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[2022] ZAECBHC 40
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M.L v Member of the Executive Council for Health, Eastern Cape (501/2017) [2022] ZAECBHC 40; [2023] 1 All SA 475 (ECB) (15 March 2022)
SAFLII
Note:
Certain
personal/private details of parties or witnesses have been
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IN THE HIGH COURT OF
SOUTH AFRICA
(EASTERN
CAPE LOCAL DIVISION,
BISHO)
REPORTABLE
Case
Number: 501/2017
Date
of Hearing: 26, 28, 29 & 30 April 2021
18
November 2021
Date
of Delivery: 15 March 2022
In
the matter between:
M[....]
L[....]
PLAINTIFF
and
MEMBER
OF THE EXECUTIVE COUNCIL FOR
HEALTH,
EASTERN
CAPE
DEFENDANT
JUDGMENT
NOTYESI
AJ:
Introduction
[1]
The plaintiff, Ms M[....] L[....], claims delictual damages in her
own name and on
behalf of her minor child, E[....] (E) against the
defendant, the Member of the Executive Council for Health, Eastern
Cape Province
(the MEC). The claim emanates from the child suffering
cerebral palsy as a consequence of a hypoxic-ischaemic event during
the
birth process. The plaintiff bases the claim on allegations of
medical negligence by the medical and/or nursing staff of Mbekweni
Health Care Centre, Vidgesville Clinic, Mthatha General Hospital
and/or Nelson Mandela Academic Hospital.
[2]
The main contention of the plaintiff is that the medical
practitioners and nursing
staff at the Vidgesville Clinic, the
Mbekweni Health Care Centre, Mthatha General Hospital and or Nelson
Mandela Academic Hospital
treated her and her child in a substandard
manner and were in many respects negligent in carrying out their
obligations towards
the plaintiff and her child and that such
substandard or negligent treatment caused the plaintiff and E to
suffer damages for which
the defendant must be held liable. The
plaintiff further contends that the substandard treatment and
negligent acts were committed
by those nursing staff and medical
practitioners who were acting within the course and scope of their
employment.
[3]
In response to the plaintiff’s case, the defendant made a
general plea in which
negligence and causality are denied. The
parties had narrowed down the trial issues to the question of
causality pursuant to the
pre-trial procedures and expert advice. The
main dispute being whether E had a pre-existing medical condition
that had caused the
cerebral palsy or whether the cerebral palsy was
caused as a result of the negligence by the medical staff and/or
nurses.
[4]
By agreement between the parties, the question of the quantum of the
plaintiff’s
claim is to stand over and at the commencement of
these proceedings, the parties sought an order separating the merits
from the
quantum.
[5]
Although I heard the evidence in this matter on 26, 28, 29 and 30
April 2021, I directed
the parties to file heads of argument and that
agreement be reached on when I could hear oral submissions. When the
parties could
not reach an agreement on a mutual date, I directed the
parties to prepare a joint practice note for the determination of the
trial
issues based on the heads of argument. In the joint practice
note received on 18 November 2021, the parties requested for the
disposal
of the matter based on their respective heads of argument.
This court is indebted to counsel for their comprehensive heads of
argument,
which has assisted in the preparation of this judgment.
Background
[6]
The allegations of negligence during the birthing process of E, child
of the plaintiff,
between the Mbekweni Health Care Centre,
Vidgesville Clinic, Mthatha General Hospital and, later Nelson
Mandela Academic Hospital
is the crux of adjudication. Unfortunately,
there are no complete official records from the hospitals and clinics
for the labour
and birth period. In this regard, I do emphasize that
there is an obligation upon the defendant’s employees to keep
clinic
and hospital notes pertaining to the plaintiff’s
treatment. This aspect will be dealt with later in the judgment.
Admissions
[7]
The parties had reached an agreement on several issues pertaining to
the trial. Briefly,
I set out some of the agreed facts:
7.1 The
plaintiff made about four antenatal visits to the Clinic prior to the
birth of E on 17 December 2007.
7.2 On
15 December 2007, at approximately 23h00, the plaintiff started to
experience labour pains.
7.3 On
16 December 2007, the plaintiff arrived at Vidgesville Clinic at
07h00and was examined soon after arrival
at about 07h30 by way of a
vaginal examination, a foetal heart rate and blood pressure tests.
7.4 The
plaintiff’s water broke at 18h00 and the “toilet like
liquid” was coming out. This is
identified as meconium.
7.5 The
plaintiff was advised that she would be transferred to Mthatha
General Hospital.
7.6 The
plaintiff arrived at the Mthatha General Hospital at 20h00. At that
stage, she was advised that her womb
is still closed and she was
admitted to the ward.
7.7 The
plaintiff was left on her own until she felt something pushing in her
vagina and this took place at approximately
04h00 on 17 December
2007. According to the plaintiff, she was assisted by a student nurse
with the delivery of E.
