|
OUTER HOUSE, COURT OF SESSION
[2006] CSOH 63
|
|
|
OPINION OF LORD HODGE
in the cause
PAULINE McKENZIE
Pursuer;
against
FIFE
ACUTE HOSPITALS NHS TRUST
Defenders:
ญญญญญญญญญญญญญญญญญ________________
|
Pursuer: Dunlop, Q.C.. Gianni; Morisons
Defenders: Stacey, Q.C., Stuart; R F Macdonald
28 April 2006
Background
[1] Kyle
McKenzie is a twelve-year-old boy who suffers from cerebral palsy which was
caused by events when his mother was in labour before his birth. He was born at 2344 hours on 25 February 1994. In the proof which I have heard the only
substantive issue between the parties was the timing of the events that caused
that condition.
Admission
of Liability
[2] The
defenders lodged a Minute of Admission of Liability in the following terms:
"That for the
purposes of this action only, and without prejudice to their rights and pleas
in relation to causation and quantum of damages, the defenders hereby admit
liability to make reparation to the pursuer, as guardian for Kyle McKenzie, for
any loss, injury and damage sustained by Kyle McKenzie as a result of his not
being born by 2140 hours on 25 February 1994".
[3] The
pursuer's contention on liability was that the defenders were negligent in
failing to deliver Kyle either two hours and thirty minutes or in any event two
hours before he was born. Shortly after
2000 hours on 25 February 1994
the cardiotocograph ("CTG") disclosed a trace of the foetal heart rate that was
non-reassuring. It was not disputed that
that should have caused the obstetricians responsible for Kyle's welfare to
investigate his condition. They should
have stopped the syntocinon infusion which was intended to stimulate the
progress of labour. A sample of foetal
blood should have been taken by about 2030 hours to test its acidity in order
to decide whether to intervene to expedite delivery. As there is no means of telling what the
reading of the acidity of the foetus's blood ("the pH reading") would have been
at 2030 hours but it is likely that a pH reading at about 2100 hours would have
revealed foetal acidity at a level which required immediate intervention, I
have to proceed on the basis that the defenders could without negligence have
postponed a decision to initiate a Caesarean section until shortly after 2100
hours. The failure to deliver Kyle by
2140 hours was admittedly negligent. The
evidence does not establish that it was negligent not to have delivered Kyle
earlier. Thus, in view of the admission
of liability, the only issue which I have to decide is one of causation. That issue is whether on balance of
probabilities the harmful event or events which caused Kyle's cerebral palsy
occurred after about 2140 hours on 25
February 1994.
The
parties' contentions on causation
[4] The
pursuer's contention was that if Kyle had been delivered two hours before he
was, he would not have suffered the cerebral palsy from which he has suffered
since birth. The defenders' contention
was that the damage to Kyle's brain was caused by an undetected event several
hours before his birth and, in particular, before 2000 hours; thus the admitted
negligence of the defenders' employee did not cause him to suffer the injury
that has caused his cerebral palsy.
The
nature of Kyle's condition
[5] Kyle's
condition is not in dispute; Dr Christopher Steer, a Consultant Paediatrician
at the Victoria Hospital,
Kirkcaldy, described his condition and was supported by other experts. Kyle suffers from cerebral palsy which is
predominantly of an extrapyramidal, dyskinetic type. That means that damage was caused to the
system of nerve tracts connecting the cerebral cortex, basal ganglia and
certain other parts of the brain, which system is mainly concerned with the
regulation of reflex muscle movements.
The result of the damage is dyskinesia; that is abnormal involuntary
movements instead of normal smoothly controlled limb and facial movements. Kyle is left with an inability, or at least a
reduced ability, to organise and execute intended movements, to coordinate
automatic movements and to maintain his posture. Damage to his extrapyramidal system has also
affected Kyle's ability to coordinate his feeding and swallowing. The cause of this damage is not in
dispute. Kyle's brain was deprived of
oxygen as a result of an interruption of the flow of his mother's oxygenated
blood into his body; in other words he suffered a hypoxic ischaemic brain
injury.
[6] The
parts of Kyle's brain that suffered the most severe damage were the basal
ganglia. These are particularly
susceptible to asphyxial damage because of their high metabolic activity. They are involved with the regulation of
voluntary movements at a subconscious level and when damaged can cause involuntary
movements of the face and limbs. He
also has suffered epilepsy and some learning difficulties which indicate that
he suffered some damage to the cerebral cortex.
There appears to be hippocampal damage, in the temporal lobe, which
could explain Kyle's cognitive impairment and epilepsy. Kyle's intellectual function has been
relatively preserved but he has difficulty in communicating. Kyle also suffered short-term mild to
moderate damage to his kidneys which manifested itself in blood in his urine
and elevated levels of urea and creatinine in the days immediately after his
birth.
