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[2022] ZAECBHC 1
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J.A obo D.M.A v Member of Executive Council for Health, Eastern Cape (C.A.& R: 8/2021) [2022] ZAECBHC 1; [2022] 2 All SA 112 (ECB); 2022 (3) SA 475 (ECB) (21 January 2022)
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IN
THE HIGH COURT OF SOUTH AFRICA
EASTERN
CAPE LOCAL DIVISION, BHISHO
REPORTABLE
CASE
NO: C.A.& R: 8/2021
DATE
HEARD: 03 SEPTEMBER 2021
DATE
HANDED DOWN: 21 JANUARY 2022
In
the matter between:
J
A[....] on behalf of
DMA
APPELLANT
and
THE
MEMBER OF EXECUTIVE COUNCIL FOR
RESPONDENT
HEALTH,
EASTERN CAPE
FULL
COURT APPEAL JUDGMENT
D
VAN ZYL DJP:
[1]
This an appeal against an order granting absolution from the
instance. The appellant’s
claim was for delictual damages on
behalf of her minor child (as is customary, I shall refer to him as
DMA to protect his identity).
The claim was founded on the allegation
that DMA suffered a brain injury, caused by the negligence of the
respondent’s employees
when the appellant gave birth to DMA at
the Andries Vosloo Hospital in Somerset East in the Eastern Cape. The
respondent admitted
that the hospital staff were negligent.
[2]
The sole issue in the appeal is that of factual causation, that is,
whether or not
it can be said that the negligent conduct of the
medical staff at the hospital was the cause of the injury suffered by
DMA. That
this was the only issue, was confirmed by the parties
during argument. On the facts, and in the context of the evidence
presented
in this matter, a determination of the primary issue in
turn raises two secondary issues. The first issue is how to deal with
a
conflict in the evidence of opposing expert witnesses, while the
second raises the question when factual causation must be found
to
have been proved in a delictual claim of this nature.
[3]
On the common cause evidence placed before the trial court, DMA had
suffered a brain
injury. His clinical condition is that he has a left
sided spastic hemiplegic type of cerebral palsy with microcephaly.
[1]
Furthermore, he suffers from epilepsy, and what is described as
severe global developmental delay. The disagreement lies in what
caused the brain injury, and of the clinical condition which resulted
therefrom. The position adopted by the parties in their respective
expert witnesses’ summaries is as follows: according to the
appellant, DMA’s condition is the result of a brain injury
known as hypoxic-ischemic encephalopathy, which he sustained during
labour, and was caused by prolonged partial hypoxic ischemia.
The
respondent’s expert witness on the other hand contended that on
the clinical evidence, DMA has an underlying neurometabolic
disorder
in keeping with Nonketotic Hyperglycinemia, which may account for his
clinical condition.
[4]
Hypoxic-ischemic encephalopathy (HIE) is a brain injury as a result
of impaired cerebral
blood flow and oxygen delivery to the brain of
the foetus during birth. Hypoxemia occurs when there is a decrease in
oxygen levels
in the blood of the foetus, and ischemia is a lack of
blood flow to the brain. The compensating response of the foetus to
hypoxia
is to redistribute oxygenated blood to more deserving organs,
such as the heart and the brain. The redistribution of blood in the
brain itself ensures that during episodes of prolonged foetal
hypoxia, blood is directed to vital brain structures at the expense
of less metabolically active structures of the brain, namely the
cerebral cortex and the white matter. This protects the brain
stem,
cerebellum and deep grey matter from injury where the vital centres
of life, like the respiratory and cardiac centres, are
situated. The
pattern of the insult that results from the directing of blood from
the areas of the brain around the vital brain
structures presents
itself as an injury to the peripheral watershed areas of the brain
where the white matter of the brain is situated.
The mechanism
responsible for the injury means that the injury takes place over a
long period of time, and can last for several
hours.
[5]
According to the literature to which the respondent’s
paediatric neurologist
made reference to in his evidence, Nonketotic
Hyperglycinemia (NKH) is a rare genetic metabolic disorder caused by
a defect in
the enzyme system responsible for breaking down the amino
acid, glycine, in the body. The defect in the system results in an
accumulation
of glycine in all the body tissues, including the brain.
There is a classical and a variant form of NKH. Classic NKH, which is
the relevant form in the present context, is caused by genetic
variants in the genes of a person, and is an inherited condition.
Based on its ultimate outcome, classic NKH can be categorised as
either severe, or a mild form of the disorder. The disorder may
be
diagnosed by elevated glycine in blood plasma and a compatible
pattern of brain imaging. Increased levels of glycine in the
spinal
fluid is highly indicative of NKH, and is consequently the preferred
diagnostic test. Based on the extent of NKH, a sufferer
may present
with intractable epilepsy and no developmental progress, or in its
attenuated form, with variable developmental progress
and treatable
epilepsy, or an absence of epilepsy.
[6]
The appellant led evidence from three witnesses, namely Professor
Lotz, Dr Murray
and Prof van Toorn. Professor Lotz is a qualified
radiologist. Dr Murray is an obstetrician and a gynaecologist, and
Prof von Toorn
is a paediatric neurologist. The defendant in turn
adduced the evidence of a paediatric neurologist, Dr Keshave. The two
neurologists
testified to the possible causes of DMA’s
condition. In addition to the oral evidence of these witnesses, the
parties placed
before the trial court the joint minutes of van Toorn
and Keshave, as well as that of the respective radiologists;
obstetricians;
and geneticists from whom the parties had commissioned
expert witness reports. The expertise of all the witnesses in their
respective
fields was not placed in issue. Except for one or two
aspects, the clinical evidence on which the expert witnesses based
their
opinions, was similarly not in dispute.
[7]
In its assessment of the evidence placed before it, the trial court
proceeded from
the premise that the respondent had admitted that DMA
suffered a brain injury, and that due to the negligence of the
respondent’s
employees, the foetus was deprived of oxygen
during the birth process. The issue to be decided, said the court,
was whether or
not the oxygen deprivation during birth was the cause
of the brain impairment which DMA was diagnosed to be suffering from
when
the action was instituted. In short, was the cause of the
admitted injury oxygen deprivation as contended by van Toorn, the
appellant’s
expert neurologist, or was it NKH as opined by
Keshave, the respondent’s expert witness?
[8]
The trial court concluded that on the evidence placed before it, it
could not decide
to its satisfaction where the truth lay, and ordered
absolution from the instance. It found that where the expert opinions
presented
by the respective parties with regard to the cause of DMA’s
injury were both capable of logical support, the matter should
not be
decided by a simple preference of one opinion over the other, and
that in the present matter, Keshave’s opinion could
not be
found not to have a logical basis. This finding was undoubtedly based
on the decision in Michael and Another v Linksfield
Park Clinic (Pty)
Ltd and Another,
[2]
where the
court dealt with a conflict in expert evidence with whether the
diagnosis and treatment in question accorded with sound
medical
practice. It held that “…
it
would be wrong to decide a case by simple preference where there are
conflicting views on either side, both capable of logical
support.”
