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[2019] ZASCA 102
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AN v MEC for Health, Eastern Cape (585/2018) [2019] ZASCA 102; [2019] 4 All SA 1 (SCA) (15 August 2019)
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THE
SUPREME COURT OF APPEAL OF SOUTH AFRICA
JUDGMENT
Reportable
Case
No: 585/2018
In
the matter between:
AN
on behalf of EN
APPELLANT
and
MEMBER
OF THE EXECUTIVE COUNCIL
FOR
HEALTH, EASTERN
CAPE RESPONDENT
Neutral
citation:
AN v MEC for Health,
Eastern Cape
(585/2018)
[2019] ZASCA 102
(15
August 2019)
Coram:
Cachalia, Tshiqi and Molemela JJA and Gorven and Weiner
AJJA
Heard
:
22 May 2019
Delivered:
15 August 2019
Summary:
Delict
–
Medical
negligence
–
failure to
monitor the appellant and foetus during labour – whether
negligence of hospital staff was causally connected to
the child’s
brain damage –
factual causation not
established
–
appeal dismissed.
ORDER
On
appeal from:
Eastern Cape
Local
Division of the High Court, Mthatha (Dawood J sitting as court of
first instance):
The
appeal is dismissed.
JUDGMENT
Gorven
AJA (Cachalia and Tshiqi JJA and Weiner AJA concurring):
[1]
There is one central issue in
this appeal. A baby was born with brain damage caused during labour.
Did the negligent failure of
the staff at All Saints Hospital,
Engcobo, (the hospital) to properly monitor the mother and foetus
during delivery cause that
brain damage? In other words, as a matter
of fact, did the harm result from the negligence?
[2]
The mother in question is the
appellant and represents her minor child, the baby. She claimed
damages arising from the brain damage.
The respondent is responsible
in law if such loss was caused by the negligent conduct of the
hospital staff. The matter was tried
in the Mthatha High Court before
Dawood J. She held that the appellant did not prove that the
negligent failure to monitor the
mother and foetus had caused the
damage. She dismissed the appellant’s claim but made no order
as to costs. This appeal is
with her leave.
[3]
It is worth
briefly sketching the legal landscape governing such a claim.
‘
[I]n
order to be liable for the loss of someone else, the act or omission
of the defendant must have been wrongful and negligent
and have
caused the loss.’
[1]
Wrongfulness
involves the breach of a legal duty. The legal duty in the present
matter arose when the mother was admitted to the
hospital in labour.
The staff assumed a duty to care for mother and fetus during the
birth process without negligence, in other
words, as would reasonable
staff in their position. More particularly, they had a duty to
monitor the condition of mother and foetus
and act appropriately on
the results. They negligently failed to do so, in breach of that
legal duty. Their conduct was thus wrongful.
But this, in and of
itself, has never been sufficient to found delictual liability. The
wrongful conduct must cause the wronged
person to suffer loss. The
first step in proving this is to prove that the wrongful conduct of
the staff caused the baby to suffer
brain damage. The appellant
accordingly bore an onus to prove this. Wrongfulness should not be
conflated with factual causation.
[2]
[4]
The
test for factual causation is whether the act or omission of the
defendant has been proved to have caused or materially contributed
to
the harm suffered.
[3]
Where the
defendant has negligently breached a legal duty and the plaintiff has
suffered harm, it must still be proved that the
breach is what caused
the harm suffered. In heads of argument and initially before us,
counsel for the appellant sought to rely
on what were termed the
majority and minority judgments in
Lee
v Minister for Correctional Services
.
[4]
[5]
Lee
concerned
an inadequate system to monitor and isolate offenders who were in the
infectious stage of tuberculosis in a correctional
facility. It was
accepted that the plaintiff probably became infected whilst
incarcerated. The causation question was whether
this
inadequate system could be said to have caused the tuberculosis. This
court held that the case had not been made out. In the
Constitutional
Court, Nkabinde J, who wrote the majority judgment, summarised the
approach to factual causation taken in this court
in that matter:
[5]
‘
The Supreme
Court of Appeal judgment . . . non-suited Mr Lee on the basis that he
failed to prove that reasonable systemic adequacy
would have
“altogether eliminated” the risk of contagion, that he
does not know the source of his infection and that
had he known the
source it is possible that he might have been able to establish a
causal link between his infection and the specific
negligent conduct
on the part of the responsible authorities.’
[6]
She
criticised this approach:
‘
The
implication of that kind of inexorable logic is that factual
causation under our law can never be proved
where
the specific incident or source of infection cannot be identified
.
This means that even wrongful and negligent conduct of correctional
facility authorities can by no means, in those instances,
lead to
delictual liability.’
[7]
(my emphasis)
She
went on to hold that the ‘but-for’ test should be more
flexibly applied.
[6]
There
has been some debate as to whether
Lee
changed the law on factual causation. Malcolm Wallis
[8]
convincingly argues that
Lee
did not do so. Professor Anton Fagan
[9]
compared what he says are the common law elements with those he says
were applied in
Lee
and comes to the opposite conclusion. Such reasoned disagreement
suggests that some of the reasoning in
Lee
muddied the waters of factual causation. The majority certainly
highlighted difficulties which might arise in the application of
the
but-for test, in particular where the wrongfulness arose from an
omission:
‘
Although
different theories have developed on causation, the one frequently
employed by courts in determining factual causation,
is the
conditio
sine qua non
theory or but-for test. This test is not without problems, especially
when determining whether a specific omission caused a certain
consequence.’
[10]
And
later:
‘
However, in
the case of an omission the but-for test requires that a hypothetical
positive act be inserted in the particular set
of facts, the
so-called mental removal of the defendant's omission. This means that
reasonable conduct of the defendant would be
inserted into the set of
facts.’
[11]
[7]
To the extent that it
might be thought that
Lee
changed the test for factual causation, this was subsequently
expressly disavowed by the Constitutional Court in
Mashongwa
:
‘
Lee
never
sought to replace the pre-existing approach to factual causation. It
adopted an approach to causation premised on the
flexibility that has
always been recognised in the traditional approach. It is
particularly apt where the harm that has ensued
is closely
connected to an omission of a defendant that carries the duty to
prevent the harm. Regard being had to all the
facts, the question is
whether the harm would nevertheless have ensued, even if the omission
had not occurred. However, where the
traditional but-for test is
adequate to establish a causal link it may not be necessary, as in
the present case, to resort to the
Lee
test.’
[12]
Mashongwa
went
on to apply the traditional but-for test.
[13]
This was in line with
Lee
which seemed to embrace a flexible approach to causation only ‘where
the specific incident or source of infection cannot
be
identified.’
[14]
[8]
However,
I do not believe it is necessary to resolve that debate here. The
present matter differs from
Lee
.
It relates more closely to
Mashongwa
.
The source of harm is known. It was an acute profound hypoxic
ischaemic
[15]
insult caused by
complete lack of oxygen to the brain for a sustained period. Based on
Lee
,
the approach to be taken is ‘that reasonable conduct of the
defendant [must] be inserted into the set of facts.’
[16]
In the present matter, the question must be asked: Would the brain
damage have been avoided if the hospital staff had properly
monitored
the mother and foetus and had acted appropriately on the results? If
so, factual causation is established. If not, factual
causation has
not been established and one is left with only wrongful conduct
without proof that it caused the harm suffered. It
must be mentioned
that, during argument, counsel for the appellant retreated from
reliance on
Lee
and accepted that in the present matter the but-for test was
applicable in order to determine factual causation.
[9]
Having surveyed the legal
terrain, attention must be directed to the facts of this matter.
There is much which is common cause or
not seriously contested. The
mother was admitted to the hospital on 2 October 2013. This was her
first birth and she had slightly
exceeded full term. The delivery
appeared uncomplicated. The apgar scores were low and alerted the
staff to the possibility of
damage. The baby sustained a brain injury
during labour. The cause was an acute profound hypoxic ischaemic
insult. Acute means
sudden, as opposed to developing over a period of
time. This occurred during labour. Ischaemia is a restriction in
blood supply.
Blood supplies oxygen to the brain. A continued
restriction in blood supply leads to a lack of oxygen supply. Where
this takes
place, bradycardia occurs. This is a slowing of the foetal
heart rate. Hypoxia results from a sustained reduction in the supply
of oxygen to the brain. The injury to the baby is described as
hypoxic-ischaemic encephalopathy. This is a form of neurological
dysfunction. In this case, the baby developed cerebral palsy.
