外科干预对高血压脑出血后脑水肿转归的影响
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摘要
目的探讨手术干预对高血压脑出血后血肿周围脑水肿形成与发展的影响。
方法选择高血压脑出血患者160例,根据其入院后治疗方式分保守组、开颅组和微创组。采用相关性分析研究入选病例入院时血肿量和入院时水肿量的相关性;保守组以患者的年龄、性别、入院收缩压、舒张压、血肿量、血肿部位、GCS、Fib和血糖为自变量,分别以入院后第1天、第3天、第7天、第14天脑水肿相对增量(relative growth of perihematomal edema volume,RE)为因变量分别采用简单线性和多元线性回归分析研究相关性;保守组中不同出血部位对第1、3、7、14天RE的影响采用方差分析研究;保守组中不同出血部位不同血肿量对第1、3、7、14天RE的影响采用方差分析研究;幕上出血微创术、开颅术和保守治疗三者间及幕下出血开颅术与保守治疗间对RE在第1-3,3-7,7-14和14-21天的影响采用方差分析研究。
结果高血压脑出血后血肿量与脑水肿发生呈正相关(R2=0.5831),与不同时间点脑水肿相对增量相关(P <0. 01);不同出血部位的RE间无统计学差异(P>0.05)。幕上小血肿的RE最大(P<0.05);幕上微创组和开颅组间的RE无明显差异(P>0.05),与保守组相比,RE较少(P<0.05);幕下开颅组与保守组相比,RE无明显差异(P>0.05)。
结论高血压脑出血后血肿量与脑水肿程度、RE密切相关,幕上小量血肿对脑水肿变化速率影响较大,手术治疗在一定程度上减轻脑水肿发展速率。
Objective To investigate the effect of Surgical intervention on brain edema formation and development after Hypertensive Intracerebral Hemorrhage (HICH).
Methods 160 patients with HICH were divided into conservative group(C group) and surgery group which includes craniotomy group(Sc group) and minimally invasive group(Sm group) . We evaluated the association between baseline hematoma and edema by simple linear regression model. For the conservative group, age, sex, SBP, DBP, GCS, Fib,baseline hematoma, location and blood glucose were independent variable, while the relative growth of perihematomal edema volume(RE) at different time points were dependent variable, all the independent variables were evaluated by simple linear regression except location and multiple linear regression model, respectively; Analysis of variance were used with different bleeding sites, the different classifications of the hematoma volume, surgical and non-surgical, surgery in different ways, different parts of the operation was on the relative growth of perihematomal edema volume.
Results There was a highly significant correlation between hematoma an d perihematomal edema volumes at baseline( R2 =0.5831) ,and between hematoma and RE at different time(P<0.01); there was no significant statistic difference between RE of different bleeding sites(P>0.05).A small quantity of supratentorial intracerebral hematoma impact largest on RE(P<0.05); There was no significant difference between RE of Sc group and Sm group, but they were significantly lower as compared with C group(P<0.05).There was no significantly difference between RE of C group and Sc group with infratentorial intracerebral Hemorrhage (P>0.05).
Conclusions The degree of perihematomal edema and RE are strongly related to the size of the baseline hematoma of HICH; A small quantity of supratentorial hematoma impacts largely on the development of brain edema; Removing hematoma by surgery can reduce the development of brain edema.
方法选择高血压脑出血患者160例,根据其入院后治疗方式分保守组、开颅组和微创组。采用相关性分析研究入选病例入院时血肿量和入院时水肿量的相关性;保守组以患者的年龄、性别、入院收缩压、舒张压、血肿量、血肿部位、GCS、Fib和血糖为自变量,分别以入院后第1天、第3天、第7天、第14天脑水肿相对增量(relative growth of perihematomal edema volume,RE)为因变量分别采用简单线性和多元线性回归分析研究相关性;保守组中不同出血部位对第1、3、7、14天RE的影响采用方差分析研究;保守组中不同出血部位不同血肿量对第1、3、7、14天RE的影响采用方差分析研究;幕上出血微创术、开颅术和保守治疗三者间及幕下出血开颅术与保守治疗间对RE在第1-3,3-7,7-14和14-21天的影响采用方差分析研究。
结果高血压脑出血后血肿量与脑水肿发生呈正相关(R2=0.5831),与不同时间点脑水肿相对增量相关(P <0. 01);不同出血部位的RE间无统计学差异(P>0.05)。幕上小血肿的RE最大(P<0.05);幕上微创组和开颅组间的RE无明显差异(P>0.05),与保守组相比,RE较少(P<0.05);幕下开颅组与保守组相比,RE无明显差异(P>0.05)。
结论高血压脑出血后血肿量与脑水肿程度、RE密切相关,幕上小量血肿对脑水肿变化速率影响较大,手术治疗在一定程度上减轻脑水肿发展速率。
Objective To investigate the effect of Surgical intervention on brain edema formation and development after Hypertensive Intracerebral Hemorrhage (HICH).
