Heparin-induced thrombocytopenia Type II in subarachnoid hemorrhage patients: incidence and complications

Heparin-induced thrombocytopenia Type II (HIT II) is the autoimmune-mediated severe form of the disease characterized by a significant reduction in platelets, and it carries a high risk of "paradoxical" serious thrombotic complications. Although HIT II has been studied in several different patient populations, the incidence of HIT II and the rate of thrombotic complications have never been reported in a neurosurgical patient population. Subarachnoid hemorrhage (SAH) patients, among neurosurgical patient populations, have a high exposure to heparin because they are in critical care units and have indwelling vascular catheters. In addition, the increase in neuroendovascular procedures with the associated use of heparinization will increase the exposure of SAH patients to heparin.

During a 3.5-year period (January 2000-June 2003), 389 consecutive SAH patients were treated at our center. We retrospectively reviewed their laboratory data and medical records and used accepted clinical criteria for the diagnosis of HIT II to determine the incidence of HIT II, thrombotic complications, management, and outcome.

Fifty-nine patients (15%) met the clinical diagnostic criteria for HIT II. The average platelet count nadir in the HIT II patients was 68,600 +/- 25,300/microl (mean +/- standard deviation). Female patients and patients with Fisher Grade 3 were more likely to develop HIT II (P < 0.01). Thirty-six patients (61%) underwent a neuroendovascular procedure. The rate of systemic thrombotic complications in the HIT II patients was 37 versus 7% in SAH patients without HIT II (P < 0.001), and the rate of new hypodensities on head computed tomographic scans was 66% in the HIT II patients versus 40% in the SAH patients without HIT II (P < 0.001). Clinical outcomes were worse in the HIT II patients. The outcome was favorable for 38% in the HIT II patients versus 52% in all SAH patients (P < 0.05), and deaths were more common (29%) in the HIT II patients than in all SAH patients (12%, P < 0.001).

The incidence of HIT II in SAH patients at a single center was 15%. The SAH patients with HIT II had significantly higher rates of thrombotic complications, new hypodensities on head computed tomographic scans, more deaths, and significantly less favorable outcomes. This is the first report of the incidence of HIT II in a neurosurgical patient population.