[7] There
is no dispute as to the cause of a dyskinetic form of cerebral palsy: it is
caused predominantly by an acute profound asphyxia. That form of asphyxia involves a relatively
sudden shutting off of a foetus's oxygen supply before its body can adapt to
the problem. This causes damage
principally to the parts of the brain such as the basal ganglia with high
metabolic activity while sparing parts of the brain with less metabolic
requirement. Dr Brian Kendall, a
Consultant Neuroradiologist at the Royal Free Hospital and honorary Consultant
Neuroradiologist at the Hospital for Sick Children and the National Hospital
for Neuroradiology and Neurosurgery, London, gave expert evidence on the damage
to Kyle's brain that was revealed by the neuro-imaging of a cranial CT scan
which had been performed in April 1997. That neuro-imaging revealed damage to
the lentiform nuclei which form part of the basal ganglia, to the pre and post
central gyri in the cerebral cortex and in the superior vermis of the
cerebellum. These three regions are
centres of high metabolism in a mature foetus and therefore vulnerable to an
acute and generalised drop of the circulation of oxygenated blood to the
brain.
[8] The
cerebral palsy was caused by an injury to his brain in the intrapartum period; that is during the course of labour. While in their written pleadings the
defenders averred that the damage occurred at least twelve hours before delivery,
the one expert witness whom they led at proof accepted that it was likely that
Kyle sustained the injury during labour.
There was no expert evidence led before me to suggest otherwise. Therefore the issue in this case is: when
during labour did that acute event occur?
To determine that I have first to summarise the facts of the pursuer's
pregnancy and labour which were established and most of which were never in
dispute.
The
pursuer's pregnancy and labour
[9] The
pursuer had an uneventful pregnancy. She
had no major risk factors except that she was a moderate smoker. But Kyle demonstrated none of the
complications associated with smoking.
Foetal growth was assessed as appropriate at all stages. There was no
evidence of reduced liquor volume. There
was no evidence of an inadequate placenta giving rise to growth
retardation. In short, there were no
obvious antenatal complications. His
birth weight was 3.26 kg, which was within the normal weight range at birth.
There was no evidence of any early intrauterine brain damage or of any
malformation of the brain. Thus in
prospect and with hindsight there was nothing which pointed to any antenatal
compromise.
[10] The pursuer was admitted to Forth
Park Maternity Hospital
at 0800 hours 24 February 1994
in the forty-second week of her pregnancy for induction of labour. This was eleven days after her expected date
of delivery. A CTG was applied
externally between 0835 and 0930 hours to record the foetal heart rate. The CTG trace was consistent with foetal
wellbeing. The CTG was recommenced at
1245 hours and continued thereafter.
The medical staff decided to give the pursuer syntocinon (a drug to
augment labour) which was administered to her from 1300 hours onwards.
[11] The pursuer's membranes ruptured spontaneously at 1200 hours. The rupture revealed liquor stained with
meconium (the contents of the foetal bowel).
Initially the defenders appeared to suggest that the meconium indicated
that Kyle might have suffered the insult to his brain which caused his cerebral
palsy at a time before he came into hospital.
But Mrs Stacey (reflecting the evidence of her expert witness) presented
her closing submissions on the basis that it was more likely that Kyle suffered
the relevant insult during the afternoon or early evening when the CTG was
recording his heart rate. She did not
invite me to treat the meconium staining at 1200 hours as
significant. This was consistent with the
evidence of Professor Greer, the Professor of Obstetrics and Gynaecology at Glasgow
University and Honorary Consultant in Obstetrics and Gynaecology at Glasgow
Royal Infirmary and Princess Royal Maternity Hospital, and Dr David Lloyd,
Consultant in Perinatal Medicine in Grampian University Hospitals NHS Trust,
who opined that the presence of meconium on the rupture of the membranes was
not unusual with babies who were delivered after their forty-week term. In support of this view I was referred to
research articles by Steer and Others (1989) and by Meis and Others (1978).
[12] The CTG was temporarily discontinued for ten minutes between
1610 hours and 1620 hours when an epidural anaesthetic was being set up. Otherwise the CTG monitored the foetal heart
rate continuously from 1245 hours and revealed that, although there were
occasional variable decelerations, it was within the normal range. This was consistent with the wellbeing of the
foetus. At 1930 hours the CTG showed a
baseline tachycardia (an increase of the heart rate above the normal) but the
heart rate had normal variability. This
did not indicate foetal distress. But
after 2000 hrs the CTG trace revealed an erratic foetal heart rate with late
decelerations. Late decelerations are
thought to be associated with foetal hypoxia.