7.8 E
did not cry at birth and was rushed to an incubator. E started having
seizures almost immediately. E was
then transferred to Nelson
MandelaAcademic Hospital.
7.9 E
was nursed in an incubator.
7.10 E had been on
treatment with Phenobarbitone to suppress seizures since then, but
the seizures are still recurring.
7.11 The road to
health chart indicates that E was born on 17 December 2007 with a
birth weight of 3 400 grams. E suffered
from meconium
aspiration, low APGAR, however the actual APGAR scores were not
given.
7.12 On a proper
calculation of time, the plaintiff was in labour for a period of more
than 22 hours prior to the birth of
E and that there was no
monitoring by nursing or medical staff at the hospital.
The
Pre-Trial Conference
[8]
In a pre-trial conference minutes dated 26 November 2019, several
helpful admissions
were also made by the parties with a view to
narrow down the trial issues. I do record these admissions, which
were confirmed by
the parties in a meeting of 25 February 2020. The
importance of the pre-trial minute is that it later forms the basis
of the expert
joint minute.
“
Pre-Trial
Minutes of 26 November 2019
1.
The parties agree that the plaintiff who is also known as N[....] was
in labour and presented at
Mbekweni Health Care Centre where she was
admitted.
2.
The parties agree that at Mbekweni Health Care Centre the plaintiff
registered herself as N[....]
L[....] and her admission took place at
approximately 06h00 on 16 December 2007 and was assessed for the
first time at approximately
07h30 and found to be 2 cm dilated.
3.
The parties agree that the plaintiff was assessed for the second time
in the evening of 16 December
2007 and a toilet like liquid was
running out of her vagina upon breaking of waters.
4.
The parties agree that the plaintiff was then transferred to Mthatha
General Hospital where she
arrived at approximately 20h00.
5.
The parties agree that at Mthatha General Hospital the plaintiff, who
was in labour with strong
contractions was admitted at the labour
ward overnight with the IV line running and was found to be 2 cm
dilated and was informed
that she was not ready to deliver.
6.
The parties agree that the plaintiff gave birth approximately 04h00
on 17 December 2007 at Mthatha
General Hospital by normal vaginal
delivery.
7.
The parties agree that the plaintiff was in labour for a period of
more than twenty two (22) hours
with no proper monitoring.
8.
The parties agree that the National Guidelines state that the fetal
heart rate should be monitored
half-hourly in labour and that a
second stage of an hour or longer should be reported to a doctor.
9.
The parties agree that the birth weight was 3.4 kg, and Apgar scores
were recorded as low and the
diagnosis recorded in the Road to Health
Chart was “Meconium Aspiration with low Apgar”.
10.
The parties agree that at birth E[....] did not cry, was weak, had
swelling on the head, immediately had seizures,
was rushed and place
in the incubator, given oxygen and was transferred to Nelson Mandela
Academic Hospital.
11.
The parties agree that at Nelson Mandela Academic Hospital, E[....]
was admitted in the neonatal high care unit,
the plaintiff was
informed that E[....] had seizure soon after birth, was floppy, had
an intravenous drip and was fed via a nasogastric
tube which was
eventually removed on 21 December 2007.
12.
The parties agree that E[....] was discharged from Nelson Mandela
Academic Hospital on 27 December 2007.
13.
The parties agree:
13.1 That the
Road to Health Chart discovered by the plaintiff be admitted as
evidence and is what it purports to be subject
to the right of either
party to dispute the correctness or authenticity thereof on notice to
the other party (which may be in medico-legal
report).
13.2 That
pursuant to the medico-legal report of defendant’s expert, Dr
Keshave, -
13.2.1
At the time of birth the following problems were noted;
13.2.1.1
MAS – Meconium Aspiration Syndrome; and
13.2.1.2
Low Apgars.
13.2.2
That based on the RTHC the presence of Meconium Aspiration Syndrome
seems the most likely cause to have resulted in the low apgars and
this would have caused the neonatal Encephalopathy.
13.2.3
That based on the first genetic test, CGH Array – done at
Ampath Laboratories on 18 March 2019 indicated that there was no
underlying abnormalities, this would make an underlying genetic
condition and also a neurometabolic condition less likely.
13.2.4
That Dr Keshave accepts that the clinical picture in the MRI scan
is
supportive of prolonged partial hypoxic ischemic injury.
14.
The parties agree that from the available hospital records, the
clinical picture and the MRI picture, there are
no antenatal or
postnatal causes that contributed to the brain injury of E[....].
15.
That pursuant to the medico-legal report of the plaintiff’s
expert Prof Lotz, the parties agree that-
15.1 The report
of Prof Lotz reflects that genetic disorders and inflammatory, brain
diseases are unlikely as causes of the child’s
brain damage.
15.2 The MRI is
supportive of a diagnosis of prolonged partial hypoxic ischaemic
injury in a brain.
16.
That pursuant to the medico-legal report of defendant’s expert
Dr Redfern, the parties agree that –
16.1 the
perinatal period is the most likely time period when brain injury may
have occurred.
