M obo M v Member of the Executive Council for Health and Social Development of the Gauteng Provincial Department (2011/41603) [2018] ZAGPJHC 513 (1 October 2018)

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[2018] ZAGPJHC 513
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M obo M v Member of the Executive Council for Health and Social Development of the Gauteng Provincial Department (2011/41603) [2018] ZAGPJHC 513 (1 October 2018)

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Certain
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REPUBLIC
OF SOUTH AFRICA
IN THE HIGH COURT OF
SOUTH AFRICA
GAUTENG LOCAL
DIVISION, JOHANNESBURG
Case
No: 2011/41603
In
the matter between:
M:
B obo
M:
K
PLAINTIFF
And
THE
MEMBER OF THE EXECUTIVE COUNCILFOR
HEALTH
AND SOCIAL DEVELOPMENT OF THE
GAUTENG
PROVINCIAL
DEPARTMENT
DEFENDANT
Summary
:
Claim for damages – arising out of injuries sustained by foetus
at birth - negligence of employees of Defendant –
test for
negligence discussed – causation – absence of hospital
records – Defendant negligent and found liable.
JUDGEMENT
CELE
AJ
Heard:
18 June 2018
Delivered:
01 October 2018
Introduction
[1]
The plaintiff sues herein in her personal and representative
capacity, as the mother and natural guardian of her minor child,
K M
(the child), who was born on […] January 2006 at the Chris
Hani Baragwanath Hospital (The Hospital).  The claim
is based
upon the alleged negligence of the medical and/or nursing staff of
the hospital, resulting in the child suffering from
cerebral palsy.
By agreement between the parties Court ordered that the issues of
liability and quantum be separated and the determination
of quantum
of damages was postponed
sine die
. The Defendant opposed the
claim by denying that any of its staff acted negligently.
Factual
Background
[2]
A pregnant Plaintiff attended antenatal clinic for at least four
times. There was no history of any deficiencies of the foetus.
A
private doctor she attended in August 2005 told her that she was
carrying a baby girl, which was to be her first born. On […]

January 2006 she woke up early in the morning, went to the bathroom,
discovered that she was bleeding (spotting) and she reported
this to
her mother with whom she lived. According to her it was still early
morning around 02h00 because it was still dark. She
never checked the
exact time. Transport was arranged by her mother to ferry her to the
Hospital. Her mother, Ms Teboho Margaret
Mbanda thought it was about
04h50 when the Plaintiff left home for the Hospital. The Plaintiff
proceeded to the labour department
where she registered her
particulars and she was offered a hospital night dress to change
into.  When asked what was wrong
with her she reported that she
was bleeding. She was made to sit on a bench and was offered porridge
to eat.
[3]
Urine testing was conducted on her by a nurse and she was taken into
a cubicle with a bed which she was made to lie on. The
Plaintiff said
that a brown belt, referring to a cardiotocograph monitor otherwise
often referred to as the CTG monitor, was connected
on her. The CTG
is used for monitoring the expectant mother and the foetal heartrate
before, during and after contractions. Any
deceleration picked up by
the CTG monitor is a symptom of foetal destress and it must
immediately be acted upon to alleviate the
distress. The CTG depicts
a graphic pattern and produces an audible sound which requires
interpretation of patterns associated
with foetal distress and it
informs the decision to intervene and accelerate birth.
[4]
By then the Plaintiff had spent more than an hour since her arrival
at the Hospital. She was then moved to another cubicle,
taking the
monitor with her. A male Doctor attended to her by conducting some
tests on her. He ordered a nurse to get an intravenous
infusion (a
drip) which was connected to her. She estimated the time to be 11h00
by then, though she had no watch. While the Doctor
continued to check
on her he spoke to another person in attendance about a Caesarean
section but she could not hear what exactly
was said. This happened
at about 11h10. Thus far, the Plaintiff had not had any labour pains.
She was then given medication to
induce labour. Some 30 minutes later
a further dosage was given to her to further induce labour. Sometime
later she was moved to
the delivery room where she was counselled
about the delivery process and was told what to do at various stages.
She thought it
was then about 14h30.
[5]
A Doctor attended to her and he broke her water as it had not yet
broken and then left. Still she had no labour pains and the
baby was
not coming. The nurse repeatedly told her to push. Time passed and
the nurse called for another Doctor who inserted his
hands into her
and appeared to feel something. The baby then presented herself. She
had a nuchal cord around her neck. The Doctor
called for a scissor
which was brought by a nurse. He clamped the nuchal cord, cut it and
he pulled the baby out. Birth was accordingly
by vertex delivery at
around 15h30 on […] January 2006.
[6]
The baby was then taken away from the mother and placed into a head
box. Most of the records pertaining to the labour and birth
periods
of the child were lost at the hands of the Hospital staff. From the
remaining birth records the newly born baby or neonate
was born with
normal anthropometrical measurements but did not immediately breath
had a reduced muscle tone and a blue coloration
requiring immediate
resuscitation, hence the immediate placement into the head box.
Saturation of the neonate then improved to
normal, at 93%.
[7]
It was only on the next day that the Plaintiff saw her newly born
baby who was still in the cubicle in the neonatal unit. On
30 January
2006 the baby were still in Hospital as she was receiving treatment.
The neonatal discharge summary notes of this baby
contained the
following information about the baby:-
1. APGAR scores were
recorded at 4/10 at one minute of life and 7/10 at 5 minutes of life;
2. Birth weight was
recorded at 3000g and the discharge weight (6 days later) at 3280g;
3. Gestational age was
recorded as term;
4. Findings in respect of
a cranial ultrasound were recorded as a bright brain, good pulsations
and no bleeds;
5. Diagnosis of perinatal
asphyxia;
6. Cord around the neck;
7. A PH was recorded as
7.23 and base excess recorded as - 8.2.
[8]
When the baby was discharged, the Plaintiff was not told anything
about the medical condition of her baby. She followed up the

