M M v Road Accident Fund (3677/2017) [2019] ZAFSHC 86 (6 June 2019)

50 Reportability
Personal Injury Law - Road Accident Fund

Brief Summary

Delict — Causation — Motor vehicle accident — Plaintiff claiming damages for injuries to minor child allegedly caused by accident — Plaintiff's evidence insufficient to establish causal nexus between accident and child's injuries — Expert testimony relied upon by Plaintiff deemed inadequate due to lack of specialization — Court finds no link between the negligent driving and the subsequent medical conditions of the child. The Plaintiff, M M, brought an action against the Road Accident Fund as the representative of her minor child, N M, claiming damages for injuries allegedly resulting from a motor vehicle accident on 2 September 2014. The Plaintiff contended that the accident caused a placental abruption leading to N's premature birth and subsequent medical issues, including hydrocephalus. The court examined the evidence presented, particularly the expert testimony, and concluded that the Plaintiff failed to establish a causal connection between the accident and N's injuries, ultimately dismissing the claim.

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[2019] ZAFSHC 86
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M M v Road Accident Fund (3677/2017) [2019] ZAFSHC 86 (6 June 2019)

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,
FREE
STATE
DIVISION,
BLOEMFONTEIN
CASE NO: 3677/2017
M
M
PLAINTIFF
v
ROAD ACCIDENT
FUND
DEFENDANT
HEARD ON:
7  MAY 2019
CORAM:
MURRAY AJ
JUDGMENT BY:
MURRAY, AJ
DELIVERED ON:
6 JUNE 2019
[1]
In this matter the Plaintiff
M M
instituted action
against the Road Accident Fund (“the RAF”) in her
capacity as natural mother, guardian and representative
of the minor
child
N M
for damages allegedly arising from a motor vehicle
accident on 2 September 2014. At the time of the collision the
Plaintiff was
32 weeks pregnant with N.  At issue is whether the
accident was the cause of N’s premature birth and subsequent
hydrocephalus.
[2]
Adv E Lubbe appeared for the Plaintiff and Adv H de la Rey for the
RAF.  Only two witnesses were called on behalf of the
Plaintiff,
namely the Plaintiff herself and Dr Kahn.  No witnesses were
called on behalf of the Defendant, but the Plaintiff’s
expert
was extensively cross-examined regarding his medical evidence and
conclusions.  By agreement Counsel filed written
argument on 16,
20 and 24 May, respectively.
[3]
Merits and quantum were separated.  For purposes of this case
the only injuries that can be relevant, would be injuries
sustained
by N, if any. The only issue to be determined regarding the merits is
the
nexus
between the accident and such ‘injuries’.
[4]
The Plaintiff’s case is that, as a result of the accident, she
suffered a placental abruption (‘
abruptio placentae’
)
and had to undergo an urgent caesarean section on 12 September 2014.
She avers that, as a result of that, N was born prematurely
and
developed a germinal matrix haemorrhage which resulted in obstructive
hydrocephalus for which she had to have a ventricular
shunt inserted,
and as a result has suffered severe developmental delays.
[5]
On the Plaintiff’s evidence, on
2 September 2014
her car
was rear-ended by the driver of the insured vehicle.  She was
wearing her seatbelt and sustained no injuries during
the collision
(“the MVA”).  The next day she drove her car from
Kroonstad to Welkom and back to arrange to have
it repaired by the
insured driver.  A few days after the incident her feet started
to swell. On
11 September 2014
, nine days after the accident
she developed abdominal pain and started to bleed.  Only on 12
September, when  the bleeding
became uncontrollable, did she go
to Welkom Medi-Clinic.  N was delivered by caesarean section on
the same day and placental
abruption was diagnosed.  N, although
born prematurely at 34 weeks, suffered no complications other than
some breathing difficulties
due to hyaline membrane disease.
[6]
Four days after her birth N was diagnosed with a Grade 1 germinal
matrix haemorrhage
[1]
(“GMH”).
Six months later, on
25
March 2015,
she started crying and vomiting and was diagnosed with a congenital
disorder, Dandy Walker Syndrome
[2]
,
and ‘associated obstructive hydrocephalus’
[3]
.
She had to have a shunt inserted, which failed, then had to
have a reduction done, and is left with severe developmental
delays.
[7]
The fact that the Plaintiff presented with placental abruption ten
days after the accident which resulted in N’s premature
birth
does not for purposes of this matter constitute injuries, nor does
her evidence take the matter any further save to confirm
that she was
not injured in the accident, that besides for swollen feet she only
started having uterine pain and bleeding nine
days after the accident
and that N was born on 12 September 2014 without complications apart
from the breathing difficulties for
which she was treated.
[8]
The Plaintiff was a credible witness regarding the accident itself on
2 September 2014. No evidence was presented for the Defendant
in that
regard.   But, although, in the absence of evidence to the
contrary, the negligence of the insured driver stands
undisputed,
that cannot render the RAF liable.  What the Plaintiff needs to
prove is that the alleged injuries suffered by
N were caused by and
arose from the accident.  What is in dispute, therefore, is
whether the accident caused N’s premature
birth, her germinal
matrix haemorrhage (“GMH”) and her hydrocephalus and
consequent developmental delays, and whether
the Court can safely
accept Dr Kahn’s version in that regard.
[9]
The Plaintiff’s own evidence did not establish a
causal
nexus
between N’s alleged injuries and the negligent
driving of the insured vehicle, however.  Her case therefore
stands or
falls on the evidence and medico-legal opinion of Dr Kahn,
a general practitioner who testified as an expert on her behalf.
[10]
Dr Kahn concluded that it was probably the germinal matrix
haemorrhage that caused the hydrocephalus and not the Dandy Walker