[3]
Whilst the nature of the conflict in the expert opinion in Linksfield
was different from the one in the present matter, the principle
expressed equally finds application.
[9]
The trial court correctly in my view approached the issue for
determination on the
basis of there being two conflicting expert
opinions with regard to what the factual cause of DMA’s injury
was. The question
in this appeal is accordingly whether the court was
correct in concluding that the two opinions were equally placed on
the evidence
before it, and that the appellant must as a consequence
be found not to have discharged the burden of proving that it was the
respondent’s
negligence that was the cause of the injury
sustained by DMA. Before I proceed to determine this issue, it may be
convenient to
say
something about how expert
opinion evidence is to be approached and evaluated when there is
conflicting or inconsistent evidence
from two or more expert
witnesses.
[10]
The opinion of a witness is generally inadmissible. “
In
the law of evidence ‘opinion’ means any inference from
observed facts, and the law on the subject derives from the
general
rule that witnesses must speak only to that which was directly
observed by them.”
[4]
Opinion is admissible if it is relevant. Relevance is in turn
determined by the issues in the matter. If the opinion can assist
the
court in determining an issue, is has probative value, otherwise it
is superfluous.
[5]
Expert
opinion evidence is received when the issues require special skill
and knowledge to draw the right inferences from the facts
stated by
the witnesses.
[6]
[11]
Conceptually there are several types of conflicts in expert evidence
that may present itself
in any given case. The first is a conflict
with regard to the assumed facts. By reason of its very nature,
expert opinion must
have a factual basis. The facts upon which an
expert’s opinion is based must be proved by admissible
evidence. An expert
opinion based entirely on inadmissible evidence
is itself inadmissible. The facts may be established by asking the
expert witness
in examination-in-chief what those facts are.
[7]
“
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.”
[8]
How those facts are proven is determined by the principles of
evidence and the usual methods used for judicial fact-finding and
rational decision-making. Where the expert him or herself observed
relevant facts, that evidence will be evidence of fact and admissible
as such.
[9]
Where the opinion
seeks to take issue on the facts with the version of direct
eyewitness evidence, credible eyewitness evidence
that conforms to
the probabilities, will generally take preference to the opinion of
an expert of what the facts are.
[10]
In the final result, the decision of what the facts are must be
founded on an assessment of the evidence as a whole and the
probabilities
as they appear therefrom.
[11]
[12]
Secondly, a conflict in the expert opinion may lie in the analysis of
the established facts and
the inferences drawn therefrom by opposing
expert witnesses. A proper evaluation of the evidence in this context
focuses primarily
on “
the
process of reasoning which led to the conclusion, including the
premise from which the reasoning proceeds…”
[12]
The reason for interrogating the underlying premise of expert opinion
lies in its nature. In essence it amounts, as in the present
context,
to a statement that established medical opinion, as the expert
witness interprets it, dictates a particular result under
an assumed
set of facts. This requires an assessment of the rationality and
internal consistency of the evidence of each of the
expert
witnesses.
[13]
“
The
cogency of an expert opinion depends on its consistency with proven
facts and on the reasoning by which the conclusion is reached.”
[14]
The source for the evaluation of this evidence for its cogency and
reliability are (i) the reasons that have been provided by the
expert
for the position adopted by him/her; (ii) whether that reasoning has
a logical basis when measured against the established
facts; and
(iii) the probabilities raised on the facts of the matter.
[15]
It means that the opinion must be logical in its own context, that
is, it must accord with, and be consistent with all the established
facts, and must not postulate facts which have not been proved.
[16]
[13]
The inferences drawn from the facts must be sound. The internal logic
of the opinion must be
consistent, and the reasoning adopted in
arriving at the conclusion in question must accord with what the
accepted standards of
methodology are in the relevant discipline.
[17]
The reasoning will be illogical or irrational and consequently
unreliable, if (i) it is based on a misinterpretation of the facts;
(ii) it is speculative, or internally contradictory or inconsistent
to be unreliable; (iii) if the opinion is based on a standard
of
conduct that is higher or lower than what has been found to be the
acceptable standard; (iv) if the methodology employed by
the expert
witness is flawed. What flows from this is that the mere fact that an
expert opinion is unchallenged, does not necessarily
mean that it
must be accepted. However, if that evidence is based on sound grounds
and is supported by the facts, there exists
no reason not to accept
it.
[14]
Other considerations relevant in this context are (i) the
qualifications and the experience of
the expert witnesses with regard
to the issue he or she is asked to express an opinion on; (ii)
support by authoritative, peer-reviewed
literature;
[18]
(iii) the measure of equivocality with which the opinion is
expressed; (iv) the quality of the investigation done by the expert;
(v) and the presence or absence of impartiality or a lack of
objectivity. What is ultimately required is a critical evaluation
of
the reasoning on which the opinion is based, rather than
considerations of credibility.
[19]
Should it not be possible to resolve a conflict in the expert opinion
presented to the court in this manner, that is, when the
two opposing
opinions are both found to be sound and reasonable, the position of
the overall burden of proof will inevitably determine
which party
must fail. It is worth emphasising that the onus as a determining
factor “
can
only arise if the tribunal finds the evidence pro and con so evenly
balanced that it can come to no such conclusion. Then the
onus will
determine the matter. But if the tribunal, after hearing and weighing
the evidence, comes to a determinate conclusion,
the onus has nothing
to do with it, and need not be further considered.”
[20]
[15]
A third type of conflict which may arise in expert evidence, is that
of competing theories of
a purely scientific nature. The choice
between two conflicting theories is informed primarily by the extent
to which the theory
is regarded as being established and has gained
general acceptance within the specific scientific community in the
particular discipline
to which it belongs. Whether or not a theory
has been sufficiently established must be measured against
considerations such as
whether it can, and has been tested; whether
it is the product of reliable principles and methods that have been
reliably applied
to the facts of the case; and whether it has been
subjected to peer review and publication.
[16]
Fourthly, a conflict may also arise in the context of what the
accepted standard of conduct of
a medical professional is in certain
circumstances. Typically medical negligence cases deal with the
situation where an injury
is alleged to be in complete discord with
the recognised therapeutic objective and techniques of the operation
or treatment involved.
Expert opinion, in this context, is aimed at
determining whether the conduct of a professional person in a
particular field accords
with what is regarded as sound practice in
that field. Again, the method adopted is to evaluate opinion evidence
with the view
of establishing the extent to which the opinions
advanced are founded on logical reasoning.
[21]
[17]
What is evident from the aforegoing is that the evaluation of expert
opinion in determining its probative value and the considerations
relevant thereto, are determined by the nature of the conflict in the
opinion, and the context provided by all the evidence and
the issues
which the court is asked to determine. In general, it is important to
bear in mind that it is ultimately the task of
the court to determine
the probative value of expert evidence placed before it and to make
its own finding with regards to the
issues raised.
