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[2021] ZAGPPHC 139
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LM obo DM v Member of the Executive Council for Health of the Limpopo Provincial Government (31261/2015) [2021] ZAGPPHC 139 (8 March 2021)
IN
THE HIGH COURT OF SOUTH AFRICA
(GAUTENG
DIVISION, PRETORIA)
Case
number: 31261/2015
Heard:
15 February - 18 February 2021
and
25 February 2021
Date
of judgment: 8 March 2021
NOT
REPORTABLE
NOT
OF INTEREST TO OTHER JUDGES
REVISED
In
the matter between:
LM
on behalf of DM
Plaintiff
and
THE
MEMBER OF THE EXECUTIVE COUNCIL
FOR
HEALTH OF THE LIMPOPO
PROVINCIAL
GOVERNMENT Defendant
JUDGMENT
SWANEPOEL
AJ:
INTRODUCTION
[1]
This is a claim for delictual damages resulting from a birth injury
that the plaintiff’s
minor child (“D”) sustained
during labour. Plaintiff arrived at the Dilokong Hospital in the
early hours of the morning
of 17 July 2010 suffering from lower
abdominal pain. She was, she believed, in the early stages of labour.
The plaintiff was assessed
as being nine months pregnant by date, and
38 weeks by palpitation. By 14h00 the plaintiff had entered the
latent first stage of
labour. Her vital signs were normal, as were
those of the foetus. By 18h00 the plaintiff was 4cm dilated, and she
entered into
the active first stage of labour. The foetus’
baseline heart rate was normal with good variables and no noted
decelerations.
[2]
Labour progressed normally until 22h00. The plaintiff was attended to
2-hourly, and
no concerns were noted. By 00h00 some concerns were
noted. Although the partogram is contradictory in that multiple
contradictory
entries were made on it, it appears that the labour had
slowed somewhat. By 01h20 there was no doubt that the progress of
labour
had slowed and had crossed the action line. The plaintiff had
not yet fully dilated and the nursing staff felt it necessary to
notify the doctor on call of the plaintiff’s condition. It
appears likely that the nursing staff were concerned about the
plaintiff’s condition because they called the doctor at 01h30
and again at 02h00. He promised he would come to see the plaintiff
but there is no evidence that he did so.
[3]
By 01h50 the membranes had ruptured and meconium-stained liquor
(grade 2) was noted.
At 02h00 it was recorded that the plaintiff was
fully dilated, and she entered the second stage of labour. The last
clinical entry
was made at 02h00 and it records that the doctor was
notified about the plaintiff’s condition. The foetus’
heart rate
was 136 – 138 bpm and regular. The plan was to
monitor the foetal and maternal condition. Thereafter there is no
further
entry in the clinical notes, and no indication that the
plaintiff was monitored at all. Plaintiff started bearing down at
either
02h15 or 03h15. The exact time is uncertain as the time on the
summary of labour form was changed at some point. D was born
at
03h35. Her 1 minute Apgar score was 5/10. Her heart rate was
satisfactory and scored 2, while she scored 0 for respiration and
muscle tone, 1 for response to stimulation, and 2 for colour. This
assessment is in itself contradictory because it is unlikely
that her
colour would have been optimal if she was having trouble breathing.
[4]
A second Apgar assessment at 5 minutes of life scored 7/10. D’s
breathing had
improved somewhat, and she had a better muscle tone.
The neonate assessment form shows that D had a slow respiration rate,
a weak
moro-reflex, and an absent grasp reflex and “cry”.
She was resuscitated and supplemental oxygen was administered via
a
headbox. D’s blood glucose was high at 11.2 mmol/L.
[5]
Later observations noted that she had suffered seizures. Her “cry”
was
still not audible, and a doctor noted hypertonia, rigidity and no
reflexes-Moro. D was ‘floppy”. The evidence was clear:
D
had suffered birth asphyxia which had caused a moderate
hypoxic-ischaemic (“HI”) injury which resulted in severe
asymmetrical mixed type cerebral palsy, predominantly dystonic.
[6]
Plaintiff’s alleges that defendant was negligent in one or more
of the following
aspects in that he:
[6.1]
Failed to employ the services of a suitably qualified medical
practitioner who could examine the plaintiff
and manage her labour;
[6.2]
Failed to ensure that a medical practitioner was in attendance at all
material times;
[6.3]
Failed to employ suitably qualified nursing staff;
[6.4]
Failed to ensure that the hospital was adequately equipped;
[6.5]
Failed to take the required steps to ensure proper, timeous and
professional assessment, monitoring
and management of patients in
labour;
[6.6]
Failed to implement steps to prevent the occurrence of a
complication;
[6.7]
Failed to avoid the complication when he could have done so by
exercising reasonable care and diligence.
[7]
Plaintiff alleges that the defendant’s employees were negligent
in one or more
of the following respects, in that they:
[7.1]
Failed to properly and sufficiently assess and examine plaintiff upon
her admission;
[7.2]
Failed to monitor plaintiff’s labour and foetal well-being
appropriately and with sufficient
regularity or at all;
[7.3] Failed to note
sufficiently, timeously or at all that plaintiff’s labour was
not progressing appropriately;
[7.4]
Failed to request assessment or examination by a medical practitioner
upon admission;
[7.5]
Failed to perform accurate and proper cardiotocographic (“CTG”)
tracings of the foetal
heart rate and maternal contractions, and/or
failed to recognize that the foetal heart pattern on the CTG was
unsatisfactory;
[7.6]
Failed to monitor the foetal heart rate appropriately, timeously or
with sufficient frequency and/or
at all, and/or failed to detect that
D was in foetal distress;
[7.7]
Failed to note and/or appreciate the significance and/or timeous
progress of labour;
[7.8]
Failed to monitor plaintiff’s labour, either appropriately,
timeously with sufficient frequency
and/or at all;
[7.9]
Failed to perform a proper and accurate partogram;
[7.10] Failed to
perform, or request to be performed, a caesarian section in
circumstances where it would have been appropriate
to do so;
[7.11] Failed to
provide the requisite reasonable medical, nursing and midwifery
services with such professional skill and
diligence as could
reasonably be expected of medical practitioners, nurses and midwives;
[7.12] Failed to
obtain a comprehensive obstetric history from the plaintiff;
[7.13] Failed to
render reasonable medical, nursing and midwifery services with
professional skill and diligence;
[7.14] Failed to
prevent D from suffering a hypoxic ischaemic incident, which resulted
in severe brain damage.
[8]
It is not in dispute that defendant had a duty of care to ensure that
plaintiff received
proper medical care and that defendant is
vicariously liable for the acts or omissions of the hospital staff.
It is also not in
dispute that plaintiff received sub-standard care.
There is no evidence that she was monitored at all from 02h00
onwards, at a
time when the protocols require constant monitoring of
the mother and foetus. Defendant accepts that the nursing staff were
negligent.
[9]
The sole question for determination is whether the negligent omission
resulted
in the hypoxic ischaemic injury and whether, with
proper care, the injury could have been prevented.
[10]
At the outset the parties moved for an order that the merits of the
matter be separated from
the quantum in terms of rule 33 (4) of the
Uniform Rules of Court. I granted the order. Therefore, it is only
the issue of liability
that has to be determined at this stage.
THE
EVIDENCE
[11]
I must point out that none of the witnesses were present at the
birth. They have formulated their
opinions based upon the plaintiff’s
medical records, the antenatal card, the partogram, other labour
records, and the neonatal
records. They also relied on an MRI scan
which was performed on 4 February 2015.
