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Hyperlactataemia induced by CVVHDF with low lactate bicarbonate-buffered solutions in patients with liver dysfunction

Ho, K.M. (2006) Hyperlactataemia induced by CVVHDF with low lactate bicarbonate-buffered solutions in patients with liver dysfunction. Nephrology Dialysis Transplantation, 21 (4). pp. 1096-1099.

Free to read: http://dx.doi.org/10.1093/ndt/gfi339
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Abstract

Critical illness is often complicated by hyperlactataemia, acute renal failure, and multi-organ failure [1]. Sodium lactate is the most commonly used nonbicarbonate buffer in both dialysate and replacement solutions and as a result, significant quantities of lactate could be transferred to the patient resulting in hyperlactataemia during continuous veno-venous haemodiafiltration (CVVHDF) [2]. Hyperlactataemia is well described during CVVHDF when the lactate load exceeds the capacity of lactate metabolism in critically ill patients [1]. The liver accounts for approximately 50% of the total lactate clearance of the body and therefore patients with liver dysfunction have a reduced capacity to metabolize lactate [1]. As such, bicarbonate-buffered solutions instead of lactate-buffered solutions are recommended in these patients [2–4]. Significant hyperlactataemia induced by the use of low lactate bicarbonate-buffered replacement and dialysate solutions during CVVHDF in critically ill patients has not been described [5]. We report on two critically ill patients, both with circulatory failure and acute liver dysfunction, who developed significant hyperlactataemia during CVVHDF with the use of low lactate bicarbonate-buffered solutions.

Item Type: Journal Article
Publisher: Oxford University Press
Copyright: © 2005 The Author
URI: http://researchrepository.murdoch.edu.au/id/eprint/34301
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