Author/Authors :
Georg-Christian Funk، نويسنده , , Daniel Doberer، نويسنده , , Valentin Fuhrmann، نويسنده , , Ulrike Holzinger، نويسنده , , Reinhard Kitzberger، نويسنده , , Nikolaus Kneidinger، نويسنده , , Gregor Lindner، نويسنده , , Bruno Schneeweiss، نويسنده ,
Abstract :
Background/Aims
Hyperlactatemia with unexplained absence of metabolic acidosis is observed in acute liver failure. In chronic liver disease offsetting metabolic acid–base disorders could be revealed by means of physical–chemical acid–base analysis. The purpose of this study was to determine whether the acidifying effect of lactate is neutralized by the alkalinizing effect of hypoalbuminemia in acute liver failure.
Methods
Serial arterial blood samples of 46 consecutive patients with non-paracetamol-induced acute liver failure were studied after admission to a medical ICU in a prospective investigation and compared to healthy controls. Acid–base state was assessed by quantitative physical–chemical analysis.
Results
Lactate was increased and albumin was decreased in patients with acute liver failure compared to healthy controls resulting in normal net metabolic acid–base state. The alkalinizing effect of hypoalbuminemia was neutralized by the acidifying effect of elevated lactate. This observation was confirmed in serial analysis during 5 days after admission.
Conclusions
The acidifying effect of lactate is neutralized by the alkalinizing effect of hypoalbuminemia in non-paracetamol-induced acute liver failure. The absence of apparent metabolic acidosis in the presence of elevated lactate can be explained by means of the physical–chemical acid–base model.