D-二聚体在心肺复苏患者自主循环恢复后的溶栓治疗

Clinical significance of D-dimer activity in thrombosis of patients with return of spontaneous circulation after cardiopulmonary resuscitation

目的 探讨D-二聚体对心肺复苏（CPR）患者溶栓治疗的临床指导意义.方法 选择有自主循环恢复（ROSC）的CPR患者,按〈2005国际CPR与心血管急救指南〉进行复苏治疗,ROSC后,患者仍昏迷不醒、生命体征不稳,予颅脑CT及胸部CT检查,排除颅内出血、主动脉夹层、气胸等溶栓治疗禁忌证,共有47例患者入选,分为A、B、C 3组,A、B组经家属同意并签字后进行溶栓治疗,于溶栓前、溶栓1、2、4、8、12 h,检测外周静脉血中D-二聚体（D-Dimer）.A组（17例）：溶栓前D-二聚体≥512 μg/L;B组（14例）：溶栓前D-二聚体＜512μg/L;C组（16例）家属拒绝溶栓治疗的患者,不论D-二聚体升高与否,作为对照组.对各组患者-般资料、D-二聚体、治愈率、格拉斯哥昏迷评分（GCS）进行统计学分析.结果 A组D-二聚体于溶栓1 h即明显升高（P＜0.05）,溶栓2 h达峰值,之后逐渐下降,最终治愈率达67%,高于B、C组,差异有统计学意义（P＜0.05）;溶栓24 h GCS高于B、C组,差异有统计学意义（P＜0.05）.B组D-二聚体溶栓4 h内基本不变（P＞0.05）,溶栓8 h后逐渐下降（P＜0.05）,治愈率较低,溶栓24 h GCS无明显升高（P＞0.05）;C组为对照组,未进行溶栓治疗,治愈率及ROSC24 h GCS均较低.结论 CPR患者ROSC后,部分患者D-二聚体（≥512μg/L）明显升高,其心脏骤停可能与血栓栓塞、循环系统血栓形成、血液流变学异常等因素有密切的关系,在初步排除溶栓治疗的绝对禁忌证后,对这部分患者进行溶栓治疗,开通梗塞的血管,改善血流循环,解除心脏骤停的病因,从而提高了CPR患者的最终治愈率.部分患者D-二聚体（＜512μg/L）无明显升高,考虑非血栓栓塞性疾病所致的心脏骤停,这时溶栓治疗不能改善患者的病情,也没有最终提高患者的治愈率,失去了溶栓治疗的意义.

Objective To investigate the clinical significance of D-dimer contents in peripheral blood for monitoring the efficacy of thrombolytic therapy in patients with return of spontaneous circulation （ROSC） of cardiopulmonary resuscitation （ CPR ） cardiopulmonary resuscitation after cardiac arrest. Methods Forty-seven patients with sudden cardiac arrest received CPR according to 2005 American Heart Association （AHA） guidelines for CPR and emergency cardiovascular care （ECC）. At the early stage of ROSC, those patients underwent head and breast CT scan if they were in a state of unconsciousness and had unstable vital signs. If intracranial hemorrhage, dissection of aorta and pneumothorax were rule out, and those patients who maintained blood circulation for over 24 hours were included. The expression of D-dimer contents in peripheral blood was determined at 0, 1, 2, 4, 8, 12 h after CPR in all patients. And the patients were randomly divided into control and experiment groups. Prior to thrombolysis, the patients whose D-dimer more than 512 μg/L were classified as Group A （n = 17 ）; those whose D-dimer below 512 μg/L Group B （ n = 14）; and the remaining control group whose family members refused thrombolytic therapy Group C （n = 16）. The general data, Glasgow coma scale, survival rate and the change of D-dimer in peripheral blood were analyzed. Results In Group A, D-dimer level began to increase significantly at CPR 1 hour. It peaked at CPR 2 hours then decreased gradually. The final survival rate was 67%. The survival rate and CCS were higher than those of Groups B and C. In Group B, the D-dimer concentrations began to increase gradually at CPR1 hour, peaked at CPR 12 hours and then decreased. The survival rate and GCS was lower than those of Group A and similar to those of Group C. Group C was control group with no thrombolysis. Conclusion For those ROSC patients with D-dimer concentrations significantly higher than usual, the pathogenesis of cardiac arrest may be concerned with thromboembolism, thrombosis in circulatory system and hyperviscosity. After an initiation of thrombolytic therapy, blocked blood vessels are recanalized,blood circulation improves and the cause of cardiac arrest is removed. Thus their survival rate becomes better. For those with D-dimer concentrations no higher than usual, the cause of cardiac arrest is not concerned with thromboembolism, thrombolytic therapy can not improve the patient outcome. And the final survival rate remains unchanged. The significance of thrombolytic therapy is none.