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Late metabolic acidosis: a reassessment of the definition
Insights
The definition of late metabolic acidosis in low birth weight (LBW) infants needs reevaluation. Studies show normal acid-base balance in healthy LBW infants, challenging previous growth correlations.
Area of Science:
- Neonatal Physiology
- Pediatric Nephrology
- Biochemistry
Background:
- The term "late metabolic acidosis" has been used to describe growth failure in apparently healthy low birth weight (LBW) infants with a base deficit.
- Previous conclusions linking hypobasemia to poor growth were drawn without sufficient data on normal acid-base variables in LBW infants.
Purpose of the Study:
- To investigate the acid-base status of healthy LBW infants.
- To determine if "hypobasemia" impacts growth in LBW infants.
- To reassess the definition of late metabolic acidosis in LBW infants.
Main Methods:
- Analysis of CO2TOT (total carbon dioxide) levels in 114 LBW infants from birth to three weeks.
- Comparison of growth rates between "hypobasemic" infants receiving bicarbonate versus saline.
- Assessment of ammonium chloride excretion capacity in relation to acid-base status.
Main Results:
- LBW infant CO2TOT levels naturally increase from birth to three weeks (mean 18.6 to 20.3 mM).
- CO2TOT distribution in LBW infants is within normal limits, with values as low as 14.5 mM falling within 2 standard deviations.
- No significant difference in growth rates was observed between infants treated with bicarbonate or saline.
- Ammonium chloride excretion was not linked to acid-base status and was similar to term infants.
Conclusions:
- The current definition of "late metabolic acidosis" in LBW infants requires reconsideration.
- Hypobasemia, as previously defined, does not appear to be a primary factor in growth failure for LBW infants.
- LBW infants possess normal acid-base regulation and excretion capabilities comparable to term infants.
Abstract:
The term "late metabolic acidosis" is generally used to define a population of apparently healthy LBW infants who fail to grow and have a base deficit in excess of 5 mEq/l (CO2TOT less than 21 mM). A relationship between hypobasemia and the lack of appropriate growth was postulated. This conclusion was reached, however, in the absence of adequate information regarding the distribution of acid-base variables in healthy LBW infants. The results of this study demonstrate that the CO2TOT of LBW infants (n = 114) rises between birth and three weeks of life from a mean of 18.6 to 20.3 mM. The frequency distribution of CO2TOT values did not show any significant deviations from normality, and 2 SD included values as low as 14.5 mM. No difference in the rate of growth was detected between "hypobasemic" infants given a solution of bicarbonate calculated to bring their blood CO2TOT to greater than 21 mM and those given similar amounts of isotonic saline solution. The ability of the LBW infants to excrete an ammonium chloride load was not related to their acid-base status and was comparable to that of term infants. It is apparent that the definition of late metabolic acidosis needs to be reconsidered.