(Kiosk 3) Cerebral Venous Sinus Thrombosis as a Consequence of Heparin-induced Thormbocytopenia from Subcutaneous Heparin Use

Case Diagnosis: This is a case of a 69-year-old female was admitted to acute rehabilitation facility after an ORIF of the right tibia plateau fracture on heparin as DVT prophylaxis, who developed hemorrhagic stroke as a consequence of Heparin Induced Thrombocytopenia.

Case Description or Program Description: 69-year-old female underwent an open reduction and internal fixation after sustaining a right tibial plateau fracture. She was then admitted for acute rehabilitation while on subcutaneous heparin for DVT prophylaxis. 7 days after admission, she was noted to be having difficulty with expressive language and command following. She was alert and oriented to person and time but not to place. No other focal neurological deficits were noted. Initially, narcotics and gabapentin were held as a possible cause of delirium. Labs demonstrated a drop in platelet count from 105k on day 6 to 75k on day 7 for which the heparin was held. CT brain demonstrated an acute right temporal lobe intracerebral hemorrhage (ICH). Patient was admitted to the neurosurgical ICU; MRV showed right sigmoid and transverse sinus thrombosis. Subsequently, serology workup confirmed HIT as Heparin-PF4 antibody was elevated.

Setting: Inpatient rehabilitation facility

Assessment/Results: Intracerebral hemorrhage in setting of heparin induced thrombocytopenia

Discussion (relevance): CVST is a rare complication of HIT with incidence of < 2%. HIT-related CVST carries a high risk of brain hemorrhage, occurring in as much as 81.8%. Diagnosis of HIT must take into consideration both clinical and laboratory evidence. Current guidelines from ACCP (American College of Chest Physicians) suggests patients receiving heparin whom the risk of HIT is >1% (eg. 4Ts score), platelet count should be monitored every 2-3 days from day 4 to 14 on heparin or until heparin is stopped. Once HIT is diagnosed, heparin products should be discontinued and a non-heparin agent such as parenteral direct thrombin inhibitor or DOAC should be initiated. In our patient, anticoagulation was changed to oral Apixaban.

Conclusions: Subcutaneous heparin use can lead to HIT-induced CVST. When patients are on subcutaneous heparin, detailed daily physical exams and monitoring of platelet counts are critical. Discontinuation of all heparin products when HIT is suspected and initiating non-heparin agent is imperative in decreasing morbidity and mortality.