Syndrome.  In his view the obstructive hydrocephalus is related
to the prematurity which was caused by the placental abruption
which,
according to him, was directly caused by the accident.
[11]
Based on that conclusion, he averred that 25% of N’s
developmental delay is due to the Dandy Walker Syndrome and 75%
is
due to the trauma causing the placental abruption and the prematurity
which led to the intra-ventricular haemorrhage and obstructive

hydrocephalus and the need for a shunt.  He then recommended
that the Defendant be held liable for the damages which N allegedly

suffered as a result of the accident.
[12]
Dr Kahn based his conclusion on the fact that the neonatal sonar done
on
16 September 2014
showed an ‘intraventricular’
haemorrhage and no evidence of a Dandy Walker Syndrome. But to
determine if that conclusion
is warranted, one needs to have regard
not only to the nature and consequences  of a Dandy Walker
Syndrome, and of a germinal
matrix haemorrhage, and the relationship
of each with hydrocephalus, as well as to the nature and causes of a
placental abruption
in the circumstances of this particular case.
[13]
A causal nexus cannot be established by some magic formula:
[4]
the enquiry as to causation is a factual one, particular to each
specific case.
[5]
In order to
succeed with her claim, the Plaintiff needs to make out a case on a
balance of probabilities to substantiate her allegations
that N’s
alleged injuries were caused by the negligent driving of the driver
of the insured vehicle.
[14]
The first enquiry is based on the application of the ‘but-for’
test to determine whether, even if the MVA had not
happened, N would
still have presented with hydrocephalus, in other words if the
negligent driving of the insured vehicle is the
sine
qua non
for
N’s hydrocephalus.  The second enquiry would then be to
determine if the wrongful act (the MVA) is linked sufficiently

closely or directly to her hydrocephalus for legal liability of the
RAF to ensue, or whether her loss is too remote for that to

happen.
[6]
[15]
It is trite that an expert is there to assist the court
[7]
and may state his opinion, but that it is the Court which must decide
whether the opinion is correct and underpinned by the correct
facts
of that particular case.
[8]
In R
v Morela
[9]
it was held
that
“…
the court … has
not the special training to enable it to act on its own opinion; it
really decides whether it can safely
accept the expert’s
opinion.”
[16]
Dr Kahn is a general practitioner, who, according to his CV, is
qualified in Occupational Health, Tropical Medicine, Community
Health
and Health Administration.  He is a certified Independent
Medical Examiner, with experience, besides his practice,
apparently
mainly in the mining industry and as a part-time medical officer at
Welkom Medi-Clinic. He conceded that he lacked
qualifications in
neurocognitive sciences and neurosurgery and that he relied on the
reports of the specialists Dr Hugo (a neurosurgeon),
Dr Verster (a
radiologist) and Dr Fourie (a paediatrician) to formulate his own
report regarding this matter.
[17]
While it is true that no experts were called by the Defendant, one
has to view Dr Kahn’s testimony in the context of
the expert
medical reports on which he, on his own version, relied for his
opinion.  Although he is an experienced general
practitioner,
his report and his evidence must therefore inevitably be evaluated in
the light of his concession that he is neither
an expert in
neurocognitive conditions or neurosurgery, nor a qualified
obstetrician.
[18]
Hydrocephalus can be caused, for instance, by a birth defect,
haemorrhage, viral infection, or by Dandy Walker cysts.

