N.K obo U.K v Member of the Executive Council for the Department of Health, Eastern Cape (CA 6/2023; 827/2019) [2024] ZAECBHC 2 (9 April 2024)

About SAFLII
Databases
Search
Terms of Use
RSS Feeds
South Africa: Eastern Cape High Court, Bhisho
SAFLII
>>
Databases
>>
South Africa: Eastern Cape High Court, Bhisho
>>
2024
>>
[2024] ZAECBHC 2
|

|

N.K obo U.K v Member of the Executive Council for the Department of Health, Eastern Cape (CA 6/2023; 827/2019) [2024] ZAECBHC 2; [2024] 3 All SA 882 (ECB) (9 April 2024)

SAFLII
Note:
Certain
personal/private details of parties or witnesses have been
redacted from this document in compliance with the law
and
SAFLII
Policy
IN
THE HIGH COURT OF SOUTH AFRICA
(EASTERN
CAPE DIVISION, BHISHO)
Reportable
Appeal
case no. CA 6/2023
High
Court case no. 827/2019
In
the matter between:
N[...]
K[...] on behalf of
U[...]
K[...]

Appellant
and
MEMBER
OF THE EXECUTIVE COUNCIL FOR THE
DEPARTMENT
OF HEALTH, EASTERN CAPE

Respondent
JUDGMENT
LAING
J
[1]
This is an appeal against the whole of the
judgment of the court
a quo
,
which previously dismissed the appellant’s claim for damages in
the amount R 28,200,000. The cause of action arose from
the alleged
negligence of the medical staff at Dora Nginza Hospital, Gqeberha,
during the birth of the plaintiff’s son, U,
on 8 March 2019.
BACKGROUND
[2]
The salient details of the parties’
respective cases, the trial proceedings, the findings of the court
a
quo
, and the application for leave to
appeal are described under the corresponding sub-headings below.
Appellant’s case
[3]
As plaintiff in the court
a
quo
, the appellant pleaded that she was
admitted to Dora Nginza Hospital on 3 March 2019 for delivery. She
endured five days of prolonged
labour before giving birth to U, who
suffers from cerebral palsy, mental retardation, and epilepsy.
[4]
It
was the appellant’s case that the defendant’s medical
staff had been negligent in their care. They had failed to,
inter
alia
,
properly assess and examine the plaintiff upon her admission,
appropriately monitor her labour and the well-being of the foetus,

and prevent U from sustaining brain damage at birth, when this could
have been avoided by exercising reasonable skill and diligence.
More
particularly, pleaded the appellant, the medical staff had failed to,
inter
alia
,
detect and prevent the onset of chorioamnionitis
[1]
and
the health complications associated therewith.
[5]
As a result of the above negligence, U has
endured pain, suffering, discomfort, the loss of amenities of life,
and total and permanent
disability. The appellant, in her personal
capacity, pleaded that she has experienced psychological shock and
trauma, limitations
on her freedom, and the loss of the joys of
parenthood.
[6]
She claimed damages in relation to U’s
future medical treatment, loss of earning capacity, and both special
and general damages.
The claim also made provision for,
inter
alia
, the costs for establishing and
administering a trust to hold any damages so awarded.
Respondent’s
case
[7]
In her plea, the defendant admitted that
the plaintiff had been at the Dora Nginza Hospital but denied that
she had endured a prolonged
five-day period of labour. If it was
found that the plaintiff had proved U’s medical condition and
injuries, then the defendant
pleaded that these could have occurred
at an antenatal stage because the plaintiff had contracted an
infection or chorioamnionitis.
This could have led to placental
insufficiency which, in turn, resulted in asphyxiation prior to the
onset of labour.
[8]
The defendant denied all allegations of
negligence. She asserted that the medical staff had,
inter
alia
, provided such care to the
plaintiff as would have been reasonably expected, including the
assessment and monitoring of the plaintiff,
and had acted in
accordance with accepted nursing and medical practice. The defendant
denied that the onset of chorioamnionitis
had been foreseeable or
that steps could have been taken to prevent it. Moreover, the
defendant denied that there had been repeated
vaginal examinations or
that these had caused the onset of chorioamnionitis. She pleaded that
the measurement of the umbilical
cord blood gas demonstrated that U
had not suffered from any fetal distress; such harm as was caused had
not occurred during labour
or delivery. The defendant pleaded that
the neurological problems suffered by U had arisen despite the
reasonable care provided
by the medical staff; there was no evidence
that the pathology which had led to U’s cerebral palsy had
emanated from labour
or that it had been preventable.
[9]
Consequently, the defendant denied that
there had been any cause of action. She denied that she was liable to
the plaintiff for
the damages claimed.
Trial proceedings
[10]
Prior to the commencement of the trial, the
parties agreed upon the admission of several joint minutes prepared
by the relevant
experts. These formed part of the trial bundle.
[11]
At the trial, the plaintiff testified on
her own behalf. She also relied on the evidence of an obstetrician
and gynaecologist, Dr
Constant Ndjapa; and a paediatric neurologist,
Dr Amith Keshave. The defendant, in turn, led the evidence of an
obstetrician and
gynaecologist, Dr Krzysztof Janowski; and a
paediatric neurologist, Dr Yavini Reddy. She also led the evidence of
a clinical manager
responsible for medico-legal matters at Dora
Nginza Hospital, Dr Ziefred McConney.
Findings of the court
a quo
[12]
The trial court held that there were two
issues for determination: the defendant’s negligence and
whether this had caused
the harm suffered. It assumed, without making
any finding, that the medical staff had indeed been negligent, and
proceeded to determine
the issue of causation, based on the medical
evidence and the plaintiff’s testimony. The trial court focused
on the question
of whether the cause of U’s brain damage had
been the onset of chorioamnionitis.
[13]
Ultimately,
the trial court found that there had been no evidence that
sub-standard monitoring had adversely affected the baby.
This was
because the plaintiff had indicated that, during the evening of 7
March 2019, prior to U’s birth on the following
day, a nurse
had checked the results of a cardiotocographic (‘CTG’)
[2]
reading and declared that everything had been satisfactory and that
the plaintiff would shortly be required to start the process
of
delivery. If there had been any problem at that stage, then the nurse
would have mentioned this. The plaintiff’s cervix,
moreover,
would not yet have been fully dilated.
[14]
The
trial court observed that the pH level for the baby, at birth, had
been normal.
[3]
There had also
been no evidence to demonstrate that reliance by the medical staff on
vacuum extraction and fundal pressure had
caused the brain damage.
The same could be said for the administration of misoprostol, used to
induce labour.
[15]
It was undisputed, said the trial court,
that the baby’s condition had been compromised at the time of
delivery. This was
in keeping with the diagnosis that his brain had
sustained an injury because of a significant lack of oxygen. The
question to be
determined was when the injury had occurred.
[16]
The
trial court accepted the evidence of the defendant’s experts,
Dr Janowski and Dr Reddy; their conclusions were based on
logical
reasoning and grounded in fact. The learned judge found as
follows:
[4]
‘…
the
answer as to when the child’s brain was injured lies in the
histological report on the evaluation of the placenta…
The
histological report would not have revealed that the chorioamnionitis
was acute and severe, exhibiting a fetal inflammatory
response with
the presence of funisitis
[5]
and vasculitis
[6]
unless the
mother contracted it a few days or weeks before the onset of labour.
That finding excludes a finding that the damage
to the child’s
brain occurred intrapartum. In the circumstances, I find that even if
it were proved that the prolonged second
stage of labour, induced
labour, and sub-standard monitoring may have caused damage to the
child’s brain, it would have happened
at a stage when the
child’s brain had already been damaged over a few days or weeks
by the insufficiency of oxygen and nutrients
from the placenta,
caused by chorioamnionitis.
…
In
other words, the probabilities indicate that the child’s brain
injury predated the prolonged second stage of labour, induced
labour,
and sub-standard monitoring. The damage to the child’s brain
might have caused or contributed to the plaintiff not
going into
labour on time, the prolonged second stage of labour, and the
difficulties with the delivery. The above finding means
that the
plaintiff failed to show that the prolonged second stage of labour,
induced labour, and sub-standard monitoring caused
the damage to the
brain of the plaintiff’s child. That being the case, the
plaintiff failed to establish that the defendant
is delictually
liable to her…’
[17]
Consequently, the trial court dismissed the
plaintiff’s claim with costs. She applied for leave to appeal.
Application for leave
to appeal
[18]
The plaintiff listed numerous grounds upon
which she based her application. She asserted that the trial court
had erred in its assessment
of the evidence and the balancing thereof
for purposes of the determination of probabilities, especially in
relation to the issue
of causation.
[19]
The trial court held that an appeal against
its findings enjoyed reasonable prospects of success. The learned
judge granted leave
to appeal against its findings that: (a) the
plaintiff had failed to prove that the damage done to U’s brain
had been caused
by the negligence of the medical staff prior to and
after the onset of labour; and (b) the plaintiff was liable for the
defendant’s
costs.
Grounds of appeal
[20]
The plaintiff asserts that the trial court
erred in failing to find that the negligence of the medical staff in
managing the intrapartum
and second stage of labour had caused the
injury to U’s brain. It also erred in its assessment of the
probabilities in relation
to the impact of chorioamnionitis on the
baby. The trial court, says the plaintiff, ought to have accepted her
undisputed evidence
that the baby had been hypoxic at birth, and that
the relevant medical staff had informed her that the injury had been
caused by
a delay in the delivery process and an insufficient supply
of oxygen to U’s brain. This contradicted Dr Janowski’s
views. These had, in turn, been at odds with those of Dr Reddy, who
had testified that the injury had been occasioned by asphyxia
or
hypoxia.
[21]
Furthermore,
contends the plaintiff, the court erred in failing to recognize the
improbability that a baby with such a serious brain
injury could have
survived
in
utero
without any indication of foetal distress. The defendant’s
experts had incorrectly conflated the presence of chorioamnionitis,

