Intrapartum risk factors for newborn encephalopathy: the Western Australian case-control studyBMJ 1998; 317 doi: https://doi.org/10.1136/bmj.317.7172.1554 (Published 05 December 1998) Cite this as: BMJ 1998;317:1554
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The paper by Badawi et al.1 goes a long way towards dispelling the
longstanding view that intra-partum asphyxia is the major cause of
neonatal encephalopathy and cerebral palsy. The fact there was no evidence
of intra-partum hypoxia in over 70% of cases of newborn encephalopathy
emphasises the need to investigate for other unusual but possible causes.
We recently experienced one such case in our unit.
A 42-year-old multiparous woman opted for a repeat caesarean section
in her second pregnancy and this procedure was performed electively at 39
weeks gestation following an uncomplicated antenatal course. Surprisingly,
caesarean section revealed thick meconium stained liquor and the baby was
delivered in poor condition. The pre-delivery foetal cardiotocograph and
post-delivery umbilical cord artery pH were normal. Early neonatal brain
scans showed marked but stable dilatation of the cerebral ventricles
consistent with an ante-partum insult. These findings were also associated
with clinical signs of neurological deficit in the neonate who was
discharged from hospital on day 13 with a presumptive diagnosis of ante-
partum hypoxia. Unfortunately he was re-admitted on day 27 with a history
of poor feeding, lethargy and hypothermia. Investigations included a
metabolic screen which revealed very high levels of urine 2-oxoglutaric
acid consistent with a diagnosis of hyper-2 oxoglutaric aciduria.
This inborn error of energy metabolism is thought to be inherited as
an autosomal recessive and is associated with an increased incidence of
seizure disorders and cerebral palsy2. Although the exact enzymatic defect
is not known and the pathological mechanisms leading to brain damage
remain obscure, the process is slowly progressive, predominantly involves
the extrapyramidal system and is compatible with survival into adulthood.
On the basis of the available evidence, we now believe this defect
accounts for the ante-partum cerebral damage observed in this case
Had this baby been delivered vaginally (as could easily have been the
case) the outcome would have been the same. Failure to perform a metabolic
screen, the presence of meconium and the poor outcome would have
encouraged a final diagnosis of encephalopathy secondary to intra-partum
foetal asphyxia, despite the actual problem lying elsewhere.
Unfortunately, under these circumstances, yet another midwife or
obstetrician would have been subjected to the trauma of accounting for the
woman’s intra-partum management. This is an example of the tightrope
midwives and obstetricians constantly find themselves walking and the
comments of Edwards and Nelson about imprecise definitions of underlying
pathophysiologies are valid and timely3.
We urge perinatologists to look harder when dealing with cases of
neonatal encephalopathy, irrespective of any evidence supporting
hypoxaemic damage. Conventionally available information may simply provide
circumstantial evidence for asphyxia whilst the truth remains hidden.
Amaju Ikomi, Senior Registrar
Panos Benardis, Senior House Officer
Susan Bateman, Consultant
Department of Obstetrics and Gynaecology,
St Peter’s Hospital, Guildford Rd,
Chertsey, Surrey KT16 0PZ
1. Badawi N, Kurinczuk JJ, Keogh JM, Alessandri LM, O’Sullivan F, Burton
PR et al. Intrapartum risk factors for newborn encephalopathy: the Western
Australian case-control study. BMJ 1998;317:1554-8.
2. Hoffmann G, Mench-Hoinowski A, Knuppel H, Langenbeck U. Hyper-2-
oxoglutaric acid in long-term mental handicap. J Ment Defic Res
3. Edwards AD, Nelson KB. Neonatal encephalopathies. BMJ 1998;317:1537-8
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Competing interests: No competing interests