[10]
In the present matter, it is
common cause that the hospital staff did not properly monitor the
labour. Accepted guidelines require
such staff to take and record the
foetal heart rate over certain periods. In well-equipped hospitals,
the foetal heart rate is
monitored with cardiotocographs (CTCs). The
hospital was not equipped with these. In such situations, the
monitoring is done by
auscultation of the foetal heart.
[11]
There are two phases of
labour; the latent phase progressing to the active phase. The active
phase has two stages. It was agreed
by the experts that no damage was
caused during the latent phase or the first stage of the active
phase. It occurred during the
second stage of the active phase. This
began at 06h00 and lasted until delivery at 06h45. The last recorded
foetal heart rate was
taken at 06h00. The damage took place during a
45 minute period. The appellant’s claim is that the failure to
monitor during
this period caused the damage.
[12]
Doctor Murray, a specialist
obstetrician called by the appellant, explained that decelerations of
the heart rate occur during contractions.
During this stage, the
foetal heart rate should be taken before, during and after alternate
contractions or every five minutes.
This is important because, after
each deceleration, the foetal heart rate should return to a normal
baseline. Any delay in doing
so signals worsening hypoxia. The
appellant contended that warning signs of this nature would have been
observed if monitoring
had taken place. If so observed, the delivery
would have been expedited. The case for the appellant was thus that:
(a) there would
have been warning signs before the sudden, damage
inducing, event; and (b) delivery would have taken place prior to
06h45 and damage
averted as a result. The case for the appellant was
that the damage resulted because no warning signs were detected.
[13]
Both parties accepted the
report of Professor Andronikou. He interpreted a Magnetic Resonance
Imaging (MRI) scan of the baby’s
brain. He concluded that the
‘[f]eatures are those in keeping with a global insult to the
brain due to hypoxic ischaemic
injury, of an acute-profound nature,
occurring at term.’ All of the experts concurred that this
means that only the deep
brain structures were damaged. The deep
brain structures are also referred to as the grey matter, or core, of
the brain. An acute
profound hypoxic ischaemic event, such as in the
present case, must be distinguished from a partial prolonged hypoxic
ischaemic
event. An acute profound event means a sudden, not
progressive, event. A partial prolonged event causes damage to the
white matter,
or peripheral structures, of the brain.
[14]
The mechanisms giving rise to
these two types of brain damage are uncontroversial. Professor Van
Toorn, Head of Paediatric Neurology
at Tygerberg Childrens’
Hospital and Stellenbosch University, was called by the appellant. He
gave clear and uncontroverted
evidence on this issue. During labour,
the blood to the brain is supplied from the placenta along the
umbilical cord (the cord).
If there is an inadequate supply of
oxygen, the brain shunts the limited blood from the peripheries to
the deep grey matter. This
is designed to protect the deep grey
matter which is the most vulnerable matter due to its higher
metabolic rate. When shunting
takes place, damage occurs to the white
matter of the brain. This means that if there is some blood supply,
but it is inadequate,
damage occurs to the white matter. If there is
no blood supply at all, none is available to shunt to the deep grey
matter. In that
instance, only the grey matter will be damaged. The
MRI scan shows only damage to the grey matter in the present case. No
damage
to white matter was evident.
[15]
Based on this reasoning, all
of the experts agreed that the damage described by Professor
Andronikou was caused by a sudden, total,
persistent lack of blood
supply to the brain. It was not caused by a reduced volume of blood
supply. If this had been the case,
damage to the white matter would
have been evident.
[16]
The
sudden, total, persistent interruption to the blood supply is usually
caused by
a
perinatal sentinel event. Such events include placental abruption,
uterine rupture, umbilical cord prolapse, shoulder dystocia
or
maternal collapse. Each of these can be verified afterwards because
they leave what was termed a footprint. Professor Smith,
a
neonatologist called by the appellant, was initially adamant that
those listed above are the only phenomena which can be termed
sentinel events. According to a study by Shankaran et al,
[17]
however, such events also include a compression of the cord which
totally interrupts blood supply for a period long enough to cause
damage (a total, persistent interruption). In Rennie &
Rosenbloom,
[18]
it is said
that the damage to the areas of the brain observed in the present
matter is regarded ‘as the imaging signature
of hypoxic
ischaemic sentinel events.’ When referred to these studies and
to his own previous use of the term for a total
cord compression,
Professor Smith finally conceded that a cord compression resulting in
a sudden, total, persistent interruption
of blood supply to the
foetus could be referred to as a sentinel event.
[17]
Whatever the nomenclature, the
experts agreed that a sudden, sustained, total interruption to the
blood supply caused by cord compression
occurred in the present
matter. For the sake of convenience, I shall refer to this as the
sentinel event. This caused the damage.
Unlike the other sentinel
events listed above, a cord compression cannot be detected after the
fact. This is because the cord does
not remain compressed when the
pressure on it is alleviated. It leaves no indication that it was
compressed. Any pressure on the
cord ceases once a baby has been
born.
[18]
The experts also agreed that
the only way to attempt to reduce the likelihood of damage when the
blood supply has been completely
disrupted is to expedite delivery of
the baby. In the circumstances obtaining at the hospital, the only
way this could have been
done would have been by a vacuum extraction.
This is because a caesarean section takes about 45 minutes to perform
and the birth
took place 45 minutes after this stage of labour
commenced.
Professor Buchmann, the
respondent’s expert obstetrician, testified that in a
well-equipped Scottish hospital with well-trained
staff, a vacuum
extraction took an average of 19 minutes. He suggested
that,
in the hospital, this would take at least 20 minutes.
[19]
The experts differed on two
main issues. First, whether there would have been any warnings of an
impending sustained total interruption
to the blood supply. If so,
the argument went, monitoring would have detected the warnings. The
birth could then have been expedited
and damage averted. Secondly,
and if not, whether it would have been possible to prevent any damage
to the brain when the sentinel
event occurred.
[20]
It was contended by the
appellant’s expert witnesses, and Professor Van Toorn in
particular, that there would have been warnings
of an impending
sentinel event. He opined that intermittent interruption to the blood
supply to the brain would have occurred during
contractions. Blood
supply would have been restored between contractions. He testified
that these would have had a cumulative effect
which ultimately led to
the sentinel event. If monitoring had taken place according to the
guidelines, therefore, a change in the
foetal condition would have
been observed. Such a change would be signalled by decelerations in
the foetal heart rate during contractions.
The delivery could then
have been expedited and the damage avoided.
[21]
There are a number of
difficulties with this opinion. First, it was entirely speculative.
There was no evidence that there was intermittent
interruption to the
blood supply during contractions. Secondly, he conceded that such
contractions would not in fact have totally
shut off blood supply to
the brain. He testified that during these periods ‘the cord is
not completely closed’. The
interruptions would then have been
partial. They would not have caused a total interruption to blood
supply but a reduction. He
was constrained to agree that, in those
circumstances, the limited blood would have been shunted to the deep
grey matter. The necessary
corollary to this is that damage to the
white matter would then have occurred. But there was none. His
opinion that, on that basis,
warnings would have been observed if
proper monitoring had been carried out does not hold water.
[22]
The
second difficulty is that authoritative, peer-reviewed literature
referred to by both parties does not support this opinion.
In a
number of studies, monitoring of the foetal heart did not support the
case that there would probably have been prior warnings
of a sentinel
event. Okumura et al
[19]
conducted a study where, in some cases, the origin of the foetal
bradycardia could not be determined. Monitoring actually indicated
the well-being of these foetuses until sudden fall of the foetal
heart rate. No warning was given. In another study, Murray et
al
[20]
studied three groups of infants where CTGs were available. The third
group, with normal CTGs on admission, suffered acute sentinel
events
without warning. Pasternak & Gorey
[21]
concluded in their study that in 9 of their 11 patients, ‘fetal
monitoring was thought to be reassuring until the onset of
the
terminal bradycardia, supporting the premise that the
hypoxic-ischaemic insult occurred at the end of labor and was acute
and severe.’ Finally, a standard text,
Williams
Obstetrics
,
[22]
warns:
‘
There are several fallacious
assumptions behind expectations of improved perinatal outcome with
electronic monitoring. One assumption
is that fetal distress is a
slowly developing phenomenon and that electronic monitoring permits
early detection of the compromised
fetus.’
The
appellant’s witnesses were unable to point to any contrary
literature. They appealed to the court a quo to accept what
they said
had been their experience. But this cannot be said to prevail in the
face of compelling peer-reviewed literature.
[23]
If there was in all probability no warning, the
issue is whether, when the sentinel event occurred, there would have
been sufficient
time to avoid the damage by expediting the delivery.