16.2 the
presence of a neonatal encephalopathy in the first few hours to days
after birth strongly points towards a perinatal
brain injury.
16.3 the
evidence suggests that, when a neonatal encephalopathy is present
after delivery, intrapartum factors can almost
always be said to be
the main cause of the encephalopathy.
16.4 the history
of seizures, and the plaintiff’s description of E[....]’s
condition after birth, suggests the
presence of a neonatal
encephalopathy even in the absence of the neonatal medical records.
Specifically, the description of E[....]
as not moving or crying, and
being unable to breastfeed and requiring tube feeds, all point
towards a diagnosis of NE, together
with the history of neonatal
seizures.
16.5 the most
likely explanation for E[....]’s neonatal encephalopathy and
subsequent brain injury was hypoxic ischaemic brain
injury, which
most likely occurred during the intrapartum period.
17.
That pursuant to the medico-legal report of defendant’s expert
Dr Mugerwa- Sekawabe, the parties agree that
–
17.1 although
the plaintiff was not advised on the reason for the transfer to
Mthatha General Hospital the description of
the colour of the
amniotic fluid which was draining, suggests that it was meconium
staining of the liquor which necessitated the
transfer.
17.2 thick
meconium stained liquor is associated with an increased risk of fetal
distress.
17.3 it is well
known that contractions during labour lead to a reduction in oxygen
supply to the placenta and in turn to the fetus.
17.4 in view of
the increased risk of hypoxia and fetal distress in setting of
meconium stained liquor, as was the case in this
matter, the non-
monitoring of the Fetal Heart Rate probably resulted in abnormalities
of the Fetal Heart Rate which accompanied
fetal acidosis going
undetected.
17.5 if there
was a proper monitoring it would have been possible to detect those
unfavourable factors which would have necessitated
interventions.
17.6 the failure
to undertake these observations, in line with acceptable standards
and also not instituting measures of clearing
the baby’s
airways of the meconium fluid at delivery so as to mitigate against
meconium aspiration amounted not only to substandard
care but was
also a breach of the duty of care.
18.
Subject to the aforegoing, in the absence of maternity records and
any grounds for dispute, it is agreed that the
medico legal reports
of Professor Lotz, and Dr Mugerwa-Sekawabe are admitted as evidence
without formal proof, including all the
opinions, facts, reported
facts and conclusions reflected therein.”
Expert
Joint Minutes
[9]
The joint minutes were signed by Dr A Redfern and Dr A Keshave dated
3 March 2020.
Dr A Redfern is a developmental paediatrician expert
for the plaintiff. Dr A Keshave is a paediatric neurologist for the
defendant.
The two experts based their joint agreement on the
admissions contained in the pre-trial minute signed on 25 February
2020. That
pre-trial minutes embodied the agreements set out in the
pre-trial of 26 November 2019, as set out above. I highlighted the
admissions
in the joint minutes and the agreement of both the experts
in relation to the admitted facts.
“
9.1
(a) The parties agree that the
plaintiff was in labour for a period of more than twenty-two hours
with no proper monitoring.
(b)
The parties agree that the birth weight was 3.4 kg, and Apgar scores
were recorded
as low and the diagnosis recorded in the Road to Health
Chart was “Meconium aspiration with low Apgar.
9.2
(a) With regards to the
possibility of a neurometabolic cause of the NE, the
experts agree
that the presence of encephalopathy from immediately after birth is
not in keeping with an inborn error of metabolism
(IEM).
9.3
(a) With regards to the results
of the metabolic tests currently available:
·
The amino acids and organic acid profiling done on 3/12/19 were
“not suggestive of an amino aciduria, amino academia or organic
aciduria.”
·
The homocysteine level was very slightly elevated, and red cell
folate and Vitamin B12 levels were normal.
·
The experts agree that the homocysteine level is not clinically
significant, and may be the result of technical factors such as lack
of fasting, or due to E[....] being on sodium valproate therapy for
treatment of her epilepsy.
9.4
(a) The experts agree that before
a final decision can be made regarding the
likely aetiology of the
child’s current condition, the results of the following
investigated should be reviewed:
(i)
Serum lactate / pyruvate ratio;
(ii)
Carnitine profile (already performed);
(iii)
Repeat serum amino acids (already performed);
(iv)
Whole exome sequencing.
9.5
The experts further agree that Prof Mary Rutherford, expert
neonatologist and neonatal neuroradiologist, should
be asked to
comment on the MRI images.
9.6
The experts agree that based on the neonatal history, the clinical
examination of the plaintiff’s child, the
MRI findings,
should
the above investigations not be conclusive of any underlying
condition
,
then prolonged partial
intrapartum asphyxia resulting in hypoxic ischaemic encephalopathy
after birth is the most probable cause
of E[....]’s
neurodisability.”
