1983Acta PaediatricaRequires access

CORD PLASMA HYPOXANTHINE AS A MEASURE OF FOETAL ASPHYXIA

Klara Thiringer

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Abstract

ABSTRACT. The clinical value of cord plasma hypoxanthine (HX) determination as a measure of foetal asphyxia was investigated. HX levels found in mixed cord plasma from 50 infants with clinical signs of perinatal asphyxia were compared to the levels found in 29 infants delivered after risk pregnancies and in 62 control neonates. All infants were assessed by three clinical scores: Apgar score, a clinical asphyxia score and perinatal reduced optimality score. In half of the infants cord blood pH, lactate and base excess were also determined. The mean cord plasma HX level in asphyctic infants was significantly higher than the mean HX level found in the two non‐asphyxiated groups. The concentration of HX correlated significantly to the clinical asphyxia score, reduced optimality score and to cumulative Apgar score, but no correlation was found to 1 and 5 min Apgar score. Cord plasma HX also correlated significantly to pH and lactate in cord blood. However, the correlation of HX to these two laboratory measures of asphyxia was no longer significant, when infants with birth weights/gestational ages below 1.0 SD were considered. This was found to be due to the lack of lactate elevation in these infants during asphyxia. Two newborn infants with substantially elevated HX levels, with only minor signs of clinical asphyxia turned out on follow‐up with spastic diplegia. It is suggested that the assay of cord plasma HX may add additional information to previously used hypoxia parameters and may be a more reliable index of perinatal asphyxia in the growth‐retarded infant, than lactate and pH at birth.

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ABSTRACT. The clinical value of cord plasma hypoxanthine (HX) determination as a measure of foetal asphyxia was investigated. HX levels found in mixed cord plasma from 50 infants with clinical signs of perinatal asphyxia were compared to the levels found in 29 infants delivered after risk pregnancies and in 62 control neonates. All infants were assessed by three clinical scores: Apgar score, a clinical asphyxia score and perinatal reduced optimality score. In half of the infants cord blood pH, lactate and base excess were also determined. The mean cord plasma HX level in asphyctic infants was significantly higher than the mean HX level found in the two non‐asphyxiated groups. The concentration of HX correlated significantly to the clinical asphyxia score, reduced optimality score and to cumulative Apgar score, but no correlation was found to 1 and 5 min Apgar score. Cord plasma HX also correlated significantly to pH and lactate in cord blood. However, the correlation of HX to these two laboratory measures of asphyxia was no longer significant, when infants with birth weights/gestational ages below 1.0 SD were considered. This was found to be due to the lack of lactate elevation in these infants during asphyxia. Two newborn infants with substantially elevated HX levels, with only minor signs of clinical asphyxia turned out on follow‐up with spastic diplegia. It is suggested that the assay of cord plasma HX may add additional information to previously used hypoxia parameters and may be a more reliable index of perinatal asphyxia in the growth‐retarded infant, than lactate and pH at birth.

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Available abstract

ABSTRACT. The clinical value of cord plasma hypoxanthine (HX) determination as a measure of foetal asphyxia was investigated. HX levels found in mixed cord plasma from 50 infants with clinical signs of perinatal asphyxia were compared to the levels found in 29 infants delivered after risk pregnancies and in 62 control neonates. All infants were assessed by three clinical scores: Apgar score, a clinical asphyxia score and perinatal reduced optimality score. In half of the infants cord blood pH, lactate and base excess were also determined. The mean cord plasma HX level in asphyctic infants was significantly higher than the mean HX level found in the two non‐asphyxiated groups. The concentration of HX correlated significantly to the clinical asphyxia score, reduced optimality score and to cumulative Apgar score, but no correlation was found to 1 and 5 min Apgar score. Cord plasma HX also correlated significantly to pH and lactate in cord blood. However, the correlation of HX to these two laboratory measures of asphyxia was no longer significant, when infants with birth weights/gestational ages below 1.0 SD were considered. This was found to be due to the lack of lactate elevation in these infants during asphyxia. Two newborn infants with substantially elevated HX levels, with only minor signs of clinical asphyxia turned out on follow‐up with spastic diplegia. It is suggested that the assay of cord plasma HX may add additional information to previously used hypoxia parameters and may be a more reliable index of perinatal asphyxia in the growth‐retarded infant, than lactate and pH at birth.

Key concepts: Medicine, Asphyxia, Apgar score, Perinatal asphyxia, Cord blood, Cord, Anesthesia, Gestational age

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