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Amino acids, uric acid, and organic acids together accounted for only 7.9% of the SIG in intensive care unit patients with metabolic acidosis.

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IntroductionMetabolic acidosis is the most frequent acid–base disorder in the intensive care unit. The optimal analysis of the underlying mechanisms is unknown.AimTo compare the conventional approach with the physicochemical approach in quantifying complicated metabolic acidosis in patients in the intensive care unitPatients and methodsWe included 50 consecutive patients with a metabolic acidosis (standard base excess ≤ -5). We measured sodium, potassium, calcium, magnesium, chloride, lactate, creatinine, urea, phosphate, albumin, pH, and arterial carbon dioxide and oxygen tensions in every patient. We then calculated HCO3-, the base excess, the anion gap, the albumin-corrected anion gap, the apparent strong ion difference, the effective strong ion difference and the strong ion gap.ResultsMost patients had multiple underlying mechanisms explaining the metabolic acidosis. Unmeasured strong anions were present in 98%, hyperchloremia was present in 80% and elevated lactate levels were present in 62% of patients. Calculation of the anion gap was not useful for the detection of hyperlactatemia. There was an excellent relation between the strong ion gap and the albumin-corrected and lactate-corrected anion gap (r2 = 0.934), with a bias of 1.86 and a precision of 0.96.ConclusionMultiple underlying mechanisms are present in most intensive care unit patients with a metabolic acidosis. These mechanisms are reliably determined by measuring the lactate-corrected and albumin-corrected anion gap. Calculation of the more time-consuming strong ion gap according to Stewart is therefore unnecessary.

In critically ill patients with metabolic acidosis, impaired renal function was associated with greater urinary SIDs. Subsequently, the higher urinary SIDs values were related to lower pH levels, illustrating the importance of renal chloride excretion to correct for acidosis.