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Ann Thorac Surg 2004;78:1880-1881
© 2004 The Society of Thoracic Surgeons
Istituto Policlinico S. Donato, Via Morandi 30, San Donato Milanese, Milan 20097, Italy
cardioanestesia{at}virgilio.it
To the Editor:
In their article, Swaminathan and associates [1] demonstrated that the lowest hematocrit during cardiopulmonary bypass (CPB) is an independent predictor of the peak postoperative change in serum creatinine, and that this association is influenced by body weight. Their interpretation is that the decreased oxygen content may induce a cellular hypoxia at the level of the renal medulla, and the authors hypothesize that minimizing bypass prime volumes should reduce anemia and therefore limit the renal risk.
As the authors correctly quoted, the first observation of an association between a low hematocrit during CPB and postoperative acute renal failure was published by our research group in 1994 [3], and we too hypothesized a cellular hypoxia at the basis of this association. Since that time, we have progressively reduced our priming volume, finally reaching, in the last years, a value of less than 900 mL. Our clinical model is, therefore, adequate to define whether a low priming volume is able to reduce the renal risk. Selecting a population (n = 2,061) with the same characteristics of the Swaminathan paper from our database of the last 3 years, we repeated the risk analysis for peak creatinine change, and obtained interesting results. Our priming volume was 856 ± 167 mL of colloid solution; preoperative hematocrit was 39.5% ± 4.3%, lowest hematocrit during CPB 26.6% ± 4%, peak creatinine change (
%) 12.9% ± 44%. Compared with the values reported by Swaminathan and associates, there is no difference in preoperative hematocrit, a significant (p < 0.001) higher value of lowest hematocrit during CPB, and a significant (p < 0.001) lower value of peak creatinine change.
We therefore can confirm that reducing the bypass prime volume exerts a beneficial effect in terms of postoperative renal function. In spite of this, our series still confirms a correlation between lowest hematocit on CPB and peak creatinine change. Selecting a population of patients weighing 75 kgs or more (n = 935), we could compare our regression analysis with the one reported by Swaminathan and associates (Fig 1). In the area between 22% and 31% of lowest hematocrit during CBP, the predicted creatinine increase is significantly lower in our low priming patients.
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References
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