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Validation of a method to partition the base deficit in meningococcal sepsis: a retrospective study

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 t...

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Detalles Bibliográficos
Autores principales: O'Dell, Ellen, Tibby, Shane M, Durward, Andrew, Aspell, Jo, Murdoch, Ian A
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2005
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1269470/
https://www.ncbi.nlm.nih.gov/pubmed/16137362
http://dx.doi.org/10.1186/cc3760
Descripción
Sumario: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 (r(2 )= 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.