accompanied by funisitis, with the occurrence of the injury. The
trial court, argues the plaintiff, erred in failing to deal with
the
MRI
[7]
results
and the joint minute of the radiologists, who had agreed that there
had been no evidence of an infective or inflammatory
disease and that
such a condition was unlikely to have been the cause of the injury.
The plaintiff asserts that the trial court
ought to have found that
the injury had been caused by the medical staff’s failure to
have monitored, properly, the foetal
heart rate; the plaintiff’s
contractions over a period of three days; and the infusion of
syntocinon.
[8]
It had also been
as a result of their unsuccessful attempt at vacuum extraction and
application of fundal pressure during a prolonged
second stage of
labour, contrary to the maternity guidelines.
[9]
[22]
The plaintiff goes on to assert that the
trial court erred in accepting Dr McConney’s evidence to the
effect that the relevant
medical records had been removed from the
Dora Nginza Hospital without consent. It was incorrect to have found
that the Department
of Health could not have been blamed for this or
the resulting paucity of information pertaining to the medical
staff’s care
of the plaintiff and her baby.
[23]
A further ground of appeal was that the
trial court erred in its determination of the issue of causation
without first having decided
the issue of negligence. It also applied
the incorrect test for causation.
[24]
The
plaintiff contended that the trial court erred in failing to find
that the injury could have occurred intrapartum, especially
when Dr
Reddy had conceded that the Volpe criteria had been met.
[10]
It ought to have rejected her reliance on the histology report
regarding the condition of the placenta, considering the MRI results

and the joint minute of the radiologists. The plaintiff argues, too,
that the trial court erred in finding that the injury had
occurred
weeks prior to the birth, because of chorioamnionitis. It erred in
placing reliance on the umbilical cord blood gas measurement
and
erred in accepting Dr Janowski’s views to the effect that the
CTG reading had indicated that everything had been satisfactory.
It
also erred, says the plaintiff, in failing to consider Dr Ndjapa’s
views regarding the plaintiff’s contractions
in relation to the
supply of oxygen to U’s brain.
[25]
On a proper weighing of the probabilities,
considering the expert evidence, the trial court ought not to have
dismissed the plaintiff’s
claim. It ought to have determined
the merits and costs of the matter in her favour.
ISSUES TO BE DECIDED
[26]
Inasmuch as the grounds of appeal serve to
delineate the issues to be determined by this court, the questions
that lie at the core
of the dispute are the following: (a) whether
the defendant’s medical staff were negligent; and (b) whether
such negligence
was the cause of the injury to U’s brain. The
court must decide whether the trial court was correct in finding that
the plaintiff
had failed to prove, on a balance of probabilities,
that the above questions had been answered in the affirmative.
[27]
Before proceeding further, it may be
helpful to reiterate the basic principles involved. This is
especially so where the determination
of the dispute involves the
analysis of a complex matrix of fact- and opinion-based evidence.
LEGAL FRAMEWORK
[28]
Regarding
appeals on questions of fact, the erstwhile Appellate Division
observed, in
R
v Dhlumayo
,
[11]
that where there has been no misdirection on fact by a trial court,
the presumption is that its conclusions are correct; the appeal
court
will only reverse such conclusions where it is convinced that they
are wrong. Furthermore, where an appeal court is required
to decide a
case purely on the record, the satisfaction of the onus becomes
all-important. Subsequently, in
Van
Aswegen v De Clercq
,
[12]
the Appellate Division held that:
‘
[where]
the trial court has reached no finding at all on the credibility of
witnesses to vitally important incidents… [t]he
appellate
court has to do its best on such material as it has before it…
The onus should not be allowed to operate in such
a case unless and
until, after all the relevant evidence has been examined to see
whether there is a sufficient balance of probabilities
on one side or
the other, the state of inability to decide is reached.’
[29]
The
Supreme Court of Appeal, within the context of a medical negligence
case such as the present, had this to say in
HAL
obo MML v MEC for Health, Free State
,
[13]
per Makgoka JA:
‘
The
presumption is that a trial court’s factual findings are
correct in the absence of demonstrable error. To overcome this

presumption, an appellant must convince the appellate court on
adequate grounds that the trial court’s factual findings were

plainly wrong. If the appellate court is merely left in doubt as to
the correctness of a factual finding, then it will uphold that

finding. It is only in exceptional circumstances that an appellate
court will interfere with the trial court’s evaluation
of oral
evidence, in the light of the advantages enjoyed by the trial court
of seeing, hearing and appraising the witnesses.’
[14]
[30]
The
above principles pertain to appeals on questions of fact.
[15]
In relation to questions of opinion, the Supreme Court of Appeal
dealt with the role of an expert witness in
Pricewaterhousecoopers
Incorporated and others v National Potato Co-operative Ltd and
another
,
[16]
where Wallis JA remarked that:
‘
Opinion
evidence is admissible “when the court can receive ‘appreciable
help’ from that witness on the particular
issue”.
[17]
That will be when:
“…
by
reason of their special knowledge and skill, they are better
qualified to draw inferences than the trier of fact. There are some

subjects upon which the court is usually quite incapable of forming
an opinion unassisted, and others upon which it could come
to some
sort of independent conclusion, but the help of an expert would be
useful”.
[18]
As to the nature of an
expert’s opinion, in the same case, Wessels JA said:
“…
an
expert’s opinion represents his reasoned conclusion based on
certain facts or data, which are either common cause, or established

by his own evidence or that of some other competent witness. Except
possibly where it is not controverted, an expert’s bald

statement of his opinion is not of any real assistance. Proper
evaluation of the opinion can only be undertaken if the process
of
reasoning which led to the conclusion, including the premises from
which the reasoning proceeds, are disclosed by the expert.”’
[19]
[31]
Wallis JA went on to remark, further, that:
‘
Lastly
when dealing with the approach to an expert witness I have found
helpful the following passage from the judgment of Justice
Marie
St-Pierre in
Widdrington
:
[20]
“
Legal
principles and tools to assess credibility and reliability
[326] ‘Before any
weight can be given to an expert’s opinion, the facts upon
which the opinion is based must be found
to exist.’
[327] ‘As long as
there is some admissible evidence on which the expert’s
testimony is based it cannot be ignored; but
it follows that the more
an expert relies on facts not in evidence, the weight given to his
opinion will diminish.’
[328] An opinion based on
facts not in evidence has no value for the court.
[329] With respect to its
probative value, the testimony of an expert is considered in the same
manner as the testimony of an ordinary
witness. The court is not
bound by the expert witness’s opinion.”
[32]
The principles described above must serve
as a rudimentary framework for the analysis of the fact- and
opinion-based evidence that
follows. The finer details of such an
analysis will attract the need to have regard to the relevant case
law that has emerged in
the field of medical negligence.
[33]
It
would be salutary to revisit the test that must be applied, as
explained by Corbett JA in
Blyth
v Van den Heever
,
[21]
where he observed:
‘
As
I see it, this case resolves itself into three main questions: (i)
what factually was the cause of the ultimate condition of
appellant’s
arm; (ii) did negligence on the part of the respondent cause or
materially contribute to this condition in the
sense that respondent
by the exercise of reasonable care and skill could have prevented it
from developing; and (iii) if liability
on the part of respondent be
established, what amount should be awarded to appellant by way of
damages?’
[34]
The
above questions are pertinent to the present matter. They provide a
useful route map for the determination of the appeal. It
is
necessary, firstly, to consider how the injury to U’s brain
occurred factually, entailing an assessment of the evidence
regarding
the medical reasons for the injury.
[22]
It is necessary, secondly, to confront the questions that lie at the
core of the dispute: whether there was negligence on the part
of the
medical staff; and, if so, then whether this caused or materially
contributed to the injury in circumstances where the medical
staff
could have prevented it by exercising reasonable care and skill.
[35]
An analysis of the evidence follows.
AVAILABLE DOCUMENTARY
EVIDENCE
[36]
It would be best to commence with an
acknowledgement that there was very little ‘hard’
evidence before the trial court.
As to how much of it was admissible
formed the subject of considerable debate on appeal.
[37]
The
available documentary evidence consisted of a Road to Health Chart,
the MRI results that informed the radiological reports,
the
histopathology report in relation to the plaintiff’s placenta,
and the arterial blood gas (‘ABG’) analysis.
[23]
During argument, the plaintiff’s counsel contended that the
defendant, at trial, proved neither the histopathology report
nor the
ABG analysis because she failed to qualify or lead the experts
responsible for the compilation thereof. Consequently, the
documents
in question amounted to hearsay and ought to have been treated as
having been of no evidential value. To that effect,
counsel referred
to
Twine
and another v Naidoo and another
,
[24]
where Vally J restated the principles applicable to the use of
experts, including the requirement that his or her evidence must
be
capable of being tested, it must be verifiable.
[25]
In
HN
v MEC for Health, KZN
,
[26]
furthermore, Koen J referred to the academic work of DT Zeffertt and
AP Paizes
[27]
to emphasise
that:
‘
[s]tatements
in the medical records that are favourable to the defendant are
hearsay where the author thereof was not called to
testify, and hence
not admissible.
…
Recordings
favourable to the plaintiff’s case in establishing negligence
and liability generally, and accordingly damaging
to the defendant’s
case, made as part of the records kept by the defendant’s
servants, are however on a different footing.
They constitute
admissions by the servants of the defendant made in the ordinary
course of discharging their duties, which are
binding against the
defendant. The defendant’s staff are obliged to make these
statements by recording the medical position
as it unfolds in the
records. They have an obligation to speak on behalf of the defendant
and dispute what is recorded, if indeed
incorrect.’
[28]
[38]
In contrast, the counsel for the defendant
asserted that both the histopathology report and the ABG analysis had
been discovered
or had formed part of the trial bundle. They had been
considered by the various experts involved and had featured
extensively,
either in evidence or argument, throughout the duration
of the trial. From the record, it is not apparent that there has ever
been
a dispute about the admissibility of either document.
[39]
The
plaintiff’s grounds of appeal made no mention of this. Counsel
referred to
S
v Waldeck
,
[29]
where Kgomo JP remarked:
‘
[o]n
a conspectus of the evidence that has been dealt with hereinbefore,
some lesser aspects not specifically, I have no reservation

whatsoever that, although the defence did not expressly agree to the
admission of the hearsay evidence, the record is replete with

evidence to support the view that the defence has by conduct agreed
or acquiesced in the State’s procuring the hearsay evidence,

and that the State was entitled to conduct its case on that
basis.’
[30]
[40]
The
legislative mechanism by which hearsay evidence can be admitted is
section 3
of the
Law of Evidence Amendment Act 45 of 1988
. The
relevant provisions permit admission when a party against whom the
evidence is to be adduced agrees thereto. This pertains
to both
criminal and civil proceedings.
[31]
[41]
There
can be no doubt that the plaintiff, through her conduct and that of
her legal team, never challenged the admissibility of
the
histopathology report or the ABG analysis during the trial. Her
counsel had complete access to the documents well in advance;
her
experts had been aware of the contents and had freely referred
thereto in their reports and their testimonies. The findings
were
tested under cross-examination. Importantly, as the counsel for the
defendant pointed out, the alleged inadmissibility of
the documents
does not constitute a ground of appeal. It would be difficult not to
find that the plaintiff has, by conduct, agreed
or acquiesced to the
admission of the documents. There is every indication that the
provisions of
section 3(1)(a)
of the
Law of Evidence Amendment Act 45
of 1988
find application. If there had been any need to repudiate the
contents of the documents, then there would have been a duty on the