discharge with a number of clinical visits. The birth of her child
was registered at Home Affairs offices and K was the name given
to
the baby. The Plaintiff never requested for an abridged birth
certificate.
[9]
The Plaintiff had to consult various doctors as time went on and it
appeared something was wrong with her baby. The baby was
diagnosed
with cerebral pulse. One such Doctor consulted was Dr Basson, an
obstetrician and gynaecologist. The Plaintiff could
not remember the
exact dates of such visitations. When K was 8 years 1 month a number
of brain scans were taken of her and presented
to Professor Jan
Willem Lotz, a Specialist Radiologist to analyse and interpret. The
Plaintiff had a one on one consultation with
Dr Basson and later also
met Dr Pearce, a paediatric neurologist on 23 June 2016.  The
case of K was then referred by the
parties to their various experts
who compiled then filed their reports. Some of the experts exchanged
their notes and formulated
joined minutes in respect of the aspects
they agreed on. Where there were points of departure these were noted
by the experts.
[10]
As the parties were preparing this matter for trial, they attempted
to narrow the issues in dispute through three pre-trial
minutes. Some
of the issues settled in the pre-trial minutes are that the Defendant
admitted that:-
1. At all relevant times
hereto and particularly during on or about January 2006:
1.
Defendant was and still is the responsible person in respect of any
and all contractual and delictual liability of the Department
of
Health and Social Development of the Gauteng Provincial Government;
2.
The Chris Hani Baragwanath Hospital was and still is the a hospital
which falls under the authority of and is controlled and
operated by
the Department of Health and Social Development of the Gauteng
Province;
2. Defendant by reason
of:
1.
The existence of the public Hospital and the fact that the Defendant,
through his Department of Health and Social Development,
held out  to
the public and particularly the Plaintiff, that the aforesaid
Hospital was a facility where reasonable medical
care, treatment and
advise is rendered and/or
2.
The Plaintiff’s admission as a patient at the said Hospital and
the undertaking by such Hospital to render medical care
and treatment
to her and her unborn child and/or
3.
The provision of section 9 (the right to equality), section 10 (the
right to dignity), section 11 (the right to life) and section
27 (the
right to health and health care services) of the Constitution of the
Republic of South Africa, Act1996 was under a legal
duty to ensure
the rendering of medical care, treatment and advise to Plaintiff with
such skill, care and diligence as could reasonably
be expected of
medical practitioners and nursing staff in similar circumstances,
obliging the Defendant to ensure proper, sufficient
and reasonable
health services are provided to members of the public, particularly
those who were obliged to make use of such services
of a public
hospital;
3. The aforesaid legal
duty of care extended to K Zoe (then as an unborn child)
4. Any and all medical
practitioners and nursing staff (whose identities are to the
Plaintiff unknown) who were involved or who
were obliged to become
involved in the admission to and the rendering of medical services
and the examination, monitoring and/or
treatment of the Plaintiff at
the aforesaid Hospital were either permanent or temporary employees
of Defendant who acted within
the course and scope of their duties as
permanent or temporary employees.
5. The main problems of
birth were, inter alia, identified and recorded as perinatal asphyxia
with a pH of 7.23 and a BE of 8.2.
In addition it was noted that the
baby was delivered with the cord around her neck.
6. Cranial ultra sounds
of the child confirmed a bright brain, good pulsations and no bleeds.
7. The MRI distribution
of changes when K was 8 years 1 month old, namely deffuse bilateral
periventricular and subcortical cystic
and non-cystic leukomalacia
and bilateral T2 hyperintensity-pulvinar, lateral thalamic and PLIC
was in keeping with hypoxic ischemic
event/s, mixed pattern
predominately of a partial prolonged type.
8. The findings of the
MRI studies suggest that genetic disorder as a cause of the child’s
brain damage was unlikely;
9. The child’s
cerebral palsy does not have a genetic/syndromic origin as per Prof
Christian’s addendum report;
10. There was no evidence
from the family history, clinical evaluation, MRI or cranial
ultrasound suggestive of a genetic, hereditary
or metabolic cause for
K’s medical condition;
11.  According to
Prof Christianson’s addendum report, the child had the
following:
11.1
Mixed cerebral palsy – dyskinetic and spactic quadriplegia;
11.2
Microcephatic;
11.3
Epilepsy not controlled;
11.4
Contractures.
12 Hyperekplexia –
this is a clinical feature associated with cerebral palsy, as such it
has no significance in this case
– as per Prof Christianson’s
addendum report.
13.  The brain
injury was suffered during the intrapartum period as per Dr
Magashoa’s summary in medico-legal report.
(Dr Mogashoa adds
that the nuchal cord contributed to the intrapartum hypoxia).
Evidence
[11]
The general onus of proof rested on the Plaintiff to satisfy Court at
least on a balance of probabilities that her version
was the truth.
Six witnesses were called to testify at the instance of the
Plaintiff. In its general nature the evidence
of the Plaintiff and
her mother is common cause and forms part of the factual background,
save to note that such evidence is contradictory
when it comes to the
time when the Plaintiff left home for Hospital on […] January
2006. On the basis of documentary and
viva voce
evidence the
other four witnesses are found to be experts in their related fields
of training and practice over many years. A summary
of the evidence
of these four witnesses shall now be outlined.
Plaintiff’s
version
Professor
Jan Willem Lotz [Specialist Radiologist]
[12]
He made a step by step presentation of sixteen slides
[1]
through which he showed in general and in specific terms how brain
injury occurs when a foetus is exposed to asphyxia at the
commencement
of and during delivery of a baby. This is determined
through a process of Magnetic Resonance Imaging (MRI) which allows an
examination
of a nucleus of an atom of the tissue be it of a skin or
muscle. This reveals a proton which has an electronic charge as it
spins
like the earth to create a magnetic field. It is the
examination of this field, by scanning through different planes, such
as the
axio, corona and the surgical or midline planes,  which
produces data that is put together to reveal any injury or assault

which might have occurred to the brain tissue.
[13]
As a result of the evolution of the brain over millions of years
there are three distinguishable parts of the brain, the Reptilian,