Professor Greer explained that the CTG trace showed a serious
tachycardia at 2012 hours, that the foetus's baseline variability was flat and
that late decelerations occurred at 2015 hours and 2026 hours. The tachycardia remained at 2100 hours, when
the pursuer was reviewed; late and
variable decelerations and reduced variability were observed. Professor Greer described the CTG trace as
showing multiple serious abnormalities consistent with foetal distress and
opined that the syntocinon infuson should have been stopped and steps taken to
deliver Kyle by Caesarean section by 2140 hours. Thereafter the CTG trace revealed baseline
tachycardia, and late decelerations following uterine contractions with reduced
baseline variability. By 2300 hours the
pursuer's cervix was fully dilated and the pursuer was encouraged to push
actively in the second stage of labour.
At around 2316 hours the CTG revealed a baseline bradycardia (a slowing
of the heart rate below the normal), a heart rate of about 100 beats per
minute ("bpm") with reduced baseline variability and late decelerations which
continued until delivery at 2344 hours.
Professor Greer described the foetal heart rate recorded on the CTG as
having been pathological for three hours and forty-five minutes, in other words
since 2000 hours.
Kyle's
condition at and after his birth
[13] As much of the dispute between the parties turned on the
interpretation of the symptoms that Kyle showed shortly after birth, it is
necessary for me to record the findings of those who treated him in some
detail. There has been no criticism of
the way in which Kyle was resuscitated and thereafter cared for. I therefore do not record his treatment
except where it is relevant as the context in which findings were made. The medical notes described Kyle on delivery
as flat, cyanosed and pale with no spontaneous movement. There were no respiratory movements. Meconium was noted in his mouth and
pharynx. At one minute after birth his
heart rate was 50 bpm. Doctors applied a
bag and mask to get oxygen into him and that rapidly increased his heart rate
to over 120 bpm. As a result his colour
improved. But at five minutes of age he
remained flat and he was still making no respiratory movements. His Apgar scores were recorded as two at one
minute after birth, three at five minutes and five at ten minutes. A registrar
arrived and intubated Kyle, noting that he was flat, but pink centrally. Irregular respiratory efforts started at
seven minutes of age. Kyle was
transferred to the Special Care Baby Unit at 0010 hours on 26 February. On arrival in that Unit he was noted to be
tense on handling at 0010 hours (twenty-six minutes of age). Arterial blood gases were taken at 0020 hours
and sent to laboratory for analysis.
That analysis revealed that Kyle had a profound metabolic acidosis: his
blood had a pH of 6.95 and a Base Excess of 22.
A metabolic acidosis arises where the foetus is deprived of oxygen and
in metabolising glucose creates acid and is consistent with a significant
hypoxic ischaemic event.
[14] Kyle commenced spontaneous movements at forty-five minutes of
age and became agitated and tense on handling.
He was recorded as making fisting and cycling movements at ninety
minutes of age and the note also recorded that no seizures were seen. Witnesses expressed differing views as to
whether the cycling movements were subtle seizures or were release phenomena -
see paragraphs [19], [32] and [33] below.
He passed urine containing blood.
Kyle was given plasma protein and sodium bicarbonate and as a result his
blood pH improved and was almost normal by 0400 hours on 26 February (four
and a quarter hours after birth). At
0430 hours (at four hours and forty-six minutes of age) it was noted that he
had been extremely agitated over the past two hours. He displayed extensor thrusting, arched his
back, clenched his hands and he was boxing with his arms. These findings were consistent with severe
cerebral irritation. At 1010 hours he
was extubated. He was noted to be very
hypertonic (stiff) and he cried when disturbed.
He was noted to be almost opisthotonic and he had stridor. Opisthotonus is extreme arching of the back
and stridor is a crowing noise made during inspiration; the former was a very
worrying sign indicating involvement of the brain stem; the latter may have
been the result of intubation.
[15] On 27 February Kyle had two epileptic seizures in the morning
and was given anticonvulsant medication.
He remained in a very arched position.
There was evidence that his kidneys were not functioning; his urinary
output was minimal and contained blood and protein; he had elevated urea and
creatinine. He was diagnosed as
suffering from acute tubular necrosis, which was a sign that the kidneys had
received a recent insult. He was
hypertonic in all four limbs; his arms were flexed and his legs were
extended. He remained hypertonic on 28
February and still did not pass significant amounts of urine. His urine had large amounts of blood and
protein in it. On 2 March 1994 he was noted to be hypertonic in
all four limbs, making cycling movements and agitated when handled. Thereafter his urine output increased and on
3 March his urine output was described as good.
Irritability, hypertonia and cycling movements persisted until 3
March. On 4 March his tone was recorded
as normal. In the following days there
were recordings of jitteriness. He was
discharged home on 10 March 1994.