DR
LINDA MURRAY
[12]
Dr. Linda Murray was plaintiff’s first witness. She is an
obstetrician and gynaecologist
in private practice at the Life
Vincent Pallotti Hospital. She lectures in obstetrics and gynaecology
at the University of Cape
Town, as well as at the University of
Stellenbosch. Dr. Murray’s expertise was not in dispute. She
testified that plaintiff
was, at the time of D’s birth, a 26
year old woman in her second pregnancy (a multigravida). She was a
so-called ‘late
booker’, only presenting herself for
examination when her pregnancy was already well advanced. She was HIV
positive, and
slightly anaemic. Plaintiff was placed on highly active
antiretroviral therapy. None of these risk factors played any role in
the
later events. Plaintiff’s pregnancy progressed normally,
and upon admission to the hospital she was classified as a ‘low
risk’ patient. The foetus was lying normally, in a cephalic
presentation. Amniotic fluid (or liquor) was normal, and the
membranes were intact. In short, there was nothing of concern during
the early part of the labour.
[13]
Dr. Murray testified that the foetus of a low risk patient may be
monitored intermittently by
auscultation, by listening to the foetal
hart rate before, during and after a contraction. She explained that
during a contraction
placental perfusion falls and there is less
oxygenated blood available in the placenta. The foetus suffers brief
episodes of hypoxia,
although under normal circumstances this does
not cause harm to the foetus. She also explained that it was
important to establish
the baseline heart rate of the foetus. During
a contraction the foetal heart rate might decelerate due to the brief
hypoxic event,
and it is important to establish whether the heart
rate returns to the baseline after a contraction. If it does not,
then there
is cause for alarm and the patient must be more closely
monitored. If necessary there must be emergency intervention to
protect
the foetus from suffering further harm, either by way of an
instrument delivery, or by way of a caesarian section.
[14]
Dr. Murray testified that there were two ‘red flag’,
indicators which should have
alerted the nursing staff that the
patient was at a heightened risk as the labour progressed. The first
was the lack of progress
in the labour. Dr. Murray said that by 01h20
the progress of labour had crossed the action line. This was in
itself unusual as
the plaintiff was a multigravida, having given
natural birth previously. The second was the presence of meconium
stained liquor
grade 2. This is a possible indicator of foetal
stress. The staff were sufficiently alarmed that they notified the
doctor of the
plaintiff’s condition. Dr. Murray is of the view
that from then onwards the foetus should have been monitored
constantly
by means of a cardiotocograph (“CTG”). There
is no evidence that a CTG was ever employed. The second stage of
labour,
commencing at full dilation at 02h00 was mildly prolonged,
but not unduly so.
[15]
Dr. Murray is of the view that there was insufficient monitoring of
the foetus after 02h00, and
that the partogram is incorrect inasmuch
as it records that the baseline heart rate was normal throughout. She
says this in light
of the fact that D was born in a compromised
state, and had to be resuscitated. The child could not have been born
in such a compromised
state if her heart rate had been normal before
birth. Dr. Murray’s opinion is in all likelihood correct given
the fact that
the partogram records that the foetus’ heart rate
was normal at 04h00, 25 minutes after the baby had already been born.
Very
little reliance can be placed on the partogram.
[16]
Dr. Murray testified that an MRI scan of the child’s brain was
performed on 4 February
2015 and was diagnostic of an
“acute-profound” (central) hypoxic ischaemic injury (“HI
injury”) of the
Basal Ganglia-Thalamic areas of the brain
(“BGT”). Often an acute-profound injury occurs fairly
quickly as a result
of a sudden sentinel event. In this case there is
no evidence of a sentinel event. In Dr. Murray’s view, the same
type of
injury may result if the foetus suffers ongoing subthreshold
hypoxia over a period of time, which builds up to a point where the
injury occurs.
[17]
It has thus far been accepted that damage to the BGT structures, the
deep grey matter of the
brain, always resulted from a sudden total
interruption of blood supply to the brain. In Dr. Murray’s
view, however, the
partial intermittent interruption of blood supply
to the brain can also result in the type of HI injury that presented
itself on
the MRI scan as an acute-profound injury.
[18]
In order to examine this theory Dr. Murray, in conjunction with
Professor Johan Smith and a number
of other medical experts,
conducted a study of ten specifically identified patients. The
purpose of the study was to investigate
cases of acute-profound HI
injuries in cases where there was no identifiable sentinel event. The
findings were published during
November 2020 in a peer reviewed
article, and concluded that:
“……
if
a non-reassuring fetal status develops during labour, and is
prolonged, a BGT pattern HI injury may result, in the absence of
a
perinatal sentinel event.”
[19]
I will deal with the study more fully hereunder. Dr. Murray pointed
out that the lack of monitoring
after 02h00 had the result that there
was no data available as to the status of the foetus, and whether it
was in distress. However,
in the absence of a sentinel event, and
given the evidence produced in the study, Dr. Murray was of the view
that the foetus must
have been in distress after 02h00, because there
is no evidence of distress before that. Prof. Lombaard, defendant’s
expert
agreed with Dr. Murray’s view in a joint minute, and
added that the insufficient monitoring of the plaintiff of the second
stage could have resulted in the foetal distress being missed. In Dr.
Murray’s opinion D’s BGT HI injury was the result
of
repeated hypoxic events which built up over a period of time between
02h00 and 03h35, and which culminated in the type of BGT
injury
commonly referred to as an acute-profound injury.
[20]
In Dr. Murray’s view the injury would likely not have occurred
just before birth. There was no
sentinel event that could have caused
a sudden injury in a short space of time. Considering the severity of
the injury, the hypoxic
episodes must have started some time before
birth, causing a gradual change in the foetal status. She was
furthermore of the view
had the foetal heart rate been properly
monitored it would have revealed that the foetus was in distress,
which would have resulted
in medical intervention in the form of an
instrument delivery. Had the foetus been delivered immediately upon
the distress being
noted, the HI injury would in all likelihood have
been prevented.
[21]
It was put to Dr. Murray in cross-examination that the injury could
have been caused by cord compression
which would have left no
footprint behind. She conceded that there would be no evidence of a
cord compression once the compression
ceases. In her view that is an
unlikely cause of the injury. Typically, a cord compression that is
equal to a sentinel event occurs
when the cord prolapses and comes
out in front of the baby’s head. This is not a sudden nor
silent event. The probability
of a cord becoming so severely
compressed that it cuts off blood supply completely is, in Dr.
Murray’s view, extremely unlikely.
In her view the injury was
the result of labour stress in a compromised foetus.
PROF.
JOHAN SMITH
[22]
Professor Johan Smith testified that he is a specialist neonatologist
in the Department of Paediatrics
at the University of Stellenbosch.
He holds the degrees MB ChB, M Med (Paed) and PhD. He attends weekly
meetings dealing with high
risk pregnancies as well as weekly
perinatal mortality meetings during which cases of stillborn babies
and neonatal deaths are
discussed. Prof. Smith’s expertise was
not in dispute. He has been a medical practitioner for 40 years, and
a neonatologist
for 27 years. Prof. Smith confirmed the correctness
of his expert summary, as well as the joint minutes between himself
and Prof
Cooper.
[23]
Prof. Smith concurs with Dr. Murray that by 1h20 the plaintiff’s
labour had crossed the action
line and thick meconium stains were
observed in the liquor, which indicated that cardiotocograph
monitoring was necessary. Between
02h00 and delivery at 03h35 the
plaintiff was in the second stage of labour and required continued
and careful monitoring. He says
that there is no evidence that the
foetus was monitored at all during the latter period.
[24]
Prof. Smith testified that at 1 minute after birth D’s Apgar
score indicated a heart rate score
of 2, which means that the foetus
had not suffered bradycardia. The baby was in respiratory distress
and required suctioning. The
baby had no grasp reflex, was
neurologically depressed, exhibited no “cry”, and was
floppy. Her blood glucose levels
were raised, which is often a stress
response. D had difficulty initiating and maintaining respiration and
required supplemental
oxygen. In Prof. Smith’s view, D
exhibited a moderate neonatal encephalopathy. All of her symptoms
were consistent with an
HI injury resulting from birth asphyxia.
The diagnosis of moderate early onset encephalopathy establishes a
‘causal
pathway’ to cerebral palsy.
