脑灌注压测量 (脑灌注压与颅内压关系)

脑外伤监测重点

久留米大学医学部神经外科 宫城知也

久留米大学医学部神经外科 森冈基浩

概述

重型脑外伤的急性期包括外伤性脑挫伤及广泛性损伤等原发性脑损伤,以及各种全身和颅内因素诱发的继发性损伤[1]。继发性损伤的诱发因素包括低血压、缺氧或体温高/低等全身因素,以及颅内血肿等导致的脑水肿或脑肿胀等局部因素。当发生脑水肿或脑肿胀时,在细胞水平会产生乳酸、炎性细胞因子和氧自由基等有害物质[2]。与继发性脑损伤关系密切的是脑缺血缺氧状态,在外伤初期脑缺血缺氧状态就开始出现[3,4],之后出现的颅内压(Intracranial pressure,ICP)升高等又加重脑缺血,从而形成恶性循环[5]。急性期患者的病情会随着时间推移发生动态变化[6],因此急性期治疗的主要目的是抑制继发性脑损伤的发生和发展,尽快改善外伤后出现的全身缺血缺氧状态,并监测脑血流代谢的动态变化。

脑外伤监护可迅速发现脑血流及代谢异常,并观察异常是否已纠正,还可以根据监护指标判定预后。ICU脑监测基本项目包括持续床边颅内压(ICP)监测、动脉压差及脑灌注压(Cerebral perfusion pressure,CPP)监测,以及呼吸循环状态监测等项目。

日本脑神经外伤学会在2006年发表《重型头部外伤治疗·管理指南(第2版)》[7]。主要内容如表1所示。本章根据该指南对脑脊髓外伤监护详细讲解。

要点脑外伤的实际治疗从入院之前就已经开始,入院后经过早期治疗转入ICU继续监护。早期治疗开始即应重视维持呼吸循环稳定,防止大脑缺血。为保护大脑,早期治疗中的呼吸循环的管理目标如表2所示。

日本脑卒中康复治疗指南,脑室引流与颅内压监测技术

颅内压与脑灌注压管理

根据日本的诊疗指南[7],成人颅内压 15~25mmHg为开始治疗的阈值。脑灌注压是平均动脉压与颅内压的差值,应维持脑灌注压在60~70mmHg以上。

注意事项在2003年发布的美国诊疗指南中,脑灌注压最低值从70mmHg调整为60mmHg,是由于维持脑灌注压在70mmHg以上时,输液量增加会使成人呼吸窘迫综合征(Adult respiratory distress syndrome,ARDS)发生率增高[29]。

要点颅内压与脑灌注压的治疗阈值随年龄变化。小儿颅内压的治疗阈值为18mmHg,婴幼儿为10mmHg。小儿脑灌注压应维持在45mmHg以上[30]。

颅内压升高患者多预后不良[31],积极控制颅内压可改善患者的预后[21]。因此,ICU的治疗逐渐以控制颅内压为主。而近年来脑灌注压的重要性也逐渐被报道[29]。脑缺血是继发性脑损伤的原因,缺血时脑血流量不足,不能满足脑耗氧量。脑血流量=脑灌注压(CPP)/脑血管阻力(Cerebrovascular resistance,CVR),脑血管自动调节功能障碍时,脑灌注压直接影响脑血流量。Rosner等报道脑血管在具备自动调节功能时,脑灌注压降低可引起脑血管扩张,继而脑血流量上升,颅内压升高,脑灌注压进一步降低,形成恶性循环,因此维持脑灌注压高值具有重要意义[29]。

瑞典的Lund治疗显示过高的脑灌注压反而加重血管性脑水肿,结果导致颅内压升高,脑灌注压的治疗阈值设定为50~60mmHg,维持在低水平上有利于治疗[33]。脑灌注压的管理目标受到脑血管自动调节功能及脑损伤程度的影响,因此临床上应结合有无脑血管自动调节功能障碍、颈内静脉血氧饱和度及脑组织氧分压等其他脑循环代谢指标综合判断。

