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A template for defining a causal relation between acute intrapartum events and cerebral palsy: international consensus statement

BMJ 1999; 319 doi: https://doi.org/10.1136/bmj.319.7216.1054 (Published 16 October 1999) Cite this as: BMJ 1999;319:1054

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Establishing probable cause in cerebral palsy

The thesis set out by Dr Little 1862 1 that cerebral palsy (CP) was
primarily due to perinatal cerebral injury did not meet with approval from
the London Obstetrical Society – an obvious conflict of interests. One
might have hoped that 137 years later a reasonably balanced view on the
role of intrapartum asphyxia in causing brain injury would have become
established but it is clear from the recent consensus statement from a
group calling themselves the International Cerebral Palsy Task Force 2
that the latter day echoes of those opposing voices still resonate. In
setting out a template for establishing the probable cause of cerebral
palsy this statement does make some useful points but there are some
aspects which most certainly require further debate.

The first is the need to recognise that in most cases where it is
possible to form a view on what caused CP this can only be done in
probabilistic terms. The question then is how much certainty is enough?
In a clinical context this will vary according to the circumstances but in
the medico-legal context the answer is clear - it is “more than 50%
certainty” (i.e. p <0.5).

In the medico-legal context the facts that intrapartum asphyxia
rarely causes CP and that CP is rarely due to intrapartum asphyxia are
irrelevant, as long as it is accepted that CP is sometimes caused by
intrapartum asphyxia. In that case, when confronted with a case of CP
which could be due to intrapartum asphyxia and in which there is evidence
of intrapartum asphyxia of potentially damaging severity, the relevant
question to ask is “are these events probably causally-related or are they
probably coincidental”? The answer is that they are more likely to be
causally related, as long as no better explanation for the CP is
forthcoming. This flows from basic probability theory dealing with
conditional probabilities. That is, the probability of events A and B
both occurring is the probability of “A” multiplied by the
probability of “B given A”. As long as event B is more likely to occur if
event A has occurred, when A and B both occur they are
more likely to be causally related than to be independent chance
occurrences.

The second point we wish to make concerns the insistence in the
consensus statement on the demonstration of a certain severity of
metabolic acidaemia in arterial blood, obtained from the umbilical cord or
the baby within an hour of birth, before considering attributing CP to
intrapartum asphyxia. We agree that this is strong evidence which it
might be necessary to have in order to form a view which approaches
certainty (e.g. p <0.05). It is not essential information for forming
a view on causation “on the balance of probabilities”. For instance, if a
baby is born by emergency caesarian section following placental abruption,
requires a lot of resuscitation at birth, suffers from an acute neonatal
encephalopathy and acute renal failure and then develops athetoid cerebral
palsy with MRI scan evidence of basal ganglia injury, then it certainly is
possible to say that acute intrapartum asphyxia is the probable cause of
disability regardless of whether or not metabolic acidaemia was
demonstrated.

This insistence on the demonstration of metabolic acidaemia is flawed
for a number of reasons, as follows:

1. Cord blood gas analysis is not universally practiced.

2. If a baby needs a lot of resuscitation and stabilization, an hour
can easily slip by before arterial blood is analysed for pH

3. Often cord venous blood is obtained and a venous pH above 7.0 or
base deficit of less than 12 mmol/L is not inconsistent with damaging
intrapartum asphyxia as a result of cord compression.

4. Sodium bicarbonate is often used as part of resuscitation and
blood from the baby after resuscitation will not reflect the acid-base
status at birth.

5. If the Task Force recommendations were to be accepted the best
defensive approach to possible litigation would be to ensure that no
assessment of acid-base status around birth is made. Then, according to
the Task Force, an intrapartum cause for cerebral palsy cannot begin to be
considered.

References

1. Little WJ. On the influence of abnormal parturition, difficult
labours, premature birth and asphyxia neonatorum on the mental and
physical condition of the child, especially in relation to deformities.
Trans Obstet Soc Lond 1862;3:293-344.

2. Alastair MacLennan for the International Cerebral Palsy Task
Force. A Template for defining a causal relation between acute
intrapartum events and cerebral palsy: international consensus statement.
BMJ 1999;319:1054-59

Competing interests: No competing interests

08 November 1999
Peter Dear
Consultants in Neonatal Medicine
Simon Newell
St James''s University Hospital, Beckett Street, Leeds LS9 7TF