[25]
Prof. Smith testified that there are different types of brain injury
which result from different clinical
causes. The first is the
so-called acute-profound injury which results from a sentinel event,
and which causes damage to the gray
matter of the brain, the BGT area
and the brain stem. The sentinel event causes an abrupt drop in the
foetal heart rate to somewhere
between 60 and 80 beats per minute.
This bradycardia lasts until delivery. The resulting lesions are
generally isolated BGT and
brainstem related. Prof. Smith says that
such injuries are rare because sentinel events are a relatively rare
occurrence.
[26]
The second type of injury results from a subacute intermittent
hypoxic insult which occurs over an
extended period of time. In his
view, this type of HI insult fluctuates above and below the threshold
for hypoxic-ischaemic injury
and results in injury to the
perirolandic and the BGT areas of the brain. Prof. Smith believes
that D’s injury falls into
this latter category.
[27]
The third type of hypoxic insult is not as devastating as, for
instance, an acute-profound incident,
and results in the brain
shunting blood from the watershed areas of the brain to the central
deep structures in order to preserve
life. This manifests in damage
to the white peripheral areas of the brain. This type of injury is
not relevant to this matter.
[28]
Prof. Smith testified that a sentinel event is a specifically
medically defined type of occurrence,
which includes uterine tears,
abruption placenta, placenta praevia, feto-maternal haemorrhage,
maternal cardio respiratory collapse,
and an umbilical cord prolapse.
In this case there was no sentinel event. In Prof. Smith’s view
this foetus suffered prolonged
intermittent hypoxia, which
accumulated and eventually resulted in the so-called acute-profound
injury. The MRI scan revealed a
Rolandic Basal Ganglia-Thalamic
injury (acute-profound pattern).
[29]
Prof. Smith says that it is well-known in the literature that in the
absence of a sentinel event an
“acute-profound” type
brain injury may occur over several hours. His contention is
partially based upon the article
which he and his colleagues have
recently published, as well as on other recent publications. He also
concedes though that there
are experts who disagree with him.
[30]
In Prof. Smith’s view D suffered repeated hypoxic insults over
at least two hours, as a result
of which the hypoxic injury developed
gradually. He also believes that the HI insults were
subthreshold/subacute and intermittent,
and that they culminated in a
final profound brain injury.
PROF.
COOPER
[31]
Prof. Peter Cooper testified for the defendant. He simply confirmed
that he had read his expert summary,
as well as the joint minutes of
the meetings between himself and Prof. Smith. He confirmed the
contents of those documents. He
gave no further evidence and he was
not cross-examined. It is a pity that he did not expound on his
opinions, as it would have
been useful to hear him on aspects on
which he disagreed with Prof. Smith.
[32]
Prof. Cooper’s summary of the events is substantially the same
as that of Dr. Murray and Prof. Cooper. He is of the view that the
plaintiff’s HIV status was a significant risk factor for
an
adverse pregnancy outcome. However, there is no evidence that the HIV
played any role in the eventual outcome. Prof. Cooper
also believes
that the foetus displayed an asymmetrical intrauterine growth
restriction which was likely due to late placental
insufficiency,
which would compromise the foetus’ ability to tolerate normal
labour.
[33]
Prof. Cooper’s view was that D was at the mild end of moderate
encephalopathy. He says that if
the encephalopathy can be traced to a
hypoxic event or events, the neurological handicap could be linked to
this. However, he points
out that there are a number of other causes
of neonatal encephalopathy, such as meningitis, metabolic causes,
vascular events and
structural brain abnormalities. Prof. Cooper
states that D was not examined for other causes of encephalopathy.
Prof. Cooper’s
expert summary does not show that he had had
sight of the radiological report of 4 February 2015, although the
joint minute of
11 February 2021 seems to suggest that he knew about
the report. The MRI report specifically states that the MRI scan
showed no
congenital abnormalities or genetic disorders, nor any
inflammatory brain disease. In this regard Prof. Cooper’s
expert summary
seems clearly contradicted by the evidence of Prof.
Smith and the MRI scan.
[34]
At best for defendant, Prof. Cooper only says that the neurological
features are suggestive of a peripartum
hypoxic ischaemic event, but
that other causes than intermittent hypoxia may have been responsible
for the injury.
[35]
The joint minute of the meeting between Professors Smith and Cooper
on 25 June 2020 records that they
agree on the basic facts relating
to the pregnancy. Prof. Cooper was of the view that the foetus
suffered from placental insufficiency,
a view that Prof. Smith agreed
with in the second minute of 11 February 2021. Both experts agreed
that D’s condition was
in keeping with birth asphyxia, although
Prof. Cooper continued to express the view that there might have been
other causes of
the respiratory distress. Both experts agreed in the
second minute that there was no evidence that infection, genetic or
anatomical
abnormalities had played a causal role in the injury.
[36]
The second joint minute also records that Professors Cooper and Smith
agree that early onset encephalopathy
establishes a “doorway in
a causal pathway between intrapartum asphyxia and cerebral palsy.”
Although Prof. Cooper
did not disagree with this basic hypothesis, he
noted that this only applied in cases of moderate encephalopathy.
However, Prof.
Cooper had already expressed the opinion in his expert
summary that D had suffered a moderate encephalopathy, albeit on the
mild
side.
[37]
Both experts agreed that there had not been a sentinel event. Prof
Smith opined that in the absence
of a sentinel event, the probable
cause of the injury was suboptimal/substandard intrapartum obstetric
management. Prof. Cooper
was of the view that substandard intrapartum
management had to be demonstrated in each specific case. Prof Cooper
also expressed
the view that current neonatal opinion was that an
acute-profound HI injury of this type could only occur in cases of
total or
near total cessation of blood flow for a period of 10 to 45
minutes.
[38]
Mr. Rossouw argued on behalf of defendant that Prof. Cooper’s
statements in the joint minutes
and in the expert summary must be
accepted as evidence, and that, in the absence of cross-examination
it stands uncontroverted.
He says so on the basis of
BEE
v Road Accident Fund
[1]
, a matter in which the
evidence contradicted the joint report of forensic accountants and
facts that had been agreed in a pre-trial
minute. I do not agree. The
following principles relating to expert witnesses can be extracted
from
BEE
and
other authorities:
[38.1]
An expert witness is there to assist the court and not to usurp the
function of the court.
[38.2]
Expert witnesses are required to lay a factual basis for their
conclusions and explain
their reasoning to the court;
[38.3]
The court must be satisfied as to the correctness of the expert’s
reasoning;
[38.4]
Absent any reasoning, the opinion is inadmissible;
[2]
[38.5]
A court is not bound by an expert’s opinion;
[3]
[38.6]
For an expert’s evidence to be helpful he or she has to be
neutral;
[4]
[39]
It is not correct therefore to understand
BEE
to mean
that a court is bound to blindly accept whatever an expert says.
[40]
Prof. Cooper states that D’s
placental insufficiency would have exacerbated any
foetal distress.
He says that if the neonatal encephalopathy was due to peripartum HI,
D’s subsequent neurological encephalopathy
could be linked to
this. However, he says, there are many other causes of neonatal
encephalopathy, such as meningitis, septicaemia,
metabolic causes,
vascular events and structural brain abnormalities. Prof. Cooper then
says:
“
There
were no details in the neonatal or follow up record to indicate that
she was investigated for other causes of encephalopathy.”
[41]
If one has regard to the documents that Prof. Cooper examined in
order to prepare
his expert report, it appears that he did not
consider the MRI scan and the three radiological reports dated 13
June 2019, 18 June
2020, and 21 January 2021 respectively. The first
joint minute refers to the “subsequent reported MRI”, and
therefore
Prof. Cooper was presumably aware at that stage that there
had been an MRI scan. The radiological report of 13 June 2019 records
that no genetic disorders or congenital anomalies were found, and no
sign of inflammatory brain disease. When Prof. Cooper says
in the
expert summary that there were no investigations into other possible
causes he is plainly wrong. Prof. Cooper contradicted
his expert
report by agreeing with Prof. Smith in the first joint minute that
there is no evidence to show that infection, genetic
or anatomical
abnormalities played a causal role.