Mammalian and Human brain. This is in slide 1 of exhibit 2. The
Reptilian core was developed first and it has all vital centres
which
keep human beings, as mammals, alive. For instance the heart bit,
breathing and swallowing processes are controlled in the
Reptilian
brain. At birth the Reptilian brain plays a vital role as it supports
life and enables the ejection of the child alive.
The Human brain on
the other side is asleep at birth. The delivery of a live child from
the mother requires a pressure wave of
blood supply to the brain of
the baby. Where there is much less oxygen in the blood noticed by too
few rings this state is referred
to as
hypoxia
. If there is a
drop in the blood pressure this is referred to as
ischemia
.
The brain injury caused by much less oxygen and a simultaneous
significant drop in the blood pressure is then called
hypoxic
ischemic assault or insult.
[14]
If there are problems such as mild asphyxia just when the child is
ready to be born (
partum period
), blood supply to the Human
brain will be shunted away first so as to preserve blood supply to
the Reptilian brain. Where the problem
is soon resolved, a recovery
process takes place with blood going back to the Human brain. The
longer the injury or insult takes
place the more there are chances
that the Human brain will suffer irreparable damage. The effect of a
mild attack is that, while
the Human brain is compromised, the
Reptilian brain is protected.
[15]
In the event of a prolonged mild blood shortage which is in the
region of 3 to 7 hours with the Reptilian brain protected the
Human
brain will pay the price of this blood shortage. He referred to this
type of damage as the
prolonged partial insult
. Where there is
sudden severe assault because of severe blood shortage to the brain
such that there is no time to shunt the blood
from the Human brain
the Reptilian brain is exposed to a deprivation of blood supply. The
injury resultant from this shortage is
referred to as the
acute
profound insult
. This results, at best, in severe brain damage
and at worst, in death of the baby to be born. The MRI helps to
detect the extent
of any such brain injury or assault.
[16]
He used slide 6 of exhibit 2 to demonstrate a prolonged partial
hypoxia-ischemia by showing normal blood supplied artery and
a
compromised blood supplied artery. The coronal view of the head has
arrows, indicating the shunting process on the Human brain,
thus the
ischemic superficial hemisphere, leaving the Reptilian brain, in the
shape of a butterfly, in the deeper central nuclei,
protected from
the injury as a result of a compromised blood supply. He also
demonstrated a foetus in utero with blood supply to
the foetus via an
umbilical cord and a partial placental abruption. There is decreased
blood pressure – moderately hypotension.
Slide 6 is a clear
indication of a prolonged partial hypoxic ischemic insult with
Reptilian brain at the centre having a butterfly
shape.
[17]
Slide 7 was used to demonstrate a sudden profound hypoxia-ischemia
with concepts of further decrease in oxygenated blood flow
leading to
cardiac arrest. There is an artery with compromised blood supply and
another with no blood supply. The coronary view
of the head shows
ischemic cerebral hemisphere, meaning the Human brain with no injury
and the ischemic deeper nuclei in the form
of a butterfly, where the
injury occurred. The foetus in utero shows a placenta separating from
the uterine wall and a decrease
in oxygenated blood supply to the
foetus via the umbilical cord. The blood oxygen concentration has
fallen - hypoxia.  Slide
8 shows a clear acute profound hypoxic
ischemic injury, that is injury to the Reptilian brain at the centre
with a butterfly shape
and a Human brain with no injury.
[18]
He said that when there is an injury to the brain, as a result of
which blood is shunted away from the area it is supposed
to go to,
those areas have cavities as a result of a loss of cells. These
spaces fill up with water such that the area looks white.
Blood in
the brain is supplied by the anterior cerebral artery, the middle
cerebral and the posterior cerebral arteries. The posterior
arteries
supply the Reptilian brain. The overlapping areas in between the
places supplied by these arteries are called the watershed
areas. It
is in these watershed areas that the shunting of blood begins. If
pressure drops further, the anterior and the middle
arteries will
constrict and the posterior arteries will dilate to allow more blood
supply to the Reptilian brain. If things go
really bad the Human
brain can be destroyed in a process to protect the Reptilian brain.
[19]
On 20 February 2014 he was presented with MRI brain scan of K with a
request to report thereon. He was not presented with any
clinical
features of the child. He preferred it that way so as to avoid such
features contaminating his investigations. He was
not concerned with
what happened, where it happened and how it happened as he was to
give the most scientific and objective report.
Slides 15 and 16 of
exhibit 2 were of K. He said that both slides showed the anterior
watershed infarction and the posterior watershed
infarction,
represented by red and yellow arrows, meaning that the injury was of
the front and back of the Human brain. He said
that this evinced a
clear case of a
prolonged partial hypoxic ischemic insult
suffered
by K.
[20]
Reference was also made by Professor Lotz to blue arrows inside the
circle on slide 15 indicated as
Pulvinars
.
He explained that when children are being looked after in the high
care, after birth, if the sugar level of a child is not
properly
monitored, the child may develop low sugar in the blood system, a
condition called
hypoglycaemia
.
Pulvinars may be found close to the Reptilian brain. He added though
that the Pulvinars do not necessarily play any part in the
acute
profound injuries. It was important to get Hospital records for K to
know if she had low sugar. If she had it, he said it
would be very
bad as she was at high care and she should have been looked after
very well. He made reference to his filed report
which he said was
last updated in 2016. He confirmed the report
[2]
and adopted it as his evidence. The discussion/Assessment according
to the report of the two experts is:
‘
The MRI
distribution of changes when K was 8 years 1 month old, namely
deffuse bilateral periventricular and subcortical cystic
and
non-cystic leukomalacia and bilateral T2 hyperintensity-pulvinar,
lateral thalamic and PLIC would be in keeping with hypoxic
ischemic
event/s, mixed pattern predominately of a partial prolonged type.’
[21]
In terms of the joint minute both he and Dr Weinstein picked up the
Pulvinars and the occipital damage to K. Both suggested
that
hypoglycaemia be excluded on K. He testified though that there were
features that pointed to a hypoglycaemic injury on K but
that did not
mean that the MRI was the last word on this aspect.  When asked
about a contribution to the injury by a nuchal
cord, he said that the
issue fell outside the scope of his expertise. By a partial prolonged
type injury he said this meant that
the child had no reserves for a
while due to circulatory collapse resulting in there being an acute
profound injury.
[22]
He then explained a
motor cortex
which he said was a strip
around the cortex like an Elis band.  Its function is to allow
the baby to move her hands, lips,
tongue etc. It allows a child to
move her head, to suckle and swallow. An injury on the cortex is
referred to as
mixed
.  It has a little bit of profound
features and is by far a
prolonged partial insult
or
injury
.
A
mixed
pattern insult
is acute profound with partial
prolonged features. When he and Dr Weinstein agreed that there was a
mixed pattern predominantly
of partial prolonged type, he understood
this to mean that 98 % of what they saw was prolonged partial type.
But there was something
in the area of the motor cortex which
suggested that there may have been a point in the development of this
situation when the
baby had no reserves and she collapses. He said
this was to come out in the neonatology.
[23]
When asked if he could determine the probable cause and timing of the
injury, he referred to the American Collage of Obstetricians
and
Gaenocologists (Acox Report) last report of 2014 which says that
Radiologists’ opinion must be placed on a big plane
of
reference, meaning all causes of this injury must be defined on
further assessment by experts of various other fields such as

