[Intramuscular pO2 monitoring in compartment syndrome--an experimental study]. / Intramuskuläres pO2-Monitoring des Kompartmentsyndroms--Eine experimentelle Studie.

HYPOTHESIS: 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. METHODS: 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. RESULTS: 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). DISCUSSION: 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.

Intramuscular partial oxygen tension monitoring in compartment syndrome--an experimental study.

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.

Effect of physical exercise on pain thresholds and plasma beta-endorphins in patients with silent and symptomatic myocardial ischaemia.

In a double-blind study, eight patients with symptomatic myocardial ischaemia and nine with asymptomatic myocardial ischaemia were compared during physical exercise under naloxone (6 mg i.v.) or placebo. Plasma beta-endorphin, cortisol and catecholamines were measured before exercise, during maximal exercise, and 10, 20 and 60 min after exercise. A tourniquet pain test (on the forearm, under control of transcutaneous PO2), and an electrical pain test (intracutaneous electrode placed in the finger with the electrical stimulus under computer control and two-interval forced-choice psychophysical technique) were performed before exercise as well as immediately after, and 60 min after exercise. Plasma beta-endorphin levels increased significantly (P less than 0.01) during exercise in symptomatic and asymptomatic patient groups; every patient showed an increase on beta-endorphins during and after exercise. However, the increase found in beta-endorphins during and after exercise was significantly larger (P less than 0.01) in asymptomatic than in symptomatic patients. After naloxone, this difference was no longer evident. Angina pectoris during exercise was reported with less latency in symptomatic patients (P less than 0.05) and occurred in two of nine asymptomatic patients following naloxone. The time course of plasma cortisol levels exhibited the same pattern as beta-endorphins with the same significant differences between symptomatic and asymptomatic groups. Electrical pain thresholds, though on average higher in asymptomatic patients (2.21 mA vs. 0.79 mA), were not affected by exercise or naloxone. Asymptomatic patients required more time to reach pain thresholds in the tourniquet pain test (P less than 0.02). After exercise, tourniquet pain thresholds were significantly lower (P less than 0.01) under naloxone compared with placebo.(ABSTRACT TRUNCATED AT 250 WORDS)