Antepartum risk factors for newborn encephalopathy: the Western Australian case-control study
BMJ 1998; 317 doi: https://doi.org/10.1136/bmj.317.7172.1549 (Published 05 December 1998) Cite this as: BMJ 1998;317:1549
All rapid responses
Rapid responses are electronic comments to the editor. They enable our users to debate issues raised in articles published on bmj.com. A rapid response is first posted online. If you need the URL (web address) of an individual response, simply click on the response headline and copy the URL from the browser window. A proportion of responses will, after editing, be published online and in the print journal as letters, which are indexed in PubMed. Rapid responses are not indexed in PubMed and they are not journal articles. The BMJ reserves the right to remove responses which are being wilfully misrepresented as published articles or when it is brought to our attention that a response spreads misinformation.
From March 2022, the word limit for rapid responses will be 600 words not including references and author details. We will no longer post responses that exceed this limit.
The word limit for letters selected from posted responses remains 300 words.
Dear Sir
The recently published paper on neonatal encephalopathy, or hypoxic
ischaemic encephalopathy (HIE) (1), and that which followed, challenged
the concept that HIE was due to the cerebral effects of the complex
responses of the mature fetus to a severe degree of intrapartum oxygen
deprivation, or asphyxia (2,3). The concept that asphyxial stress is
inherent to labour is well supported.
Correlations between reduced afferent uterine blood flows and
increasing intrauterine pressures during contractions were described in
the dog in 1947, and in ewe and in primate in 1968. An investigation in
the human in 1965, with an intravenous radioopaque dye, demonstrated
afferent vascular constriction and obliteration during the contractions of
labour, with diminished intervillous placental volume. In 1987
investigations with Doppler in the human confirmed the inverse
correlations between increasing intrauterine pressures and during
contractions and decreasing afferent flows.
The assessment of the fetal response to intrapartum asphyxial stress
requires the recognition of fetal heart rate changes observed by either
intermittent auscultation or by cardiotocograph traces. To dismiss
these well established determinants of fetal asphyxial adversity as "so
called" is unacceptable. It also demonstrates an ignorance of
fundamental obstetrical principles.
The fetal ability to withstand such stress, fetal reserve, is
affected by the identified predisposing antepartum factors (1). HIE
could only be attributed to them were it to be observed after an
antepartum abdominal delivery.
In the second article there was no report of the intrapartum
variables required to establish or negate correlations between asphyxial
stress and HIE. These should have included the intensity of the stress,
demonstrated by the record of the uterine contractions, the quality of
surveillance, the fetal responses as detected by FHR observations, and the
times between the evidence of the onset of significant irreversible and
adverse fetal reactions and those of effective interventions. The effect
of uterine overstimulation with syntocinon would have justified particular
examination.
It is not possible to determine the cause of biological events such
as HIE by the examination of the variables of associated non biological
events.
This is demonstrated by plague and malaria. There was awareness of
the predisposing factors of overcrowding and climatic conditions. Their
causes were not identified until the advent of biological sciences.
Previously the conclusions of epidemiological investigations have
been unsupported by the data (4,5). On this occasion the
investigations were also flawed by the absence of relevant data.
Intrapartum asphyxia remains unchallenged as the cause of HIE.
Yours faithfully
E.L.G.Beavis. FRCS, FRACS, FRCOG, FRANZCOG.
320 Victoria Parade
East Melbourne 3002
Victoria, Australia.
References.
1 Badawi N, Kurinczuk JJ, Keogh JM, Alessandri LM, O'Sullibvan F,
Burton PR, et al. Antepartum risk factors for newborn encephalopathy: the
Western Australian case-control study. BMJ 1998;317:1549-53.
2 Chiswick ML. Intrapartum asphyxia and hypoxic-ischaemic
encephalopathy. In Intrapartum Fetal Surveillance. Spencer JAD, Ward RHT
Editors, 1993 RCOG Press London: 181-90.
3 Longo LD; Satyseelan P. Hypoxia-ischaemia and the developing
brain: hypotheses regarding the pathophysiology of fetal-neonatal brain
damage. Br J Obstet Gynaecol 1997;104: 652-62.