确定有无脑血管自动调节功能障碍

如上所述,理论上如果脑血管自动调节功能正常,血压上升则颅内压降低。因此,我们监测一定时间内的血压与颅内压值,进行回归分析。结果显示如果为正相关(相关系数1~0)则存在自动调节功能障碍,负相关(相关系数-1~0)则自动调节功能正常(图6)。Czosnyka等人计算血压与颅内压变化的相关系数(Pressure reactivity index,PRx)发现,PRx在-0.2以下时患者预后良好[34]。我们计算9例接受35℃低体温治疗患者的PRx,结果显示预后良好的5人PRx值显著降低(表4 (图7));PRx与脑组织氧分压的关系显示PRx越接近于+1,脑组织氧分压越低。总之,脑血管自动调节功能越异常,越容易发生局部脑组织供氧障碍。

日本脑卒中康复治疗指南,脑室引流与颅内压监测技术

图6 根据颅内压及脑灌注压的变动测定脑血流自动调节功能

日本脑卒中康复治疗指南,脑室引流与颅内压监测技术

日本脑卒中康复治疗指南,脑室引流与颅内压监测技术

图7 35℃低体温治疗的PRx与脑组织氧分压的关系。

Howwells等人推荐PRx在0.13以下时应维持脑灌注压高值,采取以调节脑灌注压为主的治疗;PRx在0.13以上时应采取以调节颅内压(下调脑灌注压)为主的治疗[35]。

对10分钟内的平均血压(BP)和颅内压描点,计算相关系数。如果血压上升,颅内压也上升,则相关系数为正(0~+1),诊断为脑血流自动调节功能障碍。血压上升而颅内压下降,则相关系数为负(-1~0),诊断为脑血流自动调节功能正常。

小结

表5为颅脑外伤时各种监测指标的治疗阈值。出现监测指标异常时应立即寻找原因,尽快展开治疗。尽管监测指标繁多,但重型头部外伤患者的预后仍较差。今后应该确立合适的监护项目,开展适合每个病人的个体化治疗。

