• T Naka, R Bellomo, H Morimatsu, J Rocktaschel, L Wan, P Gow, and P Angus.
• Department of Intensive Care, Austin Hospital and Melbourne University, Melbourne, Australia.
• Int J Artif Organs. 2006 Jul 1; 29 (7): 668-74.

BackgroundContinuous renal replacement therapy (CRRT) affects acid-base balance but the influence of severe hepatic failure (SHF) on this effect is unknown.AimTo assess the effect of SHF on acid-base balance in patients receiving CVVH.DesignRetrospective laboratory investigation.SubjectsForty patients with SHF and acute renal failure (ARF) treated with CVVH and 42 critically ill patients with severe ARF but no liver disease also treated with CVVH (controls).InterventionRetrieval of clinical and laboratory data from prospective unit and laboratory databases.MethodsQuantitative acid-base status assessment using the Stewart-Figge methodology. Comparison of findings between the two groups.ResultsAlthough CVVH had a major effect on acid base balance in both groups, patients with SHF had a higher mean lactate concentrations (4.8 vs. 3.1 mmol/L; p<0.0005), a greater base deficit compared to controls (-1 vs. 4.1 mEq/L; p<0.0001) and a lower PaCO 2 tension (36.8 vs. 42.5 mmHg; p<0.0001), despite the use of bicarbonate replacement fluid. The acidifying effect of hyperlactatemia was slightly worsened by an increased strong ion gap (9.3 vs. 4.9 mEq/L; p<0.0001). It was, however, attenuated by an increased strong ion difference apparent (SIDa) (43.6 vs. 41.9 mEq/L; p<0.05) secondary to hypochloremia (96 vs. 100 mmol/L; p<0.0001) and by hypoalbuminemia, although hypoalbuminemia in SHF patients (26 vs. 23; p<0.005) was less pronounced than in controls.ConclusionThe use of CVVH does not fully correct the independent acidifying effect of liver failure on acid-base status. Increased lactate and strong ion gap values maintain a persistent base deficit despite the alkalinizing effects of hypoalbuminemia and hypochloremia. The correction of acidosis in SHF patients may require more intensive CVVH.

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