Reperfusion Injury and the NoReflow Phenomenon

The common basic problem with any failing flap is lack of nutrient blood flow. However, a compromised flap can sustain a paradoxical increase in tissue injury after the re-establishment of nutrient blood flow by a phenomenon known as reperfusion injury. Reperfusion injury occurs within seconds of blood flow being re-established to a compromised flap (Fig. 1). The primary cell responsible for reperfusion injury is the neutrophil, which is attracted to ischemic tissue by cytokines. Neutrophils migrate into the flap parenchyma and release free radicals causing cellular injury (1). Compromised reperfused flaps also exhibit the no-reflow phenomenon; the finding that blood flow does not return immediately to some parts of a flap. This is believed to be due to neutrophil plugging; however, the actual cause is unknown.

Reducing reperfusion injury is beneficial to all types of flaps (2,3) and several experimental and clinical protocols show that oxygen free radical scavengers (3), antineutrophil antibodies (4), and anti-inflammatory drugs are effective. Antiinflammatory agents including phospholipase A2 inhibitors (steroids) and lipoxygenase inhibitors are effective in reducing ischemia-reperfusion injury (5,6). However, cyclo-oxygenase inhibitors (nonsteroidal anti-inflammatory drugs [NSAIDS]) are not effective in reducing reperfusion injury (7). By inhibiting phospholipase A2, steroids including dexamethasone and hydrocortisone reduce the concentration of arachidonic acid (AA) and the formation of prostaglandins and leukotrienes. Prostaglandins are formed by the action of cyclo-oxygenase on arachidonic acid; however, inhibition of this enzyme is ineffective in reducing reperfusion injury. -g

Leukotrienes are formed by the action of lipoxygenase on arachidonic acid and inhi- |

bition of this enzyme is effective in reducing reperfusion injury (5) (Fig. 2). Systemic £

steroids are probably effective due to a reduction in the concentration the leuko-

trienes, not prostaglandins. In fact, prostacyclin (a prostaglandin) is protective in several experimental canine models of myocardial ischemia because it inhibits neu-

trophil activation and accumulation (8). Based on improved flap survival in several |

animal studies, systemic dexamethasone can improve the survival of random-pattern &

flaps if it is administered prior to, or shortly after, flap elevation. Steroids may also be beneficial in secondary ischemic events encountered in free flaps.

Figure 1 A simplified representation of reperfusion injury. Injured endothelial cells liberate a variety of cytokines. Upon reperfusion, these cytokines attract and activate circulating inflammatory cells including neutrophils. These activated cells (indicated by halos) express receptors on their surfaces that interact with endothelial cell surface receptors allowing attachment and transmigration. The neutrophils release their oxygen free radicals (respiratory burst) leading to parenchymal tissue damage. This process occurs within minutes of reperfusion.

Figure 1 A simplified representation of reperfusion injury. Injured endothelial cells liberate a variety of cytokines. Upon reperfusion, these cytokines attract and activate circulating inflammatory cells including neutrophils. These activated cells (indicated by halos) express receptors on their surfaces that interact with endothelial cell surface receptors allowing attachment and transmigration. The neutrophils release their oxygen free radicals (respiratory burst) leading to parenchymal tissue damage. This process occurs within minutes of reperfusion.

Certain pathophysiological events depend on the type of flap (random, axial, or free) because of the fundamental differences in nutrient blood flow, and in the differing methods of tissue transfer to the recipient site.

Figure 2 The phospholipase A2 pathway.
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