HEPARIN-INDUCED THROMBOCYTOPENIA PRESENTING AS INTRACRANIAL HEMORRHAGE SECONDARY TO CEREBRAL VENOUS THROMBOSIS: A MANAGEMENT DILEMMA

Abstract

SESSION TITLE: Fellows Critical Care Posters SESSION TYPE: Fellow Case Report Posters PRESENTED ON: October 18-21, 2020 INTRODUCTION: Heparin induced thrombocytopenia (HIT) is a rare disorder, but has a 20% mortality if left untreated. Thrombocytopenia and thrombosis are common findings, but bleeding diatheses can occur with intracranial hemorrhage (ICH) being a rare occurrence. ICH secondary to HIT can be caused by either lack of platelets and/or platelet dysfunction or from venous thrombosis leading to obstruction of venous drainage and subsequent venous engorgement. We present a case of a patient who developed ICH due to HIT and discuss the management complexity of initiating anticoagulation in the setting of a life-threatening bleed. CASE PRESENTATION: The patient was a 63 year-old male who underwent two-part spinal fusion for correction of his scoliosis. He was exposed to heparin products during his prolonged hospital course and on hospital day 18, he had an acute change in mental status. Vital signs were normal with a GCS of 9. Patient was also noted to have duskiness of his left-index finger with delayed capillary refill. Labs were remarkable for a profound thrombocytopenia (24K), markedly decreased from post-operative levels of 192K. Coagulation studies and fibrinogen levels were normal with no schistocytes observed on smear. HIT antibodies were pending. Non-contrast CT imaging revealed a large, acute bleed encompassing the left frontal lobe with partial effacement of the lateral ventricle (Figure 1). Given concern for HIT, a cerebral venogram was ordered which showed extensive venous sinus thrombosis from the superior sagittal sinus down to the level of left internal jugular vein (Figure 2). DISCUSSION: Clinically, the presentation was consistent with HIT (8/8 of 4T-score) with imaging supporting ICH secondary to the large venous clot burden. Knowing that anticoagulation is the definitive treatment for HIT, the management complexity of this case centered around whether to initiate anticoagulation in a patient with a high probability of HIT in the setting of a large ICH. Anticoagulation could worsen his life-threatening ICH and lead to death; however, not starting it could lead to progression of thrombotic complications and worsen venous congestion and bleeding. Based on clinical and imaging findings, available literature sources, and discussions with consultants and family, anticoagulation with argatroban was initiated. The patient's neurologic status remained stable and repeat imaging performed 12H, 24H, and 48H after the initiation of anticoagulation showed no progression of the ICH (Figure 3). No further bleeding or thrombotic complications occurred during the patient’s hospital course. CONCLUSIONS: This case demonstrates successful management of ICH secondary to venous sinus thrombosis caused by HIT. Knowledge of the etiology of the ICH allowed for use of anticoagulation, which did not increase the known hemorrhage and likely prevented further propagation of the bleed. Reference #1: n/a DISCLOSURES: No relevant relationships by John Ellis, source=Web Response No relevant relationships by Stephanie Hightower, source=Web Response No relevant relationships by Asheesh Kumar, source=Web Response No relevant relationships by Rebecca Wetzel, source=Web Response