Research
Validation of a method to partition the base deficit in meningococcal sepsis: a retrospective study
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* Corresponding author: Shane M Tibby shane.tibby@gstt.sthames.nhs.uk
1 Fellow, Department of Paediatric Intensive Care, Guy's and Saint Thomas' Hospitals, London, UK
2 Consultant, Department of Paediatric Intensive Care, Guy's and Saint Thomas' Hospitals, London, UK
3 Resident, Department of Paediatric Intensive Care, Guy's and Saint Thomas' Hospitals, London, UK
4 Consultant, Department of Paediatric Intensive Care, Guy's and Saint Thomas' Hospitals, London, UK
Critical Care 2005, 9:R464-R470 doi:10.1186/cc3760
Published: 8 July 2005Abstract
Introduction
The base deficit is a useful tool for quantifying total acid–base derangement, but cannot differentiate between various aetiologies. The Stewart–Fencl equations for strong ions and albumin have recently been abbreviated; we hypothesised that the abbreviated equations could be applied to the base deficit, thus partitioning this parameter into three components (the residual being the contribution from unmeasured anions).
Methods
The two abbreviated equations were applied retrospectively to blood gas and chemistry results in 374 samples from a cohort of 60 children with meningococcal septic shock (mean pH 7.31, mean base deficit -7.4 meq/L). Partitioning required the simultaneous measurement of plasma sodium, chloride, albumin and blood gas analysis.
Results
After partitioning for the effect of chloride and albumin, the residual base deficit was closely associated with unmeasured anions derived from the full Stewart–Fencl equations (r2 = 0.83, y = 1.99 – 0.87x, standard error of the estimate = 2.29 meq/L). Hypoalbuminaemia was a common finding; partitioning revealed that this produced a relatively consistent alkalinising effect on the base deficit (effect +2.9 ± 2.2 meq/L (mean ± SD)). The chloride effect was variable, producing both acidification and alkalinisation in approximately equal proportions (50% and 43%, respectively); furthermore the magnitude of this effect was substantial in some patients (SD ± 5.0 meq/L).
Conclusion
It is now possible to partition the base deficit at the bedside with enough accuracy to permit clinical use. This provides valuable information on the aetiology of acid–base disturbance when applied to a cohort of children with meningococcal sepsis.