[16] Kyle was admitted to hospital on 5 April 1994 because he was irritable and was arching
his back and neck. He was noted on
examination to be slightly dystonic. Dr
Steer saw Kyle regularly and expressed concern to Kyle's mother that he might
be developing cerebral palsy. He
suffered infantile spasms in August 1994 and was given anti-convulsant
drugs. On 21 December 1996 Kyle suffered a grand mal seizure and
on 29 April 1997 he
presented with status epilepticus and required intensive care. He suffered recurrent seizures in later 1997
and 1998. Throughout this period the
growth of Kyle's head appears to have been within the normal range. Kyle's mother
also gave evidence and spoke to a DVD of Kyle's condition. As revealed in her evidence and the DVD, Kyle
has dyskinetic cerebral palsy. He
suffered from fluctuating tone which is his main problem. He also has some cognitive impairment
although that poses less of a problem for him.
Her evidence was consistent with that of the medical experts who gave
evidence on her behalf.
[17] There was no significant disagreement between experts on the
categorisation of Kyle's condition at birth.
I was referred to research by Sarnat and Sarnat (1976) which was
discussed in Stevenson and Sunshine's "Fetal and Neonatal Brain Injury" (2nd
ed.1997) (chapter 18). Within the Sarnat
classification, the experts agreed that Kyle was most appropriately classified
as having Stage 2 (moderate) hypoxic ischemic encephalopathy.
The
cause of Kyle's dyskinetic cerebral palsy
(i)
The parties'
cases
[18] The pursuer's case was that there was clear evidence from the
CTG trace of an acute ischaemic hypoxic insult in the final stages of labour
which was of a nature that could cause the dyskinetic cerebral palsy from which
Kyle suffers. The acute event occurred after 2140 hours
on 25 February 1994; that
was after the time when the defenders' employee was admittedly at fault in
failing to achieve the delivery of Kyle.
There was no evidence of any earlier acute asphyxial insult which could
have caused that damage. Kyle's
neurological behaviour in the hours after his birth was not inconsistent with
the damage being caused in the final two hours of labour and in particular with
the acute event occurring from shortly after 2300 hours until his
delivery. In support of this case, Miss
Dunlop led the evidence of five medical experts of differing disciplines:
Professor Ian Greer (Obstetrics) whom I mentioned in paragraph [11] above, Dr Brian Kendall (Neuroradiology) whom
I mentioned in paragraph [7] above, Dr
David Lloyd (Perinatal Medicine) whom I mentioned in paragraph [11] above, Dr Richard Pearse, a Senior
Consultant Neonatal Paediatrician in Sheffield Teaching Hospitals NHS
Foundation Trust, and Dr Sameer Zuberi, a Consultant Paediatric Neurologist at
the Royal Hospital for Sick Children in Glasgow. I discuss the expert evidence in support of
the pursuer's submission in my decision after considering the defenders' case.
[19] The defenders' case that the acute event which caused Kyle's
dyskinetic cerebral palsy occurred during labour but before 2000 hours on 25
February 1994 rested on the expert evidence of Dr Robert McWilliam, a Consultant
Paediatric Neurologist at the Royal Hospital for Sick Children in Glasgow. He opined that it was likely that the acute
ischaemic brain insult which caused Kyle's cerebral palsy occurred not less
than six hours before his birth. He
noted that both the brain and the kidneys were compromised. While he recognized that there was
uncertainty as to the timing of perinatal insults, from observation in medical
practice he had noted that after an infant had suffered a generalised brain
insult which caused permanent neurological damage there was always a period of
almost complete inactivity of its central nervous system for between six and
twelve hours. In his oral evidence
Dr McWilliam qualified this statement by saying that the period of
inactivity was usually not less than six hours and was always greater than four
hours. He considered that what he had
observed with infants could be applied to a foetus at the final stages of a
pregnancy. Clinically the inactivity
manifested itself as hypotonia (a state of reduced tension in muscles) and lack
of responsiveness. This pattern was
evident in infants who had strokes. He
noted that Kyle was described as "tense" at twenty-six minutes of age and that
he showed extreme irritability and extensor thrusting at four and a quarter
hours of age. He associated the fisting
and cycling movements that Kyle made at ninety minutes of age with release
phenomena - movements caused by the brain stem which was not being effectively
controlled by higher centres in the brain.
He suggested that the speed with which Kyle manifested active
neurological symptoms and also recovered normal respiratory control after his
birth pointed strongly to the occurrence of a hypoxic ischaemic brain insult
many hours earlier. He opined that the
hypoxic ischaemic insult which Kyle suffered in the thirty minutes immediately
before his birth, which he described as "a potentially damaging circumstance",
did not add significantly to brain damage which was already present.
[20] In support of his view he pointed out that asphyxia at birth of
the degree that Kyle suffered occurred quite frequently (in about one in every
hundred births) without the development of a neonatal encephalopathy or
cerebral palsy. While there had been a
considerable reduction in the incidence of asphyxia in recent years, there had
been no corresponding decline in the incidence of dyskinetic cerebral palsy
which remained at one in one thousand births.
He suggested that this allowed one to infer that birth asphyxia was not
an important cause of dyskinetic cerebral palsy. Secondly, he supported his view by the
observation that the temporary damage to Kyle's renal function was an unusual
consequence of a single acute hypoxic insult.
