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SummaryThe possibility of detecting past hypoxia during the first 2 h after birth by means of blood analyses of hypoxanthine, lactate, base deficit, and pH was investigated in six infants with a 1 min Apgar score of 4 . Reference values for the four biochemical variables were obtained in 16 healthy infants with a normal 1 min Apgar score of 28. In the asphyxiated infants, elevated values for hypoxanthine were found in 48%, for lactate in 54%, and for base deficit in 46% while 21% of the pH values were lower than the reference. In the group of asphyxiated infants, significantly elevated hypoxanthine values were found during the first 20 min after birth, base deficit during 30 min, and lactate values during 120 min while lower pH values than the reference were found during the first 30 min. Significant correlations were found between hypoxanthine and lactate concentrations and also between hypoxanthine and base deficit but not between hypoxanthine and pH. It is concluded that the optimal time for detecting past intrauterine hypoxia in the newborn using the hypoxanthine test is between 10 and 20 rnin after birth, but in individual cases, significantly increased hypoxanthine concentrations may be found at any time in the 10-120 min period. We propose an equation that can be used to calculate an upper normal limit for hypoxanthine concentration in any sampling time during this period.

SummaryThe measurement of arterial plasma concentration of hypoxanthine in 16 healthy newborn infants showed a prominent increase after birth compared with the umbilical cord levels. Peak values were found 10-20 min after birth with a maximal value of 11.9 pmole/liter in the normal newborns. In five asphyxiated infants the postnatal pattern of hypoxanthine was the same as for normal infants but the increase was even more prominent. A mean peak value of 33.7 pmole/liter was noted in the asphyxiated infants. Our results indicate that the hypoxanthine concentration is influenced not only by the degree of hypoxia, but also by the peripheral circulation and the time interval between the hypoxic event and the blood sampling. It is concluded that hypoxanthine assay may be of clinical value for the detection of past hypoxia as a semiquantitative test. SpeculationIt is possible to differentiate a group of asphyxiated infants from normal infants by measurements of plasma hypoxanthine concentration. A new biochemical measure of perinatal hypoxia thus appears available. Knowledge about the change in hypoxanthine concentration is however of much greater value than that of a single plasma sample which may be &isleading.The theoretical connection between lack of oxygen, reduced cellular energy contents, and the catabolism of energy-rich phosphates (e.g., ATP, ADP) has been known for a long time. Until recently, however, the estimation of purine metabolites has not been used in clinical practice as a measure of hypoxia. With a micromethod for determination of the hypoxanthine concentration in plasma, Saugstad (18) found this metabolite to be a sensitive sign of hypoxia in experimental animals (20,21,22,23,24) and his preliminary clinical results also indicated a constant and slow decrease of this concentration after a period of fetal hypoxia. He therefore proposed that hypoxanthine measurements could be used for a retrograde estimation of past episodes of hypoxia in the newborn infant (19). In the umbilical cord plasma a hypoxanthine level of 11 pmole/liter was found to discriminate newborn infants with normal deliveries from infants with signs of intrauterine asphyxia (19). Lipp et al. (1 l), however, found that the hypoxanthine concentration in umbilical cord plasma from asphyxiated newborn infants overlapped in a rather broad range the values obtained from normal infants. This was true for both arterial and venous cord blood.In view of this discrepancy, the present study was undertaken in order to investigate the change in postnatal arterial hypoxanthine concentration in a number of normal and asphyxiated newborn infants who had been carefully monitored during delivery and in the early postnatal period. In some of these infants, the hypoxanthine concentration was also measured in venous cord blood and in the immediate neonatal period in blood samples obtained from the umbilical vein.

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Effects of obstetric regional analgesia and of asphyxia on the arterial blood gases and acid-base balance in the first two hours after birth were investigated in 85 newborn infants divided into a control group, an asphyxia group and a continuous epidural, an intermittent epidural and a paracervical + pudendal block group. Lidocaine was the drug used in the analgesia groups. In the asphyxia group the metabolic acidosis decreased and pH was normalized to the level of the control group between 10 and 30 min after birth. During this period in the asphyxia group PaO2 was higher than and PaCO2 similar to the corresponding control values. Compared with the control group, in the regional analgesia groups the metabolic acidosis tended to be less extensive and PaO2 higher, whereas PaCO2 was similar. A lower packed red cell volume in the asphyxia and in the regional analgesia groups, probably due to differences in placental transfusion, may have had influence on the results. Within the regional analgesia groups infants with hyperglycemia showed signs of an increased metabolic acidosis while infants with hypoglycemia had low base deficit and lactate values supporting the assumption that neonatal blood glucose concentration may reflect perinatal distress.