It is confirmed by an x-ray of the blood vessels (an Angiogram),
computerized tomography (a CT scan) as in N’s case, or by
way
of magnetic resonance imaging (MRI) which show cross-sectional images
of the brain and related structures.
[10]
In obstructive hydrocephalus, such as was diagnosed in N
concomitantly with the Dandy Walker diagnosis, the cerebrospinal
fluid
is blocked, which causes widening of the pathways upstream of
the block, leading to increased CSF pressure in the skull.
[19]
The first question is whether N’s hydrocephalus was caused by
the Grade I germinal matrix haemorrhage (“GMH”)
which was
diagnosed on 16 September 2014, as Dr Kahn alleged, or by the Dandy
Walker Syndrome which was diagnosed on 25 March 2017.
It is
common cause that the GMH was caused by prematurity, while the Dandy
Walker Syndrome is a congenital malformation that has
nothing to do
with prematurity.  To succeed with her claim, the Plaintiff
would need to prove on a balance of probabilities
that the
haemorrhage was due to N’s premature birth and that the
prematurity was caused by the MVA. If the cause were to
be found to
be the haemorrhage, the next question would therefore be whether the
placental abruption that resulted in the prematurity
was caused by
the MVA.
[20]
Dr Kahn in his report stated that “
An
intra-ventricular haemorrhage of the brain was diagnosed on the
16/9/2014.”
The term ‘intra-ventricular haemorrhage’ in this
particular context is misleading although in the literature
it is
often used interchangeably with the term ‘germinal matrix
haemorrhage’ as a generic term for the condition, which
is then
classified into four ‘Grades’ according to the extent of
the bleeding. The reason why it is inappropriate in
this instance is
that the report
[11]
of Dr
Verster, the diagnostic radiologist, clearly states that it was a
Grade 1 germinal matrix haemorrhage (“GMH”)
with “
no
signs of intracerebral extensions or signs of intraventricular
haemorrhage or dilatation
.”
The radiology report therefore made it clear that the
bleeding did not extend into the ventricles.
[21]
This “intra-ventricular haemorrhage” according to Dr Kahn
caused N’s hydrocephalus.  The only reason
he gives for
this conclusion is that the Dandy Walker Syndrome was not visible on
the September ultrasound yet.  To see if
that conclusion is
feasible, one needs to examine the nature of a GMH and to test the
facts or assumptions underlying Dr Kahn’s
conclusion.
[22]
Four types of haemorrhaging frequently occur in preterm babies’
brains and are graded  based on the degree of bleeding.

Grades I and II involve a smaller amount of bleeding, and was found
in the study annexed to Dr Kahn’s report to usually resolve

spontaneously, with, in most instances, no long-term problems as a
result of the bleeding.  Grades III and IV, on the other
hand,
involve more severe bleeding and are associated with progressive
hydrocephalus.
[12]
[23]
Grade I germinal matrix haemorrhage (“GMH”) is
specifically what was diagnosed in N’s case on 16 September

