Intravenous Immunoglobulin (IVIG) in Severe Heparin-Induced Thrombocytopenia (HIT) in a Traumatic Brain Injury (TBI) Patient with Cerebral Venous Sinus Thrombosis (CVST)

Alternative anticoagulation for patient with heparin-induced thrombocytopenia [15–18] Argatroban Lepirudin Bivalidrudin Fondiparinux Danaparoid Mechanism Factor II (highly selective) Factor II (highly selective) Factor II Antithrombin III-mediated inhibition of factor Xa Inhibits factor Xa and IIa Dosing Infuse 2 mcg/kg/min, infuse (max 10 mcg/kg/min); goal aPTT 1.3–3 × baseline Bolus 0.4 mg/kg (max 44 mg), infuse 0.15 mg/kg/h; goal aPTT 1.5–2.5 × baseline Infuse 0.15–0.2 mg/kg/h; goal aPTT 1.5–2.5 × baseline Subcutaneous 5 mg ( 100 kg) once daily Bolus 1,250–1,5000 U ( 90 kg); infuse 400 U/h × 4 h, then 300 U/h × 4 h Pharmacology (half-life) Hepatic metabolization (39–51 min) Renal elimination (1.3 h) Renal elimination (25 min) Renal elimination (17–21 h) Renal elimination (~ 25 h) Reversal Agent None None None; may consider None; may consider None Considerations Short 1/2 life beneficial if risk of life-threatening hemorrhage; reduce dose (0.15–1.3 mcg/kg/min) or use alternative in live failure Reduce dose in renal insufficiency; antihirudin antibodies may reduce excretion Long half-life; unable to make fine adjustments in dose We present a case of severe HIT in a TBI patient with post-traumatic CVST, which did not improve until after the administration of adjunctive IVIG. Case Description Initial Stabilization, Surgical Intervention, and Neurocritical Care Management A 44-year-old male was brought to the University of Wisconsin Emergency Department by emergency medical services after being involved in a motor vehicle collision. See PDF.] Timeline of platelet count and hematologic treatments and diagnostics Concern for HIT surfaced on POD 8 with a decline in platelet count from 92 to 53 K/μL over 24 h. Work-up involved investigating new bleeding sources (rising BUN and positive stool hemoccult elevated concern for upper gastrointestinal bleeding), HIT testing, and bilateral upper and lower venous dopplers. Aside from the development of HIT and refractory intracranial hypertension in the setting of a severe TBI and post-traumatic CSVT, the patient had a prolonged hospital course complicated by acute respiratory distress syndrome due to pulmonary contusions and Enterobacter aerogenes ventilator-associated pneumonia, bilateral pulmonary lobar collapse due to mucus plugging, and paroxysmal sympathetic hyperactivity.