plaintiff to have done so at the appropriate time and no later.
[32]
For the plaintiff only to have raised an objection in her counsel’s
heads of argument on appeal, supplemented by notes that
were
submitted during argument, suggests that this was done simply as an
afterthought; it was never an issue during the trial.
[42]
There is no basis for the contentions made
by the counsel for the plaintiff. Both the histopathology report and
the ABG analysis
must be considered to have been part of the
documentary evidence that was properly available to the trial court.
How the injury
to U’s brain occurred must, at this stage, be
the focus of further discussion.
MEDICAL REASONS FOR
THE INJURY
[43]
The views of the experts involved in the
present matter played a decisive role in the determination of the
medical reasons for the
injury. This, in turn, had a direct bearing
on the outcome of the dispute in the trial court.
[44]
In
Pricewaterhousecoopers
Incorporated
,
[33]
Wallis
JA remarked that opinion evidence is admissible when an expert can
provide ‘appreciable help’ to the court on
a particular
issue.
[34]
The
learned judge went on to emphasize, however, the importance of
fact-based reasoning. Similarly, in
AM
and another v MEC for Health, Western Cape
,
[35]
Wallis
JA discussed the role of an expert as follows:
‘
The
functions of an expert witness are threefold. First, where they have
themselves observed relevant facts that evidence will be
evidence of
fact and admissible as such. Second, they provide the court with
abstract or general knowledge concerning their discipline
that is
necessary to enable the court to understand the issues arising in the
litigation. This includes evidence of the current
state of knowledge
and generally accepted practice in the field in question. Although
such evidence can only be given by an expert
qualified in the
relevant field, it remains, at the end of the day, essentially
evidence of fact on which the court will have to
make factual
findings. It is necessary to enable the court to assess the validity
of opinions that they express. Third, they give
evidence concerning
their own inferences and opinions on the issues in the case and the
grounds for drawing those inferences and
expressing those
conclusions.’
[36]
[45]
The
learned judge proceeded further to observe:
[37]
‘
The
opinions of expert witnesses involve the drawing of inferences from
facts. The inferences must be reasonably capable of being
drawn from
those facts. If they are tenuous, or far-fetched, they cannot form
the foundation for the court to make any finding
of fact.
Furthermore, in any process of reasoning the drawing of inferences
from the facts must be based on admitted or proven
facts and not
matters of speculation. As Lord Wright said in his speech in
Caswell
v Powell Duffryn Associated Colleries Ltd
:
“
Inference
must be carefully distinguished from conjecture or speculation. There
can be no inference unless there are objective facts
from which to
infer the other facts which it is sought to establish… But if
there are no positive proved facts from which
the inference can be
made, the method of inference fails and what is left is mere
speculation or conjecture.”
[38]
’
[46]
The existence or otherwise of objective
facts must, in the present matter, determine the weight that the
trial court ought to have
attached to the inferences made by the
various experts involved. This principle must be applied to the
opinion evidence that was
presented.
[47]
The analysis that follows is based
primarily on the available documentary evidence, as interpreted by
the experts. It is divided
accordingly.
The MRI results
[48]
The parties accepted the findings of two
radiologists, Dr Bates Alheit and Dr Zuzile Zikalala, whose joint
minute, prepared on 11
March 2021, was not in dispute and was
admitted as evidence. It is useful to replicate the contents thereof
in full:
‘
1.
This joint minute has been prepared between Dr B Alheit (BA) and Dr Z
Zikalala (ZZ). This joint agreement is presented as a constructive

attempt to present to the court the imaging features of the MRI brain
scan and to advance a diagnosis for the described pattern.
2. BA refers to the body
and comment of ZZ’s report.
3. BA agrees with ZZ that
the MR study displays features of hypoxic ischaemic injury of the
brain.
4. BA agrees that the MR
findings (as described by ZZ) make the diagnosis, in the appropriate
clinical context, of a dominant watershed
zone hypoxic ischaemic
injury of the brain.
5. BA
further submits that the atrophy of central structures and the
hyperintensities in these structures suggest additional PBGT/central

hypoxic ischaemic injury of the brain.
[39]
6. Thus the findings are
in keeping with a mixed pattern of dominant watershed zone hypoxic
ischaemic (prolonged partial pattern)
and PBGT/central hypoxic
ischaemic injury.
7. The experts agree that
the findings of the MRI study suggest that genetic disorders as a
cause of the child’s brain damage
are unlikely but not excluded
in light of the signal changes of the dentate nuclei and posterior
pons. Further clinical, genetic
and metabolic assessment is advised.
8. The experts agree that
there is no evidence of current or previous infective or inflammatory
disease on the various MRI sequences
and agree that inflammatory or
infective conditions are unlikely as direct causes of the child’s
brain damage.
9. The experts agree that
a review of the clinical and obstetrical records by appropriate
specialists in the field of neonatology
and obstetrics to be
essential in determining the cause and probable timing of this
hypoxic ischaemic injury.’
[49]
There was consensus that the MRI results revealed
a hypoxic ischaemic injury to the brain
. A mixed pattern was
evident, but the experts in question were unable to comment on cause
or timing. These aspects inform the analysis
that continues below.
Histopathology
report and ABG analysis
[50]
There was, as already noted, a limited amount of real evidence upon
which the trial court
could make its findings. Both the MRI results
and the Road to Health Chart were available but it seems that the
appeal must turn,
ineluctably, on the relevance and implications of
the histopathology report and the ABG analysis. These must be
considered within
the context of the opinion evidence of the experts
involved.
Dr
Constant Ndjapa
[51]
The plaintiff’s obstetrician and gynaecologist, Dr Ndjapa, was
adamant that the injury
had occurred during the intrapartum period.
He said that it had been caused by a combination of factors:
inadequate monitoring,
the use of misoprostol for induction;
prolonged labour, with repeated vaginal examinations that had led to
intrauterine sepsis;
and the inappropriate use of fundal pressure and
vacuum extraction. These had all been high-risk factors. Dr Ndjapa
stated, in
relation to the histopathological report, that there had
been no evidence that the onset of chorioamnionitis had taken place
during
the antenatal period. Dr Reddy’s views in that regard,
he said, had been purely speculative. The factors mentioned above,

all non-speculative and based on the plaintiff’s evidence, were
the most likely causes of the chorioamnionitis, leading in
turn to
placental insufficiency and associated hypoxia.
[52]
It is not apparent from the record, however, that Dr Ndjapa properly
dealt with the full
set of findings that emerged from the
histopathology report. He never addressed the
severity
of the chorioamnionitis, and the presence of chorionic vasculitis and
funisitis, and how these factors would have had a
bearing on the
timing of the injury. Regarding the ABG analysis, Dr Ndjapa was
reluctant to comment and deferred, instead, to the
views of the
paediatric neurologists. I am left with the impression, ultimately,
that his opinion evidence was incomplete and presented
gaps in
relation to an explanation of the factual cause of the injury.
Dr Krzystof Janowski
[53]
The
defendant’s obstetrician and gynaecologist, Dr Janowski,
challenged the impact of the factors mentioned by Dr Ndjapa.
He
testified that the plaintiff had not undergone an extended period of
induction; there was no evidence that the medical staff
had repeated
the initial administration of misoprostol, if that was indeed the
medication that had been used.
[40]
They had correctly carried out vaginal examinations, using a glove
with antiseptic cream; this had been done prior to the rupturing
of
the plaintiff’s membranes. The application of fundal pressure
and attempts at vacuum extraction, moreover, did not explain
the
condition of the plaintiff’s placenta.
[54]
The value of Dr Janowski’s views lay
in the detail and logic of the reasoning that he employed. He relied
on the ACOG criteria
(2003), based on research conducted by
MacLennan, for defining the causal relation between acute intrapartum
events and cerebral
palsy. This comprised four indicators: evidence
of metabolic acidosis in the umbilical cord or very early neonatal
blood samples
(i.e. a pH level that was less than 7.0), the early
onset of moderate to severe neonatal encephalopathy for infants of
more than
34 weeks’ gestation, cerebral palsy of the spastic
quadriplegic or dyskinetic type, and the exclusion of other
identifiable
aetiologies, such as trauma, infectious conditions, or
genetic disorders.
[55]
In
that regard, Dr Janowski testified that there were two items of
evidence that prevented the fulfillment of the ACOG criteria.
The
first item was the ABG analysis, which he described, with reference
to research conducted by Higgins,
[41]
as the most objective determination of foetal metabolic condition at
birth. The analysis demonstrated the absence of metabolic
acidosis,
the pH level had been 7.33; there was no indication that the injury
had occurred during labour.
[42]
He rejected Dr Keshave’s view that a high lactate level in the
analysis had demonstrated intrapartum hypoxia, saying that
ACOG had
never recognized this as a criterion; it was too unreliable and there
was a lack of consensus about the critical value
to be used when
determining evidence of metabolic acidosis. The second item was the
histopathology report, demonstrating an alternative
and identifiable
aetiology. The severe acute chorioamnionitis, as reflected in the
report, had been responsible for placental dysfunction
and the
deprivation of nutrients and oxygen to U’s brain. It had not
been detected because it was asymptomatic; there were
clinical
features or signs of it in only 15% of cases. The presence of
chorionic vasculitis and funisitis, entailing both a maternal
and a
foetal response, underlined the severity of the chorioamnionitis and
indicated that the process had taken time to develop.
The
radiologists’ findings, including the prolonged partial nature
of the injury, supported his views.
[56]
The counsel for the plaintiff challenged Dr
Janowski’s opinion evidence primarily on the basis that it was
undermined by that
of Dr Reddy, who confirmed that metabolic acidosis
had indeed been present. A proper examination of the record suggests
that this
was not the case. The closest that Dr Reddy came to this is
apparent from the relevant portion of the joint minute prepared with