[10]
Pursuant thereto, E had been subjected to several tests at the
instance of Dr Keshave. In this
regard, I refer to the order issued
by Justice Stretch, of which I quote therefrom the relevant
paragraphs set out below:
“
1.
It is recorded that previously the defendant subjected the minor
child for some tests and the reports dated
10 April 2019, 3 December
2019 and 25 February 2020 were filed in this Court.
2.
It is further recorded that the defendant has, for the fourth time,
subjected the minor child with
some tests and the results are still
outstanding despite the fact that the defendant as ordered by this
Court on 3 March 2020 to
provide the test to the plaintiff within 30
days of the order.”
[11]
The final test was performed by Centogene Laboratory in Germany at
the instance of Dr Keshave,
who suspected genetic conditions. Out of
the Centogene test results, Dr Keshave was of the opinion that E had
AGS which led to
her brain damage. It is on the basis of this
suspicion that this court must determine:
“
Whether the
child’s brain damage was caused by a hypoxic ischemic injury
during the intrapartum period (the period from start
of labour to
birth) or whether the brain damage was caused by the genetic syndrome
contended for by the defendant.”
Expert
Evidence During Trial
[12]
During trial, only the expert witnesses testified. The medico-legal
reports of experts were filed
of record. They form part of the
evidence. The report of Dr Mugerwa-Sekawabe, including all the facts
and opinions contained therein,
was accepted by the defendant. The
report forms the basis of the admitted facts.
[13]
Dr Mugerwa-Sekawabe is a Specialist Obstetrician and Gynaecologist.
Professor Lotz (neuroradiologist),
Dr Gericke (Geneticist), Dr
MacDonald (radiologist) and Dr Redfern (paediatric neurologist) all
testified on behalf of the plaintiff.
[14]
Dr Zikalala (radiologist) and Dr Keshave (paediatric neurologist)
testified on behalf of the
defendant.
[15]
The report of Dr Mugerwa-Sekawabe is uncontested. Dr Mugerwa-Sekawabe
provides an analysis of
the assessment interview conducted with the
plaintiff on 11 February 2019, a review of available documents,
literature and gave
his conclusions and opinions. His testimony on
facts is largely based on the interviews with the plaintiff. Dr
Mugerwa-Sekawabe’s
report indicated that he had received the
identity copy of the plaintiff, birth certificate of E, hospital
notes, the medico-legal
report by Prof Lotz and medico-legal report
by Dr Redfern. Pursuant to the interview, he established that the
plaintiff started
with her antenatal visits at the Ntshele Clinic,
Mthatha from when she was 5 months pregnant. The plaintiff made at
least four
visits to the clinic and during that period, no problems
were identified.
[16]
The plaintiff had no medical or surgical problems prior to her
falling pregnant. She was a primigravida.
She started experiencing
labour pains on 15 December 2007, during the night at approximately
23h00. On 16 December 2007, she presented
to Vidgesville Clinic at
07h00, where she was examined. The examination included vaginal
examinations, fetal heart rate and blood
pressure. She was not
advised on how far dilated the cervix was. There were no further
examinations undertaken for the day. Her
water broke at 18h00 and a
toilet like liquid was coming out of her vagina. She was transferred
to Mthatha General Hospital.
[17]
The plaintiff was taken to Mthatha General Hospital by ambulance and
arrived at the hospital
at 20h00. At the Mthatha General Hospital,
she was assessed and advised that her womb was still closed. During
this time, the labour
pains were getting progressively stronger. She
cannot confirm whether an FHR test was done on admission. The
plaintiff was admitted
to the ward. Soon thereafter, she was left on
her own. Approximately at 04h00, she felt something pushing in her
vagina. The nurses
were called to assist her. A student nurse
assisted her with the delivery. The baby was then born. The plaintiff
was thereafter
put on oxygen
via
a face mask.
[18]
E did not cry at birth. The nurse who was assisting the plaintiff
showed the plaintiff the baby
and pointed out to her a swelling on
the baby’s head. The baby was then rushed to an incubator as
she started having seizures.
Pursuant thereto, the baby was then
transferred to Nelson Mandela Academic Hospital. The baby was nursed
in an incubator, had an
intravenous drip, oxygen was administered
via
nasal prongs and a nasogastric tube for feeding. The baby was
discharged from the hospital on 27 December 2007. She has been on
phenobarbitone treatment to suppress seizures. In spite of this, the
seizures are still recurring.
[19]
Dr Mugerwa-Sekawabe complains strongly about the unavailability of
the relevant records pertaining
to care during the antenatal period,
as well as management during labour. The doctor emphasized the
importance of these records
for purposes of analysis. He then gave an
analysis based on the available information and interviews of the
plaintiff.
[20]
The conclusion by Dr Mugerwa-Sekawabe in relation to the antenatal
period is that there were
no complications or untoward factors which
could be associated with her condition. In relation to the labour, Dr
Mugerwa-Sekawabe
again pointed out the importance of the Maternity
Case Records, which include the PARTOGRAM. These records are not
available. The
Maternity Care Record is the principal record of
antenatal history, intrapartum history as well as the birth and
immediate postpartum
records. The PARTOGRAM relates to all findings
of maternal and fetal conditions and progress in labour. All those
records were
not made available.
