Serum lactate is not predicted by anion gap or base excess after trauma resuscitation

The inability to normalize lactate predicts death after trauma, but lactate may not be immediately available in every center. We postulated that, in a normal acid-base environment, lactate would correlate with the anion gap and the base excess of an arterial blood gas.

We studied 52 consecutive, invasively monitored patients with trauma admitted directly to the intensive care unit (ICU) from the emergency department or operating room in our level I center to determine whether base excess and anion gap could predict lactate. Lactate, base excess, and anion gap were recorded upon admission to the ICU and 8, 16, 24, 36, and 48 hours after admission. Correlation coefficients (r2) were calculated for the total patients, the 43 survivors, and the nine non-survivors.

Serum lactate was significantly higher in nonsurvivors at 16 hours after post ICU admission (4.0 +/- 1.69 vs. 2.84 +/- 1.49, p < 0.05), and this trend persisted; the greatest difference was seen at 48 hours after admission (2.92 +/- 1.47 vs. 1.76 +/- 0.57, p < 0.001). There were no differences in base excess or anion gap between survivors and nonsurvivors. We found no consistent correlation between lactate versus anion gap, lactate versus base excess, or anion gap versus base excess.

There is no correlation between lactate, base excess, and anion gap after initial resuscitation. Neither anion gap nor base excess was capable of predicting lactate; therefore, lactate must be directly measured. The lack of correlation of anion gap with base excess or lactate suggests the presence of unmeasured anions, an impairment in acid-base regulation after injury and resuscitation, or both.