The timing of birth asphyxia is frequently at issue in allegations of medical malpractice for newborns. If asphyxia occurred within hours prior to birth, the possibility exists that alternative obstetric interventions might have affected the course of organ injury. If, on the other hand, asphyxia were long-standing then the likelihood that alternative obstetric decisions would have produced a different outcome diminishes. Circulating NRBCs are recognized to increase in chronic fetal stress syndromes (e.g., SGA, IDM). The question we addressed was whether increased NRBC values also correlated withacute fetal distress.

Method: We surveyed the medical records of 269 term (37-42 weeks gestation) AGA infants admitted to our NICU, and 56 term AGA infants admitted to our regular nursery. We attempted to determine how much of the variance in NRBC values determined on DOL 1 could be attributed to variations in traditional markers of birth asphyxia -- APGAR @ 1 minute (APGAR1), pH and base excess (BE) from umbilical cord artery and vein.

Results: NRBC did not vary at all with gestational age between 37-42 weeks (r2 = 0.000). For 56 term AGA regular nursery admissions, mode NRBC = 0%, median = 3%, 90th percentile = 10%. For 269 term AGA NICU admissions, mode NRBC = 0%, median = 6%, 90th percentile = 37%. For regressions of NRBC vs APGAR1, pHart, pHven, BEart, BEven, the amount of variance (r2) was 0.027, 0.026, 0.012, 0.006, and 0.001 respectively. For 8 infants with cord prolapse and APGAR1 < 3, median NRBC = 7%, 90th percentile = 16%.

Conclusions: 1) Variations in accepted markers of acute birth asphyxia accounted for less than 3% of the variation noted in NRBC among term newborn infants. 2) Acute birth asphyxia does not appear to `shake loose' NRBC into the circulation of term newborn infants. 3) Infants with NRBC values at the extremes of the normal population should be presumed to have an etiology other than acute asphyxia underlying the elevation in NRBC.