[21]
Dr Mugerwa-Sekawabe highlighted the consequences of the missing
clinical records and those consequences,
according to Dr
Mugerwa-Sekawabe, are that:
“
21.1
Information on the important parameters of maternal and fetal
conditions as well as the progress of labour is not available. It is
therefore not possible to ascertain what pertained during
the
intrapartum period;
21.2 Information
on medications and/or medical interventions which were provided
and/or instituted, is lacking;
21.3 Information
on whether there were any obstetric and/or neonatal complications and
what measures (if any) were instituted thereof
is not available; and
21.4 The
withholding of contemporaneous clinical records could be a deliberate
measure to shield substandard care because those
records could have
brought such substandard care to light.”
[22]
The opinion expressed by Dr Mugerwa-Sekawabe is that the transfer of
the plaintiff to Mthatha
General Hospital was necessitated as a
result of the meconium staining of the liquor (MSL). Dr
Mugerwa-Sekawabe was critical about
the fact that the plaintiff was
not referred for MSL and FHR tests on admission until the baby was
born after 04h00 on 17 December
2007.
[23]
Dr Mugerwa-Sekawabe is of the opinion that the baby suffered from
aspiration of MSL and was born
with Apgar scores that were probably
below normal. This conclusion is drawn by Dr Mugerwa-Sekawabe from
the fact that the child
did not cry at birth and it was recorded in
the Road to Health Chart under “
Problems during
pregnancy/birth/neonatally
” – “
meconium
aspiration, low Apgar
”.
[24]
According to Dr Mugerwa-Sekawabe, the accepted standards addressed
the problem of MSL and what
monitoring of the FHR ought to be. In
this regard, Dr Mugerwa-Sekawabe referred to the standards, which I
quote below:
“
[T]hin
meconium staining requires no special management. Thick [MSL] is
associated with an increased risk of fetal distress. Transfer
from
community health centre to hospital unless delivery is imminent,
monitor the fetus with a [CTG] if available, [and] when the
head
extends at delivery, thoroughly suck the infant’s mouth and
then nose before delivering the trunk.”
[25]
Dr Mugerwa-Sekawabe submitted that the management of the plaintiff’s
labour, both at the
clinic and at the hospital, were substandard,
because:
“
1.
MSL is an indication for CTG monitoring. Even in the absence of a
CTG, the FHR ought to have been checked with
a hand-held Doppler
instrument every 30 minutes, before, during and after contractions.
2.
The baby aspirated meconium during the delivery. It would appear that
the baby’s airways
were not cleared of MSL as provided in the
protocols.”
[26]
According to Dr Mugerwa-Sekawabe, contractions during labour lead to
a reduction in oxygen supply
to the placenta and in turn to the
fetus. In relation to the uterus, the reduced pressure on the uterine
arteries results in an
improvement in the blood supply to the
placenta, and a restoration of oxygenation to the fetus. In view of
the increased risk of
hypoxia and fetal distress in a setting of MSL,
as was the case in this matter, the lack of monitoring of the FHR
probably resulted
in abnormalities of the FHR which accompany fetal
acidosis going undetected. This resulted in E being born with low
Apgar scores
– one of the signs of a hypoxic ischaemic insult.
[27]
The conclusions of Dr Mugerwa-Sekawabe, pursuant to his analysis of
the facts and literature,
were that:
“
1.
In all probability pointers to intrapartum hypoxia went unnoticed,
leading the fetus to suffer from a hypoxic
ischaemic injury. Prof
Lotz is of the opinion that the fetus suffered from a global insult
of a prolonged partial nature.
2.
There appears to be a causative link between the substandard
management of labour and the hypoxic
ischaemic brain insult suffered
by E[....] L[....].”
[28]
Dr Lotz, a Neuroradiologist, also testified in support of the
plaintiff’s case. He testified
in respect of the MRI scan of
E’s brain and also testified about the CT scan which he had
analysed with Dr MacDonald. He
concluded that the neuroradiologic
features of AGS and TS are not present on E’s MRI and CT scans.
According to him, the
salient points, in this regard, are summarised
as follows:
“
1.
Intracranial calcification: The characteristic feature of AGS is
intracranial calcification, which is present
in 100% of cases.
E[....]’s CT showed no intracranial calcifications.
2.
White matter changes: The white matter changes of AGS occur
predominantly in the lobar regions,
with relative sparing of the
periventricular area, corpus callosum and optic radiations. Contrary
to this, the white matter affected
in E[....]’s MRI is almost
the exact opposite of this pattern.
3.
Cerebral atrophy: Cerebral atrophy is present in the vast majority of
AGS cases, in contrast, no
cerebral atrophy was present in E[....]’s
MRI.