The obvious first factor in this enquiry is that
counsel
for the appellant candidly admitted that it could not be proved when
the sentinel event occurred. Without being able to
do so, it could
not be said at what time monitoring would have alerted the staff to
this event.
[24]
The experts
agreed that, where a sentinel event occurs, damage takes place within
a short period of time. Professor Van Toorn testified
that a total
interruption to the blood supply gives rise to an ‘insult’.
If ‘you have a severe insult and if
that is sustained you end
up with brain damage very rapidly’. Professor Smith agreed
that, in the third group in Murray,
[23]
the average time to delivery after the observation of the sentinel
event was 22 minutes. In other words, the damage was done during
this
period. Professor Buchmann, the respondent’s expert
obstetrician, referred to Rennie
[24]
where damage began to accrue within 10 minutes of a sentinel event. I
have already mentioned that the experts agreed that an expedited
delivery in the hospital would have taken at least 20 minutes from
when it was commenced. Before commencement, a doctor would have
had
to be called. The doctor would have had to assess the situation. This
would have taken time. It is unrealistic to expect those
things to
have happened in less than 10 minutes. As already mentioned, the
authors concluded that ‘[m]ore severe encephalopathy
was
associated with . . . acute sentinel events shortly before delivery’.
Professor Buchmann testified without challenge
that the sentinel
event would probably have occurred in the 30 minutes prior to 06h45.
His
opinion is borne out by the literature referred to by both parties.
[25]
As a result, it was not proved
that there would have been sufficient time in which to deliver the
baby so as to avoid damage. Counsel
for the appellant conceded that,
as a result, causation could not be determined. When it was pointed
out that this in effect amounted
to a concession that the appellant
had not discharged the onus, he submitted that it was the negligence
of the respondent which
gave rise to this situation and the
respondent should accordingly be held liable. But, as explained
above, this is to conflate
wrongfulness and causation. Both must be
proved. When this was put to him, he did not persist in that
submission. In any event,
if the damage would probably have occurred
within the median time mentioned in Murray of 22 minutes, no remedial
action could have
averted it. An expedited delivery could not have
been performed inside that period. There is thus no basis on which
the court a
quo could find that damage could have been prevented if
monitoring had taken place.
[26]
It bears mention that the
second judgment, which I have read, concludes that the negligent
failure of the hospital staff created
risk along the lines mentioned
in
Lee
.
As I have said, it was conceded in argument that
Lee
did not apply. The matter was then argued on that basis without demur
from any members of the court. In the circumstances I do
not believe
that it is appropriate to decide it as if
Lee
does apply. In any event, I have no difficulty with the proposition
that the negligent conduct of the hospital staff in failing
to
monitor created a risk. It is, however, important to analyse the risk
which was created to evaluate whether it can be said to
have caused
the brain damage suffered by the baby. The risk created was, first,
that warnings of an impending sentinel event would
not be detected
and, secondly, that if a sentinel event did occur, this would not be
detected within a reasonable time. As to the
first, I have found that
the appellant was correctly held not to have proved that there were
any warnings of an impending sentinel
event. This risk cannot,
therefore, be said to have caused the brain damage. As to the second,
for factual causation to result,
it must be shown that if the
sentinel event had been detected within a reasonable time,
intervention within a reasonable time would
probably have prevented
the brain damage. This, too, I have concluded was not proved by the
appellant. In other words, in this
matter, it cannot be said that the
creation of risk by the negligence of the hospital staff caused the
brain damage suffered by
the baby.
[27]
The
appellant sought to rely on the minority judgment of this court in
AM
obo KM v MEC for Health, Eastern Cape
.
[25]
There, the same hospital was involved. A baby suffered cerebral palsy
as a result of hypoxia. The majority in this court held that
causation had not been established. The dissent was based on a
feature of the MRI report, also provided by Professor Andronikou,
which stated:
‘
Features are those of a chronic
evolution of a global insult to the brain due to hypoxic ischaemic
injury, of the acute profound
type, most likely occurring at
term’.
[26]
The
minority held that the words ‘chronic evolution’, when
qualifying an injury of the acute profound type meant that
‘the
acute, profound hypoxic ischaemia was not a sentinel event’.
Instead, there was ‘hypoxia and foetal distress
which
developed, undetected due to the lack of monitoring, over some time.’
The minority thus held that there would have
been forewarning prior
to the onset of the sudden, total, interruption to the blood supply.
If steps had been taken when the warnings
appeared, damage would
probably have been averted. The use of the words ‘chronic
evolution’ are absent from the MRI
report in the present
matter. Also clear, in the present matter, is that there was no
development of hypoxia and foetal distress
over a period of time
since no white matter was damaged. The case is distinguishable on the
facts and the minority judgment does
not assist the appellant.
[28]
It is appropriate to say something about the
prevalence of matters such as these. Far too often this court is
confronted with serious
and serial negligence in hospitals falling
under the respondent. Whether or not the negligence can be said to
have caused harm
in the delictual sense, it is clear that studied
neglect of standards has become pervasive in many such hospitals.
Those reliant
upon their services are receiving substandard care.
During the hearing, this situation was put to counsel for the
respondent. The
response was that this sad state of affairs and the
need for urgent remedial intervention had pertinently been brought to
the attention
of the relevant authorities. Despite this, such conduct
does not appear to have abated significantly, if at all. The
situation
is to be deprecated. In the light of this, even though the
respondent succeeded in resisting the appeal, counsel quite properly
did not seek to advance any argument for a costs award against the
appellant. No such award shall be made as a mark of displeasure.
In
addition, it is directed that this judgment be forwarded to the
respondent, and the National Minister under whom health services
fall, in the hope that this situation will be urgently addressed.
[29]
In the result, the following
order is made:
The
appeal is dismissed.
___________________
T
R Gorven
Acting
Judge of Appeal
Molemela
JA
Introduction
[30]
I have read the judgment
penned by my brother Gorven AJA (the main judgment). I agree with his
finding on wrongfulness, but respectfully
disagree with his reasoning
and conclusion in relation to causation. In my view the appeal should
succeed. The reasons for my disagreement
are set out hereunder.
[31]
The main judgment alluded to
some of the findings of this court in
AM obo
KM v MEC for Health, Eastern Cape
for
dismissing the appeal. For purposes of a proper perspective, I deem
it appropriate to mention the following differences between
that case
and the present. First, in the former, it was accepted that at a
certain critical point during labour, there was a reassuring
foetal
status, which was soon followed by lowering of the foetal heart rate.
This led to the acceptance that the foetal heart rate
would also have
been normal prior thereto. In this case, the court a quo did not
accept that there was a reassuring foetal heart
rate at 06h00. The
significance of this finding is that, unlike in
AM
obo KM v MEC
, in
the present case, there was simply no evidence of a reassuring foetal
status.
[32]
Second,
in
AM
obo KM
,
the mother of the baby did not testify, nor did any of the hospital
staff. In this matter, the appellant, who is the mother of
the baby
on behalf of whom the claim was made, testified. Her evidence was
undisputed. The extent of the negligence of the hospital
staff is
evident from her unchallenged testimony. Her evidence thus formed a
solid factual foundation to the opinions of the expert
witnesses who
testified on her behalf. Lastly, and perhaps curiously, in
AM
obo KM
,
despite the insult leading to hypoxic-ischaemic encephalopathy (HIE)
having been described as the ‘acute profound’
type, Prof
Buchmann accepted that there was no ‘sentinel event’
suffered by the woman who was giving birth and further
opined that
the hypoxic event could have been ‘related to uterine
contractions’.
[27]
In
the present case, although the brain injury was similar, Prof
Buchmann was adamant that it was most likely that there was a
sentinel event which happened without forewarning.
[33]
Turning
to the facts of this case, I am of the view that the evidence adduced
on behalf of the appellant, the contents of the article
written by
the respondent’s expert witness, Prof Buchmann, entitled
‘
Babies
who die from labour-related intrapartum hypoxia: a confidential
enquiry in South African public hospitals
’,
[28]
as well as the concessions he (Prof Buchmann) made during the trial
unquestionably prove both negligence and causation on a balance
of
probabilities.
Negligence
[34]
The
test for establishing negligence is trite.
[29]
This test rests on two bases, namely, reasonable foreseeability and
the reasonable preventability of damage.
[30]
What is or is not reasonably foreseeable in a particular case is a
fact bound enquiry.
[31]
Of
great significance is that negligence must be assessed in light of
all the circumstances.
[32]
[35]
With
specific reference to this matter, the standards that were applicable
at the time of the appellant’s admission are clearly
spelt out
in the National Maternal Guidelines (the guidelines) published in
2007. The foreword to the guidelines states that they
were reviewed
by many experts and were updated following a vast literature review.