Neonatologists. He noted that the occipital lobes were the areas
where the injury was seen and it had to be checked if K suffered
any
visual damage or visual loss. He said that a hypoxic ischemic injury
played out over a period of time and so he did not have
to look at
any earlier scans preceding her 8 years of age as the brain did not
have any regenerative ability. He testified that
monitoring the baby
at birth was very important. When there were signs of destress these
had to be attended to urgently lest the
situation complicates with
resultant irreparable harm or even death.
Professor
Johan Smith [Neonatologist]
[24]
Professor Johan Smith confirmed that he was specialising in
Paediatrics.as a Head of Department at Tigerberg Medical Hospital,
in
Stellenbosch. He said that he was very familiar with the working of
the cardiotocograph known as the CTG. In the main he relied
on the
joint minute of the Radiologists in respect of the type of brain
damage on K. He identified two types of hypoxic ischaemic
insults:-
24.1. Sudden or
acute-profound insults which occurs as a result of an insult which
does not allow for the auto regulatory shunting
of blood to the
reptilian brain;
24.2. Intermittent
hypoxia which, in a period of 60 - 90 minutes results in
decompensation. The rate of decompensation is determined
by the
quality of the foetal reserves, the duration of the insult and the
degree of the insult. He was firm in saying that the
injury on K
occurred during the intrapartum period and presented as a result of
partial prolonged hypoxic ischaemic events, which
developed and
occurred over hours resulting in a predominantly partial prolonged
insult and eventual culmination into an acute
profound injury which
he said probably occurred after sufficient depletion of foetal
reserves.
[25]
He said that it would be of importance in respect of this matter to
know whether, in fact, a CTG tracing was done in respect
of the
plaintiff during the birth. He referred to the available birth
records and confirmed that according to these records the
neonate was
born with normal anthropometrical measurements but, within an hour of
birth, did not breath, had a reduced muscle tone
and a blue
coloration. As a result, resuscitation was performed, and the neonate
commenced independent breathing after 4 minutes.
The neonate was
placed in a head box and saturation improved to 93% (normal). He
testified that having regard to the physical features
noted, the
identification of encephalopathy, the decompensation, the lack of
muscle tone and inability of primitive reflexes the
neonate was
clearly depressed and suffered from respiratory distress and was
diagnosed with asphyxia.
[26]
He said that because of the arterial blood gas obtained 42 minutes
after birth and the assessed pH of 7.23, the neonate was
clearly
acidotic, which is associated with a lack of oxygenation during the
birth process. The neonate presented with clinical
features of
metabolic acidosis, hyponatremia, raised lactate that can be caused
by oxygen deficiency to cells, increased global
muscle tone, eventual
mild respiratory distress and ultimately excessive levels of oxygen
in the blood caused by overventilation.
[27]
He said that the arterial blood gas of 13h15 on 30 January 2006
[3]
indicated:
27.1. A PH of 7.46
indicative of alkalosis (too much alkaline in the blood due to
overventilation) and still washing out too much
carbon dioxide;
27.2. Neurogenic
hyperventilation indicative of acute respiratory and neurological
compromise;
27.3. The cranial
ultrasound of the brain at 14h53 on 30 January 2006
[4]
revealed features in keeping with brain swelling (oedema).
[28]
He concluded that K was a depressed baby at birth which required
resuscitation and had clear clinical signs of additional organ
injury
and swelling of the brain.       The
hypoglycaemia may have exacerbated the intra-partum injury
but he
conceded that there may not be any brain damages as a result of
hypoglycaemia and it appears as a result of the joint radiologists'

minute that this can now be excluded. The mechanism of the mixed MRI
pattern in respect of K is best described due to the sufficient

depletion of foetal reserves.
[29]
In respect of an umbilical cord Professor Smith gave evidence that
the cord consists of a vein and two arteries of which the
arteries
have muscular walls. Compression of the vein would normally result in
an anaemic neonate. In any event any impairment
of blood perfusion
due to cord compression would have been identifiable through proper
monitoring. The presence of a nuchal cord
does not require diagnosis
through a sonar and involvement of the nuchal cord causing blood
compromise can and should be detected
through monitoring as a tight
nuchal cord might be associated with foetal distress. In reaching his
opinion he did not exclude
the nuchal cord around the neck and
remains of the opinion that the injury sustained by the neonate
probably occurred during the
intrapartum period due to undetected
foetal distress or a failure to react to foetal distress.
[30]
When asked whether the presence of a nuchal cord around the neck can
cause an acute profound brain insult, Professor Smith
explained that
it can occur only as a result of and following upon a partial
prolonged insult process culminating in depletion
of foetal reserves
and then resulting in an acute profound brain insult. Heh explained
that no sentinel event was associated with
this birth and that a cord
around the neck does not qualify as a sentinel event like a prolapse
of the umbilical associated with
falling of the umbilical through the
vagina. Although a tight cord around the neck may be a medical
emergency it does not qualify
as a Sentinel event, as Sentinel events
are associated with a sudden and severe regulatory collapse. He
dismissed reasoning put
to him that an acute profound insult to the
brain can result in a subsequent partial prolonged injury, stating
that same is based
on incorrect reasoning and not clinically sound.
[31]
In dealing with the ACOG criteria in respect of intrapartum hypoxic
ischaemic encephalopathy Professor Smith explained comprehensively

that the ACOG criteria are not available in the South African context
and as a result the ACOG template does not fit a Third World
base.
[32]
In respect of the acidosis Professor Smith gave evidence that the
base deficit and relevant predictable rates would have resolved

within 4 hours and in addition the neonate presented with an abnormal
drive to reduce carbon dioxide which is associated with asphyxia
and
part of neonatal encephalopathy.
[33]
He furthermore testified that, with proper monitoring, the distress
could and should have been detected at an early stage and
that
intervention would have led to a positive result for the neo-born.
The process of Labour should be monitored through any of
the known
mechanisms of assessment to monitor foetal heartrate patterns and the
increase and decrease thereof before, during and
after contractions.
Foetal heart rate monitoring is conducted by means of, either-
auscultation, doppler assessment or CTG which
depicts a graphic
pattern and produces an audible sound which requires interpretation
of patterns associated with foetal distress
and informs the decision
to intervene and accelerate birth. A partogram may also be used to
monitor birth as it is designed to
plot and to graphically display
the maternal and foetal condition.
Dr
Johannes Petros Hattingh Basson [Obstetrician and Gynaecologist]
[34]
Dr Basson was in full time private Obstetrical and Gynaecological
practice at MediClinic, Welkom. In 2003 to 2012 he was an
assessor
for maternal deaths in the Free State for NCCEMD appointed by the
Minister of Health. In his lifetime he delivered about
28000 babies.
He confirmed the contents of his report and a joint minute drawn by
him and Dr Peter C Koli, also an Obstetrician
and Gynaecologist (for
the Defendant). Both Doctors agreed that:
34.1. No antenatal or
intra-partum records were available;
34.2. Intra-partum
records were of the utmost importance to evaluate the intra-partum
management of the patient. It is an obligation
in terms of the Health
Act No61 of 2003 that patient records were safely kept and made
available for evaluation;
34.3. K suffered a brain
injury, most likely in the peri-partum period, resulting in severe
handicap.
[35]
His evidence and his reports were based on the available Hospital
records he received, K’s Road to Health Chat, Medico-legal

reports by Professors Lotz and Smith and on information he received
from the Plaintiff. He said that the intra-partum hypoxic ischemic

injury of a predominantly partial prolonged nature resulting in K
suffering from cerebral palsy should, as could have been detected

through proper foetal monitoring. According to him the accepted
protocol for foetal monitoring in low-risk pregnancies during the

active phase of labour requires that the foetal condition should be
assessed 30 minutes, before, during and after contractions.
[36]
He said that foetal monitoring was to be conducted through
determination of the foetal Heartrate and heartrate patterns defined