He suggested that Kyle's renal damage was a manifestation of an earlier
insult in which his body had undergone physiological changes to protect the
brain at the expense of other organs. He
also suggested that the difficulties that Kyle encountered after 2000 hours on 25 February 1994 may have been a
manifestation of earlier damage which compromised his ability to cope with the
stresses of labour. Dr McWilliam
referred in his evidence in chief to Joseph Volpe's "Neurology of the Newborn"
(4th ed. 2001), Stanley, Blair and Alberman "Cerebral Palsies:
Epidemiology and Causal Pathways" (2000) and articles by Pasternak (1993) and
Pasternak and Gorey (1998).
(ii)
Decision
[21] In deciding between the parties' contentions it is in my
opinion important to start by considering the nature of Kyle's condition and
the process that caused that condition.
As I have said, parties agreed on these matters. See paragraphs [5] to [8] above.
Dyskinetic cerebral palsy is a relatively unusual form of cerebral palsy
when a child is delivered at term. I was
referred in this regard by both parties to a paper by Lewis Rosenbloom (1994)
about a study of the connection between birth asphyxia and dyskinetic cerebral
palsy from data collected in Merseyside.
Dyskinetic cerebral palsy is caused by damage to the basal ganglia which
in turn is caused by brief near-total asphyxia, an acute event which does not
allow the foetus to adapt to the insult and which damages the structures of the
brain which have high energy requirements.
Animal studies by Myers (1972) have given rise to a paradigm discussed
by Pasternak (1993) of the acute hypoxia allowing full recovery if the insult
lasts less than ten minutes, but inflicting increasingly severe neuronal damage
when the insult lasts between ten and twenty-five minutes, and causing
irreversible vascular collapse and death after twenty-five minutes. The acute total asphyxia created in the
laboratory rarely if ever occurs in human infants; it is more common for an
acute near-total asphyxial event to be preceded by partial asphyxia caused by
the impairment of the exchange of gases between the mother and the foetus. Animal studies have shown that preceding
partial asphyxia can cause the foetus to deteriorate more rapidly when exposed
to acute asphyxia thereafter.
[22] When did the acute near-total asphyxial event occur? In recent years medical literature has warned
against an uncritical attribution of the cause of neonatal encephalopathy to
pre-birth asphyxia in the later stages of labour. Among others, Stanley, Blair
and Alberman (2000) have suggested that in the past researchers and clinicians
have overestimated the significance of birth asphyxia in the aetiology of
cerebral palsies and that an antenatal insult or condition was the cause of
most cerebral palsies. As is stated in
the template to which I refer in the next paragraph, epidemiological studies have
suggested that in about ninety per cent of cases intrapartum hypoxia could not have been the cause of cerebral palsy
and that in the remaining ten per cent intrapartum
signs compatible with damaging hypoxia might have had antenatal or intrapartum origins. Nonetheless, as Dr Zuberi pointed out,
Aicardi and Bax (1992) suggest that the incidence of perinatal factors is
higher in cases of dyskinetic cerebral palsy than in other forms of cerebral palsy.
[23] Fortunately, in this case it is not necessary to consider the
likelihood of an acute near-total asphyxial event before the onset of
labour. The pursuer's expert witnesses
all suggested that the acute event which caused Kyle's cerebral palsy occurred intrapartum (during labour). Dr McWilliam, on cross-examination, agreed
but placed the event at some time before 2000 hours on 25 February 1994.
There was thus, as I have said, no expert evidence led before me which
suggested that the damage was inflicted before the onset of labour. As a result I do not have to consider in any
detail the evidence led for and against the template for defining a causal
relation between acute intrapartum
events and cerebral palsy prepared by the International Cerebral Palsy Task
Force and published in 1999. It was not
disputed that intrapartum
complications cause cerebral palsy only infrequently, but it was also accepted
by the experts that this was one of those infrequent cases. Kyle's circumstances met all three essential
criteria in the template to define an acute intrapartum
hypoxic event and also four of the five non-specific criteria which together
suggest an intrapartum timing. Only one non-specific criterion was not met:
there was no identified sentinel hypoxic event.
In other words, as Mrs Stacey submitted, we do not know the mechanism
which reduced or cut off the supply of oxygenated blood to Kyle from his mother
and which caused his cerebral palsy.
[24] What we do know however is that the CTG trace of Kyle's heart
rate after 2300 hours on 25 February
1994 indicated a hypoxic event which was sufficient in itself to
cause the damage to Kyle's basal ganglia and cortex which in fact occurred.