2014.   It has been called the most frequent brain lesion
to be diagnosed in premature babies
[13]
and especially in those with hyaline membrane disease.
[14]
Dr Verster’s radiologic report made it clear that the bleeding
in N’s Grade 1 GMH was confined to the germinal
matrix and the
cauda-thalamic groove on the right and did not extend into the brain
or into the ventricles.  Dr Verster found
no widening
(dilatation) of the ventricles (which would have indicated blockage
or partial blockage of the ventricles) and found
that the rest of the
brain’s parenchymal, subarachnoid spaces appeared to be
normal.  He also found the midline to be
central and the basal
cisterns and posterior fossa to appear normal.
[24]
At that stage (on 16 September 2014), therefore, there was no sign of
hydrocephalus, and the signs and symptoms of Dandy Walker
Syndrome
appear not to have developed to a point where they were observable by
ultrasound yet.  They  only became apparent
in March 2015
when N started crying and vomiting.  The CT of her brain then
revealed features of Dandy Walker syndrome with
large posterior fossa
cyst (which would have blocked the ventricles and accordingly the
flow of cerebrospinal fluid above the blockage),
hypoplasia of the
cerebellum, displacement of the large venous sinuses and scalloping
of the occipital bone; as well as associated
hydrocephalus with
prominent peri-ventricular oedematous changes.
[25]
There therefore is no factual evidence that the Grade 1 GMH in N’s
case was not an ‘isolated’ of ‘confined’
GMH
that resolved spontaneously without infiltrating the ventricles since
no follow-up ultrasound appears to have been done as
Dr Verster
recommended.  There was in September no indication of
hydrocephalus (for instance dilated ventricles or irritability
or
vomiting).  On Dr Kahn’s own version the paediatrician
deemed N to be fine when she was released on 23 October 2014
and she
was already sitting at 3 to 4 months old. On the facts before this
Court, she therefore appears to have developed normally
for the first
few months. There is no evidence that anything was wrong until she
started crying and vomiting, which only happened
in March 2015.
[26]
Had the diagnosis on 26 September 2014 been one of a Grade III
haemorrhage with bleeding extending into the ventricles, or
a Grade
IV haemorrhage, also called an ‘Intraparenchymal Haemorrhage’
with the bleeding directly involving the brain
tissue, a conclusion
that the haemorrhage caused the subsequent hydrocephalus would have
been a much more feasible one.  It
would then have been much
more probable that blood clots would have formed and blocked the flow
of cerebrospinal fluid, which would
have led to increased fluid in
the brain.  An increase in the size and pressure of the fluid
spaces surrounding the brain
may then have caused obstructive
hydrocephalus.
[27]
Therefore, had it been either a Grade III or a Grade IV haemorrhage
that was diagnosed in September, the haemorrhage as cause
of the
hydrocephalus would justifiably have been regarded as a probability
rather than as a mere possibility.  The Grade 1
GMH, however,
until proven to have spread, was confined to the small area of the
brain indicated in Dr Verster’s report (a
so-called ‘isolated
or confined Grade I GMH’).  In the absence of any evidence
of progression of the bleeding
into the ventricles and other brain
structures or of any known physical evidence of hydrocephalus before
March 2015, the Grade
I GMH with which N was diagnosed, cannot be
regarded as the probable cause of the obstructive hydrocephalus.
At most it can
be a viewed as a
possibility
, and a very slight
one at that.
[28]
Furthermore, had N not suffered from the Dandy Walker Syndrome, an
inference that the GMH had caused the hydrocephalus would
have been
more logical.  But in the absence of factual proof of
progression of the bleeding into surrounding brain structures,
and in
view thereof that the hydrocephalus was diagnosed together with the
Dandy Walker syndrome, such an inference is not a reasonable
one in
this case.  Especially if regard is had to the nature of the
Dandy Walker Syndrome and the strong relationship between
it and
hydrocephalus.
[29]
It was only in March 2015 when N started to cry and vomit that
obstructive hydrocephalus and the Dandy Walker Syndrome were

