LATE METABOLIC ACIDOSIS (LMA): A REASSESSMENT

Abstract

There is substantial controversy regarding the definition and the clinical consequences of LMA. Well, low birth weight (LBW) infants fed standard formula were screened for blood tCO₂ q. 3-4 days, (n=114). Values for the entire group were normally distributed (19.1 ± 2.6 (SD) mmol/l). From 1-21 days of age the mean rose linearly from 18.2 to 19.7 mmol/l and then plateaued. 16/74 infants had “acidosis” arbitrarily defined as tCO₂ <18 mmol/l. Eight of them were matched for maturity and weight and randomly allocated to treatment either with 5% NaHCO₃ p.o. to raise tCO₂ to >21 mmol/l (E) or 0.9% NaCl (1 ml/feed) (C). The weight gain was 16.0±3.8(SE)g/kg/day in E, 17.2 ± 1.4 in C, (p>.7), and 14.4±1.21 in non-acidotic babies. Values for titratable acidity, ammonium excretion, net acid excretion (NAE) or minimum urinary pH attained during ammonium chloride loading were not different in E or C and were similar to those previously reported for non-acidotic infants. Thus: a) values of tCO₂ as low as 14 mmol/l during the first month of life fall within 2 SD for age and cannot be considered abnormal; b) the appropriate NAE for age suggests that blood tCO₂ in LBW infants reflects their HCO₃ threshold; c) LMA did not result in an increased capacity to excrete H⁺; d) since no association was found between weight gain and tCO₂, the failure to thrive of LBW infants might be spuriously attributed to low tCO₂.

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