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Delayed-Onset Heparin-Induced Thrombocytopenia With Cerebral Venous Sinus Thrombosis Following Total Knee
Megan M J Bauman1,2, Ryan M Naylor1, Ashley R Santilli3
1Department of Neurological Surgery, Mayo Clinic, Rochester, MN, USA.
Heparin-induced thrombocytopenia (HIT) is a prothrombotic state caused by autoantibodies against platelet factor 4 (PF4)-heparin complexes. Although HIT typically presents 5-10 days after the initiation of heparin, thrombosis and thrombocytopenia may occur up to several weeks following heparin withdrawal, so-called delayed-onset HIT. Although rare, there have been isolated reports of HIT-induced cerebral venous sinus thrombosis (CVST), which carry high rates of morbidity and mortality. There is a need to further characterize the etiology, clinical presentation, treatment paradigms, and outcomes of patients with HIT-induced CVST. Here, we present the case of a 57-year old female who presented to the emergency department with a headache and seizure 11 days following a right total knee arthroplasty for which she received 3 post-operative doses of enoxaparin. Work-up demonstrated acute intracerebral hemorrhage (ICH), CVST, and thrombocytopenia. Intravenous heparin resulted in rapidly deteriorating platelet count and subsequent serologic testing confirmed the diagnosis of HIT. Treatment with bivalirudin was initiated, the HIT resolved, and the patient was discharged home on hospital day 19 with long-term anticoagulation mediated by warfarin. At 3-month follow up, the patient had mild upper motor neuron pattern weakness and was living independently. This case depicts a rare case of delayed-onset HIT and CVST, highlights the importance of establishing a fluid treatment plan for managing HIT-induced CVST, and illustrates the importance of employing rapid anticoagulation despite acute ICH to achieve a desirable clinical outcome.
Heparin-induced thrombocytopenia (HIT) is a prothrombotic state caused by autoantibodies against platelet factor 4 (PF4)-heparin complexes. Although HIT typically presents 5-10 days after the initiation of heparin, thrombosis and thrombocytopenia may occur up to several weeks following heparin withdrawal, so-called delayed-onset HIT. Although rare, there have been isolated reports of HIT-induced cerebral venous sinus thrombosis (CVST), which carry high rates of morbidity and mortality. There is a need to further characterize the etiology, clinical presentation, treatment paradigms, and outcomes of patients with HIT-induced CVST. Here, we present the case of a 57-year old female who presented to the emergency department with a headache and seizure 11 days following a right total knee arthroplasty for which she received 3 post-operative doses of enoxaparin. Work-up demonstrated acute intracerebral hemorrhage (ICH), CVST, and thrombocytopenia. Intravenous heparin resulted in rapidly deteriorating platelet count and subsequent serologic testing confirmed the diagnosis of HIT. Treatment with bivalirudin was initiated, the HIT resolved, and the patient was discharged home on hospital day 19 with long-term anticoagulation mediated by warfarin. At 3-month follow up, the patient had mild upper motor neuron pattern weakness and was living independently. This case depicts a rare case of delayed-onset HIT and CVST, highlights the importance of establishing a fluid treatment plan for managing HIT-induced CVST, and illustrates the importance of employing rapid anticoagulation despite acute ICH to achieve a desirable clinical outcome.
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