98例脑挫裂伤患者纤溶亢进的相关因素研究
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摘要
目的探讨脑挫裂伤患者发生纤溶亢进的相关因素,以期优化为外科治疗提供参考依据。方法选取2016年6月—2017年6月滨洲医学院附属医院收治的成人创伤患者204例[创伤严重程度评分(ISS)≥16],分为脑挫裂伤患者98例(实验组)和颅外创伤患者106例(对照组)。将到达急诊室时D-二聚体(D-D)≥38 mg/L定义为纤溶亢进。通过与对照组比较,评估实验组患者纤溶亢进与创伤严重程度、组织损伤及血压的关系。结果两组发生纤溶亢进的患者损伤严重,即ISS更高(P<0.05);Pearson相关分析结果显示,ISS与凝血酶原时间(PT)、激活部分凝血酶时间(APTT)及D-D呈正相关(P <0.05);根据乳酸脱氢酶(LDH)和肌酸激酶(CK)水平组织损伤程度,组织损伤与两组中的纤溶亢进呈正相关(P <0.05);实验组纤溶亢进者病死率高于无纤溶亢进者(P <0.05);收缩压与纤溶亢进在实验组呈正相关(P <0.05),而在对照组呈负相关(P <0.05)。结论严重创伤患者伤后易出现纤溶亢进,并与组织损伤和创伤严重程度有关;发生纤溶亢进的脑挫裂伤患者病死率更高,并与收缩压升高有关。
Objective To investigate the related factors of hyperfibrinolysis in patients with cerebral contusion and to provide reference for its surgical treatment. Methods Totally 204 adult trauma patients with an admission ISS score more than 16 admitted to our hospital from June 2016 to June 2017 were selected, among which 98 cases with cerebral contusion were called experimental group and the other 106 cases with extracranial trauma were called control group. Hyperfibrinolysis was defined when the D-dimer level was more than 38 mg/L. Compared with the control group, the relationship between fibrinolysis and the severity of trauma, tissue injury and blood pressure in the experimental group was evaluated. Results In both groups, patients with hyperfibrinolysis were more severely damaged and got higher ISS scores. Pearson correlation analysis showed that ISS was positively correlated with PT,APTT and D-dimer, and the correlation coefficients were 0.463, 0.436 and 0.663 respectively. Tissue damage assessed by levels of lactate dehydrogenase(LDH) and creatine kinase(CK) was positively correlated with hyperfibrinolysis in both groups. In the experimental group, mortality of patients with hyperfibrinolysis was higher than that without hyperfibrinolysis. Systolic blood pressure and hyperfibrinolysis in the experimental group were positively correlated and negatively correlated in the control group. Conclusions Hyperfibrinolysis occurs in the patients with severe trauma and is related to the degree of trauma and tissue injury. The mortality of patients with cerebral contusion and hyperfibrinolysis is higher, which is related to the increased systolic blood pressure.
Objective To investigate the related factors of hyperfibrinolysis in patients with cerebral contusion and to provide reference for its surgical treatment. Methods Totally 204 adult trauma patients with an admission ISS score more than 16 admitted to our hospital from June 2016 to June 2017 were selected, among which 98 cases with cerebral contusion were called experimental group and the other 106 cases with extracranial trauma were called control group. Hyperfibrinolysis was defined when the D-dimer level was more than 38 mg/L. Compared with the control group, the relationship between fibrinolysis and the severity of trauma, tissue injury and blood pressure in the experimental group was evaluated. Results In both groups, patients with hyperfibrinolysis were more severely damaged and got higher ISS scores. Pearson correlation analysis showed that ISS was positively correlated with PT,APTT and D-dimer, and the correlation coefficients were 0.463, 0.436 and 0.663 respectively. Tissue damage assessed by levels of lactate dehydrogenase(LDH) and creatine kinase(CK) was positively correlated with hyperfibrinolysis in both groups. In the experimental group, mortality of patients with hyperfibrinolysis was higher than that without hyperfibrinolysis. Systolic blood pressure and hyperfibrinolysis in the experimental group were positively correlated and negatively correlated in the control group. Conclusions Hyperfibrinolysis occurs in the patients with severe trauma and is related to the degree of trauma and tissue injury. The mortality of patients with cerebral contusion and hyperfibrinolysis is higher, which is related to the increased systolic blood pressure.
引文
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[5]COHEN M J,BROHI K,GANTER M T,et al.Early coagulopathy after traumatic brain injury:the role of hypoperfusion and the protein C pathway[J].J Trauma,2007,63:1254-1261.
[6]BROHI K,COHEN M J,DAVENPORT R A.Acute coagulopathy of trauma:mechanism,identification and effect[J].Curr Opin Crit Care,2007,13(6):680-685.
[7]LUSTENBERGER T,TALVING P,KOBAYASHI L,et al.Early coagulopathy after isolated severe traumatic brain injury:relationship with hypoperfusion challenged[J].J Trauma,2010,69:1410-1414.
[8]KARAKUS A,KEKEC Z,AKCAN R,et al.The relationship of trauma severity and mortality with cardiac enzymes and cytokines at multiple trauma patients[J].Ulus Travma Acil Cerrahi Derg,2012,18:289-295.
[9]HAYAKAWA M,GANDO S,IEKO M,et al.Massive amounts of tissue factor induce fibrinogenolysis without tissue hypoperfusion in rats[J].Shock,2013,39:514-519.
[10]THEUSINGER O M,BAULIG W,SEIFERT B,et al.Changes in coagulation in standard laboratory tests and ROTEM in trauma patients between on-scene and arrival in the emergency department[J].Anesth Analg,2015,120:627-635.
[2]HAYAKAWA M,MAEKAWA K,KUSHIMOTO S,et al.High D-dimer levels predict a poor outcome in patients with severe trauma,even with high fibrinogen levels on arrival:a multicenter retrospective study[J].Shock,2016,45:308-314.
[3]KUTCHER M E,CRIPPS M W,MCCREERY R C,et al.Criteria for empiric treatment of hyperfibrinolysis after trauma[J].J Trauma Acute Care Surg,2012,73:87-93.
[4]MAEGELE M.Coagulopathy after traumatic brain injury:incidence,pathogenesis,and treatment options[J].Transfusion,2013,53(1):28S-37S.
[5]COHEN M J,BROHI K,GANTER M T,et al.Early coagulopathy after traumatic brain injury:the role of hypoperfusion and the protein C pathway[J].J Trauma,2007,63:1254-1261.
[6]BROHI K,COHEN M J,DAVENPORT R A.Acute coagulopathy of trauma:mechanism,identification and effect[J].Curr Opin Crit Care,2007,13(6):680-685.
[7]LUSTENBERGER T,TALVING P,KOBAYASHI L,et al.Early coagulopathy after isolated severe traumatic brain injury:relationship with hypoperfusion challenged[J].J Trauma,2010,69:1410-1414.
[8]KARAKUS A,KEKEC Z,AKCAN R,et al.The relationship of trauma severity and mortality with cardiac enzymes and cytokines at multiple trauma patients[J].Ulus Travma Acil Cerrahi Derg,2012,18:289-295.
[9]HAYAKAWA M,GANDO S,IEKO M,et al.Massive amounts of tissue factor induce fibrinogenolysis without tissue hypoperfusion in rats[J].Shock,2013,39:514-519.
[10]THEUSINGER O M,BAULIG W,SEIFERT B,et al.Changes in coagulation in standard laboratory tests and ROTEM in trauma patients between on-scene and arrival in the emergency department[J].Anesth Analg,2015,120:627-635.