High dose subcutaneous unfractionated heparin for prevention of venous thromboembolism in overweight neurocritical care patients.

Timing and dosing of chemical venous thromboembolism (VTE) prophylaxis in brain injury is controversial. Risk of bleeding while using high dose unfractionated heparin (UFH) in overweight patients to prevent VTE is also unknown. The purpose of this study was to describe the use of subcutaneous heparin 7500 units for VTE prophylaxis in overweight patients. This was a retrospective study comparing patients over 100 kg who received either 7500 units Q8 h (n = 141) (high dose group, HDG), or 5000 units Q8 h (n = 257) (traditional dose group, TDG), of UFH subcutaneously. Both groups had similar rates of bleeding complications. The incidence of drop in hemoglobin by two points in any 24 h was 14 % (20/141) HDG versus 11 % (28/257) TDG; P = 0.33. Hemoglobin drop by two points from baseline was 57 % (81/141) HDG versus 51 % (132/257) TDG; P = 0.24. The need for pRBC transfusion was 26 % (36/141) HDG versus 20 % (52/257) TDG; P = 0.22. An increase in aPTT from baseline by two times was 4 % (5/141) HDG versus 4 % (9/257) TDG, P = 0.59. Discontinuation of heparin therapy for association with progressive bleeding was not documented in any patients. No differences in minor bleeding complications were observed. There was no difference in the incidence of VTE: 5.7 % (8/141) HDG versus 9.3 % (24/257) TDG; P = 0.2. In univariate and multivariable logistic regression analysis, only the time of the initiation of heparin after admission was associated with the occurrence of VTE (median, IQR) 46 h (17-86) HDG versus 105 h (56-167) TDG; OR 1.2 (1.1-1.3); P < 0.001. High dose subcutaneous UFH was not associated with an increased risk of bleeding, nor did it decrease the incidence of VTE in overweight patients.

Plasmapheresis may be an option in urgent management of heparin-induced thrombocytopenia in the setting of acute intracerebral hemorrhage.

BACKGROUND: We report a case of heparin-induced thrombocytopenia (HIT) that was complicated by acute intracerebral hemorrhage (ICH) and bilateral adrenal hemorrhage. In the setting of worsening thrombocytopenia, the risk of expansion of ICH and additional thrombotic events is concerning; hence, we employed plasmapheresis to reduce thrombotic risk. METHODS: We followed serial daily heparin antibody enzyme-linked immunosorbent assay (ELISA) optical density measurements as well as heparin-induced platelet aggregation (HIPA) assays on both pre- and post-pheresis samples in order to objectively determine when thrombotic risk was sufficiently decreased. RESULTS: After four cycles of plasmapheresis, both heparin antibody ELISA and HIPA assays became negative. CONCLUSION: This case helps illustrate the utility of plasmapheresis in management of HIT when anticoagulation is contraindicated.

Central nervous system vasculitis secondary to systemic sclerosis.

Systemic sclerosis (SSc) or scleroderma is a connective tissue disease with a diverse array of clinical manifestations secondary to underlying fibrosis and autoimmunity. Central nervous system (CNS) impairment is uncommon in SSc. Here we report the fourth known patient with CNS vasculitis caused by SSc. In each previous report, the patient was a middle-aged to elderly female. Our patient was 24 years old at the time of presentation, significantly younger than the other reported patients. Importantly, our patient's rapidly progressive clinical course and poor response to immunosuppression have not been reported in patients with CNS vasculitis secondary to scleroderma. Although CNS vasculitis is extremely rare in SSc, our report suggests that clinicians should consider this diagnosis in the differential of SSc patients with neurologic impairment.