Seekamp A, Van Griensven M, Blankenburg H, Regel G
Unfallchirurgische Klinik, Medizinische Hochschule Hannover, Germany.
Eur J Emerg Med. 1997 Dec;4(4):185-92. doi: 10.1097/00063110-199712000-00002.
Measuring intracompartmental pressure is a well-accepted method in evaluating a compartment syndrome, which may occur after limb ischaemia followed by reperfusion. As a compartment syndrome is paralleled by a decreased microcirculation it should be possible also to evaluate a compartment syndrome by measuring intramuscular partial oxygen tension (PO2). In this study, anaesthetized 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, 4 or 6 h of ischaemia followed by 4 h of reperfusion. One further group was also subjected to 4 h of ischaemia and 4 h 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 specimens were obtained after each experiment. Two hours of ischaemia followed by 4 h of reperfusion did not result in any morphological changes and also in no significant change in compartment pressure during both phases, whereas PO2 significantly dropped during ischaemia (from 19.0 mmHg to 3.0-5.0 mmHg) and returned to normal during reperfusion. In prolonged ischaemia (4 h) morphologically a severe interstitial oedema was evident, compartment pressure increased during reperfusion (from 2.0 mmHg to 8.8 mmHg) and PO2 dropped during ischaemia to 3.0 mmHg and did not return to normal during reperfusion (10.5 mmHg versus 19.0 mmHg normal). In the case of 6 h ischaemia, partial necrosis and no interstitial oedema was 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 microcirculatory disorders preceding or following 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 where there are suspected clinical signs and risk of ischaemia 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认可的方法,筋膜室综合征可能发生在肢体缺血再灌注之后。由于筋膜室综合征伴有微循环减少,因此通过测量肌肉内的部分氧分压(PO2)来评估筋膜室综合征也应该是可行的。在本研究中,对麻醉的大鼠(通过气管切开术自主呼吸)进行肾下腹主动脉结扎。将压力导管置于一侧后肢小腿肌群的筋膜下,而对侧则植入PO2导管。除假手术组外,三个实验组分别经历2、4或6小时的缺血,随后再灌注4小时。另有一组也经历4小时的缺血和4小时的再灌注,但在再灌注时接受了筋膜切开术。每隔15分钟记录一次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。缺血2小时后再灌注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(正常为19.0 mmHg,再灌注时为10.5 mmHg)。在缺血6小时的情况下,形态学上发现部分坏死且无间质水肿。在整个研究过程中,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会导致对筋膜室综合征前后微循环障碍的假阴性解读,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,特别是在存在可疑临床体征和缺血风险但筋膜室内压力正常的情况下。