diagnosed. ‘Associated hydrocephalus’ with prominent
swelling around the ventricular system was evident on the CT scan
of
the brain which revealed the Dandy Walker Syndrome and which,
according to Dr Verster’s report, ‘may account for
the
possible acute presentation’.
[30]
The report of Dr Daniel Hugo, the neurosurgeon, one of the experts on
whose report Dr Kahn also relies, stated that N was born
with
hydrocephalus and a variety of intra-cranial problems.  He
merely found that there was a
possibility
(‘
moontlikheid’
)
[15]
not a probability (‘
waarskynlikheid’)
[16]
that the hydrocephalus
developed as a result of the MVA.   And he categorically
stated that it was impossible at that
stage to determine whether the
hydrocephalus was caused by the MVA since when he saw N, she already
presented with hydrocephalus
as well as ventriculitis.
[31]
Dr Hugo then concluded that it could be post-traumatic hydrocephalus,
or it could be hydrocephalus caused by a congenital defect
or even by
a birth injury. He held that, without pre-natal sonars which do or do
not show hydrocephalus, it would be impossible
to determine if the
MVA caused the hydrocephalus. But, even though the two prenatal
sonars which are available do not show hydrocephalus,
that does not
mean that it was the GMH that caused it and not the Dandy Walker
Syndrome, and the Plaintiff would still need to
prove on a balance of
probabilities that whatever caused the hydrocephalus was caused by
the MVA.
[32]
It is common cause that the Dandy Walker Syndrome which was diagnosed
6 months after the accident, is a congenital disorder
which can
safely be disregarded as having been caused by the accident.
Dandy Walker malformation involves the cerebellum
(back of the brain)
and one of its key features is an enlargement of the fourth ventricle
which is a small channel that allows
fluid to flow freely between the
upper and lower areas of the brain and spinal cord.  The fourth
ventricle becomes enlarged
because its outlets are partly or
completely closed and part of the cerebellum fails to develop.
[17]
It can cause obstruction of the normal drainage of cerebrospinal
fluid (CSF), resulting in a build-up of CSF and hydrocephalus.
[33]
The said congenital brain malformation occurs during early embryonic
development of the cerebellum (the movement centrum of
the brain) and
the fourth ventricle.  In several medical studies the extremely
high prevalence of hydrocephalus in persons
suffering from Dandy
Walker Syndrome has been confirmed.   In one study
conducted over a period of 30 years, for instance,
it was found that
70% of patients presented with Dandy Walker Syndrome in the 1
st
year of life and that hydrocephalus was present in
91%
of patients at the time of diagnosis of the Dandy Walker
Syndrome.
[18]
[34]
It has also been found that the signs and symptoms caused by abnormal
brain development in the majority of individuals with
Dandy Walker
Malformation are either present at birth already or develop within
the first year of life, and that they can appear
dramatically or
develop unnoticed.
[19]
As
the malformation develops, an increase in size of the fluid spaces
around the brain and an increase in pressure may develop
due to
blockage of the normal flow of spinal fluid leads which leads to
excessive amounts of fluid which then accumulates in and
around the
brain.  That leads to abnormally high pressure within the
skull.  Crying and vomiting, such as N did in
March
2015
,
are some of the symptoms of increased intracranial pressure.
[35]
It is therefore clear that the very fact that N has Dandy Walker
Syndrome makes it inevitable, or at the very least most probable,

that she would have developed hydrocephalus anyway, even if she had
not been born prematurely and regardless of the occurrence
of the
MVA.  Compared to the very high probability of hydrocephalus
having been caused by the Dandy Walker Syndrome, the slim
possibility
that it may been caused by the Grade 1 GMH, in the absence of any
evidence to support such an inference, in my view,
makes it more
probable than not that the congenital Dandy Walker Syndrome was the
cause of N’s hydrocephalus and not the
Grade I germinal matrix
haemorrhage.
[36]
But even if I should be wrong about that, I am of the view that it
has not been proven on a balance of probabilities that the
MVA was
the cause of the placental abruption and consequently of N’s
prematurity, either.  If it was not the cause,
even if the
haemorrhage were to have caused the hydrocephalus, of course there
would be no causal connection between the MVA and
the hydrocephalus.
[37]
Placental abruption occurs when the placenta partially or completely
separates from the inner wall of the uterus before delivery.
It
happens mostly in the third trimester of pregnancy, and can happen
suddenly.  Signs and symptoms of placental abruption
are,
inter
alia,
vaginal bleeding and abdominal pain.  According to Dr
Kahn’s report, as well as the hospital record of 12 September
2014,
the Plaintiff started to have uterine pain and bleeding only on
11 September 2014, nine days after the accident.  On the
Plaintiff’s
version the bleeding became ‘uncontrollable’
on 12 September and a Caesarian was performed.
[38]
The exact cause of placental abruption is often unknown, as it is in
this case, according to Dr Fourie’s report. There
are numerous
possible causes such as,
inter
alia
, a
fall or other type of blow to the abdomen, insufficient amniotic
fluid, sudden uterine decompression, high blood pressure during

pregnancy, smoking
[20]
,
cocaine or other drug use during pregnancy, infection in the uterus
during pregnancy, maternal age of 35+,
[21]
abnormalities of the uterus, abnormalities of the umbilical cord
[22]
or of the placenta, membrane ruptures.
[39]
In the present case, the Plaintiff confirmed that she was wearing a
safety belt at the time of the accident, and that she suffered
no
injury and felt no pain during the collision.
[23]
The Plaintiff is also known to have been HIV positive and on
anti-retroviral medication during her pregnancy. It is not known
whether she smoked during pregnancy.  Furthermore, it is
undisputed that the baby suffered from the congenital Dandy Walker

