CEREBRAL-CIRCULATION AND METABOLISM AFTER SEVERE TRAUMATIC BRAIN INJURY - THE ELUSIVE ROLE OF ISCHEMIA
CEREBRAL-CIRCULATION AND METABOLISM AFTER SEVERE TRAUMATIC BRAIN INJURY - THE ELUSIVE ROLE OF ISCHEMIA
复制标题
DOI：
10.3171/jns.1991.75.5.0685
复制
发表时间：
1991-11-01
影响因子：
4.1
通讯作者：
YOUNG, HF
中科院分区：
文献类型：
--
作者：
BOUMA, GJ;MUIZELAAR, JP;YOUNG, HF
虽然实验和病理研究表明，脑缺血在大多数颅脑损伤致死病例中起着重要作用，但在大多数颅脑损伤患者的脑血流临床研究中，脑缺血的发现并不多见。本研究的假设是脑缺血发生在损伤后的最初几个小时，但CBF测量还没有足够早地进行。对186例格拉斯哥昏迷评分小于或等于8分的成年颅脑损伤患者进行早期脑血流量(Xe-133静脉法)和动静脉氧分差(AVDO2)的测定，并与神经功能状态和预后相关。在伤后6小时内，脑血流量较低(22.5+/-5.2毫升/100克/分)，但在伤后24小时内显著增加。AVDO2的变化与此相反，运动评分低的患者AVDO2下降幅度最大，提示24小时后出现相对充血。运动评分与脑血流量在伤后8小时内显著相关(Spearman系数=0.69，p<；0.001)，但早在伤后12小时这种相关性就消失了。CBF和预后之间的关系也发现了类似的模式。在6小时内获得的研究中，有三分之一的研究发现脑血流低于梗死阈值(CBF小于或等于18ml/100gm/min)，此后发病率迅速下降。24小时后脑血流量降低通常与AVDO2升高无关，可能是氧化代谢低下的反映，而不是明显的缺血。在24例患者中，伤后某个时间点的脑血流量为18ml/100gm/min或更低；死亡率在这一亚组中显著较高，幸存者的情况更差。在某些情况下，通过减少过度换气或诱导动脉高压成功地治疗了缺血。这些结果支持上述假说，并提示创伤性脑损伤后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，早期过度换气或降低血压以防止脑水肿可能是有害的。
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 Xe-133 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 < 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.