日本脑卒中康复治疗指南,脑室引流与颅内压监测技术

●参考文献

[1]徳富孝志:重症頭部外傷の病態と治療. Jpn J Neurosurg, 14:425-431, 2005.[2]Bouma GJ, Muizellaar JP, et al:Cerebral circulation and metabolism after severe traumatic brain injury:The elusive roleof ischemia. J Neurosurg, 75:685-693, 1991.[3]Robertson CS, Contant CF, et al:Cerebral blood flow, arteriovenouus oxygen difference, and outcome in head injured patients.J Neurol Neurosurg Psychiatry, 55:594-603, 1992.[4]von Oettingen G, Berghot B, et al:Blood flow and ischemia within traumatic cerebral contusions. Neurosurgery, 50:781-790, 2002.[5]徳富孝志:脳損傷急性期の保護療法. 久留米医学会雑誌, 68:239-244, 2005.[6]徳富孝志:重症頭部外傷モニタリングの実際. Jpn J Neurosurg, 16:906-912, 2007.[7]日本神経外傷学会:重症頭部外傷治療·管理のガイドライン 第2版. 神経外傷, 29:1-115, 2006.[8]Bullock RM, Chesnut RM, et al:Guidelines for the surgical management of traumatic brain injury. Neurosurgery, 58:S1-50, 2006.[9]Chan KH, Miller JD, et al:The effect of changes in cerebral perfusion pressure upon middle cerebral artery blood flow velocity and jugular bulb venous oxygen saturation after severe brain injury. J Neurosurg, 77:55-61, 1992.[10]Latronico N, Beindorf AE, et al:Limits of intermittent jugular bulb oxygen saturation monitoring in the management of severe head trauma patients. Neurosurgery, 46:1131-1139, 2000.[11]Metz C, Holzschuh M, et al:Monitoring of cerebral oxygen metabolism in the jugular bulb:Reliability of unilateral measurements in severe head injury. J Cereb Blood Flow Metabol, 18:332-343, 1998.[12]Robertson CS, Narayan RK, et al:Cerebral arteriovenous oxygen difference as an estimate of cerebral blood flow in comatous patients. J Neurosurg, 70:222-230, 1989.[13]Dearden NM, Midgley S:Technical considerations in continuous jugular venous oxygen saturation measurement. Acta Neurochir Suppl(Wien), 59:91-97, 1993.[14]Valadka AB, Gopinath SP, et al:Relationship of brain tissue PO2 to Outcome after severe head injury. Crit Care Med, 26:1576-1581, 1998.[15]Meixensberger J, Dings J, et al:Studies of tissue PO2 in normal and pathological human brain cortex. Acta Neurochir Suppl(Wien), 59:58-63, 1993.[16]Menon DK, Coles JP, et al:Diffusion limited oxygen delivery following head injury. Crit Care Med, 32:1384-1390, 2004.[17]van den Brink WA, van Santbrink H, et al:Brain oxygen tension in severe head injury. Neurosurgery, 46:868-878, 2000.[18]Stiefel MF, Spiotta A, et al:Reduces mortality rate in patients with severe traumatic brain injury treated with brain tissue oxygen monitoring. J Neurosurg, 103:805-811, 2005.[19]Reinert M, Barth A, et al:Effects of cerebral perfusion pressure and intracranial fraction of inspired oxygen on brain tissue oxygen, lactate and glucose in patients with severe head injury. Acta Neurochir(Wien), 145:341-350, 2003.[20]Kampfl A, Pfausler B, et al:Near infrared spectroscopy(NIRS)in patients with severe brain injury and elevated intracranial pressure. A pilot study. Acta Nurochir Suppl, 70:112-114, 1997.[21]Shigemori M, Kikuchi N, et al:Monitoring of severe head-injuryed patients with transcranial Doppler(TCD)ultrasonography. Acta Neurochir Suppl(Wien), 55:6-7, 1992.[22]Oertel M, Kelly DF, et al:Efficacy of hyperventilation, blood pressure elevation, and metabolic suppression therapy in controlling intracranial pressure after head injury. J Neurosurg, 97:1045-1053, 2002.[23]Schmidt EA, Czosnkya M, et al:Preliminary experience of the estimation of cereberal perfusion pressure using transcranial Doppler ultrasonography. J Neurol Neurosurg Psychiatry, 70:198-204, 2001.[24]Goodman JC, Valdka AB, et al:Extracellular lactate and glucose alterations in the brain after head injury measured by microdialysis. Crit Care Med, 27:1965-1973, 1999.[25]Shiozaki T, Sugimoto H, et al:Effect of mild hypothermia on uncontrollable intracranial hypertension after severe head injury. J Neurosurg, 79:363-368,1993.[26]Tokutomi T, Morimoto K, et al:Optimal temperature for the management of severe traumatic brain injury:Effect of hypothermia on intracranial pressure, systemic and intracranial hemodynamics, and metabolism. Neurosurgery, 52:102-111, 2003.[27]Clifton GL, Miller ER, et al:Lack of induction of hypothermia after acute brain injury. N Engl J Med, 344:556-563, 2001.[28]Hutchison JS, Ward RE, et al:Hypothermia PediatricHead Injury Trial Investigators and the Canadian Critical Care Trials Group:Hypothermia Therapy after Traumatic BrainInjury in Children. N Engl J Med, 358:2447-2456, 2008.

[29]Rosner MJ, Rosner SD, et al:Cerebral perfusion pressure:Management protocol and clinical results. J Neurosurg, 83:949-962, 1995.

[30]Carney NA, Chesnut R, et al:Guidelines for the acute medical management of severe traumatic brain injury in infants,children, and adolescents. Crit Care Med, 31:S409-491, 2003.

[31]Becker DP, Miller JD, et al:The outcome from severe head injury with early diagnosis and intensive management. J Neurosurg,47:491-502, 1977.

[32]Bulger EM, Nathens AB, et al:Management of severe head injury:Institutional variations in care and effect on outcome.Crit care Med, 30:1870-1876, 2002.

[33]Eker C, Asgeirsson B, et al:Improved outcome after severe head injury with a new therapy based on principles for brainvolume regulation and preserved microcirculation. Crit Care Med, 26:1881-1886, 1998.

[34]Czosnyka M, Smielewski P, et al:Continuous assessment of the cerebral vasomotor reactivity in head injury. Neurosurgery,41:11-19, 1997.

[35]Howwells T, Elf K, et al:Pressure reactivity as a guide in the treatment of cerebral perfusion pressure in patients withbrain trauma. J Neurosurg, 102:311-317, 2005.

注:本文节选自 NS NEUROSURGERY 神经外科手术图解系列