Methods 160 patients with HICH were divided into conservative group(C group) and surgery group which includes craniotomy group(Sc group) and minimally invasive group(Sm group) . We evaluated the association between baseline hematoma and edema by simple linear regression model. For the conservative group, age, sex, SBP, DBP, GCS, Fib,baseline hematoma, location and blood glucose were independent variable, while the relative growth of perihematomal edema volume(RE) at different time points were dependent variable, all the independent variables were evaluated by simple linear regression except location and multiple linear regression model, respectively; Analysis of variance were used with different bleeding sites, the different classifications of the hematoma volume, surgical and non-surgical, surgery in different ways, different parts of the operation was on the relative growth of perihematomal edema volume.
Results There was a highly significant correlation between hematoma an d perihematomal edema volumes at baseline( R2 =0.5831) ,and between hematoma and RE at different time(P<0.01); there was no significant statistic difference between RE of different bleeding sites(P>0.05).A small quantity of supratentorial intracerebral hematoma impact largest on RE(P<0.05); There was no significant difference between RE of Sc group and Sm group, but they were significantly lower as compared with C group(P<0.05).There was no significantly difference between RE of C group and Sc group with infratentorial intracerebral Hemorrhage (P>0.05).
Conclusions The degree of perihematomal edema and RE are strongly related to the size of the baseline hematoma of HICH; A small quantity of supratentorial hematoma impacts largely on the development of brain edema; Removing hematoma by surgery can reduce the development of brain edema.
引文
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[1]张玉琪.再论微创神经外科学[J].中华神经外科杂志,2005,2(4):193-194.
[2] Krum JM, Khaibullina A. Inhibition of endogenous VEGF impedes revascularization and astroglial proliferation: roles for VEGF in brain repair [J]. Exp Neurol,2003,181(2):241-257.
[3]黄智武.高血压脑出血治疗的临床研究进展[J].医学文选,2004,23(6):814-818.
[4]徐凤科,包金锁.高血压脑出血外科治疗手术术式的研究进展[J].中国煤炭工业医学杂志,2007,10(12):1352-1353.
[5] Qureshi AI, Tuhrim S, Broderik JP. Spontaneous intracerebral hemorrhage [J].N Engl J Med ,2001, 311: 1450-1460.
[6] Flahetty ML, Haverbusch M, Sekar P. Long term mortality after intracerebral hemorrhage [J]. Neurology ,2006,66:1182-1186.
[7] Diringer MN. Intracerebral hemorrhage: pathophysiology and management [J]. Crit Care Med,2002,21:1591-1603.
[8] Kazui S, Naritomi H, Yamamoto H. Enlargement of spontaneous intracerebral hemorrhage [J]. Incidence and time course. Stroke,1996,27:1783-1787.
[9] Lee KR, Kawai N, Kim S,et al. Mechanisms of edema formation after intracerebral hemorrhage: effects of thrombin on cerebral blood flow, blood barrier permeability, and cell survival in a rat model[J] . Neurosurg ,2002,86:272-278.
[10] Zazulia AR, Diringer MN, Derdeyn CP,et al. Progression of mass effect after intracerebral hemorrhage [J].Stroke,1999,30:1167-1173.
[11] Hemphillm JL, Bonvich DC, Besmetris L,et al. A smiple, reliable grading scale for intracerebral hemorrhage [J]. Stroke, 2001,32:891-897.
[12]廖光查.高血压性脑出血微创手术治疗研究进展[J].微创医学,2007,2(4):313-315.
[13] Qureshi AI,Tuhrim S,Broderick JP,et al.Hanley DRS spontaneous intracerebral hemorrhage[J].N Engl Med,2001,344:1450-1460.
[14]孟兆鹏,张峰.高血压脑出血外科微创治疗进展[J].西南军医,2007,9(5):92-93.
[15] Gebel JM, Jauch EC, Brott TG,et al. Natural history of perihematomal edema inpatients with hyperacute spontaneous intracerebral hemorrhage [J]. Stroke, 2002,33: 2631-2635 .
[16] Zazulia AR, Diringer MN, Derdeyn CP,et al. Progression of mass effect after intracerebral hemorrhage [J].Stroke,1999,30:1167-1173.
[17] Hemphillm JL, Bonvich DC, Besmetris L,et al. A smiple, reliable grading scale for intracerebral hemorrhage [J]. Stroke, 2001,32:891-897.
[18] Xi G, Keep RF, Hoff JT,et al. Mechanisms of brain injury after intracerebral hemorrhage [J]. Lancet Neurol ,2006, 5:53-63.
[19] Juvela S, Kase CS. Advances in Intracerebral Hemorrhage Management [J]. Stroke ,2006,37: 301-304.
[20] Castillo J, Davalos A, Alvarez-sabin J,et al. Molecular signatures of brain injury after intracerebral hemorrhage [J]. Neurology ,2002, 58: 624-629.
[21] Hua Y, Xi G, Keep RF,et al. Complement activation in the brain after experimental intracerebral hemorrhage [J]. Neurosurg ,2000,92:1016-1022.
[22] Inaji M, Tomita H, Tone O,et al. Chronological changes of perihematomal edema of human intracerebral hematoma [J]. Acta Neruochir Suppl ,2003,86:445-448.
