Emergency physicians routinely encounter patients who are receiving some form of anticoagulant therapy. This population becomes increasingly challenging to treat in the face of major bleeding complications or prior to emergency surgery.
Management of anticoagulant therapy is multifaceted because of the significant individual variations in dosage requirements that make over-anticoagulation very common in this population. Additionally, because of the narrow therapeutic window for many anticoagulants such as warfarin and heparin, treatment frequently results in bleeding that can be life-threatening.
Major bleeding involving the gastrointestinal or urinary tract or the soft tissue occurs in up to 6.5% of patients on anticoagulant therapy. The incidence of fatal bleeding, such as intracranial hemorrhage, is approximately 1% annually.1 As over-anticoagulation is commonly seen and its effects are potentially harmful to the patient, emergency physicians should know the major anticoagulants routinely used in patients presenting to the emergency department, as well as the current indications, agents used, and recommendations for reversal.
Indications for Reversal
The clear risk of anticoagulation is the possibility of bleeding, which can cause death or serious morbidity.
Emergency physicians should consider reversal of anticoagulation if patients experience bleeding in the brain, the gastrointestinal tract, the deep muscles, the retro-ocular region, or the joint spaces. Emergency physicians should also consider the severity of the hemorrhage seen, reversing in cases of shock or if the patient requires blood transfusions as a result of the bleeding.
Finally, patients should undergo reversal of anticoagulation if urgent or emergent surgery is indicated, such as for ischemic surgical events, septic shock, and treatment of open fractures.2
Anticoagulants and Recommendations for Reversal
Warfarin is a commonly used oral anticoagulant used to prevent and treat many thromboembolic conditions, such as acute deep venous thrombosis, pulmonary emboli, and ischemic strokes from clots formed on mechanical valves. Warfarin blocks the activation of Vitamin K and interferes with the carboxylation of Vitamin K–dependent coagulation factors I, VII, IX, and X, which in turn blocks the extrinsic coagulation pathway. Warfarin also blocks synthesis of antithrombotic proteins C and S, which serve to inhibit the function of factors V and VII in the coagulation cascade.