Abstract
The treatment of hypoxic lactic acidosis with acute renal failure was studied in 2 neonates requiring peritoneal dialysis. In infant I pre-dialysis blood pH was 7.23, HCO3 13 mEq/L, and R fraction [(serum Na-(Cl− + HCO3)] 39 mEq/L representing accumulation of lactate, 35 mM/L. After 24 hours of peritoneal dialysis with a commercial solution containing 35 mEq/L sodium lactate, acidosis failed to improve and in fact worsened. HCO3 fell to 8 mEq/L while R rose to 47 mEq/L and plasma lactate to 40 mM/L. Increased acidosis was presumably due to loss of bicarbonate into dialysate. After dialysis with a solution containing 40 mEq/L of bicarbonate instead of lactate, acidosis was corrected with blood pH 7.45, serum HCO3 24 mEq/L, and R 22 mEq/L. In infant II predialysis blood pH was 7.18, serum HCO3 12 mEq/L, R 53 mEq/L, and plasma lactate 50 mM/L. Dialysate containing 40 mEq/L of sodium bicarbonate and no lactate was used. With concentration gradient favoring movement of HCO3 into and lactate out of extracellular fluid, serum HCO3 rose to 19 mEq/L and R fell to 39 mEq/L, blood pH 7.36. Improved circulation and oxygenation permitted metabolism of remaining lactate, producing a transient metabolic alkalosis. In acute renal failure with lactic acidosis, a peritoneal dialysate should be prepared containing sodium bicarbonate rather than lactate. Likewise acetate or other organic anions would not be metabolized effectively in hypoxic states.
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Russo, J., Nash, M. & Winters, R. NEONATAL LACTIC ACIDOSIS AND ACUTE RENAL FAILURE: THE ROLE OF PERITONEAL DIALYSIS. Pediatr Res 11, 556 (1977). https://doi.org/10.1203/00006450-197704000-01119
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DOI: https://doi.org/10.1203/00006450-197704000-01119