Bourguignon P R, Shackford S R, Shiffer C, Nichols P, Nees A V
Department of Surgery, University of Vermont College of Medicine, Burlington 05401, USA.
Arch Surg. 1998 Apr;133(4):390-8. doi: 10.1001/archsurg.133.4.390.
To evaluate the effects of delayed vs early fluid resuscitation on cerebral hemodynamics after severe head injury and uncontrolled hemorrhagic shock.
Prospective, randomized, controlled experimental trial.
Surgical research laboratory.
Immature swine (N=16) weighing 40 to 50 kg.
Twelve swine were subjected to cryogenic brain lesion and hemorrhage to maintain a mean arterial pressure (MAP) of 50 mm Hg. Animals were randomized to receive 1 L of Ringer lactate solution in 20 minutes, starting 20 minutes after injury and hemorrhage, followed by 1 L of Ringer lactate solution in 30 minutes (ER group) (n=6), or no fluid resuscitation (DR group) (n=6). The 4 control animals underwent instrumentation only. The study ended 70 minutes after head injury and hemorrhage.
Measurements of MAP, bilateral regional cerebral blood flow, serum hemoglobin level, systemic and regional cerebral oxygen delivery, and intracranial pressure performed at baseline and 20 (phase 1), 50 (phase 2), and 70 minutes (phase 3) after head injury and hemorrhage. Lesion size (percentage of ipsilateral cortex) was measured post mortem.
All animals survived the experimental period. Systemic cerebral oxygen delivery in the DR group was significantly lower at phase 3 compared with that of the ER group (31.5% vs 53.1% at baseline) (P=.03). However, bilateral regional cerebral oxygen delivery was significantly greater in the DR group at phase 3 compared with that of the ER group (71.5% vs 47.0% at baseline in the injured side; 72.9% vs 48.4% at baseline in the noninjured side) (P=.02). Bilateral cerebral blood flow was similar in all groups at all times. The ER group showed a trend toward a greater intracranial pressure elevation (6.8 vs -0.25) (P=.07) and lesion size (37.0% vs 28.6%) (P=.07). Hemoglobin level became significantly lower in the ER group at phase 2 (7.0 vs 10.7) (P=.03) and remained lower at phase 3 (6.9 vs 11.7) (P=.01).
Early fluid resuscitation with Ringer lactate solution following head injury and uncontrolled hemorrhagic shock worsens cerebral hemodynamics. Cerebral pressure autoregulation is sufficiently intact following head injury to maintain regional cerebral oxygen delivery without asanguineous fluid resuscitation.
评估延迟液体复苏与早期液体复苏对重型颅脑损伤合并失血性休克患者脑血流动力学的影响。
前瞻性、随机、对照实验研究。
外科研究实验室。
体重40至50千克的未成年猪（n = 16）。
12只猪接受低温脑损伤和出血，以维持平均动脉压（MAP）为50毫米汞柱。动物被随机分为两组，一组在受伤和出血后20分钟开始，20分钟内输注1升乳酸林格氏液，随后30分钟内再输注1升乳酸林格氏液（早期复苏组，ER组）（n = 6）；另一组不进行液体复苏（延迟复苏组，DR组）（n = 6）。4只对照动物仅接受仪器植入。研究在颅脑损伤和出血后70分钟结束。
在基线、颅脑损伤和出血后20分钟（阶段1）、50分钟（阶段2）和70分钟（阶段3）测量MAP、双侧局部脑血流量、血清血红蛋白水平、全身及局部脑氧输送量和颅内压。伤后测量病变大小（同侧皮质百分比）。
所有动物均存活至实验结束。与ER组相比，DR组在阶段3的全身脑氧输送量显著降低（基线时分别为31.5%和53.1%）（P = 0.03）。然而，与ER组相比，DR组在阶段3的双侧局部脑氧输送量显著增加（受伤侧基线时分别为71.5%和47.0%；未受伤侧基线时分别为72.9%和48.4%）（P = 0.02）。所有组在各时间点的双侧脑血流量相似。ER组颅内压升高趋势更明显（6.8对 -0.25）（P = 0.07），病变大小也更大（37.0%对28.6%）（P = 0.07）。ER组在阶段2血红蛋白水平显著降低（7.0对10.7）（P = 0.03），在阶段3仍较低（6.9对11.7）（P = 0.01）。
重型颅脑损伤合并失血性休克后早期给予乳酸林格氏液进行液体复苏会恶化脑血流动力学。颅脑损伤后脑血管压力自动调节功能足够完好，无需输血性液体复苏即可维持局部脑氧输送。
