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Acid–base changes in meningococcal sepsis revealed by partitioning the base deficit


Base deficit (BD) quantifies a metabolic acidosis without defining aetiology. Factors contributing to a metabolic acidosis include lactic acid and unmeasured anions (together known as tissue acid), hyperchloraemia and plasma albumin concentration. An equation exists to quantify the effect of albumin on BD; we have recently derived a similar equation for the effect of chloride. After partitioning the BD for these factors, the residual BD should reflect the contribution from tissue acid.


In patients with meningococcal sepsis, we aimed to: (1) validate this approach by comparing the agreement between tissue acids derived from the partitioned BD with that from the Stewart–Fencl method; and (2) use the partitioned BD to examine the temporal profile of acid base disturbance during the first 48 hours of treatment.


Sixty patients admitted to the intensive care unit with meningococcal sepsis over 2 years were studied, median (interquartile) weight 13 kg (10–20), median PIM risk of mortality 10.3% (6–16). Arterial blood was drawn at admission, and at 4, 8, 12, 18, 24 and 48 hours. BD was calculated from a standard algorithm in the blood gas analyser, and tissue acid via the Stewart–Fencl method.


(1) For the group as a whole, there was a strong association between tissue acid derived from the partitioned BD and the Stewart–Fencl method (r2 = 0.83). (2) A substantial metabolic acidosis was present at admission (mean pH 7.31, standard error of the mean 0.01, mean BD -8.9, standard error of the mean 0.5), which persisted at 24 hours. The admission BD was predominantly due to tissue acid, which was offset by an alkalinising effect of hypochloraemia and hypoalbuminaemia (Fig. 1). By 8 hours, chloride was now exhibiting an acidifying effect, which was related to the amount of chloride administered in the resuscitation fluids (r2 = 0.41).


Figure 1


The partitioned BD provides an accurate measure of tissue acid, and can be used to identify changes in the cause of a metabolic acidosis over time.

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Tibby, S., O'Dell, E., Durward, A. et al. Acid–base changes in meningococcal sepsis revealed by partitioning the base deficit. Crit Care 9, P412 (2005).

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  • Intensive Care Unit
  • Lactic Acid
  • Metabolic Acidosis
  • Base Change
  • Resuscitation Fluid