Crespo Eric M, Oliveira Gustavo B F, Honeycutt Emily F, Becker Richard C, Berger Peter B, Moliterno David J, Anstrom Kevin J, Abrams Charles S, Kleiman Neal S, Moll Stephan, Rice Lawrence, Rodgers Jo E, Steinhubl Steven R, Tapson Victor F, Granger Christopher B, Ohman E Magnus
University of Vermont, Burlington, USA.
Am Heart J. 2009 Apr;157(4):651-7. doi: 10.1016/j.ahj.2009.01.005. Epub 2009 Mar 17.
Thrombocytopenia and heparin-induced thrombocytopenia (HIT) are potentially devastating paradoxical side effects of heparin therapy. We explored the evaluation, management, and clinical consequences of thrombocytopenia occurring during heparin therapy in diverse clinical settings.
CATCH was a prospective observational study that enrolled 3,536 patients in 48 US hospitals. Data were collected on 3 strata: patients receiving any form of heparin for > or =96 hours (n = 2,420); cardiac care unit (CCU) patients treated with heparin who developed thrombocytopenia (n = 1,090); patients who had an HIT assay performed (n = 449).
Thrombocytopenia occurred in 36.4% of patients in the prolonged heparin stratum and was associated with an increased risk of death or thromboembolic complication (OR 1.5, 95% CI 1.2-1.9). Among a subset of patients whose clinical presentation suggested they were at high risk for HIT, suspicion for HIT was uncommon (prolonged heparin stratum 19.8%, CCU stratum 37.6%) and often did not arise until > or =1 day after patients developed thrombocytopenia. Often patients were not evaluated for HIT until after they had had a thromboembolic complication (prolonged heparin stratum 43.8%, CCU stratum 61%). Even after HIT was suspected, patients often continued to receive heparin. Direct thrombin inhibitor use was infrequent (prolonged heparin stratum 29.4%, CCU stratum 35.6%). Among the few patients who underwent evaluation, HIT was confirmed in 46.7% of the prolonged heparin stratum and 31.4% of the CCU stratum.
Thrombocytopenia is common among patients receiving heparin, and it is associated with substantial risk for catastrophic complications. Despite the high risk for HIT in this population, recognition, evaluation, and appropriate treatment are infrequent and delayed.
血小板减少症和肝素诱导的血小板减少症（HIT）是肝素治疗潜在的严重矛盾性副作用。我们探讨了在不同临床环境中肝素治疗期间发生的血小板减少症的评估、管理及临床后果。
CATCH是一项前瞻性观察性研究，在美国48家医院纳入了3536例患者。收集了3个层面的数据：接受任何形式肝素治疗≥96小时的患者（n = 2420）；发生血小板减少症的接受肝素治疗的心脏监护病房（CCU）患者（n = 1090）；进行了HIT检测的患者（n = 449）。
在接受长时间肝素治疗的患者层面中，36.4%的患者发生了血小板减少症，且与死亡或血栓栓塞并发症风险增加相关（比值比1.5，95%置信区间1.2 - 1.9）。在一部分临床表现提示有高HIT风险的患者中，对HIT的怀疑并不常见（长时间肝素治疗层面为19.8%，CCU层面为37.6%），且往往在患者出现血小板减少症≥1天后才出现。患者通常直到发生血栓栓塞并发症后才接受HIT评估（长时间肝素治疗层面为43.8%，CCU层面为61%）。即使怀疑有HIT，患者仍常继续接受肝素治疗。直接凝血酶抑制剂的使用并不常见（长时间肝素治疗层面为29.4%，CCU层面为35.6%）。在少数接受评估的患者中，长时间肝素治疗层面46.7%的患者及CCU层面31.4%的患者确诊为HIT。
血小板减少症在接受肝素治疗的患者中很常见，且与严重灾难性并发症风险相关。尽管该人群中HIT风险很高，但识别、评估及适当治疗却不常见且延迟。
