Acid–base changes in meningococcal sepsis revealed by partitioning the base deficit
© BioMed Central Ltd 2005
Published: 7 March 2005
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.
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.