[22]
Faced with a conflict in the expert testimony of the opposing
parties, the court is required to justify its preference for one
opinion over another by a careful and critical evaluation
thereof.
[23]
Further, the
primary function of an expert witness is to guide the court to a
correct decision on questions, which fall within
that expert’s
specialised field. To that extent, the expert witness has a duty to
provide the court with abstract or general
knowledge concerning his
or her discipline, and the criteria necessary to enable the court to
form its own independent judgment
by the application of the criteria
to the facts proved in evidence.
[24]
Accordingly,
the mere “…
pitting
of one hypothesis against another does not constitute the discharge
of the functions of an expert.”
[25]
Finally,
it is not the function of the court to develop its own theory or
thesis and to introduce on its own accord evidence that
is otherwise
founded on special knowledge and skill.
[26]
E
x
hypothesi
,
such evidence is outside the learning of the court.
The
function of the court is restricted to deciding a matter on the
evidence placed before it by the parties,
and to choose between conflicting expert evidence, or accepting or
rejecting the proffered expert evidence.
[18]
Turning to the issue raised in this appeal, the conflict essentially
lies in the opinion evidence
of the two neurologists with regard to
the cause of the injury. Van Toorn’s evidence was that the
nature of the injury, as
it was identified by the radiologists, is
consistent with the clinical records of what transpired during the
appellant’s
labour, creating the risk of a hypoxic ischemic
insult, and the clinical condition of DMA immediately after birth.
Keshave’s
hypothesis of the cause, being NKH, was in essence
premised on the following aspects: (i) the clinical features
exhibited by DMA
after birth; (ii) the fact that DMA was diagnosed
with a type of cerebral palsy that is not usually associated with
intrapartum
asphyxia; (iii) in contrast to the magnetic resonance
imaging (MRI) scan on which the radiologists based their opinion, the
report
of a radiologist on an earlier computerised tomography (CT)
scan taken a year and 6 months after the birth of DMA, showed damage
to only the one side of his brain, which in keeping with NKH, this is
indicative of an injury that is progressive in nature; and
(iv)
elevated levels of glycine found in DMA’s blood plasma.
[19]
On a critical assessment of Van Toorn’s evidence with regard to
the cause of the injury,
when measured against that of Keshave, his
evidence proves to be more reliable with there being nothing, at
least not of a material
nature, that may detract from the probative
value thereof. His evidence not only had a logical basis, but the
conclusions reached
by him were well reasoned, and consistent with
the clinical evidence, the joint reports of the expert witnesses
engaged by the
respective parties, the oral evidence of the other
expert witnesses, and the probabilities as the they arose therefrom.
[20]
The salient features of the clinical evidence on which Van Toorn and
the appellant’s other
expert witnesses based their opinions
were in summary that the appellant gave birth to DMA by way of an
emergency caesarean section.
The reason for the absence of a natural
delivery was noted as having been cephalopelvic disproportion, that
is, the foetal head
was too large, or in a position, that rendered it
difficult to pass through the pelvis. DMA was born a week past the
determined
delivery date. During labour, the foetal heart rate was
recorded as being irregular. The appellant’s labour progressed
poorly,
and she was in labour for 35 hours and 45 minutes, of which
11 hours and 15 minutes were in the latent phase, and 24 hours in the
active phase of the first stage of labour. The appellant’s
amniotic fluid liqour, when released by the rupture of the membranes
was meconium stained. Meconium is foetal bowl content that is
expelled into the amniotic fluid. The nursing staff administered
oxytocin, a drug that augments delivery by causing an increase in
contractions. DMA was born with a caput, being a soft tissue
swelling
on the head of a new born baby.
[21]
At birth DMA had a lack of muscle tone, and he had to be resuscitated
with oxygen for ten minutes.
He was nursed in an incubator. He
vomited when cup fed, but retained later feeds. The following day DMA
was reported to have had
a seizure, described as “
twitching
on the right of the body.”
Medication was prescribed and
administered intravenously on two more occasions. He was discharged
from the hospital after five
days. He received physiotherapy from
which he benefitted. At the age of one, a head measurement noted a
head circumference indicative
of substandard head growth. Six years
later DMA was diagnosed with cerebral palsy. He presented with
seizures on a number of occasions,
and was diagnosed as having
epilepsy. His epilepsy was treated with medication.
[22]
The parties placed two joint minutes from three radiologists into
evidence. Two of the radiologists,
namely Alheit and Lotz, were
engaged by the appellant, and the third, Dr Ahmed, by the respondent.
In the earlier of the two joint
minutes, Lotz and Ahmed agreed on the
following: (i) that the MRI scan demonstrates features which are, in
the appropriate clinical
context, compatible with a prolonged partial
hypoxic ischemic insult to the brain; (ii) that the injury
asymmetrically involves
the posterior watershed regions of the brain;
(iii) that in view of extensive occipital white matter damage, the
clinical records
should be evaluated for possible episodes of low
blood sugar (hypoglycaemia) postnatally; and lastly, (iv) that
genetic disorders
as a cause of the brain damage was unlikely,
according to Lotz, and less likely, according to Ahmed.
[23]
In the joint minute of Alheit and Ahmed there are four features that
stand out. The first is
that they were in agreement that the imaging
of the MRI scan of DMA’s brain presented a brain injury, which
was the likely
result of a prolonged partial hypoxic ischaemic
cerebral insult. Alheit, set the likelihood of that being the
position as “
exceedingly high.”
The second feature
is that the presence of ulegyria makes it likely that the injury is
the result of a prolonged partial hypoxic
ischaemic insult. Ulegyria
refers to mushroom shaped scarring of the brain, indicative of dead
brain cells. The third feature is
that the two radiologists agreed
that the brain imaging is consistent with additional hypoglycaemic
encephalopathy. That is, additional
brain damage caused by episodes
of low blood sugar. Alheit was of the opinion that the dominant
injury was exceedingly likely to
be prolonged partial hypoxic
ischemic in nature, while Ahmed did not want to commit himself on
which one of the two was the dominant
insult simply on the imaging,
and in the absence of clinical data. The fourth, and an important
feature of the joint minute, is
that both radiologists concluded that
the findings of the MRI study rendered genetic disorders as a cause
of DMA’s brain
damage unlikely.
[24]
The two obstetricians, Murray and Janowski, agreed that (i) the
appellant was more than 41 weeks
pregnant when she was admitted to
the maternity ward; (ii) that her labour must be regarded as having
been severely prolonged by
reason of a prolonged active phase of the
first stage of labour; (iii) that the foetus was at an increased risk
of intrapartum
hypoxia due to the prolonged labour; and (iv) that the
administering of oxytocin to augment the appellant’s labour;
the signs
of cephalopelvic disproportion; and the prolonged active
phase of the first stage of labour, were all indicators for the need
to
perform a caesarean section to prevent injury to the foetus.
