Patients treated for severe acute leg ischemia are at risk of developing reperfusion syndrome. This occurs when ischemic muscles are reperfused and metabolites from damaged and disintegrated muscle cells are spread systemically. A part of this process consists of leakage of myoglobin; it may be nephrotoxic and colors the urine red. The metabolites also affect central circulation and may cause arrhythmia and heart failure. The risk for reperfusion syndrome is higher when occlusions are proximal and the affected muscle mass is large. One example is saddle emboli located in the iliac bifurcation. The risk is also higher when the ischemia time is longer than 4-6 h.
The elevated mortality associated with severe acute leg ischemia may be due to reperfusion syndrome. Survival may therefore be improved by avoiding reperfusion and a lower mortality has been reported from hospitals where primary amputation is favored. It has also been suggested that thrombolysis saves lives by restoring perfusion gradually. For a threatened leg this is seldom an option because rapid restoration of perfusion is necessary to save it.
The best treatment for reperfusion syndrome is prevention by expeditious restoration of flow.
There are no clinically proven effective drugs but many have been successful in animal models, including heparin, mannitol, and prostaglandins. Because heparin and mannitol also have other potential benefits and few side effects they are recommended during the postoperative period. Obviously, acidosis and hyperkalemia must be corrected, and the patient needs to be well hydrated and have good urine output.
For patients with suspected reperfusion syndrome - urine acidosis and high serum myoglobin levels - alkalinization of the urine is often recommended in order to avoid renal failure despite weak support in the literature. If the urine is red, the urine pH <7.0, and serum myoglobin >10,000 mg/ml, 100 ml sodium bicarbonate is given IV. The dose is repeated until the pH is normalized.
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