[42]
In the first joint minute Prof. Smith stated that a diagnosis of
early onset encephalopathy
establishes an essential ‘doorway’
in a causal pathway between intrapartum asphyxia and cerebral palsy.
Prof. Cooper
disagreed, suggesting that the mild HI encephalopathy
found in this case would not have resulted in later major
neurological handicap
and cerebral palsy. The difficulty is that in
Prof. Cooper’s own expert report he says:
“
However that
fact that she was able to feed from a cup on the third day, was well
enough to receive her first immunizations on the
fourth day and could
be discharged on the sixth day indicated that this was at the mild
end of the spectrum
of moderate encephalopathy.
[43]
Prof. Cooper was in agreement that no sentinel event occurred.
However, he makes
no suggestion as to a possible cause of the injury.
[44]
In the second joint minute Prof. Cooper’s attention was
specifically drawn
to the study by Smith
et al.
His only
response was to say that the paper had only been published online and
only when it was published in print would peer review
be able to take
place. He said that until peer review had taken place, the paper
could not be accepted. I find it strange, in the
era of the internet,
that comment would only follow on publication in hard copy. This
criticism was also put to Prof. Smith. He
explained that the paper
had been submitted to the American Journal of Perinatology, where it
had been subjected to comprehensive
peer review before it was
published. He said that Prof. Cooper was confusing pre-publication
peer review with post-publication
comment.
[45]
I find it hard to believe that a journal of such standing would
publish a paper without
proper peer review having first taken place.
In any event, Prof. Cooper is one of Prof. Smith’s peers. If he
had any qualms
about the study, its methodology, the data, or its
interpretation, he would no doubt have raised his concerns.
[46]
Prof. Cooper failed to deal with any of the other recent publications
(ACOG and Volpe)
which contradict his position. Mr. Rossouw submitted
that these studies could not be relied upon because they based their
findings
on experiments on monkeys and sheep. Firstly, this is not
correct. The studies also included human subjects. As I understand,
Volpe
is reliant on studies by a number of experts in the field who
have observed numerous human cases. Secondly, Prof. Smith testified
that animal studies were relevant albeit that one had to be careful
what conclusions were drawn from those studies. The Smith
et al
study included animal experiments, but was also based, as Prof. Smith
explained, on his experience (and that of his co-authors)
over many
years, involving human cases.
[47]
The main bones of contention between the parties were therefore the
following:
[47.1]
Has plaintiff demonstrated that subthreshold/subacute intermittent HI
insults
that build up over an extended period
of time can cause this type of acute-profound type injury of
the BGT
and perirolandic brain structures?
[47.2]
If the answer to the above question is in the affirmative, then is
there
evidence to suggest that such insults occurred in D’s
case?
[47.3]
If there is evidence that there were such insults, then would proper
monitoring
have alerted the nursing staff to the fact that the foetus
was in distress?
[47.4]
If the nursing staff had been forewarned that the foetus was in
distress,
would immediate intervention have prevented the injury?
[48]
If all of the above questions are answered in the affirmative,
causation would have
been established.
CAN
A SUBACUTE INTERMITTENT HYPOXIC ISCHAEMIC INSULT OVER A PERIOD OF
TIME RESULT IN AN ACUTE-PROFOUND TYPE INJURY?
[49]
It has thus far been widely believed that only an acute-profound
insult such as a
sentinel event can cause this type of BGT HI injury.
In
AN
o.b.o. EN v Member of the Executive Council for Health, Eastern
Cape
[5]
the
Supreme Court of Appeal (“SCA”) dealt with a similar
claim for damages resulting from birth asphyxia where the medical
care had been substandard. The central point for determination was
whether causation had been established.
[50]
In
AN
the foetus had suffered an acute-profound HI
insult, a cord compression, which resulted in a total cessation of
blood supply to
the brain. The SCA accepted that only an
acute-profound total interruption of the blood supply could have
caused the type of BGT
injury found in that case. It accepted that if
the interruption of blood supply was intermittent, the white
peripheral matter in
the watershed areas would have been injured. In
other words, the SCA accepted the conventional view as it was at that
time. Prof.
Smith testified in that case. His evidence was rejected
as being speculative and his opinion was rejected on the basis that
it
was not supported by authoritative peer-reviewed literature.
[51]
The SCA therefore upheld the finding by Dawood J in the court
a
quo
where she said (regarding the defendant’s witness, Buchman)
[6]
:
“
Professor
Buchman however stated that although that is what he relied on, the
exclusion of that would not change his opinion since
it was still
an acute-profound event that would have occurred in the last
half an hour prior to delivery according
to the articles
relied upon and therefore even with no monitoring the outcome would
have been the same.
(h)
The sub-standard care and failure to adequately monitor was not a
causative factor in this
case according to him.
(i)
His opinion as to how the insult and resultant injury occurred and
that it was
an acute-profound is as already indicated in keeping
with the medical authorities cited and I find it the more probable
explanation
as these are the only available medical authorities at
this time that have been peer reviewed and despite the criticism
levelled
that it was not of a big enough sample and old, it is
authoritative until contrary findings and outcomes are made in peer
reviewed
published articles.
(j)
The plaintiff’s expert’s opinions in other litigated
matters accordingly
cannot be accepted as being authoritative without
knowing the full history of each case and having that data checked by
experts
in the relevant fields and peer reviewed.”
[52]
The
AN
case is distinguishable from this case for a
number of reasons. Firstly, in
AN
there had been a
sentinel event, a cord compression, which resulted in the injury.
Secondly, the latest authorities on this issue
were not yet available
to the SCA, and it based its finding on authority which is now very
much in question. Thirdly, the defendant
in
AN
called a
witness who gave convincing evidence that a sentinel event had
occurred. Prof. Johannes Buchanan testified that the injury
was
sudden, without warning and severe. Intervention by Ventouse or
forceps delivery or caesarian section could not have occurred
quickly
enough to prevent the harm in his view, and consequently there was no
causal connection between the sub-standard care and
the outcome.
[53]
In
The
Member of the Executive Council for Health, Eastern Cape v
Mpetsheni
[7]
the
SCA was faced with a similar case. The plaintiff had given birth to a
severely brain damaged baby as a result of a hypoxic ischaemic
insult. In that matter the accepted evidence was that the foetus had
suffered an acute-profound injury, probably a compression
of the
cord, akin to a sentinel event. This proposition was accepted by the
plaintiff’s expert. That matter is equally distinguishable
from
this matter as the experts agree that in this case that there was no
sentinel event.
[54]
I was handed a series of articles dealing with so-called ‘acute
profound’
injuries, commencing with Joseph Pasternak
et
al’s
publication
in 1998
[8]
. Pasternak studied
eleven infants that had sustained an acute near-total intrauterine
asphyxia at the end of labour, due to bradycardia.
Pasternak’s
study postulated that in these cases there had been an acute
near-total intrauterine asphyxia at the end of labour.
According to
Pasternak imaging studies documented a consistent pattern of injury
in subcortical brain nuclei, including thalamus,
basal ganglia and
brainstem. In contrast the cerebral cortex and white matter were
completely or relatively spared.
[55]
This study was criticized by Alistair Mc Lennan in 1999 on the
grounds that he believed
that of the eleven babies studied, ten did
not meet the strict perinatal definition for asphyxia. Prof. Smith
agrees with this
criticism. Pasternak, however, later reaffirmed his
belief that all of the babies had suffered asphyxia. Prof. Smith also
criticized
the basis of the study, and specifically Pasternak’s
claim that imaging studies documented a pattern of injury consistent
with BGT and brainstem injury, as opposed to cerebral cortex damage:
[55.1]
Of the eleven patients in the study, four had no radiological
evidence for any brain injury whatsoever;
[55.2]
Only one case had a BGT type mid-brain injury which Volpe calls the
deep nuclei stem pattern injury;
[55.3]
Three cases had BGT and perirolandic cortex deep nuclei pattern
injuries, similar to this case;
[55.4]
Three patients had an isolated BGT injury.