[25]
The question whether there was a genetic cause for DMA’s
condition, was addressed by the
two geneticists in a joint minute. Dr
Gericke and Prof Christianson were in agreement that there was no
evidence of dysmorphic
features present with DMA associated with any
recognisable genetic condition or syndromic disorder. That would
include dysmorphic
features of alcohol syndrome, or partial foetal
alcohol syndrome. Gericke pertinently noted that DMA’s ears
were not low
set, and that the presence of minor epicanthic folds
could be a normal variant physical feature. Neither of the
geneticists expressed
the need for further testing to be conducted.
They instead deferred to the other experts in their respective fields
with regard
to the cause of DMA’s condition.
[26]
The two-paediatric neurologists, Van Toorn and Keshave authored two
joint minutes. On a reading
of the preamble to the second joint
minute, the reason for the compilation of a second joint minute lies
in the fact that Keshave
in the first written summary of his
evidence, expressed the opinion that certain facts, such as the
presence of occipital white
matter injuries, and the deceleration of
DMA’s head growth, may possibly be due to other causes, which
may include genetic
metabolic disorders. Subsequently, metabolic
tests were performed which
inter alia
noted that DMA had
elevated glycine levels, followed by a recommendation that further
testing for glycine be performed to rule
out the presence of NKH. As
a consequence, the focus of the second minute between Van Toorn and
Keshave was whether NKH could be
considered as being a cause of DMA’s
condition.
[27]
Some of the aspects on which van Toorn and Keshave were in agreement
with in their joint minutes,
and which are relevant in the context of
the issue raised, are as follows: The pattern of the injury to DMA’s
brain, as shown
by the MRI images, was compatible with a prolonged
partial hypoxic ischemic injury. The developmental outcome associated
with intrapartum
asphyxia was either spastic quadriplegia or
dyskinetic cerebral palsy. Other subtypes of cerebral palsy were less
likely to be
associated with an intrapartum hypoxic ischemic event.
DMA has a left sided hemiplegia. In the case of children with
hemiplegic
cerebral palsy, the left cerebral hemisphere is usually
normal. In the case of DMA, his brain injury presented with damage to
both
the right and the left, although the left side was damaged to a
lesser extent. Van Toorn and Keshave agreed that the reason why
he
was not manifesting quadriplegia, is “
simply that his left
motor area was spared from hypoxic ischemic hypoglycaemic injury.”
They further agreed that a diagnosis of NKA should not be based
on a single elevated serum glycine level, and that the deceleration
of DMA’s head growth since birth supports an early hypoxic
ischemic injury. Finally, they agreed that features such as apnea,
poor feeding and the early onset of seizures, were compatible with
both HIE and NKH.
[28]
The oral testimony of the radiologist, Professor Lotz was that the
MRI scan of the brain of DMA
presented a typical example of a
watershed injury, which injury is the hallmark of a prolonged partial
hypoxic ischemic insult.
It is a pattern of injury that occurs at 36
weeks of gestation onwards. The injury is situated at the posterior
of DMA’s
brain, on both the left and the right side. The injury
on the right is more severe and more prominent. According to Lotz,
the brain
injury is not reflective of having been caused by a genetic
disorder, inflammation or infection, and there can be no doubt that
it is a watershed injury, which could only have been caused by a
prolonged partial hypoxic ischemic insult. The reason is to be
found
in the fact that neurological injuries have certain defined patterns.
By evaluating the pattern presented by imaging, neuroradiology
as a
field of expertise, is able to draw a conclusion with regard to the
cause of a brain injury. Accordingly, if the injury was
caused by a
genetic disorder or such, the injury would have presented itself with
a different pattern, and would have been identifiable
as such by a
radiologist. Lotz testified that MRI is an advanced technology that
gives radiologists the ability to more accurately
diagnose the nature
of a brain injury, and that it simply cannot be compared to older and
more limited technology, such as a CT
scan.
[29]
The evidence of Lotz with regard to the nature of the brain injury
sustained by DMA was not disputed
in cross-examination. Rather, the
focus of the respondent’s questioning of this witness was
limited to two aspects. The first
was whether or not the injury could
have been caused subsequent to the birth process, without proposing
what other likely cause
may account for the type of injury diagnosed
by the three radiologists. In particular, Lotz was not asked whether
the injury could
have been caused by an accumulation of glycine in
the brain of DMA as a result of him suffering from NKH. The
importance of the
failure of this having been put to Lotz, must be
assessed in the context of all three radiologists having agreed on
the nature
of the injury; the uncontested evidence of Lotz of when
and how such an injury is sustained; and importantly, the evidence of
Keshave,
with reference to the literature on which he relied, that
the injury produced to the brain of someone suffering from NKH has an
identifiable profile when it is viewed on an MRI scan. The second
aspect raised with Lotz in cross-examination was that he was
not
qualified to express an opinion on the statement that “
not
all hypoxic ischemic injuries result in cerebral palsy.”
Lotz responded to the question by firstly making the concession that
there may be other causes for cerebral palsy, and that with
regard to
what those causes may be, should more appropriately be dealt with by
someone with the necessary expertise, namely a neurologist.
[30]
There is nothing that detracts from the reliability of the evidence
of the plaintiff’s
obstetrician, Dr Murray, and none was
suggested. Her evidence was consistent with the respondent’s
admission on the pleadings
that the nursing staff allowed the
appellant’s labour to be unduly prolonged, and that it caused
DMA to sustain a hypoxic
ischemic injury. Murray expressed the
opinion that during labour there were several reasons for the foetus
to have become hypoxic.
These were as follows. Delivery took place at
about 41weeks and 3 days, which meant that the appellant was at least
a week over
her due date. A foetus that is delivered late may not be
able to manage the stresses posed by labour as well as a foetus that
is
born earlier. The fact that the appellant was over her due date
necessitated the need for careful monitoring of her labour, which
did
not happen. According to Murray, a striking feature of the
appellant’s labour was the length thereof. She testified that
she had never seen a labour as long as that of the appellant. It
meant that she gave birth nearly 24 hours later than what was
expected according to recommended norms. She was 8 centimetres
dilated for 18 hours, a length of time, which Murray described as
being incredibly long. According to Murray, it must have been fairly
obvious at an early stage of labour that delivery of the baby
was
obstructed, in that the foetal head was too big to progress through
the maternal pelvis.
[31]
Further, the appellant’s liquor was meconium stained. As
stated, meconium refers to the
faeces of the foetus, which is passed
in the uterus, and said Murray, it is considered to be a response to
stresses during labour.
Instead of performing a caesarean section,
the appellant was given oxytocin. That, Murray said, would have had
the effect of increasing
contractions, which in turn would have had
the effect of placing further stress on the foetus. She explained
that during labour
the foetus would naturally undergo brief bouts of
hypoxia when blood flow is interrupted by the mother’s
contractions. The
foetus is naturally well equipped to deal with
this. However, if the contractions are too strong, occur too often
and carry on
for too long, it may be harmful to the foetus.
