Abstract
Cerebral venous sinus thrombosis (CVST) requires anticoagulation to promote vessel recanalization. Current anticoagulation paradigms utilize plasma tests from peripheral venous/arterial samples for therapeutic monitoring. We describe a medically-refractory case of CVST in a 35-year-old woman later found to have JAK2 mutation and essential thrombocytosis. Despite therapeutic anticoagulation levels, worsening cerebral edema and progression to coma prompted endovascular treatment. Failed endovascular thrombectomy attempts led to placement of 2 separate indwelling microcatheters for continuous infusion of tissue plasminogen activator (tPA). Forty-hours of continuous-tPA in addition to systemic intravenous-heparin led to complete radiographic and clinical resolution of CVST. Whole blood coagulation testing using Rotational Thromboelastometry (ROTEM) from simultaneous samples taken intracranially (via cerebral microcatheters) and peripherally (via antecubital vein) all revealed prolonged intrinsic pathway activation clotting times consistent with heparin anticoagulation use. However, both intracranial ROTEM samples identified faster clotting times compared to the peripheral sample suggesting lower anticoagulation levels intracranially. Our findings were speculative and hypothesis generating as to whether this explained medical treatment failure. If there are coagulopathy differences at local sites of injury not adequately captured by peripheral blood draws, further investigation is required to identify better approaches to avoid under-treatment of similar cases.