创伤性脑梗死相关危险因素研究
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摘要
目的:探讨创伤性脑损伤后脑梗死(PTCI)的相关危险因素,并评估治疗效果。方法:1选择符合入选条件的新入院患者130例,在伤后12~24h内抽取静脉血,检验凝血功能[血小板、凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)、纤维蛋白原、D-二聚体]、血浆生化(Na+、K+、Ca2+、HCO2-)、白细胞计数、血沉、血黏度、红细胞比容,记录患者一般资料[性别、年龄、入院时格拉斯哥昏迷评分(GCS)];2入院时检查头部CT,并按我科常规诊疗原则进行治疗,定期第3、5、7天复查头部CT,记录发生PTCI的患者;3伤后第2天所有患者行CT血管造影检查(CTA),对发生PTCI的患者复查;4统计比较130例患者血样本检验指标、一般资料的各区间范围及不同CTA结果的患者例数及PTCI发生例数,对高危因素进行多因素回归分析;5评价比较PTCI患者2周和6周后的治疗效果。结果:1130例患者中,12例发生PTCI,发生率为9.23%;2入院时低GCS评分,血小板、PT、APTT及纤维蛋白原异常,D-二聚体增高和高DIC评分,血浆HCO2-异常及血浆黏度增高是发生PTCI的可能危险因素(P<0.05)。但其中入院时低GCS评分(OR=2 418.539,95%CI:1.182~4 947 063.228,P<0.05),血小板异常(OR=1 453.894,95%CI:2.611~809 679.718,P<0.05),PT异常(OR=1 184.697,95%CI:2.610~537 768.835,P<0.05),D-二聚体增高(OR=169.882,95%CI:3.214~8 978.776,P<0.05)及高DIC评分(OR=147.558,95%CI:2.096~10 385.975,P<0.05)与PTCI的发生密切相关;3PTCI患者往往存在脑血管纤细、血管受压、管腔狭窄(闭合)(P<0.05);4PTCI治疗2周及6周后的效果比较差异无统计学意义(P>0.05)。结论:入院时低GCS评分、血小板及PT异常、D-二聚体增高和高DIC评分是发生PTCI的独立危险因素,应及早重视并预防;另外PTCI患者往往存在脑血管变化,发生PTCI后治疗效果不佳。
Objective:Discussing the risk factors associated with posttraumatic cerebral infarction after brain injury and to assess the effect of treatment.Method:1Selected the eligible newly admitted patients(a total of 130cases),collected venous blood within 12-24 hafter injury,tested the coagulation function(platelets,PT,APTT,fibrinogen,D-dimer),plasma biochemistry(Na+,K+,Ca2+,HCO2-),white blood cell count,blood sedimentation rate,plasma viscosity,hematocrit,recorded patient demographics(gender,age,admission GCS score).2 Examed the brain CT at admission,and re-examed the brain CT at 3d,5d,7d,while conventional treatment in accordance with the principles of our department for treatment,then recorded the patients with PTCI.3Examed the CT angiography examination to all 130 cases at the second day after injury and reviewed the patients with PTCI.4Recorded the number of patients and patients with PTCI in the scope of each section of indicators of blood test and the basic information,recorded the number of patients with different result of CTA,compared all the data above,and multivariate logistic regression analysed the high risk factor.5Evaluated the effect of treatment to the PTCI patient after 2weeks and 6weeks.Result:112cases occurred PTCI in 130 patients,the incidence was 9.23%.2Low GCS score on admission,abnormal platelets,PT,APTT and fibrinogen,high D-dimer and high DIC score,abnormal HCO2-and high plasma viscosity had statistical significance to affect the occurrence of PTCI(P<0.05),and they were the suspicious risk factor for PTCI.But low GCS score on admission(OR=2 418.539,95%CI:1.182-4 947 063.228,P<0.05),platelet abnormalities(OR=1 453.894,95%CI:2.611-809 679.718,P<0.05),PT anomalies(OR=1 184.697,95%CI:2.610-537 768.83,P<0.05),D-dimer increased(OR=169.882,95%CI:3.214-8 978.776,P<0.05)and high DIC score(OR=147.558,95%CI:2.096-10 385.975,P<0.05)were closely related to the occurrence of PTCI.3Vascular thin,vascular compression,bureaucratic narrow(closed)easily leaded PTCI(P<0.05).4There was no different of PTCI patients after two weeks and six weeks treatment(P>0.05).Conclusion:Low GCS score on admission,platelets and PT anomalies,D-dimer increased and high DIC scores were high risk factors for the occurrence of PTCI,they should be actively prevent.Cerebrovascular changes easily leaded PTCI.If PTCI occured,there was a poor respons to treatment.