Professor Greer and Dr Kendall both considered that the CTG trace pointed to
the occurrence of a major hypoxic event which began after 2000 hours and became
acute in the later stages of labour. Dr
Pearse also considered the CTG trace to be evidence of asphyxia and suggested
that the period of acute asphyxia, manifested by the foetal bradycardia,
occurred within the twenty to thirty minutes before birth. Dr McWilliam accepted that the CTG after
2300 hours disclosed hypoxia that was a potentially damaging event. In substance he did not challenge the
evidence of the pursuer's experts on the potential of the hypoxia after 2300
hours to inflict the injuries that Kyle suffered; his position was that the
damage had already occurred.
[25] Mrs Stacey in her closing submission suggested that the issue
in this case was simply a question for consultant paediatric neurologists such
as Dr McWilliam and Dr Zuberi and implied that experts from other
disciplines had little to offer in helping the court to decide on the balance
of probabilities when Kyle suffered the damage which caused his cerebral
palsy. I am satisfied that that
submission is incorrect. In my opinion
it is appropriate that I should look not only at the evidence of the
neurologists as to the timing of the emergence of active symptoms after Kyle's
birth but also at the whole circumstances including the views of experts of
other medical disciplines on what may properly be inferred from the
circumstances both before and after Kyle's birth.
[26] In particular, it is significant that from 1245 hours on 25 February 1994 Kyle's heart rate
was continually monitored by CTG, except for a period of about ten minutes between
1610 and 1620 hours. On the expert
evidence before me it was not disputed that it was likely that the acute event
which damaged Kyle occurred when the CTG was operating. The CTG is a sensitive instrument and is able
to pick up events which have the potential to cause brain damage although it is
not specific as to the nature of those incidents. Professor Greer opined that the CTG picked up
babies who had problems in a very high percentage of cases. He accepted Mrs Stacey's proposition that a
CTG could suggest that a foetus was in difficulty but the baby would then be
born unharmed. CTGs gave rise to such
"false positive" results as they were sensitive but not specific. However while he recognised that CTGs could
give rise to "false negatives", he stated that it was uncommon where there had
been continuous monitoring for there to have been a normal CTG and a baby who
was flat at delivery. Although Mrs
Stacey did not ask Professor Greer about it, she referred Dr Zuberi to an
article by Steer and Others (1989) which suggested that the sensitivity of an
abnormal CTG for foetal acidosis was eighty per cent and for severe acidosis
was eighty-three per cent. This, she
suggested, supported the view that there was a significant "false negative"
rate in CTG monitoring. However, while
one must be alive to the possibility of "false negatives", I am not persuaded
that that paper establishes any percentage occurrence of the failure of CTGs to
pick up events that in fact cause cerebral palsy both because not all babies
with acidosis at birth go on to suffer cerebral palsy and also because there is
always scope for a clinician (as in this case) to misinterpret a CTG. In any event in this case the CTG did reveal
a non-reassuring trace which, as I have said, was consistent with an acute
event which (subject to questions of the timing of the onset of active
neurological symptoms following birth) would explain Kyle's cerebral palsy.
[27] Significantly, Professor Greer also opined that the borderline
tachycardia that Kyle exhibited at about 1930 hours (and for some time
thereafter) was inconsistent with his having suffered major hypoxic damage
before then: he would not have expected a severely damaged baby to exhibit
normal responses on a CTG to the stresses of labour. Dr Kendall also expressed the view that it
was improbable that Kyle suffered an acute hypoxic event which was not picked
up on the CTG. There was no evidence of
a period of bradycardia before 2000 hours and such bradycardia was needed to
inflict the damage that Kyle suffered.
He did not believe that Kyle's heart rate would have reverted to normal
after an episode of bradycardia that caused the damage that he suffered. Dr Pearse expressed the view that it was very
unlikely that Kyle suffered an acute and damaging asphyxia, made a spontaneous
recovery and then showed a normal trace on his CTG, in which his heart rate
reacted appropriately to stimuli during labour.
Dr Lloyd also relied on the absence of evidence in the CTG trace that
Kyle suffered any damage during labour before 2000 hours to support his view
that such early damage did not occur.
[28] I consider this uncontradicted evidence of distinguished medical
experts from disciplines other than paediatric neurology to be highly relevant
to the question of causation. Unless
there were persuasive and properly vouched evidence from neurologists that the
timing of the emergence of symptoms after birth meant that the acute event must
have occurred earlier during labour than the CTG suggested, I would consider
this evidence sufficient to satisfy me that the acute event that caused the
damage to Kyle's brain occurred within the final forty minutes of labour, preceded
by a period of partial asphyxia after 2000 hours. Was there such contrary evidence?
[29] In my opinion there was not.
Dr McWilliam's view, that there was invariably a period of at least four
hours after a generalised brain insult which caused permanent neurological
damage before active abnormal neurological behaviour emerged, was based on his
own observation of infants. It was not
supported by the medical literature.
