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Japanese Red Cross Society of Wakayama Medical Center; simosimo_7{at}ybb.ne.jp (Shimogai, Iranami, Yamazaki) Department of Anesthesiology; Wakayama Medical University; Wakayama City; Wakayama, Japan (Hatano)
To the Editor:
We (1) previously reported the occurrence of astroglial cell damage immediately after tourniquet deflation from bone cement. In a recent arthroscopic knee repair, tourniquet deflation was followed by a large, transient decrease in bispectral index (BIS), suggesting the release of circulating substances that altered the brain’s electrocortical activities.
A 27-year-old softball player underwent video-assisted repair of the left anterior cruciate ligament. The surgery was aided by a pneumatic tourniquet on the proximal left thigh, inflated to a pressure of 250 mm Hg. When the tourniquet was deflated, the BIS abruptly decreased to lower values, <10, for approximately 10 min (Figs. 1a and b). Then, over the next 10 min, the BIS value gradually increased, until it returned to the previous value of approximately 60. His arterial blood pressure (110–130/70–80 mm Hg), heart rate (60–90 bpm), and pupil size (5–6 mm) were unchanged during this period. End-tidal CO2 transiently increased to 58 mm Hg upon deflation, and then returned to the baseline value of 28–35 mm Hg. Anesthetic emergence was rapid and unremarkable, with no suggestion of neurological deficit.
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Tourniquet-induced limb ischemia and exsanguination lead to production of H2O2 and free radicals (2,3). Skeletal muscle is highly vulnerable to ischemia (4). Increased pressure within an osteofascial compartment, found in both acute trauma and exercise-induced elevated compartment pressure, may result in circulatory compromise (5). Indicators of skeletal muscle ischemia, including interstitial concentrations of glucose, lactate, and hypoxanthine, increase more prominently after limb exsanguination than after circulatory occlusion alone (6). Tourniquet-induced exsanguination and ischemia during limb surgery may cause more severe ischemic changes in muscular, athletic patients than in patients of average physical condition.
Glial cells and oligodendrocytes may be injured by ischemia-reperfusion events (7). These cells’ electrocortical activity is negatively correlated to the concentration of hypoxantine (8). We speculate that the transiently low BIS in this case was caused by the brain’s response to toxic substances, such as hypoxantine, produced during the tourniquet-generated exsanguination and ischemia.
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