Dr Keshave, which reads as follows:
‘
1.
AK:
[43]
Based on YR report of
March 2021, he agrees that there is spastic quadriplegic cerebral
palsy, with global developmental delay.
The clinical presentation is
in keeping with the ACOG criteria (2017), for the type of cerebral
palsy associated with intrapartum
hypoxic ischaemic injury.
YR:
Agrees with the
above statement
but would like to specify that antepartum and
postpartum hypoxic ischaemic insults can also result in the child
having spastic
quadriplegic cerebral palsy and global developmental
delay.
AK: As
per the birth anthropometry antenatally the insult is unlikely to
have occurred prior to 37 weeks gestation. Also, there
were no
postnatal insults to account for the current clinical picture. The
postnatal insult of seizures were as a result of the
neonatal
encephalopathy, and forms part of the syndrome- as described by JJ
Volpe (2018).’
[44]
[57]
As I understand it, Dr Reddy merely agreed
with Dr Keshave’s general statement that U’s condition
was typical for an
intrapartum hypoxic ischaemic injury, as envisaged
by the ACOG criteria. She immediately qualified her statement by
pointing out
that the condition could also result from both
antepartum and postpartum injuries. Dr Keshave replied in turn. This
is supported
by the explanation that she gave during
evidence-in-chief:
‘
So
I agree with Dr Keshave regarding the clinical condition of the
child. We are in full agreement with that and what I wanted to

specify is that antepartum and even postpartum… hypoxic
ischaemic insults can also result in exactly the same condition
in
the child. So you can have spastic quadriplegic cerebral palsy and
global developmental delay not only from an intrapartum insult.
There
are many causes of that condition.’
[45]
[58]
In her report, moreover, Dr Reddy referred
to the ACOG criteria (2014) and commented that:
‘
The
following neonatal signs are consistent with an acute peripartum or
intrapartum event:
·
Foetal umbilical artery pH less than 7.0,
or base deficit greater than or equal to 12 mmol/L, or both,
increases the probability
that neonatal encephalopathy, if present,
had an intrapartum hypoxic component; lesser degrees of acidemia
decrease that likelihood.
(
Not
fulfilled.
)
o
Blood gas shows a compensated metabolic
acidosis
with high lactate levels:
§
pH 7.33/ pCO2- 24.5/ pO2- 155/ Glucose-
7.1/ Lactate- 11.8/ HCO3- 16.1/ BD 13
o
If
there was acute intrapartum brain injury, the acidosis should not be
compensated. This implies that the insult may have been
prior to the
initiation of labour.’
[46]
[59]
Dr Reddy went on to emphasize:
‘
[U]
fulfils 3/6 ACOG criteria to determine an intrapartum cause of HIE.
The Apgar score and blood gas findings do not support an
acute
peripartum or intrapartum event.’
[60]
During her testimony, she stated as
follows:
‘
So
I am happy that this blood gas gives you a reasonable picture of what
the baby was at birth, I am not saying it is the most accurate

because I do not know exactly how it was taken, but I think it is
reasonable and for me the big thing here, is it was a compensated

metabolic acidosis. And what do I mean by this? I mean that this baby
had time to actually adjust to what was happening so there
was an
insult at some point but this child had the time to compensate and
that is why the pH was not lower.’
[61]
The record does not support counsel’s
contention that Dr Reddy undermined Dr Janowski’s opinion
evidence. Far from it.
If anything, the record demonstrates that the
defendant’s experts were entirely in agreement that the ABG
analysis had revealed
a compensated metabolic acidosis with a pH
level of 7.33, within the normal range.
Dr Amith Keshave
[62]
The plaintiff’s paediatric
neurologist, Dr Keshave, dealt with the ABG analysis by noting that
the lactate level of 11.6 had
been almost three times higher than
normal. This indicated severe acidosis at birth. There had been
anaerobic respiration, meaning
that, in the absence of sufficient
oxygen, U had depended on lactate to generate energy. Consequently,
Dr Keshave was of the view
that the ABG sample had not been obtained
at birth. The baby’s encephalopathic state would have led to
urgent attempts to
resuscitate and stabilize him, which would have
quickly corrected the pH level but not the lactate level, which would
have taken
considerably longer to recover. The sample could not have
been obtained from the umbilical cord because this would have been
removed
at birth, prior to resuscitation. That was the only way to
account for the ABG analysis, said Dr Keshave.
[63]
Under cross-examination, however, Dr
Keshave admitted that there was no record of the sample having been
obtained from the baby,
instead of the cord. He partially conceded,
too, the correctness of Dr Janowski’s assertion that the high
lactate level could
have been caused by an infection but asserted,
nevertheless, that it failed to account for the high oxygen level;
this could only
have resulted from resuscitation after an intrapartum
hypoxic ischaemic injury.
[64]
In
his report, Dr Keshave concluded that U’s condition at birth
had satisfied both the Volpe criteria (2018) and the ACOG
criteria
(2014) for an intrapartum hypoxic ischaemic injury. Regarding the
histopathology report, Dr Keshave addressed the presence
of
chorioamnionitis in the joint minute prepared with Dr Reddy. He
referred to an
academic
article by Harteman and others
[47]
and noted that U’s C-reactive protein (‘CRP’)
levels had been normal, suggesting that the presence of
chorioamnionitis
had played a lesser part than other factors.
[48]
He went on to assert, in testimony, that academic studies were
inconclusive in relation to the impact of chorioamnionitis on the

foetus; none of the cases considered had involved a prolonged second
stage of labour and neonatal encephalopathy. Dealing specifically

with the presence of chorionic vasculitis and funisitis, Dr Keshave
pointed out that there could be inflammation even during a
normal
pregnancy. There would have been signs of an infection, such as a
fever, but the inflammatory markers in this case had all
been normal.
There could have been changes in the markers between the time of the
collection of the placenta and the time of its
analysis at the
laboratory. U’s neonatal encephalopathy had to be considered
against the background of a prolonged second
stage of labour and the
complications that had followed, not just chorioamnionitis.
[65]
The record indicates that Dr Keshave addressed, to a limited
extent, the implications of chorionic vasculitis and funisitis. From

the opinion evidence of both Dr Janowski and Dr Reddy, these factors
had a significant bearing on the severity of the chorioamnionitis
and
the timing of the hypoxic ischaemic injury. It is not apparent from
Dr Keshave’s report, the joint minute, or his testimony,
that
sufficient attention was given to them to avoid the impression that
his views, specifically in this regard, tended to be superficial
in
nature and unsupported by any clear reference to studies or research.
Dr
Yavini Reddy
[66]
The defendant’s paediatric neurologist, Dr Reddy, expressed the
view that severe
acute chorioamnionitis with a maternal and foetal
inflammatory response, as reflected in the histopathological report,
had introduced
the possibility of placental foetal vascular
malperfusion (‘FVM’). This meant impaired foetal blood
flow and oxygenation,
thereby priming the baby’s brain for
injury. In her opinion, chorioamnionitis and the resulting foetal
inflammatory response
had led to placental insufficiency, resulting
in the hypoxic ischaemic injury that had caused U’s cerebral
palsy. It had
not been preventable. The injury, said Dr Reddy, was
likely to have occurred after 36 weeks’ gestation because there
had
been no intrauterine growth restriction, but prior to the onset
of labour. In her view, the injury would have occurred even if the

second stage of labour had not been prolonged.
[67]
At trial, Dr Reddy commented on the joint minute
that she had prepared with Dr Keshave. She testified that the ACOG
criteria were
merely guidelines; each case had to be considered
thoroughly and in its entirety. The International Cerebral Palsy Task
Force,
comprising a global affiliation of obstetric associations, had
emphasized that there must be an absence of all other proximal
factors,
i.e. factors that were present prior to the onset of labour,
before attributing neonatal encephalopathy to an intrapartum hypoxic

ischaemic injury. She testified that placental FVM was a new medical
concept, only emerging in the past ten to 15 years. There
was,
furthermore, no better way to understand what had happened at the
time of delivery than by studying the condition of the placenta;
the
histopathology report in the present case was decisive.
[68]
Dr
Reddy asserted that numerous studies demonstrated that placental
hypoperfusion, i.e. a reduced amount of blood flow through the

mother’s placenta to the foetus, can cause injury to the brain.
The process takes place over weeks. The reduced blood flow
places
stress on the foetal brain such that it cannot endure the normal
rigours of labour; there are no energy reserves to allow
the brain to
cope. The damage has already been inflicted. A reduced blood flow via
the umbilical cord has the implication that
less oxygen and fewer
nutrients reach the brain. Dr Reddy referred to an academic article
by Volpe
[49]
in
which he considered studies carried out on the role of placental FVM
in relation to neonatal HIE; the learned writer stated that,
in most
cases, it evolved over a sub-acute to chronic period prior to
delivery but not closer than approximately 48 hours. Volpe
went on to
observe that the studies also indicated that a state of impaired
foetal blood flow and oxygenation existed for many
days to weeks
prior to delivery. Consequently, said Dr Reddy, there was a basis
upon which to say that the onset of chorioamnionitis
in the present
case had not occurred over a period of hours or a day. The injury to
U’s brain had taken place during a four-week
period, after 36
weeks of gestation but prior to the onset of labour; it had not
occurred any earlier because there had been no
evidence of growth
retardation. She also referred to an article by MacLennan and
others
[50]
where
the learned writers used the findings of multiple epidemiological
[51]
studies
to contend that chorioamnionitis and funisitis were evidence of
infection that predated labour and were associated with
an increased
risk of cerebral palsy.
[69]
In relation to Dr Keshave’s reference to the
Harteman study, Dr Reddy stated that it supported her views. Studies
have shown
that milder degrees of chorioamnionitis, with only a
maternal inflammatory response, create a lower risk of injury to the
foetal
brain; in contrast, more severe degrees of chorioamnionitis,
with thrombosis and a foetal inflammatory response, create a much
higher risk. The severe acute chorioamnionitis of the placenta, as
identified in the histopathological report, created a considerably