[30] The template referred to in paragraph [23] above did not
identify the timing of the emergence of such behaviour as an indicator of a
causal relationship between an intrapartum
event and cerebral palsy. There was
considerable debate in evidence over the meaning of a passage in Volpe (chapter
9, p.333) in which he discussed the clinical aspects of hypoxic-ischaemic
encephalopathy. Among the clinical
features of severe hypoxic-ischaemic encephalopathy in the first twelve hours
after birth Volpe lists (in table 9.4) the occurrence of hypotonia with minimal
movement more than hypertonia. It was
suggested in evidence that Volpe's classification of the severely affected
infant was broadly equivalent to Sarnat and Sarnat Stage III classification,
and that appears to be correct. Volpe
goes on to state:
"The large
majority of infants at this stage are markedly and diffusely hypotonic with
minimal spontaneous or elicited movement.
Less-affected infants have preserved tone or occasionally some increase
in tone. The latter is particularly
likely with prominent involvement of the basal ganglia."
In the period from twelve to twenty
hours after birth, Volpe states that infants with involvement of the basal
ganglia may exhibit an increase in their hypertonia, especially in response to
handling. Dr McWilliam suggested that
Volpe was less specific in his views than he was but that nothing Volpe said
contradicted his opinion as to timing.
Nonetheless, what Volpe says does not unequivocally support Dr McWilliam's
view. In particular, if, as was
suggested by Dr Lloyd and Dr Zuberi, Volpe's reference to less- affected
infants with basal ganglia damage in the passage quoted above was broadly
equivalent to Kyle's classification (i.e. Sarnat and Sarnat Stage II), an
increase in tone in the first twelve hours after birth was to be expected.
[31] Studies by Constantinou and Others (1989) and by Ahn and Others
(1998) suggest that the interval between an asphyxial event and the ensuing
encephalopathy may vary considerably and that there is no reliable time
relationship between perinatal asphyxial insults and the onset of
seizures. See the chapter by Dear and
Newell on cerebral palsy and intrapartum
events (chapter 14) in Clements' "Risk Management and Litigation in Obstetrics
and Gynaecology" (2001). The study by Ahn and Others (1998) suggests that the onset of seizures after
birth does not of itself appear to be a reliable indicator of the timing of
foetal brain injury. While it was
pointed out that in that study the authors used evidence of abnormal foetal heart
rates detected by monitoring as the likely time of the hypoxic ischaemic events
(and therefore the results were not inconsistent with Dr McWilliam's thesis in
cases where an abnormal foetal heart rate was a symptom of an earlier damaging
event), the study provides no support for Dr McWilliam's position.
[32] Dr McWilliam's view on timing was also not shared by Dr Zuberi,
the only other paediatric neurologist who gave evidence. Dr Zuberi expressed the view that there was
no clear pattern of timing of the onset of abnormal active cerebral activity
and spoke of having seen hypertonia and seizures within the first hour after a
global ischaemic injury. He opined that
one could not reach conclusions with any confidence as to the timing of an
otherwise silent global ischaemic insult from the time at which such symptoms
emerged. He based his views on his own
clinical experience and his review of the literature. In his evidence he referred to Volpe (above)
and to a paper by Pasternak and Gorey (1998) which, in a study of eleven
infants born at term after an acute, near-total uterine asphyxia at the end of
labour, suggested that there was a wide range in the timing of the onset of
seizures following such an insult. I
accept that it is not possible on the published information to compare with any
accuracy the severity of the insult to each of the infants in that study to
that which Kyle suffered. Nonetheless,
the paper does not suggest that the time of onset of seizures is a reliable
guide to the timing of the causative insult.
Dr Zuberi also referred to an illustrative case in Pasternak's 1993
paper (referred to in paragraph [20] above) in which a woman suffered a uterine
rupture and had her baby delivered within twenty minutes of presentation at
hospital and her baby suffered seizures at forty-five minutes of age. I accept, as Mrs Stacey submitted, that one
cannot take very much from the case because the reader of the paper does not
know the timing of the uterine rupture before the mother arrived in hospital
and because the baby had more severe acidosis than Kyle. Nevertheless it does not appear to support Dr
McWilliam's general thesis. While Dr
Zuberi had practised in his specialty for considerably fewer years than Dr
McWilliam, he was, like Dr McWilliam, a distinguished medical practitioner and
I saw no reason to discount his evidence and to prefer Dr McWilliam's on
the ground of seniority. In my opinion
Dr Zuberi's view, that the timing of onset of hypertonia and seizures is a poor
indicator of the timing of the asphyxial event, is supported by the medical
literature to which I was referred. In
addition he was supported by the evidence of neonatologists: both Dr Lloyd and
Dr Pearse thought that the early emergence of Kyle's hypertonia was
consistent with very recent damage to his basal ganglia.
[33] For the sake of completeness, I should make clear that I am not
persuaded that it makes any difference if active symptoms such as fisting and
cycling were subtle epileptic seizures or brainstem release phenomena. Whichever they were, I am not satisfied that
their early emergence after birth is a reliable indicator that the acute insult
occurred four or more hours beforehand.