Objective:Discussing the risk factors associated with posttraumatic cerebral infarction after brain injury and to assess the effect of treatment.Method:1Selected the eligible newly admitted patients(a total of 130cases),collected venous blood within 12-24 hafter injury,tested the coagulation function(platelets,PT,APTT,fibrinogen,D-dimer),plasma biochemistry(Na+,K+,Ca2+,HCO2-),white blood cell count,blood sedimentation rate,plasma viscosity,hematocrit,recorded patient demographics(gender,age,admission GCS score).2 Examed the brain CT at admission,and re-examed the brain CT at 3d,5d,7d,while conventional treatment in accordance with the principles of our department for treatment,then recorded the patients with PTCI.3Examed the CT angiography examination to all 130 cases at the second day after injury and reviewed the patients with PTCI.4Recorded the number of patients and patients with PTCI in the scope of each section of indicators of blood test and the basic information,recorded the number of patients with different result of CTA,compared all the data above,and multivariate logistic regression analysed the high risk factor.5Evaluated the effect of treatment to the PTCI patient after 2weeks and 6weeks.Result:112cases occurred PTCI in 130 patients,the incidence was 9.23%.2Low GCS score on admission,abnormal platelets,PT,APTT and fibrinogen,high D-dimer and high DIC score,abnormal HCO2-and high plasma viscosity had statistical significance to affect the occurrence of PTCI(P<0.05),and they were the suspicious risk factor for PTCI.But low GCS score on admission(OR=2 418.539,95%CI:1.182-4 947 063.228,P<0.05),platelet abnormalities(OR=1 453.894,95%CI:2.611-809 679.718,P<0.05),PT anomalies(OR=1 184.697,95%CI:2.610-537 768.83,P<0.05),D-dimer increased(OR=169.882,95%CI:3.214-8 978.776,P<0.05)and high DIC score(OR=147.558,95%CI:2.096-10 385.975,P<0.05)were closely related to the occurrence of PTCI.3Vascular thin,vascular compression,bureaucratic narrow(closed)easily leaded PTCI(P<0.05).4There was no different of PTCI patients after two weeks and six weeks treatment(P>0.05).Conclusion:Low GCS score on admission,platelets and PT anomalies,D-dimer increased and high DIC scores were high risk factors for the occurrence of PTCI,they should be actively prevent.Cerebrovascular changes easily leaded PTCI.If PTCI occured,there was a poor respons to treatment.
引文
[1]Marino R,Gasparotti R,Pinelli L,et al.Posttraumatic cerebral infarction in patients with moderate or severe head trauma[J].Neurology,2006,67:1165-1171.
[2]Doerfler A,Engelhorn T,Forsting M.Decompressive craniectomy for early therapy and secondary prevention of cerebral infarction[J].Stroke,2001,32:813-815.
[3]沈和平,王耿焕.颅脑损伤后继发脑梗塞的相关因素分析[J].浙江创伤外科杂志,2011,16(3):294-296.
[4]Miller P R,Fabian T C,Croce M A,et al.Prospective screening for blunt cerebrovascular injuries:analysis of diagnostic modalities and outcomes[J].Ann Surg,2002,236:386-393;discussion 393-395.
[5]Tawil I,Stein D M,Mirvis S E,et al.Posttraumatic cerebral infarction:incidence,outcome,and risk factors[J].J Trauma,2008,64:849-853.
[6]Chen H,Xue L X,Guo Y,et al.The influence of hemocoagulation disorders on the development of posttraumatic cerebral infarction and outcome in patients with moderate or severe head trauma[J].Biomed Res Int,2013,doi:10.1155/2013/685174.
[7]Kumar M A.Coagulopathy associated with traumatic brain injury[J].Curr Neurol Neurosci Rep,2013,13:391-391.
[8]Nekludov M,Bellander B M,Blomback M,et al.Platelet dysfunction in patients with severe traumatic brain injury[J].J Neurotrauma,2007,24:1699-1706.
[9]Sillesen M.Coagulation changes following traumatic brain injury and shock[J].Dan Med J,2014,61:B4974.
