Hoh Brian L, Aghi Manish, Pryor Johnny C, Ogilvy Christopher S
Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, USA.
Neurosurgery. 2005 Aug;57(2):243-8; discussion 243-8. doi: 10.1227/01.neu.0000166539.02280.e5.
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.
II型肝素诱导的血小板减少症（HIT II）是一种自身免疫介导的严重疾病形式，其特征为血小板显著减少，并具有“反常”严重血栓并发症的高风险。尽管已在多个不同患者群体中对HIT II进行了研究，但从未有关于神经外科患者群体中HIT II发病率及血栓并发症发生率的报道。在神经外科患者群体中，蛛网膜下腔出血（SAH）患者因处于重症监护病房且留置血管导管，肝素暴露量较高。此外，随着神经血管内介入手术的增加以及肝素化的相关使用，SAH患者的肝素暴露量将会增加。
在3.5年期间（2000年1月至2003年6月），我们中心连续治疗了389例SAH患者。我们回顾性地查阅了他们的实验室数据和病历，并采用公认的HIT II临床诊断标准来确定HIT II的发病率、血栓并发症、治疗及结局。
59例患者（15%）符合HIT II的临床诊断标准。HIT II患者的血小板计数最低点平均为68,600±25,300/微升（均值±标准差）。女性患者及Fisher分级为3级的患者更易发生HIT II（P<0.01）。36例患者（61%）接受了神经血管内介入手术。HIT II患者的全身性血栓并发症发生率为37% versus 无HIT II的SAH患者为7%（P<0.001），HIT II患者头部计算机断层扫描上新发低密度影的发生率为66% versus 无HIT II的SAH患者为40%（P<0.001）。HIT II患者的临床结局更差。HIT II患者中结局良好的比例为38% versus 所有SAH患者为52%（P<0.05），HIT II患者中的死亡更为常见（29%） versus 所有SAH患者为12%（P<0.001）。
单一中心SAH患者中HIT II的发病率为15%。患有HIT II的SAH患者血栓并发症发生率、头部计算机断层扫描上新发低密度影发生率显著更高，死亡更多，且结局明显更差。这是神经外科患者群体中HIT II发病率的首次报道。
