Abstract
Purpose: Several variables related to tourniquet (TQ) inflation contribute to ischemic muscle injury. Among these the duration of ischemia has been identified as a primary factor. The purposes of this study were to investigate the following during and after TQ-induced ischemia during orthopedic trauma surgery:
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muscle oxygenation changes measured by near infrared spectroscopy (NIRS);
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muscle protein oxidation; and
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correlations between muscle oxygenation / hemodynamics and oxidative changes.
Method: Consented patients aged 19–69 yrs (n=18) with unilateral ankle fracture requiring surgery at our institution were recruited. A pair of NIRS probes was fixed over the midpoint of the tibialis anterior muscle (TA) on both the injured and healthy legs. A thigh TQ was applied to the injured leg and inflated to 300 mmHg. Using the NIRS apparatus coupled to a laptop with data acquisition software, changes in oxygenated (O2Hb), deoxygenated (HHb), and total hemoglobin (tHb) levels in the TA of both legs were measured before and during TQ inflation, and after release until values returned to baseline. PRE surgical biopsies were collected from the peroneus tertius muscle (PT) immediately after TQ inflation and incision. POST biopsies were collected from the same PT immediately before TQ deflation. Oxidation of PT myosin, actin, and total protein was quantified using Western blot analysis of 4-hydroxynonenal (4-HNE) modified proteins. Data are reported as mean±SD.
Results: In PRE biopsies compared to POST biopsies there were large and statistically significant increases in the PT content of 4-NE modified myosin (174.4±128%; P< 1×10-6), actin (223.7±182%; P< 5×10-9), and total protein (567.5±378%; P< 5×10-7). There was a greater increase in PT protein oxidation in male subjects than in female subjects (50.8% difference; P< 0.05). In the TA of the fractured side, there were moderate to strong linear correlations between total protein oxidation and: the relative change in tHb (r=−0.704) and O2Hb (r=−0.415) during the period of TQ inflation and the rate at which the muscle became reoxygenated following TQ release (r=0.502). There was no relationship between muscle protein oxidation and TQ time, nor between muscle protein oxidation and age of patients.
Conclusion: TQ-induced muscle ischemia for 21 to 74 min during lower extremity surgery leads to oxidative muscle injury as measured according to myofibrillar contractile protein oxidation. Importantly, we observed that when the TQ was “leaky,” local increases in muscle tHb were associated with a lower magnitude of protein oxidation, however, when local decreases in muscle O2Hb were observed, perhaps due to local blood loss below the TQ, more oxidative changes resulted. Intriguingly, gender appeared to influence the extent of muscle oxidative injury, but age did not. Surprisingly, there was no significant correlation between muscle oxidative injury and the TQ-induced ischemia interval.
FUNDING: MSFHR, COF, BCLA.
Correspondence should be addressed to: COA, 4150 Ste. Catherine St. West Suite 360, Westmount, QC H3Z 2Y5, Canada. Email: meetings@canorth.org