[56]
Therefore only 4 out of 11 cases had the deep nuclei-brainstem type
injury which
is associated with acute-profound type events according
to Volpe and the American College of Obstetricians and Gynaecologists
(“ACOG”).
Pasternak’s general statement regarding
the consistency of the injuries through the cases is shown to be
inconsistent with
the data. Only in five of the cases was a sentinel
event identified. In all of the Pasternak cases a terminal fixed
bradycardia
occurred which lasted between 10 and 45 minutes. That
distinguishes the Pasternak cases from this case where it is unlikely
that
a fixed bradycardia occurred.
[57]
Okumura
[9]
reported on a study
of two patients. Both had allegedly suffered a sudden fall in foetal
heart rate and had suffered an HI insult.
In referring to the
Pasternak study, Okumura remarked that the foetuses had suffered the
same type of sudden hypoxic incident as
in the Pasternak study. Both
cases revealed injury to the BGT areas. On this basis, Okumura
postulated that sudden acute hypoxia
leads to injury to the BGT
structures, while gradual intermittent hypoxia resulted in injury to
the watershed areas. Okumura’s
study however shows that the
second foetus did not suffer a sudden bradycardia. It displayed an
erratic heart rate which fluctuated
significantly, until the mother
suffered prolonged repeated contractions. At that point the foetus
suffered a sudden bradycardia.
[58]
Essentially only one of Okumura’s patients is comparable to the
Pasternak group.
Nevertheless, after the Pasternak and Okumura
studies were published, it seems to have been widely accepted that
only acute-profound
insults result in BGT injury. Radiologists
started referring to the pattern on an MRI scan which involved the
BGT structures as
an acute-profound injury, the name suggesting the
pathophysiology of the injury. Thereafter, when an MRI scan produced
an image
showing BGT injury, the injury was referred to as
acute-profound and it was accepted that the insult that caused the
injury had
been acute (sharp or severe) and profound (intense).
[59]
In 2011 Rennie and Rosenbloom published a study
[10]
which was aimed at determining the time from insult to foetal HI
injury in animals and human babies. The article was restricted
to the
acute-profound HI model. Again, as with Okumura, the authors accepted
the existing view that only acute-profound insults
resulted in injury
to the BGT structures. The study was aimed at determining the time
available to deliver a foetus in the event
of an acute-profound
event. In itself the study does not provide authority for the
proposition that only an acute-profound event
would result in a BGT
injury.
[60]
Deidre Murray
et
al
published a study
[11]
in 2009
which sought to examine foetal heart rate patterns during labour and
to relate those findings to neurodevelopmental outcome.
Of 35
foetuses studied, the second group relates most closely to this case:
Those were infants who had been admitted with a normal
CTG trace, who
then deteriorated over a period of time to become pathological. Only
four of the subjects of the study suffered
sentinel events. Those
insults resulted in the most severe injury, but the study did not
exclude the possibility that prolonged
and intermittent HI incidents
could result in BGT injury. Murray is neither supportive nor
dismissive of the Pasternak theory,
in my view.
[61]
Later publications discussed the possibility of injury to the BGT
areas other than
through an acute-profound incident or a sentinel
event.
Volpe’s
Neurology of the Newborn
[12]
is an authoritative publication which is referred to by
neonatologists worldwide. The major patterns of neuronal injury are
discussed
by Volpe and three are identified
[13]
:
[61.1]
The diffuse pattern involving the cerebral cortex, deep nuclear and
brain stem. In these
instances the insult is severe and prolonged.
[61.2]
The cerebral cortex-deep nuclear which is caused by a moderate
prolonged insult.
[14]
[61.3]
Deep nuclear-brain stem, in which the insult is severe and abrupt.
[62]
Volpe comments as follows:
[15]
“
In the more
prolonged and less severe insults, the diversion of blood to deep
nuclear structures occurs to a degree, and thus the
cerebral regions
are more likely to be affected. Studies in the near-term fetal lamb
indicate that the severe terminal insult that results in injury to
deep nuclear structures especially may be likely to occur after
brief, repeated hypoxic-ischaemic insults first cause a cumulative
deleterious effect on cardiovascular function that presumably
then
can result in a severe late insult…..
Term fetal monkeys
subjected to a partial rather than total interference with
respiratory gas exchange (produced by halothane-induced
hypotension)
developed physiological derangements over longer periods, so-called
prolonged partial asphyxia. The maternal event
resulted in more
slowly evolving hypoxia and acidosis, followed by decelerations of
the fetal heart rate, diminished cardiac output,
hypotension and
evidence for cerebral ischemia. Brain injury became apparent after
several hours, and the topography involved cerebral
cortex
(especially in paracentral areas), basal ganglia and thalamus, as in
human infants (see Table 19.1)”
[63]
ACOG supported this view in 2019.
[16]
The ACOG publication acknowledges that a severe partial insult of
prolonged duration or a combined partial with profound terminal
insult can cause deep nuclear neuronal injury:
“
The second form
of selective neuronal injury is the cerebral-deep nuclear neuronal
injury, which combines neuronal damage in the
deep nuclear gray
matter with injury in the cerebral cortex, usually the parasagittal
areas of the perirolandic cortex……..In
experimental
models, the mechanism responsible for this pattern is described as a
‘prolonged
partial with final total asphyxia” with
a moderate to severe insult evolving in a gradual manner leading to a
potential complete
‘asphyxia’”
[64]
The final study, that of Smith
et
al,
was
published very recently.
[17]
The authors reviewed 195 cases of neonatal encephalopathy. After
excluding a number of cases, ten were identified for inclusion
in the
study, all of them displaying term gestation neonatal
encephalopathy-cerebral palsy. None of the cases were associated with
intrapartum fever, congenital abnormalities, metabolic errors,
intracranial infections, septic shock or cranial birth trauma. None
had suffered prenatal injury. Cases with genetic disorders were
excluded. All cases displayed an acute-profound HI pattern on MRI,
had clearly documented evidence of an assessment of the foetus on
admission and underwent intermittent adequate foetal monitoring
during labour. In none of the cases was a sentinel event
identifiable. Injuries that did not involve the BGT areas, or those
with
a mixed or a watershed injury were also excluded.
[65]
The study showed that if a non-reassuring foetal status develops
during labour, is
prolonged and leads into a pathological CTG
tracing, the brain injury pattern may be the same as in the case of
an acute-profound
BGT HI injury. The authors wrote:
“
The present
case series shows that in the absence of a perinatal sentinel event,
subacute or subthreshold intrapartum HI occurs
in the human fetus and
that warning signs in the form of a NRFS, in some instances hours
before delivery, may occur. This paper
supports the notion that with
appropriate intrapartum care and timeous reaction to FHR
abnormalities and action in the form of
intrapartum resuscitation and
expedited delivery, in the majority of cases adverse BGT pattern
injury would have been prevented.”
[66]
The conclusion was:
“
This
study shows that if a nonreassuring fetal status develops during
labour and is prolonged, a BGT pattern HI injury may result,
in the
absence of a sentinel event.”
[67]
There is no substantive evidence from the defendant to refute Prof.
Smith’s
version. I would have expected defendant to put up some
evidence as to the cause of the injury. I say so in the full
understanding
that defendant does not bear an onus of proof. However,
when the plaintiff presents a well-reasoned opinion, one would expect
the
defendant to put up some version of its own.
[18]
Defendant did not even put up a version during cross-examination. I
therefore accept Prof. Smith’s evidence, that a series
of
partial intermittent, subacute/subthreshold hypoxic insults may
result in this type of injury to the BGT deep nuclear structures
including the perirolandic area.
DID
THE FOETUS SUFFER PARTIAL INTERMITTENT HYPOXIC INSULTS, AND DID THIS
CAUSE THE INJURY TO THE BGT AREAS?
