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重症监护环境下的肝素诱导的血小板减少症:诊断与管理

Heparin-induced thrombocytopenia in the critical care setting: diagnosis and management.

作者信息

Napolitano Lena M, Warkentin Theodore E, Almahameed Amjad, Nasraway Stanley A

机构信息

Acute Care Surgery, Trauma, Burn, Critical Care, Emergency Surgery, Department of Surgery, University of Michigan Health System, Ann Arbor, MI, USA.

出版信息

Crit Care Med. 2006 Dec;34(12):2898-911. doi: 10.1097/01.CCM.0000248723.18068.90.

DOI:10.1097/01.CCM.0000248723.18068.90
PMID:17075368
Abstract

BACKGROUND

Thrombocytopenia is a common occurrence in critical illness, reported in up to 41% of patients. Systematic evaluation of thrombocytopenia in critical care is essential to accurate identification and management of the cause. Although sepsis and hemodilution are more common etiologies of thrombocytopenia in critical illness, heparin-induced thrombocytopenia (HIT) is one potential etiology that warrants consideration.

OBJECTIVE

This review will summarize the pathogenesis and clinical consequences of HIT, describe the diagnostic process, and review currently available treatment options.

DATA SOURCE

MEDLINE/PubMed search of all relevant primary and review articles.

DATA SYNTHESIS AND CONCLUSIONS

HIT is a clinicopathologic syndrome characterized by thrombocytopenia (>/=50% from baseline) that typically occurs between days 5 and 14 after initiation of heparin. This temporal profile suggests a possible diagnosis of HIT, which can be supported (or refuted) with a strong positive (or negative) laboratory test for HIT antibodies. When considering the diagnosis of HIT, critical care professionals should monitor platelet counts in patients who are at risk for HIT and carefully evaluate for, a) temporal features of the thrombocytopenia in relation to heparin exposure; b) severity of thrombocytopenia; c) clinical evidence for thrombosis; and d) alternative etiologies of thrombocytopenia. Due to its prothrombotic nature, early recognition of HIT and prompt substitution of heparin with a direct thrombin inhibitor (e.g., argatroban or lepirudin) or the heparinoid danaparoid (where available) reduces the risk of thromboembolic events, some of which may be life-threatening.

摘要

背景

血小板减少症在危重症中很常见,据报道高达41%的患者会出现。对危重症中血小板减少症进行系统评估对于准确识别和处理病因至关重要。虽然脓毒症和血液稀释是危重症中血小板减少症更常见的病因,但肝素诱导的血小板减少症(HIT)是一个值得考虑的潜在病因。

目的

本综述将总结HIT的发病机制和临床后果,描述诊断过程,并回顾目前可用的治疗选择。

数据来源

对所有相关的原始研究和综述文章进行MEDLINE/PubMed检索。

数据综合与结论

HIT是一种临床病理综合征,其特征为血小板减少(较基线水平降低≥50%),通常在开始使用肝素后5至14天出现。这种时间特征提示可能为HIT,可通过HIT抗体的强阳性(或阴性)实验室检测来支持(或排除)诊断。在考虑HIT诊断时,危重症专业人员应监测有HIT风险患者的血小板计数,并仔细评估:a)血小板减少与肝素暴露相关的时间特征;b)血小板减少的严重程度;c)血栓形成的临床证据;d)血小板减少的其他病因。由于其促血栓形成的性质,早期识别HIT并迅速用直接凝血酶抑制剂(如阿加曲班或比伐卢定)或类肝素达那肝素(如可用)替代肝素可降低血栓栓塞事件风险,其中一些可能危及生命。

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