Letters

Authors' reply

Our observations tell us nothing about the potential mechanisms by which maternal thyroid dysfunction and subsequent treatment increase the risk of neonatal encephalopathy. The fetal thyroid gland does not function until late in the first trimester.¹ Current evidence suggests that small but important amounts of maternal thyroid hormone cross the placenta and have a role in the maturation of the fetal brain.² Thus maternal thyroid dysfunction may adversely affect the development of the brain in the early stages of pregnancy. We hypothesise that as fetal thyroid hormone requirements have not been established we cannot be certain that what is assumed to be adequate maternal treatment results in appropriate fetal thyroid hormone concentrations.

We agree with A M Mander and S C Leeson that serious problems with interpretation arise with several of the measures of intrapartum events used to indicate birth asphyxia in our study. Any case-control study of either neonatal encephalopathy or cerebral palsy depends on retrospective ascertainment of exposure (for example, intrapartum asphyxia) and has the added challenge of the absence of diagnostic tests. Cardiotocograms are hard to interpret and have an extremely low positive predictive value.³ Apgar scoring varies among observers and is affected by prematurity, drugs, maternal anaesthesia, and neuromuscular conditions as well as intrapartum hypoxia.

It would have been useful if cord pH had been measured in more of our study infants, but this reflects clinical practice. Furthermore, cord pH values do not correlate well with other measures of birth asphyxia and are not predictive of an adverse neurological outcome. In fact, neonates with a low Apgar score and a normal cord pH at birth may fare worse than those with a low Apgar score and a low cord pH as they may be unable to mount an appropriate biochemical response to hypoxia.⁴

Most other studies of neonatal encephalopathy have been confined to infants presumed to have been asphyxiated at birth. Our study included all infants with clinical signs of neonatal encephalopathy and then applied criteria indicating possible intrapartum asphyxia.

Paediatric research fellow Research officer Epidemiologist Senior biostatistician Director TVW Telethon Research Institute for Child Health Research, PO Box 855, West Perth 6872, Western Australia, Australia

Director Department of Neonatology, Princess Margaret Hospital for Children, Subiaco 6008, Western Australia

Nadia Badawi, Louisa M Alessandri, Jennifer J Kurinczuk, Paul R Burton, Fiona J Stanley, Patrick J Pemberton 

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