higher risk of abnormalities in the foetus than a prolonged second
stage of labour. Dr Reddy strongly asserted that the presence
of such
chorioamnionitis had led to the impairment of blood flow, meaning
that less oxygen and fewer nutrients had reached the
foetus, thereby
causing damage to U’s brain. This occurred prior to the
commencement of labour.
[70]
Whereas Dr Reddy agreed with Dr Keshave about the
importance of foetal monitoring, this did not contradict the findings
of the academic
studies that she had mentioned. A prolonged second
stage of labour led to foetal abnormalities in a much smaller
percentage of
babies when contrasted with outcomes involving the
presence of severe acute chorioamnionitis, such as that in the
present case.
[71]
Dr Reddy’s opinion evidence was influenced
primarily by the histopathology report. Her fact-based approach,
clear reasoning,
and references to studies or research to
substantiate her conclusions were indeed persuasive, as the trial
court found.
Discussion
[72]
The trial court agreed with Dr Janowski and
Dr Reddy that the answer to the question of when U’s brain was
injured lay in
the histopathological report. It found that the
conclusions reached in relation thereto by the above experts were
based on logical
reasoning that was grounded in fact. I am unable to
fault the trial court’s findings in this regard.
[73]
To a greater or lesser extent, Dr Reddy’s
opinion evidence was the fulcrum upon which the proceedings in the
trial court balanced.
Unsurprisingly, the plaintiff’s counsel
directed his attack accordingly on appeal. The main elements of his
attack must be
considered further.
Volpe and ACOG
criteria
[74]
It was argued that Dr Reddy effectively
conceded that both the Volpe and the ACOG criteria had been met. A
close examination of
the record, however, reveals this not to have
been the case; she asserted that there was no indication from either
the available
neonatal records or the plaintiff’s evidence that
there had been foetal distress; the results of the ABG analysis were
not
typical for intrapartum asphyxia. The following exchange during
cross-examination is pertinent:
‘
MR
MALUNGA:       Dr Reddy, if we then
look at the criteria of Volpe, which we all agree is almost
the Bible
for this.
DR REDDY:
No, absolutely not. Not the Bible in any
way, shape, or form. We use
it because unfortunately most people do put it in their reports so we
do use it. Volpe is a very respected
neonatal specialist… but
his criteria… it is actually not criteria, it is just his- the
things that he recommends,
it is not like [the] ACOG criteria which
have been adopted by societies all over the world.’
[75]
Counsel continued, referring to U’s
need for resuscitation, the low Apgar scores, compromise at birth,
and seizures within
48 hours:
‘
MR
MALUNGA:       And that was the
evidence of Dr Keshave that all these factors, if giving a timing
to
this particular injury…, were the factors that pointed to an
intrapartum injury.
DR
REDDY:
What I would put to you, is if Volpe had
to- remember this book, I
think it came out, these criteria, in 2016, around there, and like I
mentioned earlier, placental studies
have been recent and it is
evolving. So Volpe has not included it yet in his criteria but every
obstetric association in the world
has now included placental
histology into their assessment of a child with compromise.
So
yes, counsel, I do agree that the Volpe criteria, it is met in a very
loose way but the ACOG criteria were not met. So there
was a
discrepancy between the Volpe criteria and the ACOG criteria and I
think it is too simplistic to use three criteria when
we know that
there is a lot more happening with this case.
’
[52]
[76]
Insofar as Dr Reddy conceded that the Volpe
criteria had been met, in a ‘very loose way’, she
unequivocally rejected
the assertion that the ACOG criteria had been
satisfied. Importantly, she attached significantly more weight to the
authority of
the latter, for reasons apparent from the above
exchange.
Hypoxia at birth
[77]
The assertion was made by counsel that Dr
Reddy conceded that U had been born with hypoxia. Further examination
of the record again
indicates otherwise. She agreed that the baby had
been compromised at birth and that this had been because of a hypoxic
injury
to the brain; she also conceded that a hypoxic event may occur
during a period of sub-standard monitoring. Dr Reddy went on,
however,
to emphasize that the injury in this case took place in the
days or weeks before birth.
Thrombosis
[78]
The plaintiff’s counsel argued that
Dr Reddy’s evidence was far from consistent or entirely cogent.
She withdrew, crucially,
her submissions regarding thrombosis. The
following extract from the record is relevant:
‘
DR
REDDY:
So with the placenta, over weeks this is happening,
where the blood
flow from the mother to the child is less than it should be, it is
not optimal… it is basically the blood
flow through the
umbilical cord from the placenta, going into the brain that is
affected. It is less oxygen, less nutrients and
less flow and we know
that happened for a fact, because when you look at the placenta, the
vessels are thrombosed and what that
means when the vessels are
thrombosed, means that there is blockages. So there is actually
physical blockages where the blood needs
to flow in, it has been
blocked. And you know, that is how the damage to the brain happens.
There are other mechanisms, the inflammation
for example, causes
certain signals to go to the brain that also makes it more likely to
be damaged but the main effect is actually
lack of oxygen and lack of
blood flow.’
[79]
Dr
Reddy consequently referred to the Volpe article,
[53]
pointing out that it was published after his book and that it
addressed placental hypoperfusion directly. The extract from the

record continues:
‘
DR
REDDY:
…So Volpe did an editorial…and in
this he was looking
at a study [on]… placental [hypo]perfusion…:
“
The
placental findings of foetal vascular malperfusion…”
And
that is what I explained earlier, so not enough blood flow from the
mother to the child:
“
are
considered to be secondary to chronic, partial or recurrent
intermittent obstruction of umbilical blood flow, thereby leading
to
umbilical venous obstruction, and, as a consequence, venous
congestion, stasis, thrombosis in severe cases.”
So we have thrombosis in
this placenta, so we know that it was a severe case.
“
The
consequences for the foetus would be expected to include impaired
foetal blood flow and oxygenation, and ultimately cardiac

insufficiency…”
So if it goes on for a
certain time, the heart is also affected.
“
[a]nd
compromised cerebral blood flow and oxygenation…”
That is impaired blood
flow to the brain and what is very important is the last four lines:
“
Based
on histological features, foetal vascular malperfusion is considered
to evolve in most cases over a sub-acute to chronic period
prior to
delivery and not closer to delivery than approximately 48 hours
prior.”’
[80]
It subsequently became apparent that Dr
Reddy had misinterpreted the histopathology report in relation to the
presence of thrombosis.
She eventually conceded that it had been
absent. She remained adamant, nevertheless, that the risk of injury
to the foetus remained
significant. The following extract pertains:
‘
DR
REDDY:
Absent. Okay, so sorry, that was my- because I
understood it as
congested or thrombosed in terms of the foetal surface. So sorry, so
the thrombosis is not there,
but
it is still a severe foetal inflammatory response. So the risk may go
from 99 percent to 70 percent in terms of probability.
’
[54]
[81]
She stated further:
‘
DR
REDDY:
…So there was severe acute chorioamnionitis
with a maternal
and foetal inflammatory response; so we know that the foetal
inflammatory response gives you a much higher risk
of damage to the
placenta. So I will withdraw my statement about the foetal placental
thrombosis from the previous report. But
like I said,
severe
acute chorioamnionitis with a foetal inflammatory response still
gives you a high probability of damage to the foetus
…’
[55]
[82]
It cannot be held, as the plaintiff’s
counsel suggested, that Dr Reddy’s concession deprived her
views of consistency
or cogency. The only material effect was to
reduce the risk factor. What cannot be ignored is Dr Reddy’s
opinion evidence
that severe acute chorioamnionitis in the placenta,
with a maternal and a foetal inflammatory response, posed a
considerably higher
risk of injury to the foetus; she put this as
high as a 70% probability. The concession had no impact whatsoever on
her views regarding
the severity and timing of the injury.
Causative effect of
chorioamnionitis
[83]
The
plaintiff’s counsel went on to contend that Dr Reddy had failed
to explain, clearly, the causative effect of chorioamnionitis
on U’s
brain. She had not described how or when this had occurred. A close
examination of the record, however, reveals that
Dr Reddy described
in detail how the severe nature of the chorioamnionitis, with both a
maternal and a foetal inflammatory response,
had given rise to
placental FVM; the compromised flow of blood and oxygen from the
placenta had created the hypoxic ischaemic event
that had caused the
damage to U’s brain, manifesting, ultimately, as cerebral
palsy. This had occurred over a period of days,
if not weeks, before
birth, based on Volpe’s recent article.
[56]
She relied, too, on the article by MacLennan and others to assert
that the presence of funisitis meant that the infection had pre-dated

the commencement of labour.
[57]
The radiologists’ findings did not undermine her views.
Infective or
inflammatory disease
[84]
It
was the argument of the plaintiff’s counsel that Dr Reddy’s
evidence conflicted with that of the radiologists since
they found
that there had been no sign of any injury or condition of an
inflammatory nature. Their joint minute stated that there
was no
evidence of ‘current or previous infective or inflammatory
disease on the various MRI sequences’; they went
on to agree
that ‘inflammatory or infective conditions are unlikely as
direct causes of the child’s brain damage’.
[58]
Dr Reddy dealt with the argument as follows:
‘
DR
REDDY:
…there is direct causes, so infection is
an unlikely a direct
cause of this injury; I agree wholeheartedly with that but it needs
to be qualified and they [the radiologists]
have not explained
themselves well, unfortunately, in those joint minutes. What they are
referring [to] is direct infections of
the brain.
I
have never said the baby has a direct infection of the brain, the
infection is of the placenta, that caused impaired blood flow
to the
brain.
So I am not arguing with that
but what they are referring to is a meningitis, so infection of the
covering of the brain that can
give you certain characteristics on
MRI. They would be referring to an abscess; so if you get infection
going directly to the brain,
it can cause a brain abscess. There are
other viral infections that we know can occur in new-born babies:
CMV, toxoplasmosis…
that can give you [a] typical picture on
MRI.
So when they say that it is not due
to direct infection, it has nothing to do with chorioamnionitis. They
are talking about something
else
.
COURT:
Could
chorioamnionitis not- your evidence is that is that is the
cause.
DR REDDY:
Yes, but
it is an indirect cause
.
COURT:
Albeit
over a long time, but it is the cause, on your evidence, of
the injury.
DR
REDDY:
But you could never see it on the MRI. So
the MRI of the baby’s
brain can never give you a window into what the cause was. So that is
why they would have no way of
excluding chorioamnionitis as a cause.
They
would only be able to exclude direct infection to the brain which we
have never said that this child has
.’
[59]
[85]
The defendant’s counsel pointed out
that Dr Keshave had admitted, at trial, that a severe infection could
lead to a compromised
supply of oxygen to the brain. It was only a
direct infection of the brain, such as meningitis, that had been
ruled out.
Acute profound and
partial prolonged injury
[86]
Regarding the contention of the plaintiff’s
counsel that Dr Reddy had only addressed the question of causation in
relation
to an acute profound injury, instead of a prolonged partial
injury, this is simply not supported by the record. At best, she
indicated
that chorioamnionitis could have primed U’s brain for
a subsequent acute insult. It had, however, already damaged the brain

over a period of days if not weeks beforehand, corresponding with the
prolonged partial pattern that was identified by the radiologists.