by the influence of contractions on the foetal heartrate during the
birth process. Any decelerations in foetal heartrate should
have been
aligned with contractions and any hypoxic ischaemic complications
suffered by the foetus would present through various
foetal heartrate
patterns. These abnormalities do lead to distress and umbilical
artery acidemia. These patterns were recognisable
as problematic and
if they persisted necessitated assisted birth and or caesarean
section and or intrauterine resuscitation. He
gave evidence that
having regard of the factual evidence of continuous CTG monitoring,
the medical staff did not react on the probable
indications of foetal
distress which would have been visible from assessment of the CTG
results and failed to expedite delivery.
[37]
In respect of the incident of the nuchal cord, he testified that
nuchal cords were common and were not associated with adverse
outcome
in respect of births. The presence of a nuchal cord was associated
with an outcome of intrauterine growth restriction,
cord
infarct/stroke, foetal death, meconium aspiration syndrome, increased
rate of intrapartum foetal heartrate abnormalities.
Patients with
nuchal cords around their necks required close monitoring during
labour, preferably by continuous foetal electronic
heartrate
monitoring as tight and multiple nuchal loops were associated with
persistent variable or late decelerations. According
to him the staff
did not react to the expected indicators associated with foetal
monitoring. He said that it is highly probable
that foetal distress
was present but missed as a result. Commenting on the scores in the
patient ward control register on K he
said that 6/10 – 7/10
taken in 5 minutes was an average score. 4/10 was a bad score even
though one was not to look at one
score as the condition of the baby
improves after every 5 minutes. The score according to him should
have been 9/10 or 10/10. He
said that a tight nuchal cord could cause
asphyxia but was unlikely to lead to long term disfigurement. He said
that the absence
of meconium was not helpful as meconium was not the
only source of asphyxia.
[38]
Dr Basson and Dr Koli differed on the approach to be adopted in the
absence of intrapartum records. Dr Basson said that intrapartum

records were of utmost importance for the filing of a balanced report
on patient care in cases of known adverse outcome where access
to
records has been denied. However, collateral information may be used,
though with circumspection, to determine the standard
of care.
Dr
Debora Francis Anna Pearce [Paediatric neurologist]
[39]
She testified that she met and consulted with the Plaintiff but her
report was not limited to that consultation. She examined
K who at
that time was 10 years 5 months old. Her report has results of such
examination
[5]
. She confirmed
her report and adopted it as her evidence. She also met and consulted
with Dr Mogashoa, also  Paediatric Neurologist
(for the
Defendant).  She confirmed their joint minute. Dr Pearce’s
evidence was brief. She said that, in her opinion,
the insult was in
the intrapartum period. The agreement reached by her and Dr Mogashoa
was that there was normal foetal brain growth
prior to birth, and
that it is likely that peripartum or intrapartum hypoxic ischaemia
contributed to the pathogenesis of neonatal
encephalopathy. Dr
Mogashoa added that the nuchal cord contributed to such intrapartum
hypoxia and the final agreement is that
the child’s condition
is most likely the result of intrapartum hypoxia.
Defendant’s
version.
Professor
Keith Duncan Bolton [Paediatrician]
[40]
The defendant called only Professor Bolton to give
viva voce
evidence.  In addition to Professor Bolton’s evidence, the
defendant obtained and filed the medical legal reports from
the
following experts’ witnesses:
40.1. Dr Koll – an
obstetrician and gynaecologist who file a joint minute with Dr Basson
40.2. Dr Mogashoa–
a paediatric neurologist who filed a join minute with Dr Pearce
40.3. Dr Weinstein –
a radiologist who filed a joint minute with Prof Lotz and
40.4. The nursing sister
Smit.
[41]
Professor Bolton testified that he was employed as a part time
consultant Paediatrician at Rahina Moosa Mother and Child Hospital
in
the Gauteng Department of Health, after having been a Chief
Paediatrician there. From his stated qualifications and experience
he
is indeed an expert in his specialised field. He was furnished with
documentation on K by attorneys of the State Attorneys’
office
in Johannesburg. He confirmed and adopted as his evidence his initial
and the subsequent reports he made in this matter.
The subsequent
report was necessitated by the discovery of new documents. Commenting
on the Hospital’s Midwife’s notes
he said that the Apgar
score recorded was 6/10 – 7/10 and the nurse referred the baby
from the delivery cubicle to the “sick
bay nursery” in
the labour ward.
[42]
Commenting on the Doctor’s notes he,
inter alia
, said
that it was noted that K has the umbilical cord around her neck at
birth. Her birth weight was 3000 grams and her crown-heel
length was
53 centimetres with the head circumference of 36 centimetres. The
Doctor’s one minute Apgar score was 4/10 and
the five minute
Apgar score was 7/10. When K was brought to the sick bay, it was
noted that she was not breathing, was cyanosed
(blue) and was floppy.
She was bagged and spontaneous breathing commenced after 4 minutes.
The oxygen saturations increased from
78% to 94%. The neurological
examination after resuscitation showed that the baby was lethargic,
had poor reflexes and she was
breathing at an abnormally fast rate
(tachypnoea) . A blood gas analysis was performed 42 minutes after
birth while she was in
15 litres head box oxygen. The important
results showed pH – 7.232, pC02 – 44.2, pa02 –
65.4, B.D – 8.2.
A cranial sonar performed in the early
post-natal period showed: “bright brain, good pulsation and no
bleeds.” He took
Court into various parts of his report,
including probable/possible additional contributing factors to the
cause of cerebral palsy
in this case as partly being:
‘
Nuchal cord (NC)
one probable proximal contributing factor was the reported cord
around the neck at birth. The definition of a NC
is where the
umbilical cord is wrapped 360 degrees around the foetal neck. While
single, loose NC is common and has a benign outcome,
the same is not
true for multiple and tight loops. Non-reassuring CTG,
meconium-stained liquor, 5 minutes Apgar Scores < 7 and
NICU
transfers are and the midwife had to cut significantly more common
with tight NC.
The nuchal cord was tight
and the midwife had to cut the cord and clamp it to facilitate the
second stage of labour.
It is therefore probable
that NC played a role in this child’s birth asphyxia. The
current concept for the development of
Neonatal Encephalopathy
stresses the multifactorial and “broader perspective”
that is necessary when considering causation.
The nuchal cord was not
of the defendant’s making and antepartum diagnosis of the NC
(by ultrasound) does not justify a change
in delivery management.’
[43]
The conclusions reached by Professor Bolton were put into serious
doubt during cross-examination when taking into consideration
the
concessions made by the Defendant in the third answers to the
pre-trial minute and the agreed conclusions of the experts of
both
parties in their joint minutes. In his last remark on conclusion he
said: -
‘
However the lack
of contemporaneous notes covering the confinement, labour and early
new-born period makes it difficult to support
or refute the
Plaintiff’s version of events.’
[44]
Conclusions reached by the experts of the Defendant who did not give
viva voce
evidence were by and large in agreement with the
conclusions reached by Plaintiff’s experts with the exception
of Dr Mogashoa
who differed on three aspects from conclusions or
observations of Dr Pearce. The three situations are in respect of:-
44.1 All of the essential
criteria necessary to consider intrapartum hypoxia are present and
that a diagnosis of intrapartum hypoxia
ischemic encephalopathy can
therefore be made in terms of the evidence of, inter alia:
44.1.
1. Cerebral palsy of mixed cerebral palsy, predominantly dystonic. Dr
Mogashoa said she found mixed cerebral palsy, predominantly