[10]Tian H L,Chen H,Wu B S,et al.D-dimer as a predictor of progressive hemorrhagic injury in patients with traumatic brain injury:analysis of 194cases[J].Neurosurg Rev,2010,33:359-365;discussion 365-366.
[11]Mracsko E,Javidi E,Na S Y,et al.Leukocyte invasion of the brain after experimental intracerebral hemorrhage in mice[J].Stroke,2014,45:2107-2114.
[12]Wang J,Dore S.Inflammation after intracerebral hemorrhage[J].J Cereb Blood Flow Metab,2007,27:894-908.
[13]Chan K H,Dearden N M,Miller J D.The significance of posttraumatic increase in cerebral blood flow velocity:a transcranial doppler ultrasound study[J].Neurosurgery,1992,30:697-700.
[14]龚皓,王小兰.外伤性脑梗塞的综合治疗[J].浙江创伤外科杂志,2006,11(3):235-236.
[15]Sims N R,Anderson M F.Mitochondrial contributions to tissue damage in stroke[J].Neurochem Int,2002,40:511-526.
[16]Fehnel C R,Wendell L C,Potter N S,et al.Severe cerebral vasospasm after traumatic brain injury[J].R I Med J(2013),2014,97:45-46.
[17]Ham H Y,Lee J K,Jang J W,et al.Post-traumatic cerebral infarction:outcome after decompressive hemicraniectomy for the treatment of traumatic brain injury[J].J Korean Neurosurg Soc,2011,50:370-376.
[2]Doerfler A,Engelhorn T,Forsting M.Decompressive craniectomy for early therapy and secondary prevention of cerebral infarction[J].Stroke,2001,32:813-815.
[3]沈和平,王耿焕.颅脑损伤后继发脑梗塞的相关因素分析[J].浙江创伤外科杂志,2011,16(3):294-296.
[4]Miller P R,Fabian T C,Croce M A,et al.Prospective screening for blunt cerebrovascular injuries:analysis of diagnostic modalities and outcomes[J].Ann Surg,2002,236:386-393;discussion 393-395.
[5]Tawil I,Stein D M,Mirvis S E,et al.Posttraumatic cerebral infarction:incidence,outcome,and risk factors[J].J Trauma,2008,64:849-853.
[6]Chen H,Xue L X,Guo Y,et al.The influence of hemocoagulation disorders on the development of posttraumatic cerebral infarction and outcome in patients with moderate or severe head trauma[J].Biomed Res Int,2013,doi:10.1155/2013/685174.
[7]Kumar M A.Coagulopathy associated with traumatic brain injury[J].Curr Neurol Neurosci Rep,2013,13:391-391.
[8]Nekludov M,Bellander B M,Blomback M,et al.Platelet dysfunction in patients with severe traumatic brain injury[J].J Neurotrauma,2007,24:1699-1706.
[9]Sillesen M.Coagulation changes following traumatic brain injury and shock[J].Dan Med J,2014,61:B4974.
[10]Tian H L,Chen H,Wu B S,et al.D-dimer as a predictor of progressive hemorrhagic injury in patients with traumatic brain injury:analysis of 194cases[J].Neurosurg Rev,2010,33:359-365;discussion 365-366.
[11]Mracsko E,Javidi E,Na S Y,et al.Leukocyte invasion of the brain after experimental intracerebral hemorrhage in mice[J].Stroke,2014,45:2107-2114.
[12]Wang J,Dore S.Inflammation after intracerebral hemorrhage[J].J Cereb Blood Flow Metab,2007,27:894-908.
[13]Chan K H,Dearden N M,Miller J D.The significance of posttraumatic increase in cerebral blood flow velocity:a transcranial doppler ultrasound study[J].Neurosurgery,1992,30:697-700.
[14]龚皓,王小兰.外伤性脑梗塞的综合治疗[J].浙江创伤外科杂志,2006,11(3):235-236.
[15]Sims N R,Anderson M F.Mitochondrial contributions to tissue damage in stroke[J].Neurochem Int,2002,40:511-526.
[16]Fehnel C R,Wendell L C,Potter N S,et al.Severe cerebral vasospasm after traumatic brain injury[J].R I Med J(2013),2014,97:45-46.
[17]Ham H Y,Lee J K,Jang J W,et al.Post-traumatic cerebral infarction:outcome after decompressive hemicraniectomy for the treatment of traumatic brain injury[J].J Korean Neurosurg Soc,2011,50:370-376.