[23] Mehdiratta M, Kumar S, Hackney D,et al. Association between serum ferritin level and perihematomal edema volume in patients with spontaneous intracerebral hemorrhage [J]. Stroke ,2008,39: 1165-1170.
[24] Wu G, Xi G, Huang F,et al. Spontaneous intracerebral hemorrhage in humans: hematoma enlargement, clot lysis, and brain edema [J]. Acta Neurochir Suppl ,2006, 96: 78-80.
[25]金虎.重症高血压脑出血的超早期手术治疗[J].中国临床神经外科杂志.2003,8(1):61-62.
[26] Hemphillm JC,Bonovich DC,Besmertis L,et al. A simple,reliable grading scale for intracerebral hemorrhage[J].Stroke,2001,32(4):891-897.
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[28] Kaya RA,Turkmenoglu O,Ziyal IM,et al.The effects on prognosis of surgicaltreatment of hypertensive putaminal hematomas through transsylvia transinsular approach[J].Surgical Neurology,2003,59:176-183.
[29] Liang PC,Liang CL,Lu CH,et al.Hypertensive caudate hemorrhage:outcome,and role of external ventricular drainage[J].Stroke,2001,32(5):1195-1200.
[30] Zhao JZ,Zhou DB,Zhou LF,et al.The efficacy of three different approaches in treatment of hypertensive mtracerebral hemorrhage:a multi-center single-blind study of 2464 patients[J].Zhong Hua Yi Xue Za Zhi,2005,85(32):2238-3342.
[31]胡多利,陈忠良,朱其铮.36例脑出血微创手术前后影像学变化及临床分析[J].中华临床医学杂志,2005,6(4):31-33.
[32]李云辉,林中平,黄建龙,等.超早期锁孔血肿清除术治疗高血压基底节出血[J].中国危重病急救医学,2005,17(7):312.
[33]张延平,张攀,李业生.高血压脑出血继发重型脑室内出血的微创手术治疗[J].中国微侵袭神经外科杂志,2006,11(6):84-85.
[34]李树春,赵振华.微创手术治疗高血压脑出血临床分析[J].中国现代神经疾病杂志。2005,5(7):171.
[35]李金彩,李中秋,陆兵勋,等.脑立体定向微创手术治疗高血压脑出血[J].中华神经医学杂志,2006,5(11):855-856.
[36]闷润民,李安民,张志文,等.三种微创手术方式治疗基底核区脑出血的效果比较[J].中国微侵袭神经外科,2007,2(1);59-61.
[37]刘雨生,侯红领,洪坦娟。微创血肿清除术治疗高血压脑出血的研究进展[J].中华医学研究杂志,2005,6(4):31-33.
[2] Flahetty ML, Haverbusch M, Sekar P. Long term mortality after intracerebral hemorrhage [J]. Neurology ,2006,66:1182-1186.
[3] Diringer MN. Intracerebral hemorrhage: pathophysiology and management [J]. Crit Care Med,2002,21:1591-1603.
[4] Kazui S, Naritomi H, Yamamoto H. Enlargement of spontaneous intracerebral hemorrhage [J]. Incidence and time course. Stroke,1996,27:1783-1787.
[5]Lee KR, Kawai N, Kim S,et al. Mechanisms of edema formation after intracerebral hemorrhage: effects of thrombin on cerebral blood flow, blood barrier permeability, and cell survival in a rat model[J] . Neurosurg ,2002,86:272-278.
[6] Zazulia AR, Diringer MN, Derdeyn CP,et al. Progression of mass effect after intracerebral hemorrhage [J].Stroke,1999,30:1167-1173.
[7] Hemphillm JL, Bonvich DC, Besmetris L,et al. A smiple, reliable grading scale for intracerebral hemorrhage [J]. Stroke, 2001,32:891-897.
[8] Xi G, Keep RF, Hoff JT,et al. Mechanisms of brain injury after intracerebral hemorrhage [J]. Lancet Neurol ,2006, 5:53-63.
[9] Juvela S, Kase CS. Advances in Intracerebral Hemorrhage Management [J]. Stroke ,2006,37: 301-304.
[10] Castillo J, Davalos A, Alvarez-sabin J,et al. Molecular signatures of brain injury after intracerebral hemorrhage [J]. Neurology ,2002, 58: 624-629.
[11] Hua Y, Xi G, Keep RF,et al. Complement activation in the brain after experimental intracerebral hemorrhage [J]. Neurosurg ,2000,92:1016-1022.
[12]张玉琪.再论微创神经外科学[J].中华神经外科杂志,2005,2(4):193-194.
[13] Krum JM, Khaibullina A. Inhibition of endogenous VEGF impedes revascularization and astroglial proliferation: roles for VEGF in brain repair [J]. Exp Neurol,2003,181(2):241-257.
[14]黄智武.高血压脑出血治疗的临床研究进展[J].医学文选,2004,23(6):814-818.
[15]徐凤科,包金锁.高血压脑出血外科治疗手术术式的研究进展[J].中国煤炭工业医学杂志,2007,10(12):1352-1353.
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