Bouma G J, Muizelaar J P, Choi S C, Newlon P G, Young H F
Division of Neurosurgery, Medical College of Virginia, Virginia Commonwealth University, Richmond.
J Neurosurg. 1991 Nov;75(5):685-93. doi: 10.3171/jns.1991.75.5.0685.
Although experimental and pathological studies suggest an important role for ischemia in the majority of fatal cases of traumatic brain injury, ischemia has been a rare finding in most clinical studies of cerebral blood flow (CBF) in head-injured patients. The hypothesis of the present study was that cerebral ischemia occurs in the first few hours after injury, but that CBF measurements have not been performed early enough. Early measurements of CBF (by the 133Xe intravenous method) and arteriovenous oxygen difference (AVDO2) were obtained in 186 adult head-injured patients with a Glasgow Coma Scale score of 8 or less, and were correlated with neurological status and outcome. During the first 6 hours after injury, CBF was low (22.5 +/- 5.2 ml/100 gm/min) but increased significantly during the first 24 hours. The AVDO2 followed the opposite course; the decline of AVDO2 was most profound in patients with low motor scores, suggesting relative hyperemia after 24 hours. A significant correlation between motor score and CBF was found in the first 8 hours after injury (Spearman coefficient = 0.69, p less than 0.001), but as early as 12 hours postinjury this correlation was lost. A similar pattern was found for the relationship between CBF and outcome. Cerebral blood flow below the threshold for infarction (CBF less than or equal to 18 ml/100 gm/min) was found in one-third of the studies obtained within 6 hours, the incidence rapidly decreasing thereafter. A low CBF after 24 hours was not generally associated with a high AVDO2, and was probably a reflection of low oxidative metabolism rather than frank ischemia. In 24 patients, a CBF of 18 ml/100 gm/min or less was found at some point after injury; the mortality rate was significantly higher in this subgroup, and survivors did worse. In some cases, ischemia was successfully treated by reducing hyperventilation or inducing arterial hypertension. These results support the above hypothesis, and suggest that early ischemia after traumatic brain injury may be an important factor determining neurological outcome. Moreover, these data indicate that early hyperventilation or lowering of blood pressure to prevent brain edema may be harmful.
尽管实验和病理学研究表明，在大多数创伤性脑损伤致死病例中缺血起着重要作用，但在大多数关于头部受伤患者脑血流量（CBF）的临床研究中，缺血却是罕见的发现。本研究的假设是，脑缺血发生在受伤后的最初几个小时，但CBF测量没有足够早地进行。对186例格拉斯哥昏迷量表评分为8分及以下的成年头部受伤患者进行了早期CBF测量（采用静脉注射133Xe法）和动静脉氧分压差（AVDO2）测量，并将其与神经状态和预后相关联。在受伤后的最初6小时内，CBF较低（22.5±5.2 ml/100 gm/min），但在最初24小时内显著增加。AVDO2则呈现相反的变化趋势；运动评分低的患者AVDO2下降最为明显，提示24小时后出现相对充血。在受伤后的最初8小时内，运动评分与CBF之间存在显著相关性（斯皮尔曼系数=0.69，p<0.001），但在受伤后12小时，这种相关性就消失了。CBF与预后之间的关系也呈现出类似的模式。在6小时内进行的研究中，三分之一的患者发现脑血流量低于梗死阈值（CBF≤18 ml/100 gm/min），此后发病率迅速下降。24小时后CBF较低通常与高AVDO2无关，可能反映的是低氧化代谢而非明显的缺血。在24例患者中，受伤后的某个时间点发现CBF为18 ml/100 gm/min或更低；该亚组的死亡率显著更高，幸存者的情况也更差。在某些情况下，通过减少过度通气或诱导动脉高血压成功治疗了缺血。这些结果支持了上述假设，并表明创伤性脑损伤后的早期缺血可能是决定神经预后的重要因素。此外，这些数据表明，早期过度通气或降低血压以预防脑水肿可能是有害的。
