‘The acidosis paradox: asphyxial brain injury without coincident acidemia’
✍ Scribed by Jean-Pierre Lin
- Publisher
- John Wiley and Sons
- Year
- 2004
- Tongue
- English
- Weight
- 50 KB
- Volume
- 46
- Category
- Article
- ISSN
- 0012-1622
No coin nor oath required. For personal study only.
✦ Synopsis
Letters to the editor 'The acidosis paradox: asphyxial brain injury without coincident acidemia' SIR-Hermansen raises important clinical issues in his annotation: 'The acidosis paradox: asphyxial brain injury without coincident acidemia', 1 which provides data supporting the relative protective effect of mild to moderate lactic acidemia to the brain. By contrast, non-acidaemic babies with 1-minute Apgar score of less than 3 fared poorly.
The suggestions that asphyxiated babies with acidemia (possibly arising from a lag-time between tissue acidosis and the advent of acidemia) might benefit from cerebral vasodilatation of acidemia, ability to utilize lactate as a nutrient, the Bohr effect, or suppression of excitatory amino acids are clearly appealing explanations for more severe brain injury in those without acidemia.
Apart from lactic acid tissue sequestration, an alternative explanation for the lack of severe lactic acidosis presumably includes concomitant hypoglycaemia. This seems relevant as an inability to raise lactate levels in the face of hypoglycaemia would expose the brain to injury from lack of appropriate fuel substrate, as hepatic ketogenesis is known to be limited in the newborn, and fails to rise in the fasted newborn and in the hypoglycaemic newborn. 2 Particularly relevant is the reporting of inappropriate hyperinsulinism in postasphyxial newborns, which was associated with poor neurodevelopmental outcome. 3 In an Indian study of 2224 babies screened for hypoglycaemia the risk factors for this condition included: birth asphyxia (24.2%), diabetic mothers (23.8%), respiratory distress (13.9%) and septicaemia (11.6%). 4 This poses the question: 'How many of the babies in the various studies quoted also exhibited hypoglycaemia?'.
Low birthweight is one of the most significant predictors of asphyxia. Asphyxia occurred in 68% of babies of less than 1000g birthweight and decreased to 1.2% in babies of 3 to 4kg birthweight. 5 But gestational maturity also determines outcome since the impact of asphyxia on neonatal mortality is most pronounced in more mature babies: the mortality increasing only 3-fold in babies of less than 34 weeks' gestation but over 27-fold for babies of greater than 38 weeks' gestation. 5 This indicates different selective vulnerability to asphyxia in babies of differing birthweight and gestational age.
On a technical note, it would have been useful to know how many children, in absolute terms, fell into the high-risk categories for cohorts in Table I. In the Dennis et al. study, 6 although 9 out of 10 children with a 1-minute Apgar of less than 3 and pH>7.18 had neurodevelopmental problems, the authors state that 'The highest proportion of unimpaired children was found among those who were most severely acidotic at birth (pH ≤ 7.04; 2 standard deviations below the mean), but this finding was not statistically significant. ' Table II in Hermansen (2003) leaves the reader uncertain concerning the 'floating' numbers between columns 'pH7-7.2%', and 'pH>7.2%'.
These deliberations and the multiplicity of publications in this field should caution against reliance on single variables as predictors of outcome.