The guidelines are applicable to clinics, community
health centres
and district hospitals in South Africa. What is abundantly clear from
these guidelines is that all women who are
in labour must be
monitored closely. As regards the establishment of the guidelines,
Prof Buchmann’s article states as follows:
‘
So
to standardise care, we produced guidelines as a multidisciplinary
group with obstetricians, anaesthetists, midwives, nurses,
public
health specialists and Department of Health officials
to
get a consensus of what is feasible and best in South Africa with all
its constraints, given the best evidence available and
what we have
in terms of the resources
.’
(Emphasis added).
[36]
Under the heading of
‘management of the second stage of labour’, the
guidelines provide as follows:
‘
The second
stage commences when the cervix reaches full dilatation (10 cm).
From the time that
full dilatation of the cervix is first noted, up to 2 hours may pass
before the mother starts to bear down.
Time
can only be allowed for the head to descend onto the pelvic floor if
fetal distress and cephalopelvic disproportion have been
ruled out.
The bladder should be emptied, using a catheter if necessary. The
observations of the first stage of labour should continue. Efforts
at
bearing down are only encouraged when the fetal head starts to
distend the perineum and the mother has an urge to push.
When the mother is ready to bear down:
•
Always
communicate clearly with the mother to gain co-operation
•
Be
supportive and encouraging
•
Put the
mother in a suitable position: propped up, sitting, squatting,
kneeling, semi-Fowler’s or wedged supine. Avoid the
flat supine
position as the uterus will compress the aorta and inferior vena cava
•
Encourage
pushing only during contractions
•
Listen to
the fetal heart rate between every second contraction
•
Protect the
perineum when the head crowns
•
Gently
suction the baby’s mouth and nostrils while awaiting
restitution and external rotation
•
Record the
times of onset of the second stage, onset of bearing down efforts and
delivery.’ (Emphasis added).
[37]
Under the heading of
‘emergencies during labour’, the following is stated in
relation to foetal distress:
‘
FETAL
DISTRESS
This is suspected when the following
signs are observed:
•
Baseline
fetal heart rate ≥160 beats per minute
•
Baseline
fetal heart rate <110 beats per minute
•
Variability
persistently <5 beats per minute on CTG, in the absence of
sedating drugs
•
Late
decelerations of the fetal heart rate
Management of fetal distress
1. Explain the problem to the mother
2. Lie the mother in a left lateral
position
3. Give oxygen by face mask at 6
L/minute
4. Start an intravenous infusion of
Ringer-Lactate to run at 240 mL/hour
5. Do a vaginal examination for
cervical dilatation and to exclude cord prolapse:
- If vaginal delivery is imminent
(cervix fully dilated), deliver immediately, by vacuum extraction if
necessary
- If vaginal
delivery is not imminent, give hexoprenaline 10 micrograms IV and
prepare for immediate caesarean section. Arrange
urgent transfer from
a community health centre to hospital.’
[38]
It
is trite that the facts on which expert witnesses express an opinion
must be capable of being reconciled with all other evidence
of the
case.
[33]
The evidence of the
appellant is therefore an important consideration. The salient
aspects of the appellant’s testimony are
set out here and in
the paragraphs that follow. She testified that after her admission to
the hospital, she was taken to the labour
ward. The nurse who
attended to her performed a few vaginal examinations but did not
monitor the foetal heart rate at any stage.
During the night, she
experienced excruciating pain that rendered her unable to walk, as a
result of which she had to crawl whenever
she had to go to the
toilet. As there was no staff member at the nurse’s station
closest to her ward, she received assistance
from fellow patients
whenever she had to go to the toilet. According to her evidence, at
some point she requested that a caesarean
section be performed,
seemingly because of the severe pain she was experiencing. The
attendant nurse dismissed her request. At
06h00, a vaginal
examination was done, after which the appellant was moved to the
delivery room. This examination, too, was not
accompanied by the
monitoring of the foetal heart rate.
[39]
According to the appellant,
after examining her, the nurse told her that the baby was about to
make its arrival and instructed her
to start pushing. The nurse in
question then left the ward and never returned. The appellant was
left unattended until a member
of the cleaning staff, who happened to
be passing by, raised alarm after noticing that the baby’s head
was partially out
but seemed stuck in the vaginal opening. In
response to the cleaning lady’s call for help, a nurse came to
the scene and
delivered the baby. It is common cause that the
appellant’s baby was delivered at 06h45 by the nurse who had
just reported
for the 07h00-19h00 shift.
[40]
Dr Murray, an expert witness
who testified on behalf of the appellant, is a senior specialist in
obstetrics and gynaecology at Tygerberg
Hospital and a lecturer at
the Department of Obstetrics and Gynaecology at Stellenbosch
University. She manages the labour ward
and is a consultant that
covers obstetrics wards and obstetric clinics. Her
curriculum
vitae
further
states that she is involved in collecting data on the underlying
causes of foetal stillbirths and neonatal deaths, HIE
audits and
babies that may have come to harm during labour. Dr Murray gave
crucial evidence relating to the paucity of monitoring
during the
appellant’s latent and active stages of labour. She stated that
it has been established that some babies do not
tolerate or cope with
labour, which is why a woman’s labour must be monitored. The
foetal heart rate must be monitored throughout
labour, regardless of
the instrument used. The correct manner of assessing the foetal heart
rate is by monitoring and recording
its reading before, during and
after contractions. If there were merely random measurements of the
foetal heart rate that were
not timed to contractions, no reliable
information would be gained as to whether the foetus was coping with
labour. Thus, warning
signs would not be detected and it would not be
possible to intervene.
[41]
Dr Murray further testified
that if the uterine contractions were very strong and presented too
much hypoxic stress to allow the
foetus to stay oxygenated, the
foetus would normally show signs of hypoxia, which would manifest
themselves in a deceleration and
slow recovery of the heart rate.
A delay in returning to the normal baseline would signal worsening
hypoxia and point to
foetal distress. She pointed out that when it
comes to labour, every minute counts. Thus, even in the face of a
sentinel event,
attempts are made to mitigate the risk of harm to
both the mother and baby. Where there was a cord compression or cord
prolapse,
the delivery of the baby would have to be expedited.
Further, the mother would have had to be turned to her side to
relieve the
pressure on the umbilical cord. Under such circumstances,
a caesarean section is recommended. Where a caesarean section was the
appropriate intervention, an imminent delivery could be delayed by
turning the mother to her side. However, if the foetal head
had
already engaged in the pelvis, a vacuum extraction or forceps
delivery would have to be performed. It is of significance that
under
cross-examination, Prof Buchmann admitted that Dr Murray’s
evidence pertaining to the manoeuvres that are performed
to try and
reduce hypoxic ischemic damage constituted good practice.
[42]
I
pause to mention that the partogram signed by the night nurse reveals
that the appellant was given intravenous medication referred
to as
Ringers Lactate at 06h00. According to the maternal guidelines,
Ringers Lactate is administered as part of the management
of foetal
distress. Under the discussion on the management of foetal distress,
the guidelines state that if the cervix is fully
dilated, the baby
must be delivered
immediately
by vacuum extraction if necessary
.
Notably,
the clinical notes made by the same nurse who noted that Ringers
Lactate was administered also recorded that at 06h00,
the appellant
was experiencing ‘strong contractions’ and her uterus was
fully dilated. The respondent has not provided
any reasons explaining
why not even an attempt was made to deliver the baby at 06h00.
What is plain is that despite the existence
of foetal distress, the
appellant was left unattended at the most critical stage of labour
and this state of affairs persisted
for approximately 45 minutes. The
following extract from Prof Buchmann’s own article sounds
eerily prophetic when consideration
is paid to the facts of this
case. He stated that ‘[w]omen who are pushing in the second
stage of labour should not be left
alone, and fetal heart
auscultation must be done after each contraction to confirm return to
the baseline.
This
will allow early detection of fetal bradycardia, so that appropriate
action can be taken
.’
[34]
(Emphasis added.)
[43]
Having noted the appellant’s
evidence pertaining to her labour, Dr Murray’s conclusion was
that it was highly probable
that the hospital staff had, due to
inadequate monitoring of the appellant’s labour, failed to
notice that the foetus was
not coping and therefore failed to take
the remedial steps set out in the guidelines. This substandard care
ultimately led to the
brain injury suffered by the baby. Dr
Murray’s evidence is a very important piece of the puzzle in
relation to the
appellant’s evidence.