There was no indication, moreover, of any intrapartum hypoxic
ischaemic event, either of a prolonged partial or an acute profound

nature, based on the histopathological report and the ABG analysis.
Opinion evidence
[87]
Finally, mention must be made of the
assertion by the plaintiff’s counsel that Dr Reddy was unable
to provide opinion evidence
on possible factual causation, including
supplementary causation, during labour. The underlying premise for
this seems to have
been that a paediatric neurologist was qualified
to express a view, as an expert, on events occurring only from the
moment of birth
onwards; prior to this, i.e. during labour, the
relevant expert was an obstetrician such as Dr Janowski.
[88]
The
in
utero-
birth
divide serves as a useful distinction between the respective roles of
the experts involved. It must, however, not be treated
as a heavily
guarded border between sovereign states, preventing movement between
the two territories. There will be a transition
zone where the
expertise and experience of the experts overlap, allowing a court to
consider, at the very least, the opinion evidence
placed before it.
The court must then decide, in accordance with the usual principles
of fact-based reasoning, whether such evidence
offers ‘appreciable
help’ in the adjudication of the dispute, as Wallis JA remarked
in
Pricewaterhousecoopers
Incorporated
.
[60]
Experts in the medical field do not operate in hermetically sealed
compartments, as the learned judge went on to observe in
HAL
;
[61]
the court is entitled to the full picture.
[89]
In the present matter, the defendant’s
counsel requested Dr Reddy to respond to Dr Keshave’s view that
the management
and effect of chorioamnionitis was best commented upon
by an obstetrician or a pathologist. She stated:
‘
DR
REDDY:
So that is where I have to disagree with Dr Keshave
very vehemently.
You know, as a paediatric neurologist, it is our job to look -at
anything that can affect the brain and this is
one of the big factors
that recently have been identified as affecting perfusion to the
brain. So I would not defer comment on
this to anybody, I am happy
that I have sufficient expertise to comment on the chorioamnionitis…
MR NABELA:
So, in other words, what you are telling this court,
is that Dr
Keshave was wrong that it is only [an] obstetrician who can comment
only [sic] on chorioamnionitis?
DR REDDY:
Yes, so in terms of the chorioamnionitis,
obstetrician, yes, in terms
of the cause I would say, you know, they are probably the experts on
the cause of the chorioamnionitis,
but in terms of the effect of the
chorioamnionitis, I would argue that I am also an expert on that.’
[90]
Notwithstanding the above response, it is
vitally important not to overlook Dr Reddy’s view, based on the
article by MacLennan
and others, that the presence of funisitis
indicated that the onset of chorioamnionitis had, in fact, pre-dated
the commencement
of labour. This assertion was never properly
disputed or challenged.
What, factually, was
the cause of the injury?
[91]
Returning
to the test described by Corbett JA in Blyth,
[62]
the determination of the factual cause of the injury to U’s
brain, i.e. the medical reasons, must be decided before addressing

the question of the negligence of the medical staff involved. This is
no easy task when confronted with the specialized nature
of the
subject, the lack of consensus amongst the experts, and the almost
complete absence of proper medical records. Counsel for
the defendant
referred to
Buthelezi
v Ndaba
,
[63]
where
Brand JA observed:
‘
The
human body and its reaction to surgical intervention are far too
complex for it to be said that, because there was a complication,
the
surgeon must have been negligent in some respect.’
[64]
[92]
This is, with respect, a particularly apt
observation. It is unnecessary to strive, at one extreme, for
absolute clarity and unwavering
certainty about the reasons for an
injury and whether the medical practitioners involved must be held
accountable. The courtroom
is not a scientific laboratory. At the
other extreme, causation and delictual liability cannot be decided
merely on a balance of
possibilities. The role of the court, reduced
to its essence, is to evaluate the available evidence and to
adjudicate the dispute
based on whether the plaintiff has on a
balance of probabilities proved his or her case. Within the context
of an appeal, the court
must, of course, decide whether the trial
court successfully performed such a role and whether its findings
were indeed correct.
[93]
In the present matter, the plaintiff failed
to produce sufficiently compelling factual or opinion evidence to
persuade the trial
court that the views of Dr Reddy and Dr Janowski
were wrong. No real alternative was presented to deal, effectively,
with the pleaded
defence in relation to how the injury to U’s
brain happened.
[94]
Having
assessed, on appeal, the views of the experts in light of the
principles of fact-based reasoning, I am satisfied that the
probable
medical reason for the injury was a hypoxic ischaemic event or events
that resulted from placental FVM to which the severe
acute
chorioamnionitis, identified in terms of the histopathological
report, gave rise. This (or these) had taken place prior to
the
commencement of labour. It is also clear from the opinion evidence
that no investigation of the possible causes of a hypoxic
ischaemic
injury is complete, in circumstances such as these, without properly
considering the placental histopathology and arterial
blood gas.
[65]
[95]
It is necessary to proceed to the next
stage of the enquiry. The question to be answered is whether any
negligence on the part of
the medical staff involved caused or
materially contributed to the injury when this could have been
prevented.
NEGLIGENCE AND
CAUSATION
[96]
Negligence is the immediate issue to be
considered. If there had been negligence on the part of the staff,
then it must yet be decided
whether the requirements for causation
were met in the trial court.
Negligence
[97]
At the outset, it must be noted that the
trial court made no finding regarding negligence. The relevant
extract from the judgment
reads as follows:
‘…
To
succeed in her delictual claim, the plaintiff was required to prove
that the treating staff wrongfully and negligently caused
the damage
to her child’s brain. What was in issue were the elements of
negligence and causation. I will examine the issue
of causation
on
the assumption, without finding, that the treating staff were
negligent
by causing the plaintiff to endure a prolonged and protracted labour,
subjecting her to sub-standard care by not monitoring her
and the
child at regular intervals, attempting to vacuum extract the child
and applying fundal pressure and failing to intervene
after
misoprostol had been given to her. In the determination of causation,
the medical evidence will be considered against the
background of the
plaintiff’s evidence.’
[66]
[98]
The focus moves away at this stage from the
expert’s views to the evidence of the plaintiff herself,
necessitated by the paucity
of available documentary evidence as
already discussed. The extent to which the plaintiff’s evidence
is still relevant, after
the findings made in relation to factual
causation, must be explored further.
[99]
The
defendant’s counsel argued that the plaintiff was completely
unreliable as a witness and provided examples of why this
was so. To
this, the plaintiff’s counsel pointed out that the trial court
had never been required to determine her reliability;
the defendant’s
counsel had indicated that the dispute pertained to issues of
causation, not negligence. Consequently, asserted
the plaintiff’s
counsel, an appeal court cannot readily interfere with the trial
court’s acceptance of the plaintiff’s
evidence where it
had been undisputed. The authority upon which he relied, however,
viz.
Santam
Bpk v Biddulph
,
[67]
does
not appear to prevent this entirely. To that effect, Zulman JA held
as follows:
‘…
Whilst
a court of appeal is generally reluctant to disturb findings which
depend on credibility it is trite that it will do so where
such
findings are plainly wrong… This is especially so where the
reasons given for the findings are seriously flawed. Over-emphasis
of
the advantages which a trial court enjoys is to be avoided lest an
appellant’s right of appeal “becomes illusory”
…
It is equally true that findings of credibility cannot be judged in
isolation but require to be considered in the light
of proven facts
and the probabilities of the matter under consideration.’
[68]
[100]
The
learned judge went on to hold that the proper test was not whether a
witness was truthful or indeed reliable in all that he
or she says
but whether, on a balance of probabilities, the essential features of
his or her story were true.
[69]
The same principles potentially find application in the present
matter.
[101]
Both
Dr Ndjapa and Dr Keshave pointed out multiple high-risk factors that
were present during the labour process. These included
the
administration of misoprostol, inadequate monitoring, repeated
vaginal examinations, a prolonged second stage of labour, the

application of fundal pressure, and several failed vacuum attempts.
The key factor that emerged from the trial proceedings,
however, was
whether there had been negligence in the monitoring of the plaintiff.
The remaining factors, whether considered individually
or
collectively, did not seem to have played as important a role. There
was no conclusive evidence that the ‘mixture’
taken by
the plaintiff had indeed been misoprostol;
[70]
Dr Janowski mentioned that the plaintiff had testified that the staff
had used gloves and antiseptic cream when conducting vaginal

examinations; he also observed that she had testified that the baby’s
head had started to protrude, prompting the use of
fundal pressure
and vacuum extraction, which were the most practical options
available when preparation for a caesarean section
delivery would
have taken too long; and Dr Reddy referred to academic studies to
contend that a prolonged second stage of labour
was a low-risk
factor, between 0.4% and 1.29%, for a hypoxic ischaemic event.
[71]
[102]
The
plaintiff’s testimony that a medical practitioner had informed
her that insufficient oxygen and a delay in giving birth
had caused
the brain damage does not take the matter much further. The
plaintiff’s counsel suggested that the trial court
ought to
have applied the principles set out in
HN
,
[72]
discussed earlier, to find that the above evidence was an admission
of negligence on the part of the defendant. Considering the

histopathology report and ABG analysis, however, the medical
practitioner had no proper factual basis upon which to have made such

