Characterization of cerebral hemodynamic phases following severe head trauma: Hypoperfusion, hyperemia, and vasospasm
Characterization of cerebral hemodynamic phases following severe head trauma: Hypoperfusion, hyperemia, and vasospasm
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DOI：
10.3171/jns.1997.87.1.0009
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发表时间：
1997-07-01
影响因子：
4.1
通讯作者：
Becker, DP
中科院分区：
文献类型：
--
作者：
Martin, NA;Patwardhan, RV;Becker, DP
创伤后脑血流动力学紊乱的程度和时间对颅脑损伤患者的监测和治疗具有重要意义。本文对125例重型颅脑损伤患者的脑血流量(用Xe-133清除法测定)和经颅多普勒(TCD)进行了前瞻性研究，确定了伤后2周内三个不同的血流动力学阶段。通过测量脑动静脉氧分压差(AVDO(2))和脑氧代谢率(CMRO2)，进一步确定各时相的特征。I期(低灌注期)发生在损伤当天(第0天)，以低CBF15定义，根据15分钟的脑清除曲线(平均CBF15 32.3+/-2ml/100g/分钟)、正常大脑中动脉(MCA)血流速度(平均V-MCA 56.7+/-2.9 cm/秒)、正常大脑半球指数([HI]，平均HI 1.67+/-0.11)和正常AVDO(平均AVDO(2)5.4+/-0.5vol%)来定义。在这一阶段，CMRO2大约是正常的50%(平均CMRO2 1.77+/-0.18毫升/100克/分钟)，并在第二和第三阶段保持低水平。在II期(充血期，第1~3天)，CBF增加(46.8+/-3ml/100g/min)，AVDO(2)下降(3.8+/-0.1vol%；)，V-MCA升高(86+/-3.7 cm/s)，HI仍<3(2.41+/-0.1)。在第三阶段(血管痉挛阶段，第4-15天)，CBF下降(35.7+/-3.8ml/100g/分钟)，V-MCA进一步增加(96.7+/-6.3 cm/秒)，HI显著升高(2.87+/-0.22)。这是首次将CBF、代谢和TCD测量相结合来确定重型颅脑损伤后不同脑血流动力学阶段的特征和时间进程，并提出病因。这项研究与以前的研究结果一致并建立在此基础上，可能为组织有关创伤后脑血管和代谢病理生理学的现有知识提供一个有用的时间框架。
The extent and timing of posttraumatic cerebral hemodynamic disturbances have significant implications for the monitoring and treatment of patients with head injury. This prospective study of cerebral blood flow (CBF) (measured using Xe-133 clearance) and transcranial Doppler (TCD) measurements in 125 patients with severe head trauma has defined three distinct hemodynamic phases during the first 2 weeks after injury. The phases are further characterized by measurements of cerebral arteriovenous oxygen difference (AVDO(2)) and cerebral metabolic rate of oxygen (CMRO2). Phase I (hypoperfusion phase) occurs on the day of injury (Day 0) and is defined by a low CBF15 calculated from cerebral clearance curves integrated to 15 minutes (mean CBF15 32.3 +/- 2 ml/100 g/minute), normal middle cerebral artery (MCA) velocity (mean V-MCA 56.7 +/- 2.9 cm/second), normal hemispheric index ([HI], mean HI 1.67 +/- 0.11), and normal AVDO, (mean AVDO(2) 5.4 +/- 0.5 vol%). The CMRO2 is approximately 50% of normal (mean CMRO2 1.77 +/- 0.18 ml/100 g/minute) during this phase and remains depressed during the second and third phases. In Phase II (hyperemia phase, Days 1-3), CBF increases (46.8 +/- 3 ml/100 g/minute), AVDO(2) falls (3.8 +/- 0.1 vol%;), V-MCA rises (86 +/- 3.7 cm/second), and the HI remains less than 3 (2.41 +/- 0.1). In Phase III (vasospasm phase, Days 4-15), there is a fall in CBF (35.7 +/- 3.8 ml/100 g/minute), a further increase in V-MCA (96.7 +/- 6.3 cm/second), and a pronounced rise in the HI (2.87 +/- 0.22).This is the first study in which CBF, metabolic, and TCD measurements are combined to define the characteristics and time courses of, and to suggest etiological factors for, the distinct cerebral hemodynamic phases that occur after severe craniocerebral trauma. This research is consistent with and builds on the findings of previous investigations and may provide a useful temporal framework for the organization of existing knowledge regarding posttraumatic cerebrovascular and metabolic pathophysiology.