[44]
The
guidelines corroborate Dr Murray’s unchallenged evidence
regarding the need for proper monitoring. Prof Buchmann’s
own
article underscores the importance of monitoring a woman who is in
labour. His conclusion is that HIE- related deaths can be
prevented
if there ‘is close and careful monitoring of all women in
labour with particular attention to detail in fetal heart-rate
monitoring.’
[35]
The
following extract from the article authored by Prof Buchmann is of
significance with regards to the monitoring of a woman in
labour:
‘
The most
striking finding in this study was the failure in most of these
deaths, to detect signs of fetal distress
.
It is likely that these babies would have shown some evidence of
intrapartum hypoxia during labour. Late decelerations, the hallmark
of fetal distress, were detected in just over one quarter of these
cases…. It appears that there is a serious deficiency
in
intrapartum fetal monitoring in the hospitals studied, and probably
in most other state hospitals in South Africa. It seems
likely that
insufficient time and care is taken with auscultation, and that the
early signs of fetal hypoxia – fetal heart
decelerations –
are frequently missed.
. . .
Labour-related
intrapartum hypoxia is common
and
avoidable
cause of perinatal death in South Africa, and the majority of these
deaths occur in low-risk situations where labour appears to
be
normal. The overwhelming problem seems to be failure to detect
evidence of fetal distress. To prevent these unnecessary deaths,
the
emphasis in the labour ward care should be close and careful
monitoring of all women in labour,
with
particular attention to detail in fetal heart rate monitoring.
’
[36]
(Emphasis added.)
[45]
The appellant’s
unchallenged evidence revealed that the monitoring of her labour was
hopelessly inadequate. The most crucial
part of the monitoring,
namely the assessment of the foetal heart rate against the uterine
contractions, fell far short of the
applicable standards. On the odd
occasion on which the heart rate was recorded in the partogram, it
was not done in accordance
with the guidelines as it failed to
reflect the foetal heart rate before, during and after contractions.
The nurse who recorded
that the foetal heart rate was normal at 06h00
did not testify, which left the evidence of the appellant relating to
the failure
to monitor the foetal heart rate, undisputed. Notably,
the entry in the partogram did not reflect any measurements of the
foetal
heart rate taken during, before or after uterine contractions.
This, in my view, is a clear indication that the foetal heart rate
was not monitored. On this aspect, the court a quo found, correctly
in my view, that the recording that the foetal heart rate was
normal
at 06h00 could not be accepted. As stated before, the court a quo’s
finding on that aspect was not attacked by the
respondent on appeal.
The main judgment’s finding that the last recorded foetal heart
rate was taken at 06h00 unfortunately
fails to take that finding into
account. In my view, this finding impacts on the respondent’s
case as it puts paid to Prof
Buchmann’s theory that it was
unlikely that there were any decelerations of the foetal heart rate
before 06h00. It follows
that once that theory is discarded, his
reliance on it as a basis for refuting the probability of prior
warnings of foetal distress
must follow suit.
[46]
The evidence shows that the
nurses who attended to the appellant during labour are nursing
sisters. Despite that, the manner in
which they dispensed medical
care to the appellant during the most critical part of labour fell
below the standard of reasonably
competent nursing sisters. That a
nursing sister in their position would have foreseen harm is
unquestionable. A nursing sister
in their position would undoubtedly
have taken steps to prevent harm by expediting the delivery of the
appellant’s baby.
Given that the hospital in question falls
under the category of level 1, it can be accepted that a doctor was
present in the maternity
ward at all material times of the
appellant’s delivery. Thus, it can be accepted that had there
been any difficulties that
the attendant nurses could not handle,
they would have been escalated to a doctor on duty. It is clear from
the evidence that at
no stage was the assistance of a doctor sought.
Having considered the evidence in totality, I am satisfied that all
the grounds
of negligence pleaded by the appellant have been proven
on a balance of probabilities.
Causation
[47]
I
now turn to the contentious issue of causation. In the context of
this case, the question is whether there was a causal link between
the failure of the hospital staff to monitor and manage the
appellant’s labour in accordance with the stipulations of the
guidelines, on the one hand, and the baby’s brain damage which
led to acute cerebral palsy, on the other.
[37]
In my view, there is. Indeed, the fact that the medical staff’s
conduct was wrongful and negligent does not necessarily resolve
the
question concerning whether liability should be imputed to it,
thereby rendering the respondent vicariously liable. A successful
delictual claim entails the proof of a causal link between a
defendant’s actions or omissions and the harm suffered by a
plaintiff.
[38]
[48]
In
Minister
of Safety and Security v
Van
Duivenboden
,
[39]
this court stressed that a plaintiff is not required to establish the
causal link with certainty, but only to establish that the
wrongful
conduct was probably a cause of the loss, which calls for a sensible
retrospective analysis of what would probably have
occurred, based
upon the evidence and what can be expected to occur in the ordinary
course of human experience. In
Minister
of Finance & others v Gore NO
[40]
this court aptly held that the application of the ‘but-for’
test is not based on mathematics, pure science or philosophy. Rather,
it is a matter of common sense, based on the practical way in which
the ordinary person’s mind works against the background
of
everyday life experiences. The flexible approach reflected in the
above judgments was adopted by the Constitutional Court in
Lee
.
[49]
The
issue of causation recently received attention in the case of
Mashongwa
v PRASA
.
In
Mashongwa,
the Constitutional Court pointed out that
Lee
never
sought to replace the pre-existing approach to factual causation,
rather, it adopted an approach to causation premised on
the
flexibility that has always been recognised in the traditional
approach
[41]
as reflected in
the authorities referred to above. In re-stating the ‘but-for’
test in
Mashongwa,
[42]
the Constitutional Court settled the law on this aspect. It pointed
out that the imputation of liability to the wrongdoer depends
on
whether the harmful conduct is either too remotely or sufficiently
closely connected to the harm caused. It emphasised that
where the
traditional but-for test is adequate to establish a causal link, it
may not be necessary to resort to the
Lee
test. It is the facts of the case that will dictate which test is
more appropriate. That being the case, it follows that a wrong
concession by counsel regarding the test that is to be applied will
not be binding on the court.
[43]
[50]
Before canvassing all the
evidence showing that the nurses’ negligence probably caused
the brain injury sustained by the baby,
I deem it convenient to first
address myself to the court a quo’s evaluation of expert
evidence. It is necessary to do so
because I am of the view that its
approach was flawed and thus led to a wrong conclusion regarding
causation. I will therefore
briefly discuss the principles applicable
to the evaluation of expert evidence.
[51]
The
correct approach to the evaluation of expert evidence was
authoritatively laid down by this court in
Michael
& another v Linksfield Park Clinic (Pty) Ltd & another
,
[44]
which endorsed the approach followed by the House of Lords in
Bolitho
v City and Hackney Health Authority
.
[45]
This court pointed out that is required in the evaluation of expert
evidence is to determine whether the opinions advanced by the
experts
are founded on logical reasoning and, if so, to what extent. If the
court concludes that the opinion is one that can reasonably
be held
on the basis of the facts and the chain of reasoning of the expert
,
the threshold will be satisfied.
[46]
[52]
Prof van Toorn, a paediatric
neurologist, supports Dr Murray’s conclusion as to the probable
cause of the baby’s injury.
The court a quo expressed several
misgivings about Prof van Toorn’s evidence in relation to the
proximate cause of the baby’s
injury. It rejected some of his
evidence on the basis that it was not documented in peer-reviewed
publications. Further criticism
of his evidence is canvassed in the
main judgment. As I demonstrate below, that criticism is, in my view,
unwarranted.
[53]
Logically,
there was nothing wrong with the evidence of Prof van Toorn
pertaining to the pattern of brain injuries and the impact
of
intermittent interruption of the supply of oxygenated blood to the
brain resulting in hypoxia. Nor were there any flaws relating
to his
reliance on the studies on animal models as a basis for his thesis.
That evidence is corroborated by the Rennie & Rosenbloom
article,
[47]
alluded to in the
main judgment, where it is stated, in relation to animal models of
acute profound damage, that ‘[r]epeated
short umbilical
occlusions can also cause damage to the striatum (equivalent to the
deep grey matter) in lambs and may be closer
to the insult that often
affects the human fetus’.
[54]
In
relation to humans, the same article states the following: ‘[t]hese
data support the evidence provided by the primate studies
regarding a
worse outcome if an acute near-total insult is superimposed on a
previous episode of partial hypoxia’.