an assertion at the time.
[103]
Returning
to the monitoring of the plaintiff, it is apparent from her testimony
that CTG readings were indeed taken. She testified
that a ‘machine’
had been placed on her stomach twice in a day but whether this was
done in accordance with the benchmark
was highly contested.
[73]
Significantly,
Dr Janowski conceded that the monitoring had indeed been
sub-standard. What is clear from the record, however, is
that at no
stage was there any indication of foetal distress. The plaintiff
stated that, as late as the evening of 7 March 2019,
when she had
already been admitted to the labour ward, the ‘machine for
heartbeat’ was applied and the following ensued,
as indicated
in the record:
‘
MS
KETSHE:
After some time, she [the nurse] came up and looked at a
print-out
that was coming out of that machine; then she said everything was
becoming alright [sic] and I was going to start pushing.
[104]
There is simply no evidence that the
condition of the baby, at any stage prior to birth, gave cause for
concern, notwithstanding
possible sub-standard monitoring. The chief
contention made by the plaintiff’s counsel was that proper
monitoring, including
the conducting of regular CTG readings, would
have alerted the staff to signs of foetal distress during the
intrapartum period,
allowing necessary action to be taken in good
time. This never happened. They failed, argued counsel, to prevent
injury that occurred.
[105]
Dr Janowski and Dr Reddy both expressed the
view, however, that the injury had not occurred during the
intrapartum period. The facts
and reasoning upon which their view was
based were canvassed at some length in the investigation of the
medical reasons for the
injury.
[106]
Each of the defendant’s experts,
moreover, expressed the view that the nature of the chorioamnionitis
had been asymptomatic.
The following extract from the
cross-examination of Dr Janowski pertains:
‘
MR
MALUNGA:       Doc, how long would it
take for the onset of acute chorioamnionitis?
DR JANOWSKI:
To develop?
MR MALUNGA:
Yes.
DR JANOWSKI:
We do not know, because there are no symptoms, but definitely before
the onset
of labour.
MR MALUNGA:
I think the first part of your answer, Doc, is you do not know,
because it
does not have symptoms?
DR JANOWSKI:
Yes, it is asymptomatic. Patient did not have any symptoms. And as I
have said
yesterday only in 15 percent of acute chorioamnionitis
there are symptoms of- symptoms of clinical chorioamnionitis like a
tenderness,
temperature is high- high temperature and a high pulse
rate.’
[107]
He went on to deal with the timing of the
onset of chorioamnionitis before returning to the question of whether
proper CTG monitoring
would have detected it. The relevant extract
from the record reads:
‘
MR
MALUNGA:       Whilst… you would
exclude the hypoxic event occurring between the sub-standard

monitoring… do you agree… you could not time when the
chorioamnionitis happened?
DR
JANOWSKI:       Yes, I will repeat
myself. We do not know
because
there were no signs
;
that is why I will repeat again, that is why we keep the placenta as
a black box which can tell us what was happening.
[74]
We do not know, but taking into consideration that that result, the
presence of maternal response, foetal response, the severity
of that
acute chorioamnionitis and I will say it clear, M’Lord, it did
not happen with that short period of time when she
was admitted or
when she was induced or when she was five times examined with
unsterile gloves and… when somebody tried
to rupture the
membranes, no, no. That is not, it cannot happen like this, not that
severity of acute chorioamnionitis, it takes
time, it has to develop
over certain- how long before delivery? Maybe two weeks, maybe week,
maybe three weeks, we do not know.
And even more… is just to
add, M’Lord…
the
problem is that there are no tools right now, even doing CTGs, to
predict that maybe there is an infection
.
There are no tools because it is like the typical pattern that
something is happening…
Unfortunately
that is the problem, that is why it is silent, there are no warning
signals, it is happening without any warning,
that is why it is so
important to check the placenta
…’
[75]
[108]
From Dr Janowski’s evidence, CTG
monitoring was an inadequate tool for the proper detection of an
infection and the onset
of chorioamnionitis in circumstances such as
these. The examination of the placenta, after delivery, was
imperative.
[109]
The limitations of CTG monitoring were
emphasized, too, by Dr Reddy. She was asked, under cross-examination,
whether the CTG reading
would have been normal in a situation where,
upon admission of the mother for labour management, the foetus had
already been compromised.
She stated:
‘
DR
REDDY:
Yes, and I will give you a good example, we deal
with it all the
time. Children with a perinatal stroke… if the child has had a
stroke
in utero
,
it might have occurred at any time; or a child that is… born
without half [of] the brain… the CTG is completely
normal
because the injury did not occur at that time. So you can have severe
brain malformations and severe problems with the brain
and you can
have a normal CTG… Because you must remember that the foetal
heart rate is actually controlled from the brain
stem. So not the top
part of the brain, it is where the little stem that comes down, that
controls [the] heart rate and unless
there is specific damage there
or there is something acute happening, you can actually a very
compromised brain injury and a normal
CTG…’
[110]
Her explanation also addresses the argument
made by the plaintiff’s counsel that it was a fundamental
improbability that U
could have survived
in
utero
for such a lengthy period without
any signs of foetal distress. From Dr Reddy’s opinion evidence,
this was indeed a possibility,
at the very least.
[111]
Dr Reddy commented, moreover, on the
potentially asymptomatic nature of chorioamnionitis. The following
exchange took place during
cross-examination:
‘
MR
MALUNGA:       Okay, now as to the
timing of that injury, you testified that the probable timing
is
anything from 37 weeks to birth… I put to you, Doc, that if
the chorioamnionitis had occurred during that period, there
would
have been infective markers with the mother in that there would have
been a temperature, a fever… if it happened within
four weeks
prior to… [intervenes]
DR
REDDY:
No, I disagree. As Dr Janowski mentioned,
this
is sub-clinical chorioamnionitis or histological chorioamnionitis,
which is far more common than clinical chorioamnionitis
.
So clinical chorioamnionitis is where there is a fever in the mother,
you can have abdominal pain, the septic markers go up. That
is
actually very unusual so it is actually more common to have
sub-clinical or silent chorioamnionitis like in this case.
So
you would not have actually seen any signs in the mother with this
acute chorioamnionitis
.’
[76]
[112]
The mostly asymptomatic nature of
chorioamnionitis, as described by Dr Janowski and Dr Reddy, countered
Dr Keshave’s observation
that U’s inflammatory markers
had been normal, i.e. there had been no overt signs of infection. The
evidence of chorioamnionitis
only emerged in the histopathological
report, after the plaintiff’s placenta had been sent away for
analysis.
[113]
The plaintiff’s experts conceded that
there were limitations to CTG monitoring. Dr Ndjapa admitted that a
CTG reading may
indicate a normal foetus but the outcome could be an
abnormal baby. Dr Keshave seemed to have gone further, admitting
that, despite
proper CTG monitoring, a baby could indeed be born with
neonatal encephalopathy, especially where there was an infection.
[114]
In relation to the missing medical records,
the plaintiff’s counsel suggested that this had resulted from
an attempt by the
medical staff to conceal sub-standard care. Dr
McConney’s testimony, however, did not support this. The trial
court was correct
to have found that there was no reason to blame the
Department of Health for the absence of the records. Nothing, in the
end, turned
on it.
[115]
I am not persuaded that the plaintiff
proved, on a balance of probabilities, that the staff had been
negligent. The enquiry should
end there. Nevertheless, considering Dr
Janowski’s concession in relation to the CTG monitoring that
was (or was not) carried
out, I deem it necessary to address,
briefly, the final issue, viz. causation.
Causation
[116]
Both
parties referred to
Lee
v Minister for Correctional Services
,
[77]
where
the Constitutional Court dealt with the test for causation. Nkabinde
J held:
‘…
The
point of departure is to have clarity on what causation is. This
element of liability gives rise to two distinct enquiries.
The first
is a factual enquiry into whether the negligent act or omission
caused the harm giving rise to the claim. If it did not,
then that is
the end of the matter. If it did, the second enquiry, a juridical
problem, arises. The question is then whether the
negligent act or
omission is linked to the harm sufficiently closely or directly for
legal liability to ensue or whether the harm
is too remote. This is
termed legal causation.’
…
This
element of liability is complex and is surrounded by much
controversy. There can be no liability if it is not proved, on a

balance of probabilities, that the conduct of the defendant caused
the harm. This is so because the net of liability will be cast
too
wide. A means of limiting liability, in cases where factual causation
has been established, must therefore be applied. Whether
an act can
be identified as a cause depends on a conclusion drawn from available
facts or evidence and relevant probabilities.
Factual causation,
unlike legal causation where the question of the remoteness of the
consequences is considered, is not in itself
a policy matter but
rather a question of fact which constitutes issues connected with
decisions on constitutional matters as contemplated
by s 167(3)(b) of
the Constitution.
…
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. According to this test the enquiry to determine a causal
link, put in its simplest formulation, is whether “one
fact
follows from another.”’
[78]
[117]
Nkabinde J held, further, that the rule
regarding the application of the test was not inflexible. There were
situations where its
strict application would result in injustice.
[118]
The
plaintiff’s counsel contended that a flexible approach should
be adopted in the present matter, as endorsed by the Constitutional

Court in
Mashongwa
v Passenger Rail Agency of South Africa
.
[79]
As Mogoeng CJ pointed out, however, the decision in
Lee
never sought to replace the pre-existing approach to factual
causation, premised on the flexibility always recognized in the
common
law.
[80]
[119]
In
ZA
v Smith and another
,
[81]
Brand JA observed:
‘
What
it [the but-for test] essentially lays down is the enquiry- in the
case of an omission- as to whether, but for the defendant’s

wrongful and negligent failure to take reasonable steps, the
plaintiff’s loss would not have ensued. In this regard this

court has said on more than one occasion that the application of the
“but-for test” is not based on mathematics, pure
science
or philosophy. It is a matter of common sense, based on the practical
way in which the minds of ordinary people work, against
the
background of everyday-life experiences. In applying this
common-sense, practical test, a plaintiff therefore has to establish

that it is more likely than not that, but for the defendant’s
wrongful and negligent conduct, his or her harm would not have

