Hyperchloremia is the dominant cause of metabolic acidosis in the postresuscitation phase of pediatric meningococcal sepsis.

Objective: Metabolic acidosis is common in septic shock, yet few data exist on its etiological temporal profile during resuscitation; this is partly due to limitations in bedside monitoring tools (base excess, anion gap). Accurate identification of the type of acidosis is vital, as many therapies used in resuscitation can themselves produce metabolic acidosis.

Design: Retrospective, cohort study.

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 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.