4 Stanley FJ, Watson L. Trends in perinatal mortality and cerebral
palsy in Western Australia, 1967 TO 1985. BMJ 1992; 304: 1658-63.
5 Glynn J, Leon D. [Letter]. Trends in cerebral palsy in Western
Australia. BMJ 1992; 305: 525.
Competing interests: No competing interests
Editor,
Badawi and colleagues important case control study of neonatal
encephalopathy (NE) in Western Australia(1) demonstrates that clinical
evidence of central nervous system dysfunction in newborn infants is
associated with a wide range of disorders which, for most of their study
population, have origins prior to the onset of labour. We have two
concerns however about comparing and generalising their findings to other
populations: their definition of NE, and the greater importance of
intrapartum risk factors for NE in poorer populations in the developing
world.
The omission of intrapartum criteria from the case definition of
neonatal encephalopathy has been previously advocated and removes an
important bias affecting other studies(2) . The investigators' broad
clinical definition of neonatal encephalopathy does however make
comparison with prevalence studies in other settings problematic. For
instance isolated neonatal seizures are a notoriously difficult entity to
clinically ascertain(3) . What proportion of the 109 infants reported to
have seizures had interictal evidence of neurological dysfunction? Since
other investigators have chosen to exclude established causes of
encephalopathy such as overt congenital infection or hypoglycaemia from
prevalence studies it would be helpful for comparative purposes to know
what proportion of their cases had evidence of recognised causes of
neonatal morbidity. Finally the inclusion of 37 infants with birth defects
(23% of the case group) clearly has implications for the subsequent
analysis of likely time of insult.
From our own work on neonatal encephalopathy in a low income setting(4)
we would sound a note of caution on the generalisability of the
intrapartum risk factor study to other settings(5) . Using the same
criteria as the authors we found evidence of possible intrapartum hypoxia
in 63 (68%) of 92 infants with neonatal encephalopathy in a hospital
population based study in Kathmandu (unpublished data). It seems likely in
a high income setting with almost universal antenatal care and a
relatively low stillbirth rate that livebirth of neurologically impaired
fetuses will be maximised. In many low income countries, mothers are
stunted, do not access antenatal care, suffer high stillbirth rates and
receive poor obstetric care. Under these conditions it is likely that
intrapartum factors remain more important in the causation of neonatal
encephalopathy.
yours etc,
Matthew Ellis Lecturer in Child Health
Institute of Child Health
Royal Hospital for Children
St Michael's Hill
Bristol BS2 8BJ.
Anthony M de L Costello Reader in International Child Health
Centre for International Child Health
Institute of Child Health
30 Guilford Street
London WC1N 1EH.
Corresponding author
References
1. Badawi N, Kurinczuk JJ, Keogh JM, Alessandri LM, O'Sullivan F, Burton
PR, Pemberton PJ, Stanley FJ. Antepartum risk factors for newborn
encephalopathy: the Western Australian case-control study. BMJ
1998;317:1549-53.
2. Editorial. Birth Asphyxia: a statement. Developmental Medicine and
Child Neurology 1993;35:1022-24.
3. Connel J, Oozer R, DeVries L, Dubowitz LMS, Dubowitz V. Continuous
EEG monitoring of neonatal seizures: diagnostic and prognostic
considerations. Arch Dis Child 1989;64:452-458.
4. Ellis M, Manandhar N, Manadhar DS, Wyatt JS, Costello AM de L.
Incidence and severity of neonatal encephalopathy in Nepal, a least
developed country(abstract). Paediatr Perinat Epidem 1996;10:A17.
5. Badawi N, Kurinczuk JJ, Keogh JM, Alessandri LM, O'Sullivan F,
Burton PR, Pemberton PJ, Stanley FJ. Intrapartum risk factors for newborn
encephalopathy: the Western Australian case-control study. BMJ
1998;317:1554-8.