[32]
Oxytocin, said Murray, is a dangerous drug that must be used
cautiously. If not properly monitored,
it may cause contractions
which may be too much for the foetus to deal with. On a whole,
Murray’s evidence was that the foetus
was likely in distress
during labour, and that all the risk factors for hypoxia were
present. This, according to Murray, is a reflection
of a labour that
was grossly mismanaged, poorly monitored, and allowed to continue for
too long before a caesarean section was
performed despite the obvious
presence of an obstructed labour and a non-reassuring foetal
condition.
[33]
In his oral testimony, Van Toorn agreed with the obstetrician, Dr
Murray, that the risk of this
type of injury was created by (i) the
severely prolonged obstructed labour that was characterised by poor
progress; (ii) the administering
of oxytocin under those
circumstances; (iii) the presence of meconium stained liquor; and
(iv) the advanced gestational age and
the poor monitoring of the
appellant’s labour. Clinical evidence of the type of injury
identified by the radiologists was
the fact that DMA was not
breathing at birth, and had to be resuscitated with oxygen. Van Toorn
testified that the most common
cause of the seizures suffered by DMA
shortly after birth were hypoxia ischemia and hypoglycaemia, both of
which cause the death
of cells in the brain, as is evidenced by the
MRI imaging of DMA’s brain. His further evidence was that the
presence of ulegyria
in the MRI imaging was further consistent with
hypoxia ischemia and hypoglycaemia.
[34]
Van Toorn was asked to deal with Keshave’s opinion that DMA has
an underlying neurometabolic
disorder that may account for his
clinical condition. According to van Toorn there exists identifiable
differences between an injury
caused by a hypoxic insult, and that
which is caused by a neurometabolic disorder, such as NKH. Both
causes would present itself
with identifiable abnormalities that will
be evident from an MRI scan. In the instant matter, the damage to the
brain of DMA as
seen on the MRI scan, and confirmed by all the
radiologists, was consistent with a hypoxic ischemic brain injury.
The changes to
DMA’s brain was of a destructive nature, which
was supported by the presence of ulegyria, something that is seen
with a hypoxic
ischemic brain injury. Importantly, this type of
injury is static in nature, whereas a metabolic disorder is
progressive, in that
it raises glycine levels in the body tissues
causing damage over time. Consequently, it presents with conditions
which get worse
over time, and a regression of developmental
milestones.
[35]
With regard to the expert report on an earlier CT scan, on which
Keshave relied for arriving
at his opinion that the brain injury was
of a progressive nature in keeping with NKH, van Toorn agreed with
Lotz that it does not
necessarily exclude the existence of an injury
to both sides of the brain having been present as indicated on the
later MRI scans.
He agreed with the undisputed evidence of Lotz that
MRI is a much more advanced technology when compared to a CT scan,
which is
a much older and more limited technology. The limitations
posed by a CT scan, and the likelihood postulated by these two
witnesses
that the injury to the one side of the brain did not show
on the CT scan, is supported by the fact that the injury to DMA’s
brain was found by the radiologists to have been more pronounced on
the right side of the brain than on the left.
[36]
Van Toorn further testified that although the type of epilepsy which
DMA has presented is less
likely associated with the type of injury
identified by the radiologists, the fact is that his brain was
damaged on both sides,
and the presence of only a left sided
hemiplegia, as in the present matter, is not inconsistent with the
other side of the brain
having been able to overcome the injury. This
is something, according to van Toorn, that is typically seen in
children. With regard
to the elevated glycine levels, the most likely
cause of this, said van Toorn, was the fact that DMA was using
medication for his
epilepsy. The medication in question is known to
raise the glycine levels in the blood of its users.
[37]
Van Toorn stood firm in his opinion that although some features, like
apnea and seizures after
birth are similar to HIE and NKH, there are
marked differences between the clinical profile of the two, and that
NKH could be excluded
as a cause of DMA’s injury. The imaging
of the MRI scan was also not in keeping with NKH, and there was no
need, according
to him, to perform any further tests to exclude a
neurometabolic disorder as a cause of DMA’s condition. The
accepted medical
practice, according to him, is that further testing
is only required if there is a clinical presentation of NKH, which
was absent
in this case. If DMA was suffering from a milder form of
NKH, symptoms of the condition, according to the publications on
which
Keshave had based his opinion, would only have manifested
itself after 3 months. That was not the case with DMA. Also, visual
impairment
and the making of unusual movements, which were similarly
absent, would have been indicative of the presence of NKH. Further,
NKH
causes symmetrical spasticity. That was similarly absent in the
case of DMA. According to van Toorn, NKH is a very rare metabolic
condition that he has only seen twice in his 20 years of experience.
[38]
That brings me to Dr Keshave’s evidence. A closer examination
of his expressed opinion
on what the cause of DMA’s injury and
clinical condition is, shows that it does not support a defensible
conclusion when
measured against the facts and the other largely
uncontested evidence. He wavered between different opinions; he
sought to draw
inferences which were tenuous; he expressed views on
aspects he was not qualified to do, and he gave evidence that was
largely
of a speculative nature. I will proceed to illustrate this.
For a start, in the written summary of his expert opinion he
expressed
the opinion that there exists “
the possibility of
an underlying genetic/neurometabolic disorder”
that needed
to be considered. He later supplemented his written report by the
positive statement that DMA “
has an underlying
neurometabolic disorder”
that could account for his current
clinical condition. In his oral testimony he ended up saying, in
cross-examination, that the
possible cause of DMA’s
neurological impairment may either be an underlying neurometabolic
disorder
or
a hypoxic injury.
[39]
The profound change in opinion in his written opinions was premised
on the results of the blood
test showing that DMA had elevated serum
glycine levels. This fact alone could not in my view support the
inference, which Keshave
sought to draw in the summary of evidence.
As stated, it was an accepted fact that DMA was prescribed medication
for his epilepsy
that is known to raise glycine levels in the body.
As Van Toorn, as a matter of logic pointed out in his evidence, he
would not
have expected this type of medication to have been
prescribed by a medical practitioner if DMA’s glycine levels
were already
raised by reason of him suffering from NKH. It would
only have exacerbated his seizures, of which there was no evidence.
Further,
Keshave in his subsequent joint minute with van Toorn,
agreed that a diagnosis of NKH should not be based on a single
elevated
level of blood serum glycine. He however sought to speculate
in the minute, and again in his oral testimony, that DMA’s
caregivers
may not as regularly have given him his medication as they
were supposed to, the suggestion being that the reason for the raised
glycine levels must lie elsewhere. This is nothing more than
speculation. Inferential reasoning is an accepted technique that is
utilised in judicial fact-finding. However, the inference sought to
be drawn must be capable of being drawn from the admitted or
proven
facts, and not matters of speculation.
[27]
If tenuous, or far-fetched, it cannot form the foundation for the
court to make any finding of fact.
[28]
Further, the inference must be based on, and be consistent with all
the admitted or proved facts, and not be matters of speculation.