Syndrome which affects the embryonic brain structures.  It is
known that babies with a brain defect are at high risk for pre-term

birth.
[24]
[40]
Yet Dr Kahn categorically stated that it
was
the motor vehicle
accident that caused the placental abruption which was diagnosed 10
days after the accident.  That constitutes
a quantum leap in his
reasoning, as did his conclusion that the Grade I germinal matric
haemorrhage caused the hydrocephalus.  There
is no evidence to
support such a conclusion. Dr Kahn maintained that the other experts
did not disagree with him.  But, that
is not correct. He was the
one who used their reports to compile his, not the other way round.
[41]
The report of Dr Fourie, the obstetrician on whose report Dr Kahn by
his own admission relied for his conclusion regarding
the placental
abruption, for instance, did
not
conclude that the accident did cause the abruption.  Dr Fourie
categorically stated that
it
is difficult to determine the exact cause of the placental abruption
‘since there may have been a couple of reasons’
of which blunt trauma, like an MVA,
[25]
can
contribute to an occult placental abruption which then leads to
preterm birth.  She, in other words, mentioned trauma as a
possibility
.
She also added that the Plaintiff’s
medical
condition could also contribute,
in
other words another
possibility
.
Although Dr Fourie said that there is no literature that confirms
that Dandy Walker Syndrome is associated with placental

abruption,
[26]
she did add
that there is evidence that preterm labour is associated with
congenital abnormalities
[27]
.
Dr Kahn conceded as much.
[42]
Mr Ettienne van Lille, a clinical psychologist who assessed the
Plaintiff and studied the reports of Drs Hugo, Verster and
Fourie,
furthermore, in his report noted with regards to the Plaintiff’s
HIV status and use of anti-retroviral medication
during the
pregnancy, that research has shown that the HIV status of the mother
and the use of certain retro-viral medications
may increase the
vulnerability to or lead to an increased risk of pre-mature birth of
the foetus.  He stated that in his opinion,
within the context
of the pre-natal, peri-natal and postnatal conditions, to support a
premise of the accident as the sole cause
of the client’s
current condition and functioning is questionable.
[43]
Furthermore, there is no factual evidence whatsoever of ‘blunt
trauma’ to the Plaintiff’s abdomen.
The Plaintiff
herself insisted that she was wearing a seat-belt.  On her own
version she was unhurt.  It is also undisputed
that the
Plaintiff suffered from HIV and was using anti-retroviral medication
at the time of the accident.  There is no evidence
that the
Plaintiff’s use of ARV’s during pregnancy was properly
controlled. As set out above, therefore, the Plaintiff
had several
risk factors for preterm labour and as is evident  from the
medical literature, there are numerous potential causes
for placental
abruption other than an MVA.
[44]
In view of the absence of any factual evidence of blunt trauma to the
Plaintiff’s abdomen, the 10 day lapse between the
MVA and the
abruption, and the undisputed evidence of the presence of other risk
factors such as the Plaintiff’s HIV status
and her use of AVR’s
during pregnancy, it is not possible to find that the MVA is anything
more than simply one of several
possible
causes of N’s
preterm birth.  Furthermore, there is no evidence that the MVA
can be linked to the congenital Dandy Walker
Syndrome and its
associated hydrocephalus.
[45]
Regarding Dr Kahn’s evidence, I respectfully agree with Seriti
JA’s remark in
Glen
Marc Bee v Road Accident Fund
[28]
that:

Expert witnesses
are required to lay a factual basis for their conclusions and explain
their reasoning to the court.  The court
must satisfy itself as
to the correctness of the expert’s reasoning…  An
expert’s opinion must be underpinned
by proper reasoning in
order for a court to assess the cogency of that opinion.  Absent
any reasoning, the opinion is inadmissible…
For  an
opinion to be underpinned by proper reasoning, it must be based on
correct facts … the correct analysis of
the facts is paramount
for proper reasoning, failing which the court will not be able to
properly assess the cogency of that opinion.”
[46]
Unfortunately I have to agree with Mr de la Rey that specific parts
of Dr Kahn’s evidence and medico-legal report and
his
subsequent conclusions are void of a factual basis, are not
substantiated by the factual evidence and are based on selective