4.
The MRI and CT scan features essentially exclude a diagnosis of AGS.”
[29]
Dr Lotz confirmed that WES failed to detect an alternative
explanation for E’s brain injury.
Also, on this basis, he
agreed with other experts that the most likely cause of E’s
brain injury and neurodisability is a
hypoxic ischaemic injury
sustained during the intrapartum period. Dr Lotz came to the
conclusion that the case of E indicates that
there was a hypoxic
ischemic insult to a term brain which caused the injuries seen in E.
He further explained that when there is
a partial prolonged insult,
it means that the blood flow to the brain is interrupted at times by
way of both hypoxia (not enough
oxygen in the blood) and ischemia
(not enough pressure in the flow of blood) to the brain.
[30]
Dr Lotz dealt in his evidence with AGS extensively. He dealt with
calcification and showed the
slides where there is calcification and
not.
[31]
Dr Gericke also testified in support of the plaintiff’s case.
He is the only qualified
genetic expert that has been called in the
case. I must indicate though that Dr Keshave, a paediatric
neurologist, had informed
this court that he can testify about
genetics as well. That aspect is dealt with later.
[32]
Dr Gericke is a specialist clinical geneticist. Broadly speaking, his
evidence was not challenged
on material aspects. His testimony
related to the issue of genetics. In his testimony, Dr Gericke
excluded AGS presence on E. He
directly responded to the Centogene
report, an aspect to which I deal with later. He firstly indicated
that the Centogene report
indicates that E has a genetic result of no
functional significance, for it is of unknown significance and as
such, it is not diagnostic
of AGS. According to Dr Gericke, the
sequencing results from the testing performed by Centogene indicate
two ‘variants of
uncertain significance’ (VOUS or VUS)
relating to non-disease causing, incomplete changes in genes involved
with Aicardi
Goutieres syndrome and tuberous sclerosis II complex are
just that, they are of uncertain significance. VOUS are graded
according
to whether there is much available information (Classes 2
and 4), but the described variants in this instance are associated
with
‘scarce information’. Of the VOUS, Class 3 is the
most numerous one, comprising about 40% of all VOUS variants
discovered.
[33]
E’s family pedigree, medical history, neurodevelopmental
course, MRI findings and genetic
testing
do not
demonstrate
any of the known clinical features or TREX1 or TSC2 mutations that
are associated with Aicardi Goutieres Syndrome of
Tuberous Sclerosis
respectively.
[34]
In summary, the presented genetic sequencing results are not
informative and cannot be used in
any way to even remotely suggest
that they relate to the patient’s adverse neurological
presentation.
[35]
Dr MacDonald, an Adjunct Professor of Radiology, also testified for
the plaintiff. He testified
on the MRI brain and CT brain scans.
According to Dr MacDonald, the CT and MRI brain scans demonstrate
that there are no calcifications,
effectively excluding AGS as a
possible diagnosis. According to him, the white matter damage seen in
E is in a typical watershed
distribution, specifically sparing the
temporal lobes and there is a severe cortical thinning in the
watershed regions.
[36]
In his testimony, Dr MacDonald explained that AGS is rare and
thereafter outlined what is expected
in a neuroimaging diagnosis of
AGS. He draws the court’s attention to the following aspects:
“
1.
Brain calcifications
1.1
The study by Ugetti was 100% of 36 patients and La Piana of 121
patients but 97.5% of 112 patients where CT scans
were available. CT
is more sensitive for calcification than MRI and is the gold standard
for demonstrating brain calcification.
1.2
The result of this is in 98% of the cases where there is AGS
calcification will be present. This is a percentage
which would mean
that for this theory of the defendant to work, the child must by
chance fall within the 2% that does not show
calcification.
2.
Leukoencephalopathy (abnormal white matter)
2.1
Ugetti showed 100% of 36 patients and La Piana 90% of 121 patients.
2.2
The cortex is preserved. In a patient with AGS, the cortical
thickness is preserved (as opposed to what we see in
E[....], where
the cortex is severely thin in the watershed regions).”
[37]
Dr MacDonald is of the opinion that for the defendant’s
proposition to work, E must, first
of all, fall within the 2% with no
calcification and then further fall into the miniscule percentage
with no leukoencephalopathy.
In addition, thereto, E would be one of
the first cases (if not the first) where the cortex is not preserved.
The CT and MRI for
E therefore demonstrate none of the features
expected for AGS.
[38]
Dr Redfern, a paediatric neurologist, also testified on behalf of the
plaintiff. In his testimony,
he indicated that E does not display the
necessary clinical features to suggest a diagnosis of TREX1 related
AGS. E’s neuroimaging
is completely not compatible with a
diagnosis of AGS. The most probably cause of E’s disability is
hypoxic ischaemic brain
injury sustained in the perinatal period.
[39]
That was the plaintiff’s case.
[40]
The defendant called two expert witnesses, Dr Keshave and Dr
Zikalala.
