Vanderbilt University, Nashville, Tenn.
Vanderbilt University, Nashville, Tenn.
J Thorac Cardiovasc Surg. 2014 Feb;147(2):808-13; discussion 813-5. doi: 10.1016/j.jtcvs.2013.09.051. Epub 2013 Nov 13.
Causes of profound thrombocytopenia (platelet count <60 K) developing days after cardiac surgery include heparin platelet factor 4 antibodies, thrombotic thrombocytopenic purpura-like antibodies, and endotoxin generated by pulmonary infections. Modulation of immune-mediated profound thrombocytopenia with intravenous immunoglobulin could be efficacious for any of these conditions.
From 2002 to 2010, profound thrombocytopenia developed in 20 consecutive patients within days after cardiac surgery; 19 patients underwent valve or aortic operations, and 1 patient underwent coronary bypass. Risk profiles were high preoperatively: Patients' mean age was 73 years, 50% underwent nonelective procedures, 100% had comorbidities, and 25% underwent reoperations. When decreasing platelet counts approached 60 K, intravenous immunoglobulin was started at 1.5 g/kg intravenously over 5 days. Anticoagulation and platelet transfusions were avoided. In 1 patient, profound thrombocytopenia failed to reverse promptly, and daily plasmapheresis was introduced. Platelet counts before and after interventions were assessed with linear regression analyses over time, including a spline function and statistical knot coincident with starting intravenous immunoglobulin.
In 19 of 20 patients, profound thrombocytopenia stabilized and rebounded within 2 to 4 days after initiating intravenous immunoglobulin. In the remaining slow-responding patient, addition of plasmapheresis was associated with rapid recovery. In every patient, coincident multiorgan failure reversed, and 19 of 20 patients recovered uneventfully and survived hospitalization with no limb ischemia or tissue loss. No complications of intravenous immunoglobulin therapy or plasmapheresis were observed.
Although mechanisms of profound thrombocytopenia after cardiac surgery are poorly understood, they likely relate to inappropriate autoimmune moieties causing peripheral platelet aggregation and multiorgan failure. A protocol involving immunomodulation with intravenous immunoglobulin supplemented by plasmapheresis appeared safe and efficacious. Direct immunologic interventions for profound thrombocytopenia could improve postoperative outcomes.
心脏手术后数天发生的严重血小板减少症（血小板计数＜60K）的原因包括肝素血小板因子 4 抗体、血栓性血小板减少性紫癜样抗体和肺部感染产生的内毒素。静脉注射免疫球蛋白对这些情况中的任何一种的免疫介导的严重血小板减少症的调节都可能有效。
2002 年至 2010 年，在心脏手术后数天内，连续 20 例患者出现严重血小板减少症；19 例患者接受了瓣膜或主动脉手术，1 例患者接受了冠状动脉旁路手术。术前风险较高：患者平均年龄为 73 岁，50%为非选择性手术，100%合并有合并症，25%为再次手术。当血小板计数降至接近 60K 时，开始静脉内给予 1.5g/kg 的免疫球蛋白，连续 5 天。避免抗凝和血小板输注。在 1 例患者中，严重血小板减少症未能迅速逆转，随后开始每日进行血浆置换。通过线性回归分析评估干预前后的血小板计数，包括时间上的样条函数和与开始静脉内免疫球蛋白吻合的统计结。
在 20 例患者中的 19 例，在开始静脉内免疫球蛋白后 2 至 4 天内，严重血小板减少症稳定并反弹。在剩余的反应缓慢的患者中，加入血浆置换与快速恢复相关。在每个患者中，多器官衰竭同时逆转，20 例患者中有 19 例顺利恢复，无肢体缺血或组织损失，安全出院。未观察到静脉内免疫球蛋白治疗或血浆置换的并发症。
尽管心脏手术后严重血小板减少症的机制尚不清楚，但它们可能与导致外周血小板聚集和多器官衰竭的不适当自身免疫成分有关。涉及免疫调节的方案，包括静脉内免疫球蛋白补充血浆置换，似乎是安全有效的。直接针对严重血小板减少症的免疫干预可能会改善术后结局。