[48]
In the article authored by Pasternak, which has already been alluded
to in the main judgment, the following statement, made in
relation to
term infants who had sustained a brain injury from an acute
near-total intrauterine hypoxic insult, lends credence
to Prof van
Toorn’s evidence:
‘
. . .
therefore we were unable to determine the precise duration of the
bradycardia
or
even be confident that these patients had not experienced a
significant subacute insult before the terminal bradycardia
.
. . We believe that the similarity of their clinical features and
imaging studies to those of the other nine patients [who had
sustained an acute and severe hypoxic brain insult at the end of
labour] supports the assumption that all 11 patients represent
a
homogenous population’.
[49]
(Emphasis added.)
[55]
The excerpts from these
published articles not only give a backdrop to Prof van Toorn’s
logical process of reasoning, but
also serve to show that his
reasoning was scientifically valid. They fortify the view he
expressed in relation to intermittent
occlusions and their impact.
The undisputed evidence about the sequence of events during the
appellant’s labour
fits in neatly with the conclusion reached
by Prof van Toorn. This obviously has a bearing on the probabilities.
[56]
There
was a difference of opinion between Prof Buchmann about the
occurrence of intermittent episodes of a diminished supply of
oxygenated blood to the foetus and the impact thereof on the foetus.
It is well-established that where there are conflicting opinions
of
experts in the field, the court’s determination of negligence
must depend on an analysis of the cogency of the underlying
reasoning
which led the experts to their conflicting opinions.
[50]
Prof van Toorn testified that a foetus is normally able to adjust or
compensate for the periods of hypoxia caused by the
normal
contractions. This is known as the auto-regulation of the foetus.
According to him, an extended exposure to such hypoxia
could
compromise the ability of a foetus to recover from those intermittent
episodes. He emphasised the importance of making a
distinction
between an insult and an injury. According to him, not every insult
equates to an injury. The reaction to the insults
differs from baby
to baby. Foetal reserve, which relates to the ability of the foetus
to withstand insults, plays a significant
role. He testified that if
the foetus was exposed to prolonged periods of intermittent hypoxia,
the auto-regulation of the foetus
could fail due to the depletion of
foetal reserves. If a woman was not properly monitored, the
intermittent decelerations of the
foetal heart rate would not be
observed and consequently, no intervention would be made. In the
absence of any interventions, those
intermittent decelerations of the
foetal heart rate would culminate in a final insult to the brain of
the foetus. The extent of
the insult would depend on its duration,
extent and foetal reserves.
[57]
Prof
van Toorn’s evidence on this aspect is bolstered by the study
of animal models that is alluded to in the Rennie and Rosenbloom
article.
[51]
This article
acknowledges that in human cases of acute profound hypoxic ischaemia
‘there is clear variability both in the
fetal reserve and in
the duration and degree of the insult’. In the book entitled
Neonatal
Encephalopathy and Neurological Outcome
[52]
it is acknowledged that ‘[d]ifferences exist in the fetal
effects of hypoxic stresses associated with late and variable
decelerations, and different fetuses may have differing thresholds
for damaging degrees of metabolic academia’. Given the
views
expressed in these articles, the cogency of Prof van Toorn on this
aspect survives scrutiny and is unassailable. The court
a quo
therefore erred in finding that there was no basis for Prof van
Toorn’s thesis. The following remarks made by this
court in
Linksfield
are apposite:
‘
The court is
not bound to absolve a defendant from liability for allegedly
negligent medical treatment or diagnosis just because
evidence of
expert opinion, albeit genuinely held, is that the treatment or
diagnosis in issue accorded with sound medical practice.
The
court must be satisfied that such opinion has a logical basis, in
other words that the expert has considered comparative risks
and
benefits and has reached “a defensible conclusion”. If a
body of professional opinion overlooks an obvious risk
which could
have been guarded against it will not be reasonable, even if almost
universally held.’
[53]
[58]
The
court a quo similarly erred by disregarding Prof van Toorn’s
evidence pertaining to the 15 cases which supported his conclusions
on the features of injuries sustained as a result of intermittent
episodes of hypoxia culminating in an acute profound injury.
The
court disregarded that evidence on the basis that his thesis had not
been documented in peer-reviewed articles. The court a
quo failed to
appreciate that expert
witnesses
are not confined to express views based on literature alone. Experts
are required to lay a factual basis for their conclusions.
[54]
Prof
van
Toorn’s evidence on those 15 cases is part of his own practical
as a paediatric neurologist and ought to have been considered.
[55]
Inexplicably, while disregarding Prof van Toorn’s evidence as
to his practical experience, the court a quo seemingly accepted
Prof
Buchmann’s. I could not find any basis for this disparity.
[59]
It is trite is that a court
may not rely on the opinion of an expert whose evidence is stretching
beyond the limits of his or her
own field of expertise. Prof Buchmann
conceded that he had no expertise on certain fields of radiology that
fell within Prof van
Toorn’s expertise as a paediatric
neurosurgeon. Despite this concession, the court a quo remarked that
‘[p]
rofessor
Buchman quite eloquently satisfied this court that he was
sufficiently qualified to give expert opinion on areas that partially
infringed upon the expertise of the paediatric neurosurgeon’.
This remark, is in my view misplaced.
[60]
Moreover, the court a quo
failed to take note of a clear inaccuracy in Prof Buchmann’s
evidence when he erroneously stated
that Dr Andronikou’s report
made reference to injuries to the basal ganglia. The court a quo thus
erred when it found that
the MRI depiction and the radiologist’s
report and description of the injury supported Prof Buchmann’s
views. The following
exchange between the appellant’s counsel
and Prof Buchmann, relating to the MRI features canvassed in
Pasternak’s article
is apposite:
‘
MR
WESSELS
:
Yes, well let’s look at what the imaging shows. The first one
CT and that’s
all. Then we have MRI … (intervention).
WITNESS
:
No, the … (intervention).
MR
WESSELS
:
Defuse(?) T2 abnormality basal ganglia and thalamus.
WITNESS
:
That’s the CT on days
2 and 4, normal, which one often sees
because the CT doesn’t – isn’t spec –
sensitive to the changes. The
MRI is better.
But
this is radiology territory, I grant you that.
But the MRI is there, it’s got abnormality in the basal ganglia
and thalamus. That’s the typical acute profound picture.
The
baby did badly, died on day 12.
. . .
MR
WESSELS
:
Not all basal ganglia and thalamus are acute profound.
WITNESS
:
That’s – no,
that’s the pattern.
Basal
ganglia thalamus injuries are the signature of an acute profound
insult and Prof Andronikou’s report states that, gives
the
description and says these are in keeping with an acute profound.
That’s the MRI signature of an acute profound, basal
ganglia
thalamus, or also known as deep grey matter.’
(Emphasis added.)
[61]
Despite having conceded that
he had no expertise in radiology, Prof Buchmann persisted in
expressing an opinion on the features
of the injuries that would have
resulted and the patterns that would be depicted on the MRI scan if
Prof van Toorn’s thesis
were to be accepted as correct.
During cross-examination, when it was pointed out to Prof Buchmann
that Dr Andrinokou had
not used the term ‘basal ganglia’
anywhere in his report, Prof Buchmann was adamant that the images
depicted in the
scan showed an injury to the basal ganglia. This is
borne out by the following testimony with specific reference to the
brain injuries
sustained by the appellant’s baby:
‘
MR
WESSELS
:
But that is not necessarily exclusive,
if you have those two, then you have acute profound, you can have
those injuries with other
conditions as well.
WITNESS
:
No, no, it’s the watershed
injuries that can go with other
conditions such as infections and metabolic disorders. The acute
profound is the signature –
I mean, the basal ganglia thalamus
injury, deep grey matter, is the signature of the acute profound
insult. And Prof Andronikou’s
report states it like that.
And
there are really no other causes as far as I know. But yes, I’m
now going to radiology territory.
MR
WESSELS
:
Which is not your field.
Professor…”
MR
WESSELS
:
Yes, M’Lady. (Pause). Bilateral symmetric abnormal high signal
on
T2/FLAIR the caudate nuclei, putamina, thalami, posterior limbs of
the internal capsules focally, corona radiata and periorolantic
regions, hippocampi, abnormal high signal … (indistinct) flare
and volume loss noted focally involving the left cerebral
hemisphere,
the corpus collasum is thin around the … (indistinct) no
significant ventricum(?) megelli(?).
That
is what he found, there’s no basal ganglia reference here.
WITNESS
:
No, the basal ganglia involved there, I
will defer to radiologists on that,
but
that is –
this is the basal
ganglia thalamus injury.
That’s
the deep grey matter that he’s referred to, but I’m not
going to go and look in a textbook now and say
to you this is a basal
ganglia or that’s not a basal ganglia.’
