Regional cerebral blood flow trends in head injured patients with focal contusions and cerebral edema.

M J Alexander, N A Martin, R Khanna, M Caron, D P Becker
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引用次数: 24

Abstract

Focal contusions following head injury may be associated with focal or diffuse cerebral edema. Early global hyperemia and perifocal hyperemia may play a role in cerebral edema, although causal relationships have yet to be clearly been defined. We studied 27 patients with head injury (admission GCS 3-12) resulting in focal contusions (without evidence of subarachnoid, intraventricular or intraparenchymal hemorrhage by CT). Patients were studied with ICP monitors, head CTs, and intravenous 133Xenon regional cerebral perfusion studies serially over several days post injury. Low cortical blood flow and a low mean CBF15 flow were evident on the day of the injury. Additionally, F1 analysis indicated significantly (p < 0.05) greater cortical blood flow in the surrounding brain (mean 60 cc/100 g/min) compared to the contusion area (mean 43 cc/100 g/min) on the day of trauma. Mean regional CBF remained below normal in the contused areas (CBF15 < 35 cc/100 g/min), however the cortical flow increased in the first few days post-injury (peak F1 = 95 cc/100 g/min on day 3) then decreased to sub-normal levels. The mean CBF in the surrounding brain was low on the day of injury (CBF15 = 29 cc/100 g/min), although higher than the contused area, and increased to a peak of 45 cc/1009/min on day 3 posttrauma. Cortical flow in the surrounding brain, however, exhibited a different trend. The mean F1 was low on the day of trauma and significantly higher one day after trauma (mean 105 cc/100 g/min). Only 15 of the 27 patients with focal contusions had evidence of cerebral edema. Eleven of these exhibited focal edema and 4 exhibited diffuse edema. Focal edema developed over the first few days posttrauma as seen in followup CT, whereas patients with diffuse edema exhibited edema on the admission CT. Initial oligemia in the contused areas was associated with a subsequent hyperemic rim about the contusion. Focal hyperemia was associated with focal edema in 41% of the patients, whereas diffuse edema appeared to be independent of the hyperemic response in contusions.

脑损伤局灶性挫伤伴脑水肿患者脑血流变化趋势。
头部损伤后的局灶性挫伤可能与局灶性或弥漫性脑水肿有关。早期全身充血和局部充血可能在脑水肿中起作用,尽管因果关系尚未明确定义。我们研究了27例头部损伤(入院GCS 3-12)导致局灶性挫伤(CT未发现蛛网膜下腔、脑室或脑实质出血)的患者。在损伤后数天内,对患者进行ICP监测、头部ct和静脉133氙局部脑灌注研究。损伤当天皮质血流量低,平均CBF15流量低。此外,F1分析显示,创伤当天,与挫伤区(平均43 cc/100 g/min)相比,周围脑皮质血流量(平均60 cc/100 g/min)显著(p < 0.05)增加。损伤区平均脑血流仍低于正常水平(CBF15 < 35 cc/100 g/min),但损伤后头几天皮质血流增加(第3天峰值F1 = 95 cc/100 g/min),然后降至亚正常水平。损伤当天周围脑区的平均CBF较低(CBF15 = 29 cc/ 100g /min),但高于挫伤区域,并在创伤后第3天增加到45 cc/1009/min的峰值。然而,周围大脑的皮质流表现出不同的趋势。平均F1在外伤当天较低,外伤后1天显著升高(平均105 cc/100 g/min)。27例局灶性挫伤患者中只有15例有脑水肿的迹象。其中11例表现为局灶性水肿,4例表现为弥漫性水肿。随访CT显示,局灶性水肿发生于创伤后最初几天,而弥漫性水肿患者在入院CT上表现为水肿。挫伤区域的初始低血凝与随后挫伤周围的充血有关。41%的患者局灶性充血与局灶性水肿相关,而弥漫性水肿似乎与挫伤的充血反应无关。
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