The four groups were differentiated by the base deficit values detected in the children's cord artery blood: children with a base deficit of 4 8, 8 12, 12 16, and >16 mmol/l.
In this study, 4 predictors were independently associated with an increased risk of death: acidosis indicated by a large base deficit, cerebral manifestations of malaria (coma and/or convulsions), an elevated blood urea nitrogen, or signs of chronic illness on admission.
Using admission data, metabolic acidosis was defined by a positive base deficit and was categorized by quartiles.
We then selected patients who evidenced a metabolic acidosis at ICU admission, defined by a positive base deficit, as described above.
Metabolic acidosis was defined by a positive base deficit (i.e., negative base excess).
Our initial findings indicate that HMGB1 levels increase with increasing ISS (P < 0.0003 by rank and P < 0.0001 by trend) and base deficit (P = 0.0019 by rank and P < 0.0001 by trend).
Interestingly, in this large cohort analysis of presentation SBE, the 50% lethal dose for the acid load indicated by base deficit shifted to a substantially lower level for a given age when combined with a traumatic brain injury; it is unknown whether this is true for other injuries in isolation or combination.
Adequacy of fluid repletion can initially be judged by simple physiological measures, guided by the base deficit and plasma lactate.
There is no evidence base to support the use of one fluid over another, provided they are given in sufficient quantity, but adequacy of fluid repletion can initially be judged by simple physiological measures guided by the base deficit and plasma lactate.
The magnitude of the metabolic acidosis is generally quantified by the base deficit or base excess, which is defined as the amount of base (or acid) that must be added to a litre of blood to return the pH to 7.4 at a partial pressure of carbon dioxide (PCO2) of 40 mmHg.
