Blaisdell F William
Department of Surgery, University of California, Davis, Medical Center, 2221 Stockton Ave, Sacramento, CA 95817-2214, USA.
Cardiovasc Surg. 2002 Dec;10(6):620-30. doi: 10.1016/s0967-2109(02)00070-4.
There are two components to the reperfusion syndrome, which follows extremity ischemia. The local response, which follows reperfusion, consists of limb swelling with its potential for aggravating tissue injury and the systemic response, which results in multiple organ failure and death. It is apparent that skeletal muscle is the predominant tissue in the limb but also the tissue that is most vulnerable to ischemia. Physiological and anatomical studies show that irreversible muscle cell damage starts after 3 h of ischemia and is nearly complete at 6 h. These muscle changes are paralleled by progressive microvascular damage. Microvascular changes appear to follow rather than precede skeletal muscle damage as the tolerance of capillaries to ischemia vary with the tissue being reperfused. The more severe the cellular damage the greater the microvascular changes and with death of tissue microvascular flow ceases within a few hours-the no reflow phenomenon. At this point tissue swelling ceases. The inflammatory responses following reperfusion varies greatly. When muscle tissue death is uniform, as would follow tourniquet ischemia or limb replantation, little inflammatory response results. In most instances of reperfusion, which follows thrombotic or embolic occlusion, there will be a variable degree of ischemic damage in the zone where collateral blood flow is possible. The extent of this region will determine the magnitude of the inflammatory response, whether local or systemic. Only in this region will therapy be of any benefit, whether fasciotomy to prevent pressure occlusion of the microcirculation, or anticoagulation to prevent further microvascular thrombosis. Since many of the inflammatory mediators are generated by the act of clotting, anticoagulation will have additional benefit by decreasing the inflammatory response. In instances in which the process involves the bulk of the lower extremity, amputation rather than attempts at revascularization may be the most prudent course to prevent the toxic product in the ischemic limb from entering the systemic circulation.
再灌注综合征有两个组成部分，它发生在肢体缺血之后。再灌注后的局部反应包括肢体肿胀，这有可能加重组织损伤，以及全身反应，这会导致多器官功能衰竭和死亡。很明显，骨骼肌是肢体中的主要组织，但也是最易受缺血影响的组织。生理和解剖学研究表明，不可逆的肌肉细胞损伤在缺血3小时后开始，6小时时几乎完全形成。这些肌肉变化与微血管的渐进性损伤同时出现。微血管变化似乎是跟随骨骼肌损伤而非先于其发生，因为毛细血管对缺血的耐受性因再灌注的组织而异。细胞损伤越严重，微血管变化就越大，随着组织死亡，微血管血流在数小时内停止——即无复流现象。此时组织肿胀停止。再灌注后的炎症反应差异很大。当肌肉组织死亡均匀时，如在止血带缺血或肢体再植后，几乎不会产生炎症反应。在大多数血栓形成或栓塞性闭塞后的再灌注情况下，在可能有侧支血流的区域会有不同程度的缺血损伤。该区域的范围将决定炎症反应的程度，无论是局部还是全身的。只有在这个区域，治疗才会有任何益处，无论是进行筋膜切开术以防止微循环受压闭塞，还是进行抗凝以防止进一步的微血管血栓形成。由于许多炎症介质是由凝血过程产生的，抗凝通过减少炎症反应将有额外的益处。在该过程累及下肢大部分的情况下，截肢而非尝试血管重建可能是最谨慎的做法，以防止缺血肢体中的毒性产物进入体循环。