ensued. The plaintiff is not required to establish this causal link
with certainty.’
[82]
[120]
If the test is applied to the present
matter, then it cannot be said that the plaintiff proved that, but
for the negligence of the
medical staff, U would not have suffered
harm. Based on the plaintiff’s evidence and the opinion
evidence of the various
experts involved, I am satisfied that the
baby’s cerebral palsy was, on a balance of probabilities,
caused by a hypoxic ischaemic
injury that occurred before the
commencement of labour and which was the result of placental FVM.
This had arisen from severe acute
chorioamnionitis, accompanied by
chorionic vasculitis and funisitis; it had been asymptomatic in
nature.
[121]
Consequently, I am not persuaded that any
negligence on the part of the staff caused or materially contributed
to the injury to
U’s brain when this could have been prevented
by exercising reasonable care and skill. There was simply no causal
link.
RELIEF AND ORDER
[122]
The trial court found that the plaintiff
failed to establish that the defendant was delictually liable to her.
For the reasons set
out above, I am of the view that there is no
basis upon which to interfere with such a finding. The appeal cannot
succeed on any
of the grounds listed by the plaintiff.
[123]
Regarding costs, there is no reason why the
general rule should not apply. The defendant is entitled to recover
the expenses involved.
[124]
The following order is made:
(a)
the appeal is dismissed; and
(b)
the plaintiff is directed to pay the
defendant’s costs, including those of two counsel.
J LAING
JUDGE OF THE HIGH
COURT
I agree.
L RUSI
JUDGE OF THE HIGH
COURT
I agree.
I BANDS
JUDGE OF THE HIGH
COURT
Appearances
For
the appellant:
Adv
AG Dugmore SC and Adv Y Malunga
Instructed
by:
S
Booi & Sons Attorneys
6A
Sansom Road, Vincent, EAST LONDON
Ref:
K58/10/19
Tel:
043 721 1701
Email:
sbooi@telkomsa.net
c/o
Luvuyo Solvern Attorneys
Office
no. 2, 1
st
floor, Old King Theatre
QONCE
(King William’s Town)
Tel:
043 642 4922
Email:
solvernattorneys@gmail.com
For
the respondent:
Adv
PJ de Bruyn SC and Adv N Nabela
Instructed
by:
State
Attorney
Old
Spoornet Building
17
Fleet Street, EAST LONDON
Ref:
1085/19-P6 (Ms Dlanjwa)
c/o
Office of the Premier
32
Alexandra Road
QONCE
(King William’s Town)
Date
for final submissions:
18
December 2023
Date
of delivery of judgment:
9
April 2024
[1]
Chorioamnionitis
is defined as inflammation and infection of the inner and outer
fetal membranes, often after pre-term premature
rupture of the
membranes. See Elizabeth Martin (
et
al
),
Concise
Medical Dictionary
(Oxford University Press, 10ed 2020), at 146.
[2]
Cardiotocography
is defined as the electronic monitoring of the fetal heart rate and
the frequency of uterine contractions.
Op
cit
,
at 122.
[3]
The reading was 7.33, which, according to the experts, was within
the normal range.
A
pH reading is a measure of the acidity or alkalinity of a solution;
a pH of 7 indicates a neutral solution, below 7 indicates
acidity,
and above 7 indicates alkalinity.
Op
cit
,
at 588.
[4]
NK
on behalf of UK v MEC for Department of Health
(unreported,
case no. 827/2019, Eastern Cape Division, Bhisho, delivered on 11
October 2022), at paragraphs [44] and [45]. The
identities of the
plaintiff and her minor child have been concealed.
[5]
Funisitis
means inflammation of the connective tissue of the umbilical cord
that occurs with chorioamnionitis. See
https://en.wikipedia.org/wiki/funisitis
(accessed
on 31 January 2024).
[6]
Vasculitis
is defined as a patchy inflammation of the walls of blood vessels
that leads to damage and thrombosis. Martin,
op
cit
,
at 808.
[7]
MRI
or magnetic resonance imaging is defined as a diagnostic imaging
technique based on the emission of electromagnetic waves
from the
body when the patient is placed in a strong magnetic field and
exposed to radiofrequency radiation.
Op
cit
,
at 456.
[8]
Syntocinon
is understood to be the trade name for medication that is used to
cause the contraction of the uterus to start labour,
increase the
speed of labour, and to stop bleeding following delivery. See
https://en.wikipedia.org/wiki/oxytocin_(medication)
(accessed
on 31 January 2024).
[9]
National Department of Health, ‘Guidelines for Maternity Care
in South Africa’ (4ed 2015).
[10]
The
criteria were developed by the renowned physician, Dr Joseph Volpe,
of the Harvard Medical School, Boston, MA, USA. His work
is often
quoted in matters such as the present.
[11]
1948
(2) SA 677
(A), at 705-6.
[12]
1960
(4) SA 875
(A), at 881-2.
[13]
2022
(3) SA 571 (SCA).
[14]
At
paragraph [72].
[15]
See,
in general, the discussion in AC Cilliers (
et
al
),
Herbstein
and Van Winsen: Civil Practice of the High Courts and the Supreme
Court of Appeal of South Africa
(5ed, 2009, ch39), at 1251-2.
[16]
[2015]
2 All SA 403 (SCA).
[17]
Gentiruco
AG v Firestone SA (Pty) Ltd
1972
(1) SA 589
(A), at 616H.
[18]
Coopers
(South Africa) (Pty) Ltd v Deutsche Gesellschaft für
Schädlingsbekämpfung MBH
1976
(3) SA 352
(A), at 370G-H.
[19]
At
paragraph [97].
[20]
The reference is to the Canadian case of
Widdrington
(Estate of) v Wightman
2011
QCCS 1788 (CanLII).
[21]
1980
(1) SA 191
(A), at 196E.
[22]
T
he
question must be distinguished from the issue of factual causation,
being one of the two primary elements of causation in the
law of
delict, the other being the issue of legal causation. See JR
Midgley, ‘Delict’, in
LAWSA
(Vol 15 3ed, 31 March 2016), at paragraph 175.
[23]
This
is understood as an assessment of the acid-base ratio or pH level in
relation to arterial blood obtained from the umbilical
cord.
[24]
[2018]
1 All SA 297 (GJ).
[25]
At
paragraph 18 (q).
[26]
(1287/2014)
[2018] ZAKZPHC 8 (4 April 2018).
[27]
DT
Zeffertt and AP Paizes,
Hoffman
and Zeffertt’s
The
South African Law of Evidence
(4ed), at 183ff.
[28]
HN
,
at paragraphs [8] and [9].
[29]
2006
(2) SACR 120
(NC).
[30]
At
paragraph [24].
[31]
Section
3(1)(a)
of the
Law of Evidence Amendment Act 45 of 1988
. See, too,
S
v Ndhlovu and others
2002 (2) SACR 325
(SCA), at paragraph [12].
[32]
McWilliams
v First Consolidated Holdings (Pty) Ltd
1982
(2) SA 1
(A), at 10E-G;
Seeff
Commercial and Industrial Properties (Pty) Ltd v Silberman
2001 (3) SA 952
(SCA), at paragraph [19].
[33]
See
n 16,
supra
.
[34]
Gentiruco
AG
,
n 17,
supra
.
[35]
2021 (3) SA 337 (SCA).
[36]
At
paragraph [17].
[37]
At
paragraph [21].
[38]
[
1939]
3 All ER 722
(HL), at 733E- F, cited in
Motor
Vehicle Assurance Fund v Dubuzane
1984 (1) SA 700
(A), at 706B- D.
[39]
In
a footnote to the joint minute, ‘PBGT’ is equated to
‘perirolandic, basal ganglia and thalamus’.
[40]
The plaintiff appears to have used the terms ‘misoprostol’
and ‘syntocinon’ interchangeably.
See
n 8,
supra
.
[41]
Chris
Higgins, ‘Umbilical-cord blood gas analysis’ (October
2014, downloaded from acutecaretesting.org).
[42]
Dr
Janowski also pointed out that the CTG reading, obtained on the
evening of 7 March 2019, just before birth on the following
day, had
not given reason for concern; no abnormalities in the foetal heart
rate had been seen.
[43]
The
abbreviation is a reference to Dr Amith Keshave; similarly, ‘YR’
refers to Dr Yavini Reddy.
[44]
Emphasis
added.
[45]
Sic.
[46]
Emphasis
added.
[47]
Johanna
Harteman (et al), ‘Placental Pathology in Full-Term Infants
with Hypoxic-Ischemic Neonatal Encephalopathy and Association
with
Magnetic Resonance Imaging Pattern of Brain Injury’, Journal
of Pediatrics (October 2013), at 968-75.
[48]
C-reactive
protein is a protein with plasma concentrations that are raised in
infections and inflammatory states and in the presence
of tissue
damage or necrosis. Martin,
op
cit
,
at 184.
[49]
Joseph
Volpe, ‘Placental assessment provides insight into mechanisms
and timing of neonatal hypoxic-ischemic encephalopathy’,

Journal of Neonatal-Perinatal Medicine 12 (2019), at 113-6.
[50]
Alastair
MacLennan (et al), ‘Cerebral palsy: causes, pathways, and the
role of genetic variants’, American Journal
of Obstetrics &
Gynecology (December 2015), at 779-88.
[51]
The term, ‘epidemiological’, is used here as an
adjective; it is derived from the noun, ‘epidemiology’,

which is defined as the study of the distribution of diseases and
determinants of disease in populations. Martin,
op
cit
,
at 262.
[52]
The
reference was to the three Volpe criteria that Dr Keshave identified
in his report, viz. evidence of foetal distress or risk
of hypoxia
or ischaemia, a need for resuscitation and low Apgar scores, and an
overt neurological syndrome in the first 24 hours
of life. Emphasis
added.
[53]
See n 49,
supra
.
[54]
Emphasis
added.
[55]
Emphasis
added.
[56]
See
n 49,
supra
.
[57]
See
n 50,
supra
.
[58]
At
paragraph 8 of the joint minute.
[59]
Sic.
Emphasis added.
[60]
See
n 16,
supra
.
[61]
See
n 13,
supra
,
at paragraph [222].
[62]
See
n 21,
supra
.
[63]
2013
(5) SA 437 (SCA).
[64]
At
paragraph [16].
[65]
The
significance of the placental histopathology was acknowledged in
Magqeya
v Member of the Executive Council for Health, Eastern Cape
2018 JDR 1667 (SCA).
[66]
At
paragraph [18]. Emphasis added.
[67]
2004
(5) SA 586 (SCA).
[68]
At
paragraph [5].
[69]
At
paragraph [10].
[70]
The
plaintiff mentioned, in her testimony, the administration of
‘maiso’; there was no documentary or opinion evidence

presented during trial proceedings to corroborate or clarify this.
[71]
Both
Dr
Reddy and Dr Keshave referred to Sandström (et al), ‘Durations
of second stage of labor and pushing, and adverse
neonatal outcomes:
A population-based cohort study’, Journal of Perinatology
(2017). The article was, however, excluded
from the appeal record.
[72]
See n 26,
supra
.
[73]
The
‘Guidelines for Maternity Care in South Africa’ (n 9,
supra
)
is generally recognized as the benchmark for the subject in
question. See, too,
Nkamela
v Member of the Executive Council for Health: Eastern Cape Province
2022 JDR 1522 (ECB), at paragraphs [9] to [11].
[74]
The
reference to a ‘black box’ is understood as the flight
data recorder that facilitates the investigation of aviation

incidents. See
https://en.wikipedia.org/wiki/Flight_recorder
accessed
on 22 March 2024.
[75]
Emphasis
added.
[76]
Emphasis
added.
[77]
2013
(2) SA 144 (CC).
[78]
At
paragraphs [38] to [40].
[79]
2016
(3) SA 528 (CC).
[80]
At
paragraph [65].
[81]
2015
(4) SA 574 (SCA).
[82]
At
paragraph [30].