Gastrointestinal (GI) disease complicates anticoagulation by simultaneously increasing bleeding risk and maintaining high thromboembolic vulnerability. Mucosal injury, portal hypertension, malignancy, inflammatory bowel disease, and vascular lesions predispose to hemorrhage, whereas interruption of therapy increases the risk of stroke, venous thromboembolism, and stent thrombosis. Contemporary management follows an indication-first, risk-balanced approach that integrates thrombotic urgency, GI disease phenotype, and patient-specific bleeding-risk factors. Direct oral anticoagulants demonstrate heterogeneous GI bleeding profiles, with higher risk observed with dabigatran and rivaroxaban, while apixaban is comparatively safer in high-risk populations. Periprocedural management is guided by procedural bleeding risk, renal function, and drug pharmacokinetics, with strategies emphasizing appropriate interruption and minimal use of bridging. In acute GI bleeding, management prioritizes hemodynamic stabilization, restrictive transfusion strategies, and early endoscopic or interventional radiology–guided source control, with selective use of reversal agents in severe cases. Adjunctive measures, including proton pump inhibitor therapy and Helicobacter pylori eradication, reduce recurrent bleeding risk. Resumption of anticoagulation is generally associated with improved survival and reduced thromboembolic events when timed appropriately. Key knowledge gaps remain regarding optimal reversal strategies, lesion-specific restart timing, and management in cirrhotic populations.
Alkasabrah et al. (Wed,) studied this question.