dyskinetic and spastic quadriplegic;
44.1.2
Exclusions of other identifiable causes: infection CPR noted to be
26. Blood cultures negative. LP not done. No infection
confirmed or
disproved. Dr Pearce: the current literature suggests that CPR may be
elevated in some non-infectious conditions (prolonged
rupture of
membranes, maternal fuver during labour, foetal distress, perinatal
asphyxia, shock, intraventricular haemorrhage, pneumothorax,

pneumothorax and meconium aspiration pneumonitis). Dr Mogashoa agreed
but deferred to Neonatologists to comment on CPR.
44.1.3
Having regards to ACOG 2014 it is likely that peripartum or
intrapartum hypoxic ischemia contributed to the pathogenesis
of
neonatal encephalopathy. Dr Mogashoa agreed but added that it was her
opinion that nuchal cord contributed to the intrapartum
hypoxia.
However both agreed that K’s condition was most likely the
result of intrapartum hypoxia.
Evaluation
[45]
As already alluded to the civil onus rests on the Plaintiff to
satisfy Court that its version is more probable and consists
of
credible evidence as compared to that of the Defendant.
In
AA Onderlinge Assuransie Assosiasie Beperk v De Beer
[6]
the Court dealt with and indicated that the balancing of
probabilities means:
45.1
To select a conclusion which deems to be the more natural, or
plausible, conclusion;
45.2
From amongst several conceivable ones;
45.3
Even though that conclusion may not be the only reasonable one.
Negligence
[46]
This claim is based on the negligence of the medical and/or nursing
staff of the Hospital, resulting in the child suffering
from cerebral
palsy. Proof of negligence depends on whether conduct, in the
circumstances of each case, falls short of that of
a reasonable man.
The test for negligence appears in the following dictum of Holmes JA
in Kruger v Coetzee:
‘
For
the purpose of liability culpa arises if-
(a)
A diligens paterfamilias in the position of the Defendant:
(i)
Would foresee the reasonable possibility of his conduct injuring
another in his person or property and causing him patrimonial
loss;
and’
(ii)
Would take reasonable steps to guard against such occurrence;
and
(b)
The Defendant failed to take such steps.’
[47]
Following
this judgment, there were a number of Supreme Court of Appeal
judgments reformulating this requirement.  Thus,
Olivier
JA,
said this in Mukheiber v Raath and Another
[7]
:
‘
For
the purposes of liability culpa arises if –
(a)
A diligence paterfamilias in the position of the defendant –
(i)
Would have foreseen harm of the general kind had actually occurred;
(ii)
Would have foreseen the general kind of causal sequence by which that
harm occurred;
(iii)
Would take reasonable steps to guard against it; and
(b)
The defendant failed to take those steps.’
[48]
In Standard Chartered Bank of Canada v Nedperm Bank Limited
[8]
the principle was stated as follows:
‘
In
delict, the reasonable foreseeability test does not require that the
precise nature or the exact extent of loss suffered or the
precise
manner of the harm occurred and should have been reasonably
foreseeable for liability to result.  It is sufficient
if the
general nature of the harm suffered by the plaintiff and the general
manner of the harm occurring was reasonably foreseeable.’
[49]
Neethling
and
Potgieter
[9]
state, with reference to these decisions:
“
From
this it can be concluded – and this is important – that
because both the concrete and abstract approaches require

foreseeability of the general nature of the consequences and the
general manner in which it occurred. Both approaches should as
far as
negligence is concerned, produce the same result.”
[10]
Inferential
reasoning
[50]
The case of the Plaintiff is largely reliant on circumstantial
evidence in deciding whether any Hospital personnel acted negligently

as a result of which K suffered cerebral palsy. The direct evidence
of the Plaintiff is limited.
When
an inference of negligence would be justified and to what extent
expert evidence would be necessary would depend on the facts
of the
particular case. A court is not called upon to decide the issue of
negligence until all of the evidence is concluded. Thus,
any such
explanation as may be advanced by a defendant forms part of the
evidential material to be considered in deciding whether
a plaintiff
has proved the allegation that the damage was caused by the
negligence of the defendant.
[11]
[51]
In Ratcliffe v Plymouth and Torbay Health Authority
[12]
at paragraph 48 Lord Justice Brooke made the point that:
‘…
surrounding
a procedure which led to an unexpected outcome for a patient. If such
a case should arise, the judge should not be diverted
away from the
inference of negligence dictated by the plaintiff's evidence by mere
theoretical possibilities of how that outcome
might have occurred
without negligence: the defendants' hypothesis must have the ring of
plausibility about it. .
It
is likely to be a very rare medical negligence case in which the
defendants take the risk of calling no factual evidence, when
such
evidence is available to them, of the circumstances.’
[52]
It suffices for plaintiff to convince the court that the inference
that he or she advocates is the most readily apparent and
acceptable
inference from a number of possible inferences.
[13]
In Caswell & Powell Duffryn Associated Collieries
[14]
at 169 – 170, Lord Wright remarked: -
‘
Inference
must be carefully distinguished from conjecture or speculation. There
can be no inference unless there are objective facts
from which to
infer the other facts from which it is sought to establish. In some
cases, the other facts can be inferred with as
much practical
certainty as if they had been actually observed. In other cases, the
inference does not go beyond reasonable probability.
But if there are
no positive proved facts from which the inference can be made, the
method of inference fails and what is left
is mere speculation or
conjecture.’
Negligence
and causation
[53]
Patients of public health institutions are entitled to be treated in
the same way as patients in private medical institutions.
What is
required is a public health delivery system that recognises the
dignity and rights of those who are compelled to use its
facilities.
It is that basic sensitivity that the Constitution demands.
[15]
It needs only be foreseeable that the plaintiff will suffer damages
and the precise nature of the damages need not be precisely

foreseeable at that stage.
[16]
Although the onus of proving negligence is on the plaintiff, the
plaintiff does not have to adduce positive evidence to disprove
every
theoretical explanation which is exclusively within the knowledge of
the defendant, however unlikely, that might be devised
to explain in
a way which would absolve the defendant and his employees of
negligence.
[17]
[54]
Sometimes, however, a plaintiff is not in position to produce
evidence on a particular aspect. Less evidence will suffice to

establish a
prima
facie
case where the matter is peculiarly in the knowledge of the
defendant. In such situations, the law places a shifting evidentiary

