• C P Carvounis and D A Feinfeld.
• Department of Medicine, Nassau County Medical Center, East Meadow, NY 11554, USA.
• Am. J. Nephrol. 2000 Sep 1; 20 (5): 369-72.

BackgroundThe serum anion gap (serum [Na(+)]-Cl(-)]-[CO(2)]) is still the first-line approach to metabolic acidosis. However, while it is generally acknowledged that hypoalbuminemia mandates a downward adjustment of the expected anion gap, a specific correction factor for the anion gap in the face of low serum albumin has never been demonstrated.MethodsWe reviewed initial laboratory data from 432 consecutive patients admitted or transferred to the medical intensive care unit at Nassau County Medical Center over a 6-month period and correlated the serum albumin with the anion gap and the serum [tCO(2)] using multivariate analysis. We looked at the anion gap as a function of delta (albumin), the difference between normal and actual serum albumin, defined as 4.0 - measured serum albumin g/dl. We also assessed [tCO(2)] as an independent variable.ResultsFor patients with normal or high serum tCO(2), the ratio of change in anion gap (delta anion gap) to delta (albumin) was 1.46 and 1.45, respectively. For patients with serum tCO(2) <22 mEq/l this ratio was 1.89. In the latter group, anion gap was best predicted taking both delta (albumin) and serum tCO(2) into account: anion gap = 36.2 - serum tCO(2) - 2.3 x delta (albumin) (r = 0.71, p < 0.0001).ConclusionFor intensive care patients with normal or high serum tCO(2) (>21 mEq/l) a simple bedside adjustment of the anion gap by subtracting 1.5 times the difference between measured serum albumin and the 'normal' level of 4.0 g/dl gives a close estimate of the actual anion gap. For intensive care patients with serum tCO(2) <22 mEq/l, correction of the anion gap is well predicted by adding about twice the Delta (albumin) to the calculated gap.Copyright 2000 S. Karger AG, Basel

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