[68]
Prof. Smith and Dr. Murray approached this question by applying
inferential reasoning. They considered
the observed and admitted
facts, eliminated all other possible causes, and then deducted that
the most likely cause of the injury
was partial intermittent hypoxia.
Two undisputed facts are important. Firstly, labour in itself is
stressful, and during a contraction
the foetus may suffer brief bouts
of hypoxia. Some foeteses are inherently better equipped to cope with
the stresses of labour.
Others cannot cope as well, and may suffer
some form of injury. Secondly, it is common cause that this
particular foetus suffered
from placental insufficiency.
[69]
It is also common cause that there was no sentinel event. The
plaintiff displayed certain risk factors
(HIV and anaemia), but there
is no evidence to suggest that these risk factors played any role in
the outcome. The plaintiff suffered
a brief bout of raised blood
pressure at 18h00 for which she received medication. There is no
evidence that the hypertension persisted,
and it is not of
significance to the outcome.
[70]
At 1h50 meconium (foetal stool) grade 2 stained liquor was observed.
Meconium staining is an indicator
of possible foetal stress. If the
foetus were to suffer a severe enough bout of hypoxia, the shunting
of blood would move the available
oxygenated blood to the brain and
away from the gut, causing the relaxation of the foetal anal
sphincter, thus releasing meconium.
It is possible that the foetus
was under some stress at that stage already, but it is Dr. Murray and
Prof. Smith’s view that
in all likelihood the serious hypoxic
bouts occurred between 02h00 and birth at 03h35.
[71]
The “Summary of Labour” form records that a
retroplacental clot was observed. This could
imply that a placental
abruption occurred, which would have resulted in heavy bleeding. In
such cases the mother displays signs
of shock and a hard and
distended uterus. Dr. Murray could not completely exclude the
possibility of a placental abruption, but
the fact that there was
minimal blood observed at delivery (150 ml), and no bleeding reported
during labour, causes her to deduct
that it is unlikely that there
was a placental abruption. It is common for a clot to form after
delivery due to the separation
of the placenta from the placental
bed. The available studies reveal no cases that demonstrate that a
mild abruption may cause
HIE, or cause the baby to require advanced
resuscitation, or result in a low 5-minute Apgar score. Most likely
placental abruption
did not cause the injury. Prof. Lombaard, the
defendant’s obstetrician agrees that there is no evidence to
suggest that there
was a significant abruption, according to the
joint minute of 8 February 2021.
[72]
There was a further suggestion that the foetus had perhaps suffered a
bradycardia of unknown origin.
Prof. Smith testified that if the
foetus had suffered a total cut-off of blood flow, it would have
resulted in a fixed bradycardia
that would have persisted until
birth. At 1 minute of life the baby’s heart rate scored 2 on
the Apgar test, in other words,
it was normal. It is highly unlikely,
according to Prof. Smith, that the foetus could have experienced a
fixed bradycardia which
persisted until birth, and which resolved
itself in the 1 minute until the Apgar test was performed. If there
had been a fixed
bradycardia, it would have occurred in the 10 to 20
minutes before birth. In this case there is no evidence of a fixed
bradycardia.
[73]
It was suggested to Prof. Smith in cross-examination that a cord
compression might have occurred which
would not have left a
footprint. He testified that while a cord compression was not
strictly speaking a sentinel event, if it were
complete and sustained
it could have the same effect as a sentinel event. That would have
meant that there was a cord compression
in the 20 minutes before
delivery which was sustained, resulting in a bradycardia (the heart
rate falling to 60 to 80 beats per
minute). If that were so, in Prof.
Smith’s opinion the bradycardia could not have resolved itself
so quickly that at 1 minute
of life, when the first Apgar test was
performed, the heart rate was normal.
[74]
Mr. Rossouw submitted that there was no evidence that the foetus was
in any distress prior to birth.
He makes this submission on the
premise that the partogram is correct. The problem with this argument
is two-fold. Firstly, the
partogram is in dispute. It is patently
wrong in some respects, even to the point of recording a foetal
heartbeat after delivery.
Secondly, the condition of the baby at
birth leaves no doubt that the foetus must have been in distress
during the second stage.
[75]
Mr. Rossouw criticized the method used by plaintiff’s experts
in coming to their conclusion,
calling it ‘backward’
reasoning which, he said, is impermissible. He referred to
Goliath
(
supra
) as authority for the proposition. In my view
Goliath
is not authority for that proposition. That case concerned the
application of the
res ipsa loquitur
principle to establish
negligence.
[76]
In a minority of cases (because they are rare), the cause of the
injury is obvious: A placental abruption,
uterine tear etc. In some
instances the cause would not be obvious, and would have to be
determined, if possible, on the available
circumstantial evidence,
and considering the probabilities. In
South
African Post Office v De Lacy and another
[19]
it
was held:
“
The
process of inferential reasoning calls for an evaluation of all the
evidence and not merely selected parts. The inference that
is sought
to be drawn must be ‘consistent with all the proved facts: If
it is not, then the inference cannot be drawn’
and it must be
the ‘more natural, or plausible, conclusion from amongst
several conceivable ones”
[77]
In this case, the fact that there was no sentinel event eliminates
the possibility of an acute-profound
insult. The latest studies
support the plaintiff’s experts in their view that an
intermittent sub-acute repeating hypoxic
event may cause such an
injury. All of the admissible evidence points to such an event being
the most probable cause in this case.
No evidence of any moment was
presented by defendant and Prof. Cooper’s opinion can be
criticized on a number of grounds.
Defendant never put forward any
case whatsoever, save to say that plaintiff cannot provide direct
evidence as to what caused the
injury, and that plaintiff was
speculating.
[78]
Mr. Rossouw argued that there was no evidence as
to what happened after 02h00. In this regard he is correct,
but the
cause of the lack of evidence is the appalling record keeping by the
nursing staff. I was urged by Mr. Ströh to draw
a negative
inference against defendant for not calling any witnesses who were
present during the labour. Mr. Rossouw argues that
plaintiff is
equally to blame for not calling witnesses. This issue was discussed
in
Munster
Estates (Pty) Ltd v Killarney Hills (Pty) Ltd
[20]
:
“
See,
eg, Elgin Fireclays Ltd v Webb 1947 (4) SA 744 (A)
in which WATERMEYER CJ stated (at 749, 750):
"It
is true that if a party fails to place the evidence of a witness, who
is available and able to elucidate the facts, before
the trial Court,
this failure leads naturally to the inference that he fears that such
evidence will expose facts unfavourable
to him. (See Wigmore ss
285 and 286.) But the inference is only a proper one if the evidence
is available and if it would
elucidate the facts."
In
my opinion, however, it is to be doubted whether WATERMEYER CJ
intended laying down a general and inflexible rule to be applied
without more in every case where a party fails to call as his witness
one "who is available and able to elucidate the facts".
Whether the inference, that the party failed to call such a person as
a witness because he "fears that such evidence will
expose facts
unfavourable to him", should be drawn could depend
upon the facts peculiar to the case where the question
arises. It was
pointed out in Webranchek v L K Jacobs & Co
Ltd 1948 (4) SA 671 (A) at 682 that
it might
appear that the person concerned was equally available to both
parties, and that the inference could then be drawn against
both
parties. VAN DEN HEEVER JA also stated:
‘
After
all, plaintiff was entitled to rest his case upon evidence which he
considered adequate to discharge the onus which
lay upon
him.’”
[79]
The trial was held nearly eleven years after the fact. There is no
evidence that any of defendant’s
potential witnesses were
available to testify. In these circumstances I am not inclined to
draw any inference against either of
the parties for not calling the
nurses or the doctor.
[80]
Mr. Rossouw submitted that Prof. Smith has a proverbial ‘dog in
the fight’, and that
as a forensic expert he stands to gain if
his evidence were to be accepted, because the State would then be
swamped by claims.
Prof. Smith is a medical practitioner and
specialist of many years’ standing. He is evidently well
regarded in his field.