[41]
Dr Keshave, in his testimony for the defendant, informed this court
that he is a paediatric neurologist.
[42]
Dr Keshave testified that he assessed E on 28 February 2019. He had
also considered documents
submitted to him, such as the Road to
Health Card, medico-legal report by Dr Zikalala, a radiologist and
the Ampath Laboratory
genetic results. In his neurological or
developmental assessment, Dr Keshave prepared his reports. I quote
below from his report
dated 31 October 2019, and as amended on 25
February 2020:
“
16.
Summary of Neurological/Developmental Assessment
E[....] is a 12
year old female with Microcephalic Spastic Quadriplegia with feathers
of Autistic Spectrum Disorder complicated
by Global Developmental
Delay, Intellectual Disability, Symptomatic Epilepsy and a pseudo
bulbar palsy.
The addition of
the radiologist report – indicates that there is cystic
encephalomalacia. This would support the presence
of neonatal
encephalopathy at the time of birth – however the aetiology of
neonatal encephalopathy is vast and includes the
following
conditions:
1)
Metabolic Conditions
2)
Infectious
3)
Toxin and Drugs
4)
Perinatal Stroke Syndrome
5)
Congenital Anomalies
6)
Vasculopathies
7)
Genetic Syndromes
8)
Hypoxic Ischemic Encephalopathy
Based on the
RTHC the presence of Meconium Aspiration Syndrome seems the most
likely cause to have resulted in the low apgars (actual
score not
documented) and this would have caused the Neonatal Encephalopathy.
I also strongly
feel that there is an underlying genetic condition – in view of
the strong Autistic Spectrum Disorder features
that are showed by
E[....] – one would need to exclude an underlying genetic
condition. As the severity of the MRI brain
does not match the
clinical picture noted in E[....] at age 12 years of age.
Based on the
genetic test, CGH Array – done at Ampath Laboratories on the
18
th
March 2019 indicated that there was no
underlying abnormalities, this would make an underlying genetic cause
for E[....]’s
condition less likely. Although the genes have
returned negative for the common South African genetic mutations for
children with
ASD – this does not totally exclude an underlying
genetic disorder, as mentioned in the final comment on the genetic
results
from Ampath Laboratory.
However in view
of the lack of medical records it is still very difficult to predict
what would have caused E[....]’s current
clinical condition, as
mentioned before the presence of Neonatal Encephalopathy does not
singly handily indicate Birth Asphyxia
other conditions that still
need to be excluded include:
16.1 Metabolic
Conditions
16.2 Infectious
16.3 Toxin and
Drugs
16.4 Perinatal
Stroke Syndrome
16.5
Vasculopathies”
[43]
Dr Keshave made a recommendation for a neurometabolic screening to be
done to exclude possible
aetiology, following which the most likely
diagnosis would then be birth asphyxia. He complained as well about
the lack of medical
records, which records, in his opinion, would
have assisted with determining the underlying cause. Notwithstanding
the production
of various laboratory reports, Dr Keshave had a
suspicion about the existence of some other medical conditions in
“E”,
and he called for further metabolic and genetic
tests. One test that led Dr Keshave to amend his first report, was
the Centogene
test report.
[44]
The Centogene report, contained the following observations under the
heading “
Interpretation
”:
“
A
heterozygous variant of uncertain significance was identified in the
TREX1 gene. The genetic diagnosis of autosomal dominant
Aicardi-Goutieres syndrome 1 is possible.
A heterozygous
variant of uncertain significance was identified in the TSC2 gene.
The genetic diagnosis of autosomal dominant Tuberous
sclerosis type 2
is possible. However, further analysis is necessary.”
[45]
The Centogene report, however, proposed further testing and other
investigations for the confirmation
of their suspicions. These
included:
“
45.1
Clinical correlation.
45.2 Parental
carrier testing to establish whether the detected TREX1 and TSC2
variants are inherited or de novo.
45.3 Carrier
testing for all informative family members to establish whether the
detected variants are associated with the disorder
or not. Basic
clinic information and relationship for each analysed family member
is needed for a comprehensive evaluation of the
data.”
[46]
Based on the Centogene report, Dr Keshave requested the defendant’s
radiologist, Dr Zikalala,
to review the earlier findings. In essence,
Dr Keshave maintains that there is a suspicion that “E”
suffers from Aicardi-Goutieres
(AGS) and that, according to Dr
Keshave on the interpretation of the Centogene report, the condition
is genetic and the AGS caused
the insult to the brain of “E”.
The family history had shown no genetic conditions.
[47]
The defendant further called Dr Zikalala, a radiologist, to testify
with regards to the MRI and
CT scans. Dr Zikalala had prepared two
expert reports. The first report is dated 4 February 2019 and the
amended report is dated
27 November 2020. In her testimony, Dr
Zikalala dealt with the two reports. In respect of the first report,
she made the comment
below:
“
Cystic
encephalomalacia in the anterior and posterior watershed zones. In an
appropriate context, this is seen as the sequelae of
partial hypoxia
of prolonged duration in term infants. These findings need further
correlation with clinical history and findings.