(Emphasis
added.)
[62]
It is clear from the above exchange that even though Dr Andronikou
did not find that there was an injury to the basal ganglia,
Prof
Buchmann remained adamant that the patterns depicted in the MRI scan
showed that the basal ganglia had indeed been injured.
It bears
emphasis that even though Dr Andronikou categorised the baby’s
injury as one of an acute profound type, he did not
find that a
sentinel event had occurred. The injuries referred to in the article
authored by Rennie & Rosenbloom, which were
considered to be the
‘imaging signature of hypoxic ischaemic sentinel event’
included injuries to the basal ganglia.
Given the fact that the basal
ganglia are not listed in Dr Andronikou’s report, the Rennie &
Rosenbloom article cannot
be considered as a basis for Prof
Buchmann’s conclusion that there was a sentinel event.
Similarly, that article cannot be
considered as a basis for
disregarding Prof van Toorn’s thesis that intermittent episodes
of hypoxia can culminate in an
injury of an acute profound type. As
Prof Buchman is not an expert in radiology and paediatric neurology,
his evidence regarding
the features of the injuries and the
neuroimaging that would be depicted on the MRI scans if Prof van
Toorn’s theory were
to be accepted, amounted to speculation and
was therefore of no value. There was no basis for accepting Prof
Buchmann’s evidence
as a justification for rejecting Prof van
Toorn’s thesis. The court a quo therefore erred in rejecting
Prof van Toorn’s
plausible evidence.
[63]
In this matter, it is undisputed that the appellant’s
ante-natal records showed that she was generally in good health
and
that the health of the foetus was not at risk. It is undisputed that
she was in good health when she was admitted to All Saints
hospital.
Prof Smith’s unchallenged evidence served to exclude the
possibility of any congenital factors or genetic abnormalities
that
could have predisposed the baby to HIE. With regard to the possible
interventions that could have been resorted to and whether
such
interventions were likely to avert the harm suffered by the baby,
there is simply no evidence suggesting that on the day in
question,
the appellant’s baby could not have been delivered within the
agreed upon median of 22 minutes. The hospital falls
into the
category of level 1 hospitals that have properly trained and
qualified staff (doctors and nurses), medical equipment,
24-hour
labour and delivery service and a theatre to provide proper obstetric
care. Prof Buchmann’s evidence that there was
insufficient time
available for a vacuum-extraction delivery was not supported by any
evidence. Similarly, his evidence that a
forceps delivery was
probably not possible because of lack of expertise by the nurses was
not substantiated. There is no factual
foundation supporting his
conclusion that the injury was not preventable.
[64]
A conclusion that the baby’s injury was not preventable would
perhaps have been tenable if there was evidence that some
attempts
were made, albeit unsuccessfully, to deliver the baby in accordance
with the procedures stipulated in the guidelines.
No such evidence
was adduced. On the contrary, the evidence shows that, despite the
nurse who delivered the baby being an advanced
midwife who, in terms
of the guidelines, could do a vacuum-extraction delivery, there was
no attempt to expedite the baby’s
delivery in that fashion. No
reasons were advanced for not expediting delivery. Clearly, the
appellant and the foetus did not receive
appropriate medical care. It
is a crying shame that a woman who was admitted to a hospital more
than 12 hours before the delivery
of her baby was neglected to the
extent that the appellant and her baby were. I echo the following
sentiments expressed by this
court in
Premier
of the Province of KwaZulu-Natal v Sonny and another
:
[56]
‘
In
our country poverty and a lack of literacy abound. Masses of our
people attend public health facilities. Their lack of sophistication
and the vulnerability that accompanies poverty are factors that
cannot be ignored. ... What is required is a public health delivery
system that recognises the dignity and rights of those who are
compelled to use its facilities. It is that basic sensitivity that
the Constitution demands.’
[65]
Prof Buchmann postulated that despite the substandard medical care
dispensed to the appellant, the baby’s injury was
not
preventable because the MRI scan showed that the injury was of an
acute profound pattern. This seems to suggest that (1) there
can be
no intervention during obstetric emergencies and (2) that substandard
management of a patient’s labour automatically
becomes
irrelevant once a hypoxic ischemic insult of an acute profound nature
has been identified as a cause of the HIE. Taken
to its logical
conclusion, it in essence, exempts the hospital staff from exercising
the requisite reasonable care and skill and
absolves them from
liability once an obstetric emergency occurs during labour. I find
this proposition perplexing. None of the
articles relied upon by the
expert witnesses suggested that there is a stage when intervention
becomes irrelevant because of an
obstetric emergency. The fact that
the guidelines lay down management procedures (interventions) in
respect of ‘emergencies
during labour’ renders that
proposition nugatory. That proposition is, in any event, at odds with
Prof Buchmann’s own
written article in which he concludes that
HIE-related death
can
be prevented
through close and careful monitoring. If that is accepted, then by
parity of reason, brain injury must also be preventable.
This
accords with the following proposition made in
Neonatal
Encephalopathy and Neurological Outcome
:
‘All women in labour should be monitored in an attempt
to
prevent “asphyxial” injury
and intrapartum death’.
[57]
(Emphasis added).
[66]
Even on the acceptance that there was a sentinel event in the form of
a cord compression, this did not exempt the respondent’s
medical staff from intervening. Dr Murray testified that a cord
compression shows itself by bearing down efforts which can be
observed if there is adequate monitoring. All experts agreed that a
severe cord compression is normally accompanied by marked
decelerations
of the foetal heart rate. The upshot is that if the
appellant’s labour had been properly monitored, these
decelerations would
have been observed and the intervention of
expedited delivery would probably have been executed. Dr Murray
emphasised that
in an emergency situation, the promptness of hospital
staff is key and every minute counts. She testified that even in
catastrophic
sentinel events such as the rupturing of the uterus or
the placenta, babies have been saved by prompt intervention of
hospital
staff. That evidence was undisputed.
[67]
As correctly stated in the court a quo’s judgment, Prof
Buchmann conceded that adequate monitoring would have been able
to
detect when the change in the foetal heart rate occurred. When the
evidence of the appellant is juxtaposed with the evidence
of all the
experts, the most plausible inference is that there were indeed
forewarnings, in the form of foetal decelerations, throughout
the
active phase of labour but these decelerations were not detected and
recorded due to the inadequate monitoring. On the basis
of the
undisputed evidence, it is highly probable that a caesarean section
would have been performed successfully before 06h00
if the
appellant’s labour had been properly monitored and managed.
[68]
Further, the guidelines provide that ‘time can only be allowed
for the head to descend onto the pelvic floor if fetal
distress and
cephalopelvic disproportion have been ruled out’.
[58]
As stated before, the partogram noted that Ringers Lactate, which
according to the guidelines is one of the interventions made
when
foetal distress is suspected, was being intravenously administered to
the appellant. The evidence shows that the other procedures
for the
management of foetal distress were not followed and no attempt,
whatsoever, was made to expedite delivery of the baby despite
the
attendant nurse having noted strong contractions and a full dilation
of the cervix at 06h00. In my view, the acute profound
insult that,
according to Prof Buchmann, occurred in the last thirty minutes of
labour would most probably have been averted if
the provisions of the
guidelines quoted in the afore-going paragraphs of this judgment had
been followed. In other words, the injury
would probably not have
resulted, but for the negligence of the hospital staff.
[69]
Nevertheless, I must say that it is of significance that Dr Buchmann
conceded, albeit with some qualification, that
the
risk of sub-standard monitoring was that ‘you will miss
something which you could act upon and prevent a bad outcome’.
On probabilities, this is exactly what happened in this case.
By failing to properly monitor the appellant’s labour
in
accordance with the provisions of the guidelines (the importance of
which has been emphasized by all the expert witnesses including
Prof
Buchmann), the hospital staff created a situation that placed the
foetus at a serious risk of HIE and its attendant
sequelae
.
This risk
precluded
the timeous execution of any measures designed to avert injuries
consequent upon suffering HIE. If that had been done,
the acute
profound injury that, according to Prof Buchmann, occurred in the
last 30 minutes of the appellant’s labour would
have been
averted. If a caesarean section was no longer an option due to the
foetal head having already been engaged, an expedited
vacuum
extraction delivery would probably have been successfully performed
at 06h00.
[70]
The study done by Yamada
[59]
and Prof Buchmann’s article are both relevant to probabilities
in relation to causation. Both studies conclude that sub-optimal
intrapartum care was the probable cause of HIE in the majority of the
studied cases. On probabilities, the brain injury sustained
by the
appellant’s baby would not have occurred had the appellant and
the foetus been properly monitored and managed by the
hospital staff.