Competing interests: No competing interests
A variable that has generated a good deal of controversy here is the
position of the mother for delivery. The Dorsal Lithotomy and Semisitting
positions, in which weight is borne on the sacrum, constricting the bony
birth canal, is very common in jurisdictions with high rates of
complication and C-Section. This or a similar study of a population using
various positions as alternatives to sacral weight bearing in many of the
studied births would allow better analysis of this factor.
Competing interests: No competing interests
Neonatal encephalopathy
Dear Sir
The recently published papers on neonatal encephalopathy, or hypoxic
ischaemic encephalopathy (HIE),[1] and that which followed, challenged the
currently held view that HIE, was due to a severe degree of intrapartum
asphyxia having affected the mature or nearly mature fetus.[2] [3]
In 1947 it was demonstrated in the anaesthetised dog that afferent uterine
arterial flow reduced with increasing uterine muscular activity. Similar
observations were made in the ewe and primate in 1968, and in the human in
1987.
In 1965 radiological studies in the human demonstrated arterial
constriction and obliteration within the uterine musculature during
contractions, with diminished intervillous placental volume.
The complex vascular and biochemical responses of the fetus to severe
intrapartum asphyxia, the selective vulnerability of areas of the fetal
cerebrum, and the changes resulting in neuronal injury, are now well
understood.[3] [4] The fetal response is best detected by the examination
of cardiotocograph (CTG) traces.[5] The dismissal of this well recognised
determinant of fetal adversity as "so called" by the authors of the papers
is unjustified.
The fetal ability to withstand asphyxial stress, fetal reserve, is
affected by the recognised predisposing antepartum. factors which were
identified.[1] HIE could only be attributed to these factors were it to be
observed alter an antepartum uncomplicated abdominal delivery.
There was no reported examination of the variables required to
establish or negate correlations between intrapartum asphyxial stress and
HIE. These included the intensity of the stress shown by the uterine
contractions, the mode and quality of intrapartum surveillance, the fetal
responses as detected by FHR observations,, and the times between the
onset of irreversible adverse fetal reactions and those of effective
interventions.
Epidemiology identifies the frequency of adverse biological events,
and the relative significance of associated events. It cannot identify
their biological causes. 'EMS is illustrated by the examples of plague and
malaria, where no degree of awareness of associated factors could reveal
their underlying biological causes.
The investigators failed to examine the variables required to
substantiate their hypothesis, and to justify their conclusions. This
methodological flaw was compounded by the extrapolation of epidemiological
data to the area of biological cause, beyond the realms of logic and of
the scientific method.
Although susceptible to Predisposing adverse factors intrapartum
asphyxia remains unchallenged as the cause of HIE, Fetal susceptibility is
subject to recognised antepartum factors, the role of chorioamnionitis in
the exacerbation of intrapartum asphyxial stress would require further
investigation.
Yours faithfully
E.L.G.Beavis. FRCS, FRACS, FRCOG, FRANWOG.
320 Victoria Parade
East Melbourne 3002
Victoria, Australia.
References
1 Badawi N, Kurinczuk JJ, Keogh JM, Alessandri LM, O'Sullibvan F,
Burton PR, et al. Antepartum risk factors for newborn encephalopathy. the
Western Australian case-control study. BMJ 1998;317:1549-53.
2 Chiswick ML. Intrapartum asphyxia and hypoxic-ischaemic
encephalopathy. In Intrapartum Fetal Surveillance. Spencer JAD, Ward RHT
Editors, 1993 RCOG Press London - 181-90.
3 Longo LD, Satyseelan P. Hypoxia-ischaemia and the developing brain
hypotheses regarding the pathophysiologly of fetal-neonatal brain darnage.
Br J Obstet Gynaecol 1997;104:652-62.
4 Rutherford MA, Pennock JM, Schweiso JE, Cowan FM, Dubowitz LMS.
Hypoxic ischaemic encephalopathy: early magnetic resonance imaging
findings and their evolution. Neuropediatrics 1995;26:183-91.
5 Parer JT. Handbook of fetal heart rate monitoring. 2nd ed. W.B.
Saunders (Harcourt Brace) 1997.
Competing interests: No competing interests