reasoning.  As stated above, his continued explanation for the
discrepancies between his opinion and those of the other experts,

namely that “
the other experts don’t disagree with
him”
has no merit, since on his own evidence he based his
opinion on information obtained from the other experts, not the other
way around.
[47]
At best for the Plaintiff, therefore, evidence of
possibilities
was placed before the Court, but no credible evidence on which
the Court can find on a balance of probabilities that causality and

legal liability of the RAF have been established.  The
Plaintiff’s claim therefore cannot succeed.
[48]
Costs normally follow the outcome.  In this case, however, in
view of the particular circumstances of the case, such as,
for
instance the fact that the RAF did not immediately reject the
Plaintiff’s serious injury report, and Dr Kahns’

conclusions about the cause of N’s prematurity and
hydrocephalus, the Plaintiff would have had reason to believe that
she
might succeed with a claim on behalf of N. The Plaintiff can
therefore not be blamed for bringing the matter to court.  In
my
view it would therefore be an injustice if she were to be ordered to
pay the RAF’s costs.
[49]
In the circumstances I therefore intend to make no order as to costs.
WHEREFORE
the following order is made:
1. The Plaintiff’s
claim is dismissed.
__________________________
H
MURRAY,  AJ
On
behalf of the Plaintiff:

Adv E G Lubbe
Instructed by B L
Kretzmann Attorneys
c/o McIntyre & Van
der Post
12 Barnes Street
BLOEMFONTEIN
On
behalf of the Defendant:

Adv H de la Rey
Instructed by Mr J
Dlamini
Maduba Attorneys
Unit 1, Ground Floor
Canterbury Park
65 – 67 Pres Reitz
Ave
Westdene
BLOEMFONTEIN
[1]
Such a haemorrhage can occur due to perinatal asphyxia in preterm
neonates.
[2]
A congenital disorder that can lead to obstructive hydrocephalus
[3]
Obstructive hydrocephalus is an abnormal accumulation of
cerebrospinal fluid (CSF) in the ventricles and spaces around

the brain caused by blockage of the ventricles.
[4]
Lee v Minister of Correctional Services 2013 (2) SA 144 (CC); 2013
(1) SACR 213 (CC)
[5]
International Shipping Company (Pty) Ltd v Bentley
1990 (1) SA 680
(A) at 700 E-I
[6]
Miller v RAF [1999] 4 All SA 560 (W)
[7]
Stock v Stock 1981 3  SA 1280 (A)
[8]
Road Accident Appeal Tribunal & Others v Gouws & Another
[2017] ZASCA] 188l
[2018] 1 All SA 701
(SCA) at par
[33]
;  See
also Michael & Another v Linksfield Park Clinic (Pty) Ltd and
Another
[2002] 1 All SA 384
(A) at par [34];  S v Gouws
1967 4
SA 527
(E) 528 D,  Schmidt: Law of Evidence, at pages 17-9 –
17-20.)
[9]
1947 3 SA 147
(A) at 153
[10]
National Organisation for Rare Disorders. Database.
[11]
At p. 4 thereof.
[12]
Burstein, J
et
al.
Intraventricular
Hemorrhage and Hydrocephalus in Premature Newborns: A Prospective
Study
with CT AJR 132: 631 – 635, April 1979.
[13]
S Robinson, Neonatal posthemorrhagic hydrocephalus from prematurity:
Pathophysiology and current treatment concepts.  Rainbow
Babies
and Children’s Hospital, Neurological Institute, University
Hospitals of Cleveland, Case Western Reserve University,
Cleveland
Ohio.  Journal of Neurosurgical Pediatrics 2012 March 9(3):
10.3171/2011.
[14]
Agamanoulis, D: Neuropathology: Perinatal Ischemia and Stroke.
[15]
Bosman, Van der Merwe & Hiemstra:  Bilingual Dictionary,
Tafelberg Uitgewers, 1984, at p 329 translates ‘
moontlik

and ‘
moontlikheid

as ‘
possible,
possibly, perhaps, could conceivably happen, maybe’
and as  ‘
possibility,
off-chance’..
.
The New Shorter Oxford English Dictionary, Vol 2, at p. 2302 in turn
defines ‘
possible

and ‘
possibility

as ‘
it
can or may happen or can perhaps happen, it is conceivable that it
may
happen’.
[16]
Bosman, Van der Merwe & Hiemstra
:
Bilingual
Dictionary at p. 623 translates ‘
waarskynlik

