• A Seekamp, M Van Griensven, H Blankenburg, and G Regel.
• Unfallchirurgische Klinik, Medizinische Hochschule Hannover, Germany.
• Eur J Emerg Med. 1997 Dec 1; 4 (4): 185-92.

AbstractMeasuring 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.

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