There is a crisis affecting maternity care in many countries. Both caesarean
section rates and medical defense premiums are increasing. New options for the care of pregnant women (e.g., birthing units)
may fail because midwives, general practitioners and smaller hospitals may be unable to afford adequate insurance to continue
crisis is fuelled by widespread beliefs that cerebral palsy is often caused by injuries sustained during labour and birth
and that cerebral palsy may therefore be the result of inappropriate obstetric care. There is now considerable evidence to
suggest that these beliefs are unfounded. A conference of Australian and New Zealand specialists in this area was convened
to review the relevant literature and offer a consensus statement to help parents, counsellors, lawyers and health professionals
understand what is known and what is not known about the origins of cerebral palsy.
Cerebral palsy is not a single entity but covers neurological impairments
characterised by abnormal control of movement or posture resulting from abnormalities in brain development or an acquired
non-progressive cerebral lesion.
Cerebral palsy is the most common physical disability in childhood, occurring
in about 2-2.5 per 1000 children born. The frequency of cerebral palsy has not changed over the last 40 years, despite a fourfold
drop in both perinatal and maternal mortality. In some countries there is an increase in the occurrence of cerebral palsy,
attributable mostly to the increased survival of very low birth weight infants.
There are many antenatal factors that may lead to cerebral palsy and often there
may be several contributing factors.2,3
Examples are shown in Box 1. There are also strong associations between cerebral palsy and intrauterine growth restriction,
antenatal death of co-twin/triplet and extreme prematurity.
fetus is designed to withstand the stress of labour, which usually involves a reduction in the amount of oxygen in the blood
(hypoxaemia) and the amount of blood reaching the brain (ischaemia) during passage through the birth canal. If these reductions
are too great, a normal fetus is more likely to die than survive with cerebral palsy.4 These normal
reductions of blood supply and oxygen can compound the detrimental effects of any chronic hypoxia already experienced during
the antenatal period.4 Cerebral palsy
occurring after birth is also uncommon and is caused by, for example, complications of prematurity, untreated rhesus disease
(kernicterus), meningitis, accidents or near drowning.3
Timing the onset of pathological brain lesions
It should be clearly stated that, currently, fetal brain development (or
maldevelopment) cannot be monitored during pregnancy. Only examination of the brain at autopsy can identify the full extent
of injury in some cases. In other cases of cerebral palsy no pathological lesion is identifiable. The neuropathological lesions
leading to cerebral palsy are various and include maldevelopments (cerebral dysgenesis), germinal matrix-intraventricular
haemorrhage, cerebellar haemorrhages, grey matter damage, white matter damage (periventricular leukomalacia), hypoglycaemic
neuronal injury, thromboembolic injury (including vasculitis secondary to infection) and kernicterus.
immature brain has only a limited number of ways of responding to acute or chronic injury and these essentially consist of
neuronal and white matter loss and glial proliferation. These changes occur over many days and weeks. They may later be modified
by secondary changes such as posthaemorrhagic or postinflammatory hydrocephaly or white matter atrophy. By the time a child
presents with cerebral palsy during the first years of life, the neuropathological effects of any hypoxic-ischaemic injury
or other injury will have become modified by these changes and by further postnatal brain development. Even if that child
were to die during its first year and the brain was made available for expert examination, it would be impossible, on this
basis, to determine the exact timing of the original neurological insult.
suggestions that the condition of the placenta could be used as a surrogate marker of antepartum fetal injury are based largely
on anecdotal argument and have not yet been fully evaluated; such techniques are fraught with observer and sampling bias.
Imaging of the brain
Antenatal ultrasound scans may detect gross brain changes, but a normal
scan does not exclude antenatal neuropathology. Few infants undergo brain imaging, either because there is no clinical suspicion
that cerebral palsy may develop or because there are no imaging facilities available. A neonatal ultrasound examination may
not demonstrate longstanding microscopic changes but can detect major acute lesions or secondary changes. Acute lesions may
appear as periventricular flare, oedema and intracranial haemorrhage. Periventricular and caudothalamic notch cysts, porencephaly,
parenchymal calcification and intraventricular adhesions may also be demonstrated in the early neonatal period and imply events
occurring more than two weeks previously.
period from 26 to 34 weeks' gestation is critical for neurodevelopment. The patterns of brain injury, and therefore imaging
features, are similar in fetuses and neonates, and late investigations cannot separate brain injury occurring in utero
from perinatal or postnatal events. Magnetic resonance imaging of limited numbers of cerebral palsy patients5,6 suggests that
the adverse neurodevelopmental event occurs prenatally in up to 50% of cases.
