly greater percentage were not taking NSAIDs (61.9%) compared to those that were (38.1%; p<0.001). Patients who taking NSAIDs were significantly older (69.9 years old vs. 57.9 years old; p<0.0001), required significantly more units of red blood cell transfusion (2.4 units vs. 1.7 units; p=0.03), and had higher admission BUN levels (33.8 mg/dL vs. 24. 3 mg/dL; p=0.002). The most common diagnoses in the NSAID group were duodenal ulcer (14.06%), gastric ulcer (7.03%), and small bowel angioectasia (6.25%). In the non-NSAID group, the most common diagnoses were gastric ulcer (6.25%, esophageal varices 5.7%, and duodenal ulcer 5.3%). In patients on proton pump inhibitors PPI or H2 receptor antagonists, gastric ulcers were seen in 3.2% of the NSAID group and 4.8% of the non-NSAID (p=0.68), and duodenal ulcers were seen in 9.8% of the NSAID group and 2.4% of the non-NSAID group (p <0.05). In patients not on a PPI or H2 blocker, gastric ulcers were seen in 10.4% of the NSAID group and 7.1% of the non-NSAID group (p=0.22), and duodenal ulcers were seen in 17.9% of the NSAID group and 7.1% of the non-NSAID group (p<0.01). Conclusion: Analysis of a 12-month cohort of patients with GIB demonstrates that we have found that NSAIDs continue to play an important role in those with GIB. We also found that those taking NSAIDs still had bleeding from peptic ulcers even when taking a PPI or H2 receptor antagonists, suggesting that protection from peptic ulcer disease is incomplete and that the diagnosis of peptic ulcer should still be considered when evaluating patients taking NSAIDs.