He gave evidence which was well reasoned, and
he supported his opinions with facts. He made concessions where it
was appropriate
to do so. As much as the Supreme Court of Appeal has
warned against imputing bias to a witness in
Mpetsheni
(
supra)
,
it is also important not to impute self-interest to a witness of high
standing, as a motive for his evidence.
[21]
I decline to make such a finding.
[81]
Plaintiff must establish her case on a preponderance of
probability.
[22]
Plaintiff
does not have to establish what caused the injury on any level above
what is most probable. In my view plaintiff has
established:
[81.1]
that the BGT type injury shown on the MRI scan can be caused by a
subthreshold/subacute,
intermittent series of HI insults; and,
[81.2]
that, on the probabilities, such HI events caused the injury to the
foetus’
BGT and perirolandic areas.
CAUSATION
[82]
The final question is whether the negligent omission by the
defendant’s employees to properly
monitor the plaintiff, and to
take emergency action by instrument delivery or caesarian section
caused the harm.
[83]
In
Minister
of Police v Skosana
[23]
the Court said the following on causation:
“
Causation
in the law of delict gives rise to two rather distinct problems. The
first is a factual one and relates to the question
as to whether the
negligent act or omission in question caused or materially
contributed to (see Silva’s Fishing
Corporation (Pty.) Ltd. v. Maweza,
1957 (2) S.A.
256
(A.D.) at p. 264; Kakamas Bestuursraad v. Louw,
1960 (2) S.A. 202
(A.D.) at p. 222) the harm giving rise to the
claim. If it did not, then no legal liability can arise and cadit
quaestio. If
it did, then the second problem becomes relevant,
viz. whether the negligent act or omission is linked to the harm
sufficiently
closely or directly for legal liability to ensue or
whether, as it is said, the harm is too remote. This is basically a
juridical
problem in which considerations of legal policy may play a
part. The distinction between these two enquiries is well explained
by Prof. Fleming, The Law of Torts, 4th ed., p. 169, as follows:
“
The
first involves what may broadly be called the ‘factual’
question whether the relation between the defendant’s
breach of
duty and the plaintiff’s injury is one of cause and effect in
accordance with ‘scientific’ or ‘objective’
notions of physical sequence. If such a causal relation does not
exist, that puts an end to the plaintiff’s case, because
no
policy can be strong enough to warrant the imposition of liability
for loss to which the defendant’s conduct has not in
fact contributed.
The
second problem involves the question whether, or to what extent, the
defendant should have to answer for the consequences which
his
conduct has actually helped to produce. There must be a reasonable
connection between the harm threatened and the harm done.
As a matter
of practical politics, some limitation must be placed upon legal
responsibility, because
[24]
the
consequences of an act theoretically stretch into infinity. The task
is to select those factors which are of sufficient significance
to
justify the imposition of liability and to draw a boundary along the
line of consequences beyond which the injured party must
either
shoulder the loss himself or seek reparation from another source.”
[84]
In the colloquial, the first leg of the test is
called the “but for” test.
[25]
The plaintiff has to prove on a balance of probabilities
[26]
that the harm would not have ensued but for the act or omission. The
second part of the test is whether the act or omission is
so remote
from the harm that legal liability should not follow.
[85]
When considering whether an act is causally linked to the harm, the
act is eliminated and one
then considers whether the harm would still
have ensued. However, an omission cannot be thought away, and a
positive act must be
inserted into the facts.
[27]
It was held in
Lee
(supra)
that
the application of the test should not be inflexible. In some
instances the inflexible application of the rule would result
in an
injustice. Each case, the Constitutional Court said, had to be
decided on its own facts. In
Minister
of Safety and Security v Van Duivenboden
[28]
the court said:
There
are conceptual hurdles to be crossed when reasoning along those lines
for once the conduct that actually occurred is mentally
eliminated
and replaced by hypothetical conduct questions will immediately arise
as to the extent to which consequential events
would have been
influenced by the changed circumstances. Inherent in that form of
reasoning is thus considerable scope for speculation
which can only
broaden as the distance between the wrongful conduct and its alleged
effect increases.”
[86]
It is in these kind of cases therefore necessary to import into the
equation the conduct that
one would reasonably have expected from
trained medical personnel, and then to determine whether the outcome
would have been different.
[87]
Dr Murray testified that a hypoxic event would in all likelihood be
triggered by a contraction
and would result in a sudden deceleration
of the heart rate. The labour protocols require the use of a CGT
monitor, or proper auscultation
if a CTG is not available, to monitor
the heart rate of the foetus and the contractions simultaneously,
more especially in high
risk cases (which this was from 1h20
onwards). If a CTG is not employed, auscultation must be done before,
during and after each
contraction, to confirm that the heart rate has
returned to the baseline.
[88]
If the foetus suffered an HI event, and such event was repeated
intermittently, it would inevitably
have had an effect on the foetal
heart rate in the form of a deceleration, and there would have been
indications of distress which
would have been revealed by proper
monitoring. Considering that the injury was not sudden, and was
likely sustained over a long
period of time, proper monitoring would
most likely have resulted in emergency intervention. Dr. Murray and
Prof. Lombaard agree
that the foetal condition changed between 02h00
and 03h35. They agree that had the foetus become distressed during
the second stage
of labour (after 02h00) then proper management would
have included a prompt recourse to an instrument delivery. In a
multiparous
patient, with the foetus’ head being engaged, such
an intervention would probably have been successful. Prof. Lombaard
specifically
recorded that the insufficient monitoring of the second
stage could have caused the foetal distress to be missed.
[89]
If one were to insert proper medical care and monitoring of the
foetus and the plaintiff into
the scenario, it is probable that the
foetal distress would have been recognised, and appropriate action
would have been taken
which probably would have prevented the harm
that eventually ensued. Factual causation has thus been established.
In this case
the harm is not remote from the omission, and there is
no question that it was foreseeable that improper care and monitoring
might
result in the foetus suffering an injury. Legal causation is
also established.
[90]
Mr. Rossouw argued that if the plaintiff were to succeed not only
would it have the effect of the State being held strictly
liable in
cases where no discernible sentinel event was present, but it would
also bankrupt the State.
[91]
As for the first proposition, this case must be decided on the facts
before the Court. In this
particular case the evidence points to
defendant being liable for the damages suffered. In the cases
referred to above,
AN
and
Mpetsheni
other
facts were presented, and the claims were dismissed. If a plaintiff
can produce sufficient evidence to prove her claim, she
is entitled
to a judgment. Conversely, if the plaintiff cannot produce evidence
to support her claim, she will not succeed. I do
not believe that his
case would open the floodgates of litigation.
[92]
As for the second proposition, that the State would be bankrupted if
this claim succeeds, I must
emphasize that I fully realise the
importance of this matter for the State. However, the effect of a
case on the fiscus is not
a consideration in a delictual matter.
[93]
I consequently find that the omission by the nursing staff of the
hospital to properly monitor
the plaintiff and the foetus, to
recognise that the foetus was in distress, and to take immediate and
urgent steps to deliver the
foetus, caused the subacute intermittent
Hypoxic-Ischaemic insults to build up to a point where the BGT and
perirolandic
areas of the foetus’ brain were injured.
That injury resulted in D now suffering from
severe
asymmetrical mixed type cerebral palsy, predominantly dystonic.
COSTS
OF 27 JULY 2020
[94]
The matter was previously set down for hearing on 27 July 2020 but
was postponed by agreement
between the parties, costs being reserved
for determination during the trial.
[95]
Plaintiff argued that defendant had caused the postponement, and in
support of this contention
it presented a letter dated 3 August 2020
in which plaintiff’s attorney wrote that;
[95.1] Defendant’s
expert report in respect of its paediatric neurologist and the signed
joint minute of the paediatric
neurologists were only delivered to
plaintiff on the afternoon of 22 July 2020, five days before the
trial;
[95.2] Prof.
