Seekamp A, Blankenburg H, van Griensven M, Regel G
Unfallchirurgische Klinik, Medizinische Hochschule Hannover.
Zentralbl Chir. 1998;123(3):285-91; discussion 291-2.
Measuring intracompartmental pressure is a well accepted method in evaluating a compartment syndrome, which may occur after limb ischemia followed by reperfusion. As a compartment syndrome is paralleled by a decreased microcirculation it should be possible to evaluate a compartment syndrome also by measuring intramuscular pO2.
Anesthetized rats (spontaneous breathing via tracheotomy) were subjected to infrarenal ligation of the aorta. A pressure catheter was placed subfascial in the crural muscle group of one hind limb, whereas the contralateral side was prepared with a pO2 catheter. Besides a sham operated group, three experimental groups were subjected to either 2 hrs, 4 hrs or 6 hrs of ischemia followed by 4 hrs of reperfusion. One further group was also subjected to 4 hrs of ischemia and 4 hrs of reperfusion but received a fasciotomy at the time of reperfusion. Compartment pressure and intramuscular pO2 were recorded every 15 min. For histological examination muscle specimen were obtained after each experiment.
Two hours of ischemia followed by 4 hrs of reperfusion did not result in any morphological changes and also not in any significant change in compartment pressure during both phases, whereas pO2 significantly dropped during ischemia (from 19.0 mmHg to 3.0-5.0 mmHg) and returned to normal during reperfusion. In prolonged ischemia (4hrs) morphologically a severe interstitial edema was evident, compartment pressure increased during reperfusion (from 2.0 mmHg to 8.8 mmHg) and pO2 dropped during ischemia down to 3.0 mmHg and did not return to normal during reperfusion (10.5 mmHg versus 19.0 mmHg normal). In case of 6 hrs ischemia, partial necrosis and only little interstitial edema were found morphologically. There was no significant change in compartment pressure throughout the study; and pO2 remained significantly decreased even during reperfusion (2.0-3.0 mmHg).
Normal compartment pressure could mislead to false negative interpretation of compartment syndrome, whereas pO2 clearly identifies the microcirculatory state of the muscle. Thus, intramuscular pO2 monitoring presents a valuable method in evaluating compartment syndrome, especially in case of suspect clinical signs but normal compartment pressure.
测量筋膜室内压力是评估筋膜室综合征的一种广泛接受的方法,该综合征可能发生在肢体缺血再灌注后。由于筋膜室综合征与微循环减少同时出现,因此通过测量肌肉内的氧分压(pO2)来评估筋膜室综合征应该是可行的。
对麻醉大鼠(通过气管切开术自主呼吸)进行肾下腹主动脉结扎。在一侧后肢的小腿肌群筋膜下放置压力导管,而对侧则准备放置pO2导管。除假手术组外,三个实验组分别经历2小时、4小时或6小时的缺血,随后再灌注4小时。另一个组也经历4小时的缺血和4小时的再灌注,但在再灌注时进行了筋膜切开术。每隔15分钟记录筋膜室内压力和肌肉内pO2。每次实验后获取肌肉标本进行组织学检查。
2小时缺血后再灌注4小时,未导致任何形态学变化,且两个阶段的筋膜室内压力均无显著变化,而pO2在缺血期间显著下降(从19.0 mmHg降至3.0 - 5.0 mmHg),并在再灌注期间恢复正常。在长时间缺血(4小时)时,形态学上明显出现严重的间质水肿,再灌注期间筋膜室内压力升高(从2.0 mmHg升至8.8 mmHg),pO2在缺血期间降至3.0 mmHg,且在再灌注期间未恢复正常(10.5 mmHg对比正常的19.0 mmHg)。在6小时缺血的情况下,形态学上发现部分坏死且仅有少量间质水肿。整个研究过程中筋膜室内压力无显著变化;即使在再灌注期间,pO2仍显著降低(2.0 - 3.0 mmHg)。
正常的筋膜室内压力可能导致对筋膜室综合征的假阴性解读,而pO2能清楚地识别肌肉的微循环状态。因此,肌肉内pO2监测是评估筋膜室综合征的一种有价值的方法,特别是在临床体征可疑但筋膜室内压力正常的情况下。