and ‘
waarskynlikheid

as  ‘
probable,
probably, ‘doubtless’, no doubt’, likely
’.
The New Shorter Oxford English Dictionary, Vol 2, p. 2362 in turn
defines ‘
probable

and ‘
probability

as ‘
having
the appearance of truth or fact’
‘a degree of likelihood’ ‘may reasonably be
expected to happen or be the case’ and ‘
Probability”
an event judged likely to happen/be true a probable event/a thing
likely to be true or to happen.’
[17]
Hydrocephalus Association, USA
[18]
Drs RK Osenbach and AH Menezes, Division of Neurological
Surgery, University of Iowa Hospitals and Clinics, Iowa, USA;

“Diagnosis and Management of Dandy-Walker Malformation: 30
Years of Experience” Pediatric Neurosurgery 1992 ; Vol
18: No.
4, pp 179 - 189
[19]
National Institute of Neurological Disorders and Stroke (NIH);
The Dandy Walker Alliance, USA. The webpage of the American
Dandy
Walker Association claims that most children with Dandy Walker
Syndrome will develop hydrocephalus from the CSF build-up
in the
brain before their first birthday and the webpage of the Department
of Neurosurgery of the University of California, Los
Angeles,
estimates that hydrocephalus occurs in up to
90%
of
Dandy Walker cases.
[20]
Shobeiri F
et
al
The
Association between maternal smoking and placenta abruption: a
meta-analysis, Journal of Maternal Fetal Neonatal Medicine.
2017; 30
(16):1963. E-published 30 Sept 2016.
[21]
Mayo Clinic, Patient Care & Health Information, USA; William’s
Obstetrics, 22
nd
Ed, Cunningham F,  Gary
et
al
EDS;
Schmidt P, Raines DA: Placental Abruption (Abruptio Placentae),
2019.
[22]
Though in this instance from the medical records that the umbilical
cord was normal, we do not know that the placenta itself
was.
[23]
On their pregnancy web page the American Mayo Clinic Association
specifically advises pregnant women to always wear a safety
belt in
a moving vehicle to prevent direct abdominal trauma.
[24]
William R Brown, Dept of Radiology, Dept of Pathology, Wake Forest
University School of Medicine. Winston-Salem, NC, p.4 found
that
babies with brain defects have a high risk of preterm birth.
He even went so far as to say that the study suggests
that babies
with brain defects are predisposed to be born preterm. This was
confirmed by MA Honein, et al. in The Association
between Major
Birth Defects and Preterm Birth Maternal Child Health Journal (2009)
13: 164 – 175 in a study which found
that babies with brain
defects have a strong propensity to be born preterm and that either
the brain defects themselves or the
underlying cause of the defects
may be inducing preterm birth.
[25]
In a study done on 317 pregnant patients evaluated for
minor
trauma, of the 256 for whom the delivery information was available,
only one patient suffered a placental abruption.  In
another
study it was found that while minor abdominal injury has a small
possibility of causing preterm labour, the risk of placental

abruption rose with the severity of the abdominal injury.
[26]
In a 2013 study of nine babies with Dandy Walker Syndrome, for
instance, four of the babies with a Dandy Walker variant had
combined umbilical cord abnormality and one with classic Dandy
Walker Syndrome had combined placental abnormality. The conclusion

was that, in addition to complex pathogenesis and possible genetic
and environmental antigenic etiologies, placental and umbilical

abnormality may even be related to the development of the Dandy
Walker Syndrome. X Zhang, C
et
al
Dandy
Walker Syndrome: A Clinical Pathological Study 01/12/2013. US
Federal Science Topics.
[27]
See the studies of Brown and Honein,
supra
.
[28]
[2018] ZASCA 52
at paras [22] – [23].  See also Masstores
(Pty) Ltd v Pick ‘n Pay Retailers (Pty) Ltd
[2015] ZASCA 164l
2016 (2) A 586 (SCA) at par [15]; Jacobs v Transnet Ltd t/a
Metrorail
[2014] ZASCA 113
;
2015 (1) SA 139
(SCA) at paras [15] and
[16];  Coopers (South Africa) (Pty) Ltd v Deutsche Gesellschaft
für Schädlings-bekämpfung
mbH
1976 (3) SA 352
(A) at
371F.