Can obstetric care prevent cerebral palsy?
If better obstetric care could prevent cerebral palsy then lower rates of cerebral
palsy would be associated with good obstetric care rather than with bad obstetric care. There is very little good evidence
for this supposition. Several decades ago, new technologies such as electronic fetal monitoring were introduced into obstetrics,
without adequate assessment by randomised trials. It was assumed that early detection of fetal distress would allow early
delivery (e.g., by caesarean section), thus avoiding damage to the fetal brain and cerebral palsy. Although it is probable
that some perinatal deaths have been prevented by such techniques, there is no evidence that they have reduced the prevalence
of cerebral palsy, despite increased use of fetal monitoring and rising caesarean section rates.7
In view of the likely antenatal origins of most cases of cerebral palsy, this is not surprising. However, the mistaken belief
that birth injury is a major cause of cerebral palsy may have stemmed from:
- The high rate of non-specific fetal heart rate aberrations detected by electronic fetal
- The lack of tests which are specific for damaging levels of intrapartum hypoxia,
- The more intense medical observation during labour and delivery than antenatally.
Thus, any signs of possible fetal distress resulting from antenatal neurological injuries may not be detected until the commencement
of labour or until the normal stresses of labour uncover signs of a compromised fetus.
These factors may lead to the assumption that the fetus was healthy before labour and that it was only in
labour or at birth that problems occurred. However, events causing or predisposing to cerebral palsy may occur from conception
onwards, as shown in the Figure. Any one event or any combination of events could be the cause of the cerebral palsy.
The term fetal distress is imprecise and non-specific.9
No antenatal or intrapartum monitoring technique can clearly tell whether a fetus is unhealthy or whether the condition is
acute or chronic. Tests such as electronic fetal heart rate monitoring poorly predict fetal outcome. Up to 79% of fetal heart
rate traces during labour show some type of variation that has been described as abnormal,8
but the vast majority of such infants are born without signs of perinatal asphyxia or cerebral palsy.10
Clinical signs and test results predict only the possibility of distress and, as distress has no agreed definition
in this context, it is preferable to avoid the term fetal distress and instead describe the observed signs or the variation
in the test results.
normal fetal heart rate is generally predictive that there is no acute hypoxaemia, but variations from the normal pattern
are not good predictors of hypoxaemia. Even prolonged late decelerations with reduced variability have a less than 50% chance
of being associated with major fetal acid-base changes, which themselves are only poorly correlated with cerebral palsy.11 Similarly, meconium-stained
liquor is a common finding in labour, but only a minority of babies from these labours are born with a low umbilical arterial
blood pH. Finally, Illingworth has suggested that there is an undue readiness to ascribe brain damage to umbilical cord problems.12 Earn found a
loop around the neck of the fetus in 23% of 5676 consecutive births, without significant effect on fetal outcome, except for
one neonatal death where the cord was wound eight times around the baby's neck.13
Birth asphyxia is not a well-defined term.14
It implies some sort of dysfunction resulting from a lack of oxygen supply to the baby's tissues during the birth process.
The term should not be used clinically because of the difficulty in ascribing clinical signs and symptoms in the neonate to
an event during birth. Low pH and/or low Apgar scores at birth are supportive evidence of asphyxia but should not be used
alone to make the diagnosis.15,16
Until more information is available, perinatal asphyxia is the preferred term to describe a neonate in whom there is:
- An event or condition during the perinatal period that is likely to severely reduce
oxygen delivery and lead to acidosis (e.g., major antenatal haemorrhage or cord prolapse); and
- A failure of function of at least two organs (usually the brain and kidneys) consistent
with the effects of asphyxia.17
even these criteria are not specific for recent hypoxia and can be the result of any of the antenatal causes of cerebral palsy.
They are minimum requirements to suggest the possibility of asphyxia but do not prove its intrapartum origin.
Does cerebral palsy ever originate in labour?