[29]
[40]
Keshave’s opinion that the nature of the injury to DMA’s
brain is supportive of a
conclusion that he is suffering from NKH, is
not supported by the evidence. The fact that DMA after birth
presented with features
such as apnea and seizures, standing alone,
is insufficient to draw an inference for a diagnosis of NKH. It was
agreed by Keshave
to be equally consistent with HIE. The other
factors he sought to place reliance on, also do not serve to justify
such an inference.
As stated earlier, he
inter alia
sought to
base his opinion on the report of an earlier CT scan that only made
mention of an injury to the one side of the brain.
He further
testified that there were features on the later MRI scan, such as the
posterior areas of the brain that were damaged,
which was consistent
with the features of an injury that was caused by NKH. The difficulty
with this is that Keshave’s reliance
on the report of the CT
scan clearly did not account for the inferior quality of the
technology involved, a fact that was not disputed.
It is further
inconsistent with the fact that he agreed with Van Toorn in their
first joint minute that the changes to DMA’s
brain were
compatible with a prolonged partial hypoxic ischemic injury, which
injury Van Toorn testified is, otherwise than that
caused by NKH, not
a progressive, but a static injury. Further, Ahmed, the defendant’s
own expert radiologist, agreed with
both Lotz and Alheit that the
injury is consistent with a prolonged partial hypoxic ischemic
cerebral insult, and that genetic
disorders as a cause of the brain
damage was unlikely.
[41]
An important aspect in assessing the reliability of Keshave’s
opinion, is that Lotz was
not referred to either the report, or the
CT scan itself on which Keshave based his opinion, neither of which
seemed to have been
admitted into evidence. It could accordingly not
be tested in cross-examination, and very little, if any, weight can
be accorded
to it. It was not suggested to Lotz that the injury was,
or may have been progressive in nature, or that it is consistent with
an injury caused by NKH. This failure must be assessed in the face of
Lotz’s undisputed evidence that neurological injuries
have
certain predictive patterns that can be identified from the imaging
presented by a MRI scan. NKH, according to the literature
on which
Keshave relied, similarly presents with a compatible pattern of brain
injury. As a radiologist, Lotz was clearly qualified
to have dealt
with this in his evidence and it should, of necessity, have been
raised with him.
[42]
It is further evident from Keshave’s testimony that he
expressed his opinion with regard
to the cause of the injury, without
having had regard to what either the radiologists, or the two
geneticists, agreed to in their
respective joint minutes. He
surprisingly acknowledged in cross-examination to not having had
sight of the joint minutes. Furthermore,
the drawing of conclusions
from the imaging of either the CT and MRI scans, or from the imaging
contained in the publications on
which Keshave sought to place
reliance, clearly fell outside his field of expertise. This is an
aspect which the defendant’s
radiologist should have dealt with
in evidence. The defendant however chose not to call Ahmed as a
witness and was consequently
otherwise not allowed to simply depart
from what the radiologists had agreed to in their joint minutes.
[43]
In BEE v RAF
[30]
and the cases
referred to therein, it was held that in the absence of a timeous
repudiation, a party is bound to the facts agreed
to in a joint
minute, and that agreement reached on a matter of opinion, may
likewise not simply be departed from. “
Where
the parties engage experts who investigate the facts, and where those
experts meet and agree upon those facts, a litigant
may not repudiate
the ‘agreement unless it does so clearly and, at the very
latest, at the outset of the trial’ (para
11). In the absence
of a timeous repudiation, the facts agreed by the experts enjoy the
same status as facts which are common cause
on the pleadings or facts
agreed in a pre-trial conference (para 12). Where the experts reach
agreement on a matter of opinion
the litigants are likewise not at
liberty to repudiate the agreement. The trial court is not bound to
adopt the opinion but the
circumstances in which it would not do so
are likely to be rare (para 13). Sutherland J’s exposition has
been approved in
several subsequent cases, including in a decision of
the full court of the Gauteng Division, Pretoria, in Malema v Road
Accident
Fund [2017] ZAGPJHC 275 para 92.”
[44]
Keshave’s evidence that the form of cerebral palsy with which
DMA was diagnosed was not
typical of an injury caused by a hypoxic
ischemic type of insult must be assessed against the fact that he
agreed with Van Toorn
in their joint minute that the form of cerebral
palsy was
less likely
, not that it is incompatible with the
nature of the injury. He also agreed with Van Toorn that the reason
why DMA was not manifesting
a quadriplegia, was simply that his left
sided motor area was spared by the injury. This is consistent with
Van Toorn’s oral
evidence that DMA in all likelihood managed to
overcome the injury on the other side of his brain.
[45]
In its assessment of Keshave’s evidence, the trial court
credited him with the fact that
he had performed a physical
examination of DMA. The question is whether this placed him in a
better position than Van Toorn to
make a diagnosis. Apparently not.
The court found that having physically examined DMA, Keshave was able
to determine that he had
dysmorphic features indicative of an
underlying genetic disorder. DMA was however subsequently examined by
the two geneticists,
namely Dr Gericke and Professor Christianson
who, as stated earlier, concluded that the child did not have any
dysmorphic features
of any genetic or syndromic nature. In fact,
Gericke pointed out in the joint minute that DMA’s ears were
not low set as
stated by Keshave in the written summary of his
evidence, and that the epicanthic folds to which Keshave also made
reference to,
can be attributed to a normal variant physical feature.
Christianson chose not to disagree with this observation of Gericke.
[46]
In addition to having relied on incorrect facts, a feature of
Keshave’s testimony, as previously
stated, is the speculative
nature thereof. In the written summary of his evidence, he was of the
opinion that the degree of weakness
to the left side of DMA’s
body would indicate that the insult to his brain occurred after
delivery, rather than as a result
of a hypoxic injury during birth.
His oral testimony on the contrary was that the cause of the injury
could possibly have been
either an underlying metabolic disorder, or
a hypoxic injury, the timing of which he would leave to the
radiologists. With regard
to the clinical conditions presented by
DMA, he was unable to say, “
How much of it could have been
from his NKH, from the hypoxic injury, from the alcohol. I am not
sure. I cannot put a definitive
answer to that. However, I do not
think you can rule it out.”
His mention of alcohol appears
to have arisen from a note by a therapist that the appellant had
consumed alcohol during her pregnancy.
When it was pointed out to
Keshave that the two geneticists have excluded any likelihood of the
presence of foetal alcohol syndrome,
he gave the unmotivated response
that there are a range of disorders that may arise from the use of
alcohol during pregnancy. What
the range of disorders are, was not
stated. He disagreed in a similar fashion, in cross-examination, with
the two geneticists when
it was put to him that they were in
agreement that they could not find any evidence of a genetic or
metabolic disorder. His response
was simply that “
those are
their opinions.”
He gave a similar unreasoned response when
confronted in cross-examination with the opinion the joint minute of
the two radiologists
that a genetic disorder as a cause of the injury
was unlikely.