Lombaard, defendant’s obstetrician and gynaecologist, raised
the issue of the positioning of the foetus
being inconsistent with an
assisted delivery at the last minute, only to concede in a joint
minute which only became available
on 24 July 2020 that assisted
delivery could have succeeded within 20 minutes of the detection of
distress.
[96]
In an email dated 6 August 2020 defendant’s counsel, Ms.
Pretorius, denied that defendant’s
actions had caused the
postponement, and she emphasized that defendant had been ready to
proceed. She alleged that plaintiff had
sought the postponement.
Plaintiff’s allegations regarding late delivery of the expert
summary, and the raising of contentious
issues shortly before trial
were not answered in the email.
[97]
I do not know what was discussed between the parties prior to them
agreeing to the postponement,
nor does the joint practice note cast
any light on the events. What is undisputed is that defendant
delivered an expert summary
that was substantially out of time, which
may well have caused the plaintiff to agree to postpone the matter.
Therefore it is,
in my view, proper to follow Mr. Ströh’s
suggestion and to order that the wasted costs occasioned by the
postponement
on 27 July 2020 be costs in the cause.
CONCLUSION
[98]
Mr. Ströh presented me with a lengthy draft order which details
the exact costs that are
to be paid. Most of the suggested terms of
the order are matters that are resolved on taxation. I will therefore
make the customary
order in respect of costs.
[99]
I consequently make the following order:
[99.1]
Defendant is declared
to be liable for payment of 100% of the proven
or agreed damages resulting from the brain injury sustained by D on
18 July 2010
and the consequent cerebral palsy from which she
suffers.
[99.2]
Defendant shall pay
the taxed or agreed costs of the action thus far
on the High Court scale, including the costs of senior and junior
counsel and
the reasonable taxable preparation, qualification,
travelling and reservation fees, if any, of the following experts:
[99.2.1]
Dr. L Murray (obstetrician and gynaecologist);
[99.2.2]
Prof. J Smith (neonatologist);
[99.2.3]
Dr. B Alheit (radiologist);
[99.2.4]
Dr D Pearce (paediatric neurologist).
[99.3]
The wasted costs occasioned
by the postponement of the matter on 27
July 2020 are costs in the cause.
[99.4]
In the event that the
costs are not paid within 30 days of taxation
or settlement, then interest may be levied thereon at the applicable
mora
rate.
[99.4]
The question of quantum is postponed
sine
die.
JJC
Swanepoel
ACTING
JUDGE OF THE HIGH COURT
GAUTENG
DIVISION OF THE HIGH COURT, PRETORIA
Electronically
submitted therefore unsigned
Delivered:
This judgement was prepared and authored by the Judge whose name is
reflected and is handed down electronically
by circulation to the
Parties/their legal representatives by email and by uploading it to
the electronic file of this matter on
CaseLines. The date for
hand-down is deemed to be 8 March 2021.
PLAINTIFF’S
COUNSEL:
Adv. J. Ströh SC
Adv. M. Coetzer
PLAINTIFF’S
ATTORNEYS:
W.M. Krynauw Attorneys Inc
Mr.
J. Coetzer
Mr.
C. Rapson
DEFENDANT’S
COUNSEL:
Adv. A. Rossouw SC
Adv. L. Pretorius
DEFENDANT’S
ATTORNEYS:
The State
Attorney
Mr. D. Olwage
HEARD
ON:
15 – 18 February 2021
25
February 2021
JUDGMENT
ON:
8 March 2021
[1]
2018 (4) SA 366 (SCA)
[2]
Masstores (Pty) Ltd v Pick and Pay Retailers (Pty) Ltd 2016 (2) SA
586 (SCA)
[3]
Road Accident Appeal Tribunal v Gouws and another
[2017] ZASCA 188
;
[2018] 1 ALL SA 701
(SCA); Michael and another v Linksfield Park
Clinic (Pty) Ltd and another [2002] 1 ALL SA 384 (A); 2001 (3) SA
1188 (SCA)
[4]
Stock v Stock
1981 (3) SA 1280
(A) at 1296 E-F; Jacobs v Transnet
Ltd t/a Metrorail
2015 (1) SA 139
(SCA);
[2014] ZASCA 113
[5]
[2019] ZASCA 102; [2019] 4 ALL SA 1 (SCA)
[6]
[2018] 2 ALL SA 678 (ECM)
[7]
[2020] ZASCA 169
(14 December 2020)
[8]
Pasternak, J and Gorey, M:
The
Syndrome of Acute Near-Total Intrauterine Asphyxia in the Term
Infant
,
Pediatr Neurol 1998 18: 391-398
[9]
A Okumura, F Hayakawa, T Kato & K Watanabe,
Bilateral
Basal Ganglia-thalamic Lesions Subsequent to Prolonged Fetal
Bradycardia
,
(2000) 58 Early Human Development 111
[10]
Rennie J and Rosenbloom L,
How
long have we got to get the baby out? A review of the effects of
acute and profound intrapartum hypoxia and Ischaemia,
The
Obstetrician & Gynaecologist, 2011 13: 169 - 174
[11]
Murray, D, O’Riordan, M, Horgan, R, Boylan, G, Higgins, J,
Ryan, C:
Fetal
Heart Rate in Neonatal Hypoxic-Ischemic Encephalopathy: Relationship
with Early Cerebral Activity and Neurodevelopmental
Outcome
,
Am J 2009;26:605-612
[12]
Volpe, J et al, 2018
Volpe’s
Neurology of the Newborn
,
6
th
Ed
[13]
Chapter 19
[14]
This is the injury found in the present case.
[15]
At page 502 and 503
[16]
American College of Obstetricians and Gynaecologists;
American
Academy of Pediatrics
:
Neonatal
Encephalopathy and Neurological Outcome
,
2
nd
Ed, Chapter 10.
[17]
Smith J, Solomons R, Vollmer L, Langenegger E, Lotz, J, Andronikou,
A, Anthony, J, and Van Toorn R:
Intrapartum
Basal Banglia-Thalamic Pattern Injury and Radiologically termed
“Acute-profound Hypoxic-Ischaemic Brain Injury”
are not
Synonymous, Am J Perinatol 2020 Dec 15. Doi: 10.1055/s –
0040-1721692
[18]
Goliath v Member of Executive Council for Health, Eastern Cape
2015
(2) SA 97
(SCA) par. 19: “
That
being so, the MEC, in failing to adduce any evidence whatsoever,
accordingly took the risk of a judgment being given against
him.
After
all, it was open to the MEC to adduce evidence to show that whilst
Ms Goliath was undergoing surgery, reasonable care had
indeed been
exercised by his employees. That he did not do.”
See
also: Ntsele v MEC for Health, Gauteng Provincial Government
[2013]
2 ALL SA 356
(GSJ) at par. 42
[19]
2009 (5) SA 255
(SCA)
[2009] ZASCA 45
at par. 35; See also R v Blom
1939 AD 158
at 202 – 203; Ocean Accident and Guarantee
Corporation Ltd v Koch
1963 (4) SA 147
(A); Gordhan and others v
Public Protector and others [2020] ZAGPPHC, 777 (17 December 2020),
par 83
[20]
1979 (1) SA 621
(AD);
[1979 3 ALL SA 485
(AD)
[21]
Mpetsheni par. 39
[22]
Miller v Minister of Pensions
1947 2 ALL ER 372
at 373: “
If
the evidence is such that the tribunal can say: ‘We think it
more probable than not” the burden is discharged,
but, if the
probabilities are equal, it is not.”
[23]
1977 (1) SA 31 (A); [1977 1 ALL SA 219 (A)
[25]
De Klerk v ABSA Bank Ltd
2003 (4) SA 315
(SCA);
[2003] 1 ALL SA 651
(SCA)
[26]
International Shipping Co (Pty) Ltd v Bentley
1990 (1) SA 680
(A) at
700 E – 701 F; [1990] 1 ALL SA 498 (A)
[27]
Lee v Minister of Correctional Services 2013 (2) SA 144 (CC); [2012]
ZACC 30
[28]
2002 (6) 431 (SCA)