Most infants who develop cerebral palsy are born from uncomplicated pregnancies
and are delivered without signs of fetal heart rate abnormalities. They do not have low Apgar scores or acidosis at birth
or any abnormal neurological signs in the neonatal period.19,20
Two major studies of children with cerebral palsy have been reported in which their labour, delivery and neonatal records
were in agreement in finding that, for 90%-94%, their disability could not be related to intrapartum hypoxia.20-22
This does not mean that in 6%-10% of labours hypoxia beginning in labour is the cause of cerebral palsy. In cases in
which severe intrapartum hypoxia was documented, it may not have been preventable and earlier delivery may not always have
been possible. Pre-existing neurological deficit can contribute to intrapartum hypoxia, or be associated with chronic hypoxia.23
It is our opinion that the lesions causing cerebral palsy are rarely initiated in labour and are rarely preventable.24,25
What little evidence exists suggests that less than 2% of cerebral palsy could be attributed
to suboptimal intrapartum care.26
It is the opinion of this conference that this figure could be lower.
Causation and fault
To determine causation, Australian courts have had regard to what is known as
the but for test, where a plaintiff seeks to establish that, without (or but for) a defendant's breach of duty,
he or she would have remained uninjured. It is recognised that applying this test becomes difficult when there are a number
of events which may have influenced an outcome.31
There must also be an application of common sense to the facts of each particular case.32
Causation will be a very difficult matter to determine in cerebral palsy cases because most are caused by an antenatal condition
which often may not have declared itself before or immediately after birth. An absence of major risk factors, such as intrauterine
growth restriction, extreme prematurity, twin gestation or known antenatal viral infections, does not exclude congenital or
acquired neurological deficit during fetal development.
Chief Justice of the Australian High Court, Justice Mason, has talked about important conceptual differences between causation
in law and causation in science.
. . . [In]
science, the concept of causation has been developed in the context of explaining phenomena by reference to the relationship
between conditions and occurrences. In law, on the other hand, problems of causation arise in the context of ascertaining
or apportioning legal responsibility for a given occurrence . . . a person may be responsible for damage when his or her wrongful
conduct is one of a number of conditions sufficient to produce that damage. [However,] . . . it is for the plaintiff to establish
that his or her injuries are "caused or were materially contributed to" by the defendant's wrongful conduct. . . . Generally
speaking, that causal connection is established if it appears that the plaintiff would have not sustained his or her injuries
had the defendant not been negligent.33
Given our understanding of the rarity of preventable intrapartum causes of cerebral palsy and the difficulty
of detecting antenatal causes before labour, it should not be necessary for a defendant to prove the likelihood of neurological
abnormality of the fetus before labour or birth. The inability of a defendant to provide such details in retrospect should
not allow the assumption that the origins of the cerebral palsy began in labour. It is for a plaintiff to prove the causative
link between a putative breach and injury, not for a defendant to prove, in hindsight, the precise antenatal cause and timing
of this condition.
The standard of care required of health professionals is " . . . that to be expected by an ordinarily careful
and competent practitioner of the class to which the practitioner belongs".34,35 Whether a medical
professional has acted in accordance with a standard of reasonable care " . . . is a question for the Court [to decide] and
the duty of deciding cannot be delegated to any profession or group in the community".36 Standards of
care will be determined by the courts, not in isolation, but with regard to the evidence of expert witnesses who should give
opinion based on scientific evidence.
There is no evidence that current obstetric practices can reduce the risk
of cerebral palsy. The origins of many cases of cerebral palsy are likely to be antenatal. While obstetric interventions in
the presence of signs of possible hypoxia may prevent fetal death, there is no evidence that they will limit the prevalence
or severity of cerebral palsy. The antenatal signs of hypoxia and the methods to monitor hypoxia in labour are still imprecise.
This can lead to over-diagnosis of severe hypoxia and, even when correctly diagnosed, early delivery by caesarean section
may not change the risk of cerebral palsy. All expert witnesses and the public should recognise that the belief that caesarean
section will prevent many cases of cerebral palsy is incorrect. There is a great need for further research into the antenatal
origins and the prevention of cerebral palsy. This will include more cerebral palsy registries, improved methods of assessing
the development and well being of the fetus throughout pregnancy and labour, and better methods of assessing the neurological
integrity of the baby before and after birth.