[47]
From a reading of Keshave’s evidence and what he agreed to in
the two joint minutes with
Van Toorn, it is evident that he was not
able to raise NKH as a cause of the injury any higher than it being a
mere possibility.
The reason for this seems to lie in the fact that
his approach to the issue was that he was required to say
definitively, or at
least with a measure of certainty, what the cause
of DMA’s condition was. His view that where the clinical
features overlap
between two possible causes, the net must be thrown
wider before a diagnosis was made, appear to have been motivated by
his “
fear … that we always put the disability that
the child presents with as hypoxic ischemic injury and then forget to
investigate
everything else the child could have.”
[48]
The fact is that Keshave was not required to say with scientific or
medical certainty what the
cause of the injury was. The most commonly
employed technique for determining factual causation is the “
but
for”
test. This means that the appellant had to prove on a balance of
probabilities that, “
but
for”
the negligent actions or omissions of the respondent, the injury
would not have occurred.
[31]
The test for factual causation was explained simply and precisely by
Lord Denning in Cork v Kirby MacLean Ltd:
“
[I]f you can
say that the damage would not have happened BUT FOR a particular
fault, then that is in fact the cause of the damage;
but if you can
say that the damage would have happened just the same, fault or no
fault, then the fault is not the cause of the
damage.”
[32]
[49]
T
he
test need not be applied rigidly.
[33]
It also does not require factual causation to be determined with
scientific precision.
[34]
The
reasons for this is that factual causation is a requirement of the
substantive law for delictual liability, and its existence
is
determined by the rules of evidence, more particularly, the legal
standard set by the burden of proof. It accordingly requires
a
finding based on the legal standard of proof, and not a higher
standard that requires proof with any scientific precision.
[35]
“
It
has often been said that the legal concept of causation differs from
philosophical and scientific notions of causation. That
is because
‘questions of cause and consequence are not the same for law as
for philosophy and science’, as Windeyer
J pointed out in The
National Insurance Co. of New Zealand Ltd v Espagne
[1961] HCA 15
;
(1916) 105 CLR
569
, at p 591. In philosophy and science, the concept of causation
has been developed in the context of explaining phenomena by
reference
to the relationship between conditions and occurrences. In
law on the other hand, problems of causation arise in the context of
ascertaining or apportioning legal responsibility for a given
occurrence. The law does not accept John Stuart Mill’s
definition
of cause as the sum of the conditions, which are jointly
sufficient to produce it. Thus, at law, a person may be responsible
for
damage when his or her wrongful conduct is one of a number of
conditions sufficient to produce that damage.”
[36]
[50]
The burden of proof in a civil case requires a plaintiff to prove his
case no higher than on
a balance of probabilities. The probabilities
are determined upon the facts and an element of experience and common
sense.
[37]
It
calls for a sensible retrospective analysis of what would probably
have occurred, based upon the evidence and what can be expected
to
occur in the ordinary course.
[38]
Applying
the standard of proof to the test for factual causation, the enquiry
is directed at identifying the more plausible of any
one cause
against the backdrop of the negligent act found proved, including the
available evidence as a whole, which in a matter
such as the present,
will include, but is not limited to, expert opinion.
In
Linksfield
[39]
the court
pointed to the fact that expert scientific witnesses tend to assess
the likelihood of something in terms of scientific
certainty, and
stated that the “
Essential
difference between the scientific and the judicial measure of proof
was aptly highlighted by the House of Lords in the
Scottish case of
Dingley v The Chief Constable, Strathclyde Police 200 SC (HL) 77 and
the warning given at 89 D-E that ‘(o)ne
cannot entirely
discount the risk that by immersing himself in every detail and by
looking deeply into the minds of experts, a
judge may be seduced into
a position where he applies to the expert evidence the standards
which the expert himself will apply
to the question whether a
particular thesis has been proved or disproved – instead of
assessing, as a Judge must do, where
the balance of probabilities
lies on a review of the whole of the evidence.”
[51]
The
aforementioned shortcomings in the evidence of Keshave were not
considered by the trial court in its assessment of his evidence.
This
resulted in an uncritical acceptance of his evidence as having a
logical foundation, a finding that cannot stand. Keshave’s
evidence was speculative and incapable of throwing any doubt on the
otherwise acceptable expert opinion of the appellant that was
based
on sound grounds and supported by the basic facts. Material factual
errors that no doubt led to the aforementioned conclusion
of the
trial court, were (i) that the result of the blood tests was that DMA
was suffering from an underlying neuro-metabolic disorder,
which
accounted for his clinical position, as opposed to the result simply
indicating that he had raised glycine levels in his
blood; and (ii)
that it was common cause that the imaging patterns of DMA’s
brain did not typically follow the prescribed
patterns seen in
perinatal HIE. This finding is inconsistent with what was agreed to
by the radiologists.
[40]
[52]
The question is then whether the appellant had proved her case.
On
the whole, the clinical evidence supports the appellant’s
expert opinion that it is more likely than not that the brain
injury
sustained by DMA, and the disabilities that later followed, were the
result of prolonged partial hypoxic ischemia during
labour, as
opposed to NKH. The injury is consistent with the conduct of the
respondent in allowing a severely prolonged obstructed
labour of the
appellant to continue, which exposed the foetus to a real risk of
sustaining a hypoxic type of brain injury. It further
accords with
the clinical condition of DMA immediately following his birth. The
conduct of the respondent’s employees created
a risk of harm,
and the more plausible explanation is that the injury occurred within
that area of risk. The opinion of Van Toorn
was further supported by
the uncontradicted evidence of the radiologist Lotz, namely that the
type of brain injury with which DMA
had been diagnosed, could only
have been caused by a prolonged partial hypoxia ischemic cerebral
insult during the birth process.
As stated, Ahmed, the respondent’s
own radiologist, agreed in his joint minutes with both Lotz and
Alheit, not only with
the diagnosis of the type of brain injury
sustained by DMA, but also with the opinion that the likely cause of
the injury was a
hypoxic ischaemic insult.
[53]
For these reasons, the appeal must succeed with costs, which costs
are to include the costs occasioned
by the postponement of the appeal
on 2 August 2021 by reason of the respondent’s failure to
attend the hearing. The order
of the trial court is set aside, and it
is substituted with the following order:
“
It
is ordered that:
1.
The defendant is liable to compensate the plaintiff in her
representative capacity as the mother and natural guardian of DMA for
the damages claimed in this action in such sum as may be agreed to or
determined in due course.
2.
The defendant pay the plaintiff’s costs of the action, such
costs to include the costs
occasioned by the declaration hereby made
that the plaintiff’s expert witnesses who testified, including
Dr G S Gericke,
were necessary witnesses.