burden upon the defendant to show what steps were taken to comply
with the standards to be expected. The general
onus
nevertheless remains with the plaintiff.
[18]
In Vallaro obo Barnard v MEC
[19]
which is full bench decision of this division Court held, with
reference to McIntosh v Premier, Kwazulu-Natal and Another
[20]
in para 12 , inter alia, that:
‘
The
second inquiry is whether there was fault, in this case negligence.
As is apparent from the much-quoted dictum of Holmes JA
in Kruger v
Coetzee
1966 (2) SA 428
(A) at 430E-F, the issue of negligence itself
involves a twofold inquiry. The first is: was the harm reasonably
foreseeable? The
second is: would the diligens paterfamilias take
reasonable steps to guard against such occurrence and did the
defendant fail to
take those steps? The answer to the second inquiry
is frequently expressed in terms of a duty. The foreseeability
requirement is
more often than not assumed, and the inquiry is said
to be simply whether the defendant had a duty to take one or other
step, such
as drive in a particular way or perform some or other
positive act, and, if so, whether the failure on the part of the
defendant
to do so amounted to a breach of that duty. But the word
‘duty’, and sometimes even the expression ‘legal
duty’,
in this context, must not be confused with the concept
of ‘legal duty’ in the context of wrongfulness which, as
has
been indicated, is distinct from the issue of negligence
.
[14]
The crucial question, therefore, is the reasonableness or otherwise
of the respondents’ conduct. This is the second leg
of the
negligence inquiry. Generally speaking, the answer to the inquiry
depends on a consideration of all the relevant circumstances
and
involves a value judgment which is to be made by balancing various
competing considerations including such factors as the degree
or
extent of the risk created by the actor’s conduct, the gravity
of the possible consequences and the burden of eliminating
the risk
of harm. …’
[55]
Commenting on an approach to factual causation as stated in Lee v
Minister for Correctional Service
[21]
Mogoeng CJ in Mashongwe v Prasa,
[22]
inter
alia
,
said:
‘
[65]
Lee never sought to replace the pre-existing approach to factual
causation. It adopted an approach to causation premised on
the
flexibility that has always been recognised in the traditional
approach.  It is particularly apt where the harm that has
ensued
is closely connected to an omission of a defendant that carries the
duty to prevent the harm.  Regard being had to
all the facts,
the question is whether the harm would nevertheless have ensued, even
if the omission had not occurred. However,
where the traditional
but-for test is adequate to establish a causal link it may not be
necessary, as in the present case, to resort
to the Lee test.’
[56]
With all these legal principles in mind, I turn to the evidence
adduced by the parties on the issue of negligence. The Plaintiff

testified that she spent more than an hour waiting in the first
cubicle where urine testing was done and the CTG monitor was
connected
on her apparently by the first nurse she came into contact
with. It was at this cubicle that some doctors spoke about a
Caesarean
section. At that stage she had not felt labour pains yet.
She was, for some time, left in that cubicle as she said she was not
taken to theatre. Another nurse came to her to give her the first
doze of medicine to induce labour. That nurse returned later to
give
her the second doze, still to onset labour. She was thereafter moved
to the delivery room where a doctor broke her water.
The next person
to attend to her was a different nurse who told her when and how to
push. Still the Plaintiff was feeling no labour
pains and the baby
was not coming and it took quite a while. Then that nurse called for
a doctor. It was a different doctor from
the one she met before. The
doctor called for a pair of scissors. The nuchal cord was clamped,
cut and the baby was pulled out.
The rest is the history testified to
by various witnesses which history includes that:
‘
When
K was brought to the sick bay, it was noted that she was not
breathing, was cyanosed (blue) and was floppy. She was bagged
and
spontaneous breathing commenced after 4 minutes. The oxygen
saturations increased from 78% to 94%. The neurological examination

after resuscitation showed that the baby was lethargic, had poor
reflexes and she was breathing at an abnormally fast rate
(tachypnoea).’
[23]
[57]
The estimated time when the Plaintiff met the first doctor was around
11h00 and K was born at 15h30. While an attempt was made
to challenge
times taken during delivery, no counter evidence was adduced on this
aspect by the Defendant. I accordingly accept
the times estimation
given by the Plaintiff on events from 11h00 to 15h30, notwithstanding
a discrepancy on the Plaintiff’s
version of when she left home
for the Hospital. I have already found that most of Plaintiff’s
evidence became common cause
during the trial.
[58]
There is no direct evidence of when intrapartum commenced. Yet the
first doctor to attend to the Plaintiff at around 11h00
already had a
reason to be concerned about her health status such that a
consideration of a caesarean section was made. At this
stage, the
only source for concern would be the recording on the CTG monitor
whose records have gone missing. The Plaintiff testified
about nurses
and doctors who came to her and what they did on her. Her evidence
clearly indicates that there are moments when she
was left alone. In
the absence of labour pains she was well orientated to see what was
happening around her. One can also glean
from the patients ward
control register that between 24 January 2006 and 25 January 2006 no
less than 13 baby deliveries were made
and attended to by the labour
ward staff.
[24]
I note that
the dates and times of birth were not registered sequentially and
some of the required information is lacking from
the register.
Understandably, the labour ward staff might have been fairly busy
moving from one patient to another. Yet certain
minimum standards had
to be observed and followed.
[59]
I find that the consideration of a caesarean section was either as a
result of warning signs depicted on the CTG monitor or
from the
condition of the Plaintiff at the time, such as might be the dilation
of her vertex.  None of the attendant doctors
or nurses came to
testify to negate this irresistible conclusion. In my view, had
facilitated methods of delivery, such as the
caesarean section, been
resorted to around 11h30, K would have been born much earlier than
15h30. Time of birth could have been
around 12h15 to 12h30. Among
such facilitated methods, a caesarean section, would then have had
the advantage of avoiding K presenting
herself with a nuchal cord. It
remained common cause that K was a healthy baby just before the
delivery process commenced. The
probabilities of a child born without
suffering asphyxia in this case are very high, had early
interventions, such as caesarean
section, been resorted to, in
response to those early warnings depicted from the CTG. The
consideration of the caesarean section
was a manifestation by the
doctors that they foresaw a complicated delivery for which a
caesarean section was the solution. They
however, and without any
given explanation, failed to carry out the reasonable procedure to
alleviate the impending harm. It has
to be borne in mind, as
testified by Professor Smith, that with proper monitoring, the
distress to the foetus could and should
have been detected at an
early stage and that intervention would have led to a positive result
for the neo-born. The CTG monitor
produces an audible sound which
requires interpretation of patterns associated with foetal distress
and informs the decision to
intervene and accelerate birth. Clearly
this information was either missed out by the attendant doctors
and/or nurses or was picked
up but no reacted to. By failing to
resort to that early intervention procedure, they failed to do what a
reasonable person, possessed
with information they had, would have
done in the circumstances. Their omission was therefore negligent.
[60]
The failure of the doctors to intervene as soon as a need for it
arose had the effect of prolonging the birth of K by not less
than
3hours. After such a delay, K was lethargic, had poor reflexes and
she was breathing at an abnormally fast rate (tachypnoea).
K had
bright brain, good pulsation and no bleeds. She was not breathing and
was cyanosed (blue). She could only breathe on her
own after 4
minutes of resuscitation after birth. She was diagnosed with cerebral
palsy. Professor Bolton testifying for the Defendant
said this
condition was probably due to a tight nuchal cord around the neck of
K at birth. This could have been avoided by an earlier
intervention.
In any event, the patients ward control register refers to the cord
being slightly tight. Besides this evidence no
witness came forward
from the Defendant to testify on the degree of tightness of the cord.
To therefore rely on a cord that was
slightly tight, without giving
more details of this, is rather conjecture.
[61]
Professor Lotz was the most impressive of all witnesses who gave
viva
voce
evidence in this matter. In much simpler terms he explained
how blood in the human brain was shunted to protect the reptilian
brain
and the significance of the injuries in the two areas of the
brain. With slides he showed the coronal view of the head of K having