On this matter I accept the evidence of Dr Zuberi.
[34] I can deal briefly with the other points that Dr McWilliam made
in support of his theory, which I summarised in paragraph [20] above.
I am not persuaded that the decline in birth asphyxia and the absence of
a corresponding decline in dyskinetic cerebral palsy would allow me to infer
that birth asphyxia is not an important cause of that type of cerebral
palsy. As only a small proportion of
cerebral palsies is caused by birth asphyxia, and as dyskinetic cerebral palsy
is a relatively unusual form of cerebral palsy, I would not necessarily expect
an overall decline in birth asphyxia to give rise to a detectable decline in
the incidence of dyskinetic cerebral palsy.
Secondly, the temporary renal damage that Kyle suffered, an acute
tubular necrosis that resolved within about six days, does not appear to be
inconsistent with an acute event. I note
that in Pasternak and Gorey's study (1998) three of the eleven infants who
suffered acute near-total intrauterine asphyxia had oliguria (unusually low
urine output) lasting more than thirty-six hours and two others had an elevated
creatinine. Dr Pearse described Kyle's renal
damage as "mild to moderate" and this categorisation was consistent with
Pasternak and Gorey's observation that in the context of an acute insult,
injury to non-brain organs, when present, is usually mild. Thirdly, although it is possible that
problems revealed by a CTG trace may be a manifestation of damage caused by an
earlier insult, in Kyle's case the absence of any evidence of a sustained
bradycardia in the afternoon of 25 February 1994 persuades me that, on the
balance of probabilities, Kyle did not suffer an acute hypoxic insult at the
time that Dr McWilliam suggested that it was likely that he did.
Conclusion
[35] I accept that there is much to learn about the effect of a
hypoxic insult on a foetus and that it is therefore necessary to be cautious
before one concludes that there is a causal link between intrapartum events that manifest themselves as a non-reassuring
foetal heart trace on a CTG and the emergence of neonatal encephalopathy. Nonetheless,
I am satisfied on the balance of probabilities that in Kyle's case the hypoxic
insult which caused his dyskinetic cerebral palsy was an acute event that
occurred at the end of labour after 2300 hours on 25 February 1994.
The acute event had been preceded by a partial asphyxia which started at
about 2000 hours on that date which may have weakened Kyle's ability to cope
with stresses of the later phase of labour and may also explain the damage to
his kidneys. But the damaging acute
event occurred later that evening.
[36] Accordingly, if the obstetric registrar, who was the defenders'
employee, had acted with reasonable care by stopping the syntocinon infusion
and arranging the prompt delivery of Kyle by 2140 hours on that date, I
consider that Kyle would not have suffered the brain damage which has given
rise to this action. I conclude
therefore that the admitted negligence of that employee caused that damage.
[37] I therefore sustain the pursuer's first plea-in-law, repel the
defenders' second and third pleas-in-law and allow a proof before answer on the
quantification of loss.
References
Ahn MA, Korst LM, Phelan JP, Martin GI. Clinical Pediatrics
1998. Vol 37. 673.
Aicardi J and Bax M. Diseases of the Nervous System in
Childhood. Clinics in Developmental Medicine No 115/118 (1992). 330.
Constantinou, JE,
Gillis, J, Ouvrier, RA, Rahilly PM. Archives of Disease in Childhood
1989. Vol 64. 703
Dear PRF and Newell SJ in Clements RV "Risk Management and
Litigation in Obstetrics and Gynaecology" (2001) ch 14.
Maclennan A and Others. British Medical Journal 1999. Vol
319. 1054.
Meis PJ, Marshall Hall III, Marshall JR, Hobel CJ. American
Journal of Obstetrics and Gynaecology 1978. Vol 131. 509
Myers RE. American Journal of Obstetrics and Gynaecology
1972. Vol 112. 246.
Pasternak JF.
Pediatric Clinics of North America 1993. Vol 40.
No 5. 1061.
Pasternak JF and Gorey MT.
Paedriatric Neurology. 1998. Vol
18. 397.
Rosenbloom L. Developmental Medicine and Child Neurology.
1994. Vol 36. 285
Sarnat HB and Sarnat MS Archives of Neurology 1976. Vol 33.
696
Stanley F, Blair
E and Alberman E. "Cerebral Palsies: Epidemiology and Causal Pathways" (2000)
ch 9.
Steer PJ, Eigbe F, Lissauer TJ and Beard RW. Obstetrics and
Gynaecology 1989. Vol 74. 715
Stevenson DK and Sunshine P. Fetal & Neonatal Brain
Injury. (2nd ed) (1997) ch 36 by Robertson CMT.
Volpe JJ. "Neurology of the Unborn" (4th ed)
(2001) chs 5 & 9.
