INTRAMUSCULAR PO(2) MONITORING IN COMPART MENT SYNDROME - AN EXPERIMENTAL-STUDY

Citation
A. Seekamp et al., INTRAMUSCULAR PO(2) MONITORING IN COMPART MENT SYNDROME - AN EXPERIMENTAL-STUDY, Zentralblatt fur Chirurgie, 123(3), 1998, pp. 285-291
Citations number
15
Categorie Soggetti
Surgery
Journal title
ISSN journal
0044409X
Volume
123
Issue
3
Year of publication
1998
Pages
285 - 291
Database
ISI
SICI code
0044-409X(1998)123:3<285:IPMICM>2.0.ZU;2-8
Abstract
Hypothesis: Measuring intracompartimental pressure is a well accepted method in evaluating a compartment syndrome, which may occur after lim b ischemia followed by reperfusion. As a compartment syndrome is paral leled by a decreased microcirculation it should be possible to evaluat e a compartment syndrome also by measuring intramuscular pO(2). Method s: Anesthetized rats (spontaneous breathing via tracheotomy) were subj ected to infrarenal ligation of the aorta. A pressure catheter was pla ced subfascial in the crural muscle group of one hind limb, whereas th e contralateral side was prepared with a pO(2) catheter. Besides a sha m 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 re perfusion but received a fasciotomy at the time of reperfusion. Compar tment pressure and intramuscular pO(2) were recorded every 15 min. For histological examination muscle specimen were obtained after each exp eriment. Results: Two hours of ischemia followed by 4 hrs of reperfusi on did not result in any morphological changes and also not in any sig nificant change in compartment pressure during both phases, whereas pO (2) significantly dropped during ischemia (from 19.0 mmHg to 3.0-5.0 m mHg) and returned to normal during reperfusion. In prolonged ischemia (il hrs) morphologically a severe interstitial edema was evident, comp artment pressure increased during reperfusion (from 2.0 mmHg to 8.8 mm Hg) and pO(2) dropped during ischemia down to 3.0 mmHg and did not ret urn to normal during reperfusion (10.5 mmHg versus 19.0 mmHg normal). In case of 6 hrs ischemia, partial necrosis and only little interstiti al edema were found morhologically. There was no significant change in compartment pressure throughout the study, and pO(2) remained signifi cantly decreased even during reperfusion (2.0-3.0 mmHg). Discussion: N ormal compartment pressure could mislead to false negative interpretat ion of compartment syndrome, whereas pO(2) clearly identifies the micr ocirculatory state of the muscle. Thus, intramuscular pO(2) monitoring presents a valuable method in evaluating compartment syndrome, especi ally in case of suspect clinical signs but normal compartment pressure .