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J Thorac Cardiovasc Surg 1997;113:426
© 1997 Mosby, Inc.
LETTERS TO THE EDITOR |
Department of Cardiovascular Surgery
Albert-Ludwigs-Universität Freiburg
79106 Freiburg, Germany
Reply to the Editor:
My colleagues and I thank Drs. Sakakibara and Mitsui for their interest in our work and for raising the important question of the effluent return to the systemic circulation.
Undoubtedly, the venous effluent of limbs reperfused after several hours of complete ischemia contains greater amounts of myoglobin, free hemoglobin, creatine kinase, and potassium than do control limbs. After complete ischemia, this has been shown in experimental
1 and clinical
2 studies. To a lesser degree, this increase was also measurable after revascularization for incomplete ischemia.
3
These components in the venous effluent are a consequence of the severe local damage of skeletal muscle (rhabdomyolysis, edema) and are the cause for systemic complications (hyperkalemia, myoglobinemia, acute renal failure, acidosis, multiorgan failure, and death) following revascularization after prolonged periods of limb ischemia.
Our limb reperfusion strategy has been developed to decrease the skeletal muscle reperfusion injury after revascularizations for prolonged ischemia. Less local damage will result in reduced concentrations of potassium, creatine kinase, and hydrogen ions in the venous effluent, which could be demonstrated in an experimental study.
1 Nevertheless, the venous effluent, even after controlled limb reperfusion, still contains significant amounts of end products of the rhabdomyolysis, which can only be prevented from entering the systemic circulation by discarding the venous effluent. Simply discarding the venous effluent is not possible because of the large amount of blood that would be lost. The same is true for any filtering process. The only possibility is to separately cannulate the femoral arteries and veins and use an extracorporeal circulation including oxygenator and roller pumps. This approach was recently described by Vogt and coworkers
2 from the Zürich group in a patient with complete ischemia for 24 hours.
The concentrations of myoglobin, potassium, and creatine kinase in the venous effluent are related to the severity of ischemia (complete/incomplete) (1/3) and the duration of ischemia (2/4). The more severe the ischemic insult, the more pronounced is the reperfusion damage, resulting in higher concentrations in the venous effluent. In our three-center study,
4 we were able to reduce the concentrations of myoglobin, potassium, and creatine kinase to a level that did not produce systemic hyperkalemia or renal failure. However, Vogt and coworkers
2 have used a complete extracorporeal circuit (including an oxygenator) for a patient with complete ischemia for 24 hours and achieved excellent results with this approach. In patients with complete ischemia exceeding 24 to 36 hours, it might very well be necessary to discard the venous effluent and use an extracorporeal circuit to prevent severe systemic side effects. In our study with a mean ischemic time of 26 hours (range 6 to 39 hours), we did see systemic increases in potassium, creatine kinase, creatinine, and blood urea nitrogen; however, this did not produce remote organ failure. Even though we did not measure myoglobin concentrations in our patients, the fact that none had severe renal failure shows that there was no major renal tubular dysfunction.
Ideally, future refinements in the technique of controlled limb reperfusion will elucidate criteria, identify which patients will need controlled limb reperfusion without complete extracorporeal circulation, and define those patients who need controlled reperfusion with venous effluent discardment.
12/8/77666
References
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