I am satisfied that the evidence adduced on behalf of the appellant,
bolstered by Prof Buchmann’s concessions,
points to a causal
connection between the substandard care the appellant received from
the hospital staff during labour and the
acute profound hypoxic
injury sustained by her baby. Put in the language used by the court
in
Mashongwa
,
there is a ‘sufficiently close connection’ between the
negligence of the nurses that attended to the appellant and
the
damage that resulted. In the circumstances, causation has been
established on a balance of probabilities.
Conclusion
[71]
For all the reasons mentioned above, I would uphold the appeal with
costs.
_________________
MB
Molemela
Judge
of Appeal
APPEARANCES:
For
the Appellant: JJ Wessels SC
Instructed
by:
Nonxuba
Incorporated Attorneys, Rivonia
Webbers,
Bloemfontein
For
the Respondent: PJ De Bruyn SC (with him M Rili)
Instructed
by:
State
Attorney, Mthatha
State
Attorney, Bloemfontein
[1]
Telematrix
(Pty) Ltd t/a Matrix Vehicle Tracking v ASASA
2006 (1) SA 461
(SCA);
[2006] 1 All SA 6
;
[2005] ZASCA 73
para 12.
[2]
Mashongwa
v Passenger Rail Agency of South Africa
2016 (3) SA 528
(CC);
2016 (2) BCLR 204
;
[2015] ZACC 36
para
64.
[3]
Silva’s
Fishing Corporation (Pty) Ltd v Maweza
1957 (2) SA 256
(A);
[1957] 2 All SA 313
at 264A-B.
[4]
Lee
v Minister for Correctional Services
2013 (2) SA 144 (CC); 2013 (1) SACR 213; 2013 (2) BCLR 129; [2012]
ZACC 30.
[5]
Minister
for Correctional Services v Lee
2012 (3) SA 617
(SCA);
2012 (1) SACR 492
;
[2012] 2 All SA 586
;
[2012] ZASCA 23.
[6]
Lee
para 42.
[7]
Lee
para 63.
[8]
MJD
Wallis ‘Revel without a cause – Delictual liability
after Lee?’ (2019)
SALJ
165.
[9]
A
Fagan
Undoing
Delict: The South African Law of Delict under the Constitution
(2017) 216.
[10]
Lee
para 40.
[11]
Lee
para 41.
[12]
Mashongwa
para 65.
[13]
Mashongwa
para 66.
[14]
Lee
para 63.
[15]
There
are different ways of spelling the medical terms for foetus (fetus)
ischaemic (ischemic) etc. I have used the English spelling
in the
text but have retained the original spelling when used in quotes.
[16]
Lee
para 41.
[17]
S
Shankaran,
A
R Laptook,
S
A McDonald
,
S
R
Hintz
,
P
D
Barnes
,
A
Das
&
R
D
Higgins
‘
Acute
Perinatal Sentinel Events, Neonatal Brain Injury Pattern, and
Outcome of Infants Undergoing a Trial of Hypothermia for Neonatal
Hypoxic-Ischemic Encephalopathy’ (2017)
The
Journal of Pediatrics
180
275 at 276.
[18]
J
Rennie & L Rosenbloom ‘How long have we got to get the
baby out? A review of the effects of acute and profound intrapartum
hypoxia and ischaemia’ (2011)
The
Obstetrician and Gynaecologist
169 at 170.
[19]
A
Okumura, F
Hayakawa, T
Kato, K
Kuno
& K Watanabe
‘
Bilateral
basal ganglia-thalamic lesions subsequent to prolonged fetal
bradycardia’ (2000) 58
Early
Human Development
111.
[20]
D
Murray, M N
O'Riordan, R
Horgan, G Boylan, J R Higgins, C A Ryan
‘Fetal Heart Rate Patterns in Neonatal Hypoxic-Ischemic
Encephalopathy: Relationship with Early Cerebral Activity and
Neurodevelopmental Outcome’ (2009)
American
Journal of Perinatology
26:8 605 at 608.
[21]
J
F Pasternak & M T Gorey ‘The Syndrome of Acute Near-Total
Intrauterine Asphyxia in the Term Infant’
Pediatric
Neurology
18(5) 391 at 396.
[22]
F
G Cunningham, K J Lenovo, S L Bloom, C Y Spong, J S Dashe, B L
Hoffman, B M Casey & J S Sheffield
Williams
Obstetrics
24 ed (2014) at 496.
[23]
D
Murray et al op cit.
[24]
J
Rennie et al op cit.
[25]
AM
obo KM v MEC for Health, Eastern Cape
[2018] ZASCA 141.
[26]
AM
obo KM
p
ara
8.
[27]
AM
obo
KM
para 63.
[28]
E
J Buchmann and R C Pattinson ‘Babies who die from
labour-related intrapartum hypoxia: a confidential enquiry in South
African public hospitals’ (2006) 36
Tropical
Doctor
88.
[29]
Kruger
v Coetzee
1966 (2) SA 428
(A);
[1966] All SA 490
(A).
[30]
Jacobs
v Transnet Ltd t/a Metrorail
2015 (1) SA 139
(SCA);
[2014] ZASCA 113
para 6.
[31]
Pitzer
v Eskom
[2012]
ZASCA 44
para 24.
[32]
Kruger
at 430G.
[33]
Bee
v Road Accident Fund
2018 (4) SA 366
(SCA);
[2018] ZASCA 52.
[34]
Buchmann
and Pattinson at 10.
[35]
Ibid.
[36]
Ibid.
[37]
Mashongwa
para
63.
[38]
International
Shipping Co (Pty) Ltd v Bentley
1990
(1) SA 680
(A) at 700F-I.
[39]
Minister
of Safety and Security v
Van
Duivenboden
2002 (6) SA 431
(SCA) para 25.
[40]
Minister
of Finance & others v Gore NO
2007
(1) SA 111 (SCA); [2007] 1 All SA 309; [2006] ZASCA 98 para 33.
[41]
Mashongwa
para 65.
[42]
Mashongwa
para
68.
[43]
See
Matatiele
Municipality v President of RSA
2006 (5) SA 47
(CC);
2006 (5) BCLR 622
(CC);
[2006] ZACC 2
para 66.
[44]
Michael
& another v Linksfield Park Clinic (Pty) Ltd & another
2001 (3) SA 1188
(SCA);
[2002] 1 All SA 384
;
[2001] ZASCA 12
para
36.
[45]
Bolitho
v City and Hackney Health Authority
[1998]
AC 232
;
[1997]
UKHL 46
;
[1997] 4 All ER 771
;
[1997] 3 WLR 1151
at 241-242. Also
see
Daubert
v Merrell Dow Pharmaceuticals Inc
[1993] USSC 99
;
509
US 579
(1993).
[46]
See
Imperial
Marine Company v Motor Vessel Pasquale della Gatta & another;
Imperial Marine Company v Motor Vessel Filippo Lembo
& another
2012
(1) SA 58
(SCA);
[2012] 1 All SA 491
;
[2011]
ZASCA 131
para 26.
[47]
Rennie
and Rosenbloom at 171.
[48]
Rennie
and Rosenbloom at 173.
[49]
Pasternak
and Gorey at 396.
[50]
Buthelezi
v Ndaba
2013 (5) SA 437
(SCA);
[2013] ZASCA 72
para 1.
[51]
Rennie
and Rosenbloom at 173.
[52]
American
College of Obstetrics and Gynecologists & American Academy of
Pediatrics
Neonatal
Encephalopathy and Neurological Outcome
2ed (2014) at 90.
[53]
Linksfield
para
37.
[54]
Bee
v RAF
supra para 22.
[55]
See
Schneider
N.O. & others v AA & others
2010 (5) SA 203
(WCC);
[2010] 3 All SA 332
;
[2010] ZAWCHC 3
at 203 &
211.
[56]
Premier
of the Province of KwaZulu-Natal v Sonny and another
2011 (3) SA 424
(SCA);
[2011] ZASCA 6
para 33.
[57]
American
College of Obstetrics and Gynecologists & American Academy of
Pediatrics
Neonatal
Encephalopathy and Neurological Outcome
at 88.
[58]
See
excerpt of the guidelines at para 36 of this judgment.
[59]
T
Yamada, K Cho, M Morikawa, T Yamada and H Minakami ‘Intrapartum
risk factors for neonatal encephalopathy leading to cerebral
palsy
in women without apparent sentinel events’ (2015) 41(10)
Journal
of Obstetrics and Gynaecology Research
1 at 3.