D
VAN ZYL
DEPUTY
JUDGE PRESIDENT OF THE HIGH COURT
I
agree:
B
MAJIKI
JUDGE
OF THE HIGH COURT
I
agree:
T
MALUSI
JUDGE
OF THE HIGH COURT
Counsel
for the Appellant: Mr G Austin
Instructed
by:
GARY AUSTIN INC
c/o GORDON McCUNE
ATTORNEYS
140 Alexander Road
KING WILLIAMS TOWN
Counsel
for the Respondent: Adv H J van der Linde SC
Ms T Mqobi
Instructed
by:
The State Attorney
c/o SHARED LEGAL SERVICES
OFFICE OF THE PREMIER
32 Alexander Road
KING WILLIAMS TOWN
[1]
Microcephaly is when the brain develops abnormally, causing the head
of the child to be smaller than expected for the child’s
age.
[2]
2001 (3) SA 1188
(SCA) (Linksfield) at para [37].
[3]
Supra at para [39].
[4]
Cross on Evidence 7
th
Ed
at page 489. See also Schmidt and Rademeyer Law of Evidence at page
17 – 4 and McGregor and Another v MEC for Health
Western Cape
(1258/2018)
[2020]
ZASCA 89
(31
July 2020) (McGregor) at para [21].
[5]
Ruto Flour Mills (Pty) Ltd v Adelson (1)
1958
(4) SA 235
(T)
at 237 A – B. See generally Schwikkard v van der Merwe
Principles of Evidence 3
rd
Ed
at page 83 and 87.
[6]
Menday
v Protea Assurance Co Ltd
1976
(1) SA 565
(E)
at 569 and Coopers (South Africa) (Pty) Ltd v Deutsche Gesellschaft
Für Schädlingsbekämpfung Mbh
1976
(3) SA 352
(A)
(Coopers) at 370 F – G.
[7]
Cross
op cit at page 494. See also Schmidt and Rademeyer op cit at page 17
– 14.
[8]
Coopers
at 371 F-H.
[9]
AM
and Another v MEC for Health, Western Cape (1258/2018) [
2020]
ZASCA 89
(31
July 2020) at para [17].
[10]
Mapota
v Santam Versekeringsmaatskappy Bpk
1977
(4) SA 515
(A)
from 527 to 528; Stacey v Kent
1995
(3) SA 344
(E)
(Stacey) at 348 to 349; Motor Vehicle Assurance Fund v Kenny
1984
(4) SA 432
(E)
and Representative of Lloyd’s and Others v Classic Sailing
Adventures (Pty) Ltd
2010
(4) All SA 366
(SCA)
at para [60].
[11]
Stacey
supra.
[12]
Coopers
at 371 H.
[13]
Linksfield
supra; Oppelt v Department of Health
2016
(1) SA 325
(CC)
(Oppelt) at para [36]; and Masstores (Pty) Ltd v Pick’n Pay
Retailers (Pty) Ltd and Another
2016 (2) SA 586
(SCA) at para [15].
[14]
MEC
for Health and Social Development, Gauteng v TM obo MM
(380/2019)
[2021]
ZASCA 110
(10
August 2021) at para [125]. Also Buthelezi v Ndaba
2013 (5) SA 437
(SCA) (Buthelezi) at para [14].
[15]
Oppelt
supra at para [35].
[16]
MEC
for Health and Social Development, Gauteng v TM obo MM supra at para
[126] and BEE v Road Accident Fund
2018 (4) SA 366
(SCA) at para
[23].
[17]
Schwikkard
and van der Merwe op cit at page 99 and the authorities referred to
in fn 102.
[18]
AN
v MEC for Health, Eastern Cape
[2019]
4 All SA 1
(SCA)
at para [22] and MEC for Health and Social Development, Gauteng v TM
obo MM supra at para [126].
[19]
Oppelt
supra at para [36].
[20]
Robins v National Trust Co (4) [1927] AC at 520.
[21]
Linksfield
supra
at para [37] and [38]; Medi-Clinic v Vermeulen
2015 (1) SA 241
(SCA)
(Medi-Clinic) at paras [4] to [8] and MEC for Health and Social
Development, Gauteng v TM obo MM supra at para [125].
[22]
Van
Wyk v Lewis
1924
AD 438
at
447; S v Gouws
1967
(4) SA 527
(E)
at 528D and Buthelezi supra at para [14]. See also Schmidt and
Rademeyer op cit at page 17 – 16.
[23]
Medi-Clinic supra at para [5].
[24]
See
the authorities referred to in Stacey supra at 348 to 359 F. See
also AM and Another v MEC for Health supra at para [17].
[25]
Stacey
supra at 350 G-H.
[26]
MEC
for Health, Eastern Cape v ZM obo LM (576/2019)
[2020] ZASCA 160
(14
December 2020) at paras [12] and [13].
[27]
The inference must be the readily apparent and acceptable inference
from a number of possible inferences. See AA Onderlinge Assuransie
Bpk v De Beer
1982 (2) SA 603
(A) at 620 E – G; Cooper and
Another NNO v Merchant Trade Finance Ltd
2000 (3) SA 1009
(SCA);
Goliath v MEC for Health, Eastern Cape
2015 (2) SA 97
(SCA) and M
and Another v The MEC for Health, Western Cape (1258/2018) [2020]
ZASCA (31 July 2020) at para [21]. “
Evidence
does not include contention, submission or conjecture.”
Great
River Shipping Inc v Sunnyface Marine Limited
1994 (1) SA 65
(C) at
75 I – 76 C.
[28]
Imperial Marine Co v Deiulemar Compagnia Di Navigazione Spa
2012 (1)
SA 58
(SCA) at para [24] and Motor Vehicle Assurance Fund v Dubuzane
1984 (1) SA 700
(A) at 706 B – D.
[29]
McGregor supra at para [21].
[30]
BEE
v Road Accident Fund supra at para [64]. See also Thomas v B D
Saracens (Pty) Ltd [2012] ZAGPJHC 161.
[31]
Lee v Minister for Correctional Services
2013 (2) SA 144
(CC) (Lee)
at para [40].
[32]
[1952] All ER 402
CA at 407.
[33]
Lee v Minister of Correctional Services supra at para [44].
[34]
Oppelt supra at paras (36) to (38). See also Minister of Safety and
Security v Van Duivenboden
2002 (6) SA 431
(SCA); Minister of
Finance and Others v Gore NO 2007 (1) SA 111 (SCA).
[35]
Ocean Accident and Guarantee Corporation Ltd v Koch
1963 (4) SA 147
(A) at 157 C – D and Blyth v Van den Heever
1980 (1) SA 191(A)
at 2088.
[36]
Mason CJ in March v E and MH Stramare (Pty) Ltd
[1991] HCA 12
;
[1991] 171 CLR 506
([1991] HCA 12).
[37]
Za v Smith and Another
[2015] 3 All SA 288
(SCA) at para [30]. Lee
supra at para [39].
[38]
Minister of Safety and Security v Van Duivenboden
2002 (6) SA 431
(SCA) at para [25]. See also Lee supra at para [39].
[39]
Supra at para [40].
[40]
See paras [22] and [23] of this judgment.