arrows, indicating the shunting process on the Human brain and the
resultant ischemic superficial hemisphere, leaving the Reptilian

brain, in the shape of a butterfly, in the deeper central nuclei,
protected from the injury as a result of a compromised blood
supply.
He said that the blood shunting process he observed through the MRI
on K would have endured for a minimum of about 3 hours
but not more
than 7 hours. He referred to the process as prolonged partial insult
as opposed to a sudden severe assault because
of severe blood
shortage to the brain such that there is no time to shunt the blood
from the human brain, resulting in the acute
profound insult. The 3
hours delay of birth caused by a failure to implement a caesarean
section co-insides with the minimum period
of a prolonged partial
insult.
[62]
Professor Lotz said it repeatedly that the loss of oxygenated blood
to the human brain is inevitably at a price. The areas
where the
blood is stolen from in the human brain control various sites. I
accept the undisputed evidence of Professor Lotz and
Dr Weinstein
that in the brain injury of K there was a mixed pattern predominantly
of partial prolonged type, meaning that 98 %
of what they saw was
prolonged partial type. But there was something in the area of the
motor cortex which suggested that there
may have been a point in the
development of this situation when the baby had no reserves and she
might have collapses.
[63]
Further I accept the uncontroverted evidence of both Drs Basson and
Koli who agreed that, while there were no antenatal or
intra-partum
records available; such records were of the utmost importance to
evaluate the intra-partum management of the patient
and it was an
obligation in terms of the Health Act No 61 of 2003 that patient
records were safely kept and made available for
evaluation, K did
suffer a brain injury, most likely in the peri-partum period,
resulting in severe handicap. The brain handicap
suffered by K was of
a cerebral palsy. On the total probabilities of this matter, I find
that the negligent conduct of the employees
of the Defendant caused K
to suffer from the cerebral palsy.
Findings
1.
The neo-natal signs were consistent with
an intrapartum event predominantly of the partial prolonged type with
features associated
with acute profound insult and that this resulted
from a failure to intervene in time. if the birth was properly
managed the stressful
situation facing the foetus could and should
have been recognised and reacted upon.
2.
Court finds for the Plaintiff –
the Defendant acted negligently causing K to suffer from cerebral
palsy.
3.
Defendant is ordered to pay the costs of
two counsel.
Order
[64]
As the issue of quantum was made to stand over by agreement of the
parties, the Draft order is made an order of Court.
_______________________
H
Cele
Acting
Judge Gauteng
Division
of the High Court
Appearances
For
the Plaintiff:
Adv.N
Van Der Walt SC
Assisted
by:

P Uys and R Andrews
Instructed
by:

Renefouche Attorneys
For
the Defendant:
Adv. N Makopo
Assisted
by:

Adv. B Shabalala
Instructed
by

State Attorney
[1]
See
exhibit 2 with 16 slides.
[2]
This
is a joint minute of two Radiologists Prof Lotz (for the Plaintiff)
and Dr A Weinstein (for the Defendant) as per Bundle
E pages 1 –
3 dated 15 August 2016.
[3]
(Page 22, Bundle F)
[4]
(Bundle F, Page 23).
[5]
See
Bundle C p24 to p28.
[6]
1982(2) SA 603 (A).
[7]
1999(3) SA 1065 (SCA), para [31] (emphasis added)
This
was apparently applied in
Sea Harvest Corporation (Pty) Ltd and
Another v Duncan Dock Cold Storage (Pty) Ltd and Another
2000(1)
SA 826 (SCA), paras  [21] and [22]
In
Mkhatswa v Minister of Defence
2000(1) SA 1004 (SCA), paras
[19] to [23], Smal­berger JA referred, with approval, to
the point Scott JA articulated
in
Sea Harvest
(paras [21] and
[22])
[8]
1994(4) SA 747 (A), at 65
[9]
op cit
Chapter 4, footnote 130
[10]
The concrete approach originated in
Boberg
,
“
The
Law of Delict
”,
p. 390
See,
also,
Barnard v Santam Bpk
1999(1) SA 202 (SCA), 213-215
[11]
Goliath v Member of the Executive Council for Health, Eastern Cape
(085/2014)
[2014] ZASCA 182
;
2015 (2) SA 97
(SCA) (25 November
2014).
[12]
[1998] EWCA Civ. 2000.
13AA
Onderlinge Assuransie-Assosiasie Bpk v De Beer
1982
(2) SA 603
(A); see
also Cooper &
another
NNO v Merchant Trade Finance Ltd
2000
(3) SA 1009
(SCA).
[14]
[1940] AC 152.
[15]
Premier, KwaZulu-Natal v Sonny and another
2011 (3) SA 424
(SCA) in
paras 33 and 34.
[16]
Botes v Van Deventer
1966 (3) SA 182
(AD) at 191A – G.
[17]
Naude N.O. v Transvaal Boot and Shoe Manufacturing Co
1938 AD 379
at
392-3).
[18]
Monteoli v Woolworths (Pty) Ltd
2000 (4) SA 735
(W) at [27].
[19]
Appeal case no A5009/16, Gauteng Local Division, Johannesburg.
[20]
2006 (6) SA 1 (SCA).
[21]
2013
(2) SA 144
(CC).
The
point of departure is to have clarity on what causation is. This
element of liability gives rise to two distinct enquiries.
The first
is a factual enquiry into whether the negligent act or omission
caused the harm giving rise to the claim. If it did
not, then that
is the end of the matter. If it did, the second enquiry, a juridical
problem, arises. The question is then whether
the negligent act or
omission is linked to the harm sufficiently closely or directly for
legal liability to ensue or whether
the harm is too remote. This is
termed legal causation.
[22]
2016
(3) SA 528 (CC).
[23]
See
Prof Bolton’s evidence.
[24]
See
pages 73 – 74 of bundle F. We do not have information on
preceding and succeeding pages. There could be deliveries during

this period.