”
[48]
Almost a year later on 27 November 2020, after receipt of Dr
Keshave’s amended report which
suggests AGS, Dr Zikalala
amended her initial comments to read:
“
Cystic
encephalomalacia in the anterior and posterior watershed zones.
Differentials include metabolic conditions, infections and
hypoxic
ischaemic encephalopathy. However, correlation with clinical history,
pediatric assessment, biochemistry and genetic testing
confirmed
Aicardi-Goutieres syndrome, making the other causes less likely.
The findings in
our case are similar to documented cases of Aicardi-Goutieres
syndrome which include:
·
Abnormal white matter signal intensity with a diffuse
frontotemporal anteroposterior gradient, and periventricular
distribution
·
Cystic areas in the temporal and/or frontal lobes
·
Cerebral atrophy with dilatation of ventricles
·
Deep white matter cysts
·
Although calcifications, mainly in the basal ganglia, lobar white
matter, and dentate nuclei are not a dominant feature in our case,
some case reports have reported absence or resolution of
calcifications with time.”
[49]
Dr Zikalala, in her evidence, testified that the amendment was
necessitated by a report because
there were a few changes in the scan
that resembles some of the things that are described in the
literature of AGS. She indicated
that she was informed by the team
and the information brought by a paediatric neurologist, who carried
out the test on the child
and she disputed allegations which
suggested hearsay about the AGS. Dr Zikalala, in her evidence,
supported Dr Keshave that the
conditions, as depicted on the MRI scan
did not correlate with the clinical presentation of the child.
[50]
Dr Zikalala, in her evidence, indicated that she was informed that
there was genetic testing
which suggested AGS or similar cases in the
literature of AGS. The entire second report of Dr Zikalala, according
to her, is based
on the proposition that AGS had been positively
diagnosed and therefore, she had to review the first report. Indeed,
the first
report was reviewed and the second report suggests the
presence of AGS.
[51]
That was the case of the defendant.
The
Applicable Law
[52]
To obtain a judgment holding the defendant liable to pay delictual
damages, the court in
Minister
of Safety & Security v Van Duivenboden
[1]
state that the plaintiff must prove, on a balance of probabilities,
that the act(s) or omission(s) of the defendant is wrongful
and
negligent, and have caused loss. The approach in our law to the
plaintiff’s claim is not controversial. It is trite that
in
order to succeed in her delictual claim for damages, the plaintiff
must establish that the wrongful and negligent conduct of
the
province’s nursing and medical staff, acting within the course
and scope of their employment, caused her harm.
[2]
[53]
In
Kruger
v Coetzee
[3]
it was held:-
“
For the
purposes of liability culpa arises if –
(a)
a diligens paterfamilias in the position of the defendant (or his
employees) –
(i)
would foresee the reasonable possibility of his (their) 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 (or his employees) failed to take such steps.”
[54]
In
Naude
NO v Transvaal Boot and Shoe Manufacturing Co
[4]
it was held –
”
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
(his paraplegia) in a way which would absolve the defendant and his
employees of negligence.”
[55]
In
Mitchell
v Dixon
[5]
it was held –
“
A medical
practitioner is not expected to bring to bear upon the case entrusted
to him the highest possible degree of professional
skill, but he is
bound to employ reasonable skill and care; and he is liable for the
consequences if he does not.”
[56]
In
Monteoli
v Woolworths (Pty) Ltd
[6]
the court confirmed that the onus, nevertheless, remains with the
plaintiff. The defendant has an evidential burden to show what
steps
were taken to comply with the standards to be expected.
[57]
In
Minister
of Safety & Security & Another v Carmichele
[7]
where the court confirmed that causation has two elements –
“
1.
The factual issue to be established on a balance of probabilities by
the plaintiff by using the “but
for” test would involve
the mental elimination of the wrongful conduct in the posing of the
question as to whether upon such
hypothesis, the plaintiff’s
loss would have ensued or not;
2.
The legal causation, namely whether the wrongful act is linked
sufficiently closely or directly
to the loss for legal liability to
ensue or whether, as it is said, the loss is too remote. This is a
juridical problem and considerations
of policy may play a part in the
solution thereof.”
[58]
In
Caswell
v Powell Duffryn Associates Collieries
[8]
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.”
[59]
The expert witnesses who had testified are experienced. As a result
of the expert reports and
testimonies, the issues were narrowed down
to the question of what the factual cause of E’s condition was.
The starting point
would be to evaluate and resolve the conflict in
the testimony of the experts for the plaintiff and for the defendant.
In
J
Afrikander on behalf of
DMA v
The MEC for Health
.
[9]
“
The
opinion of a witness is generally inadmissible. ‘In the law of
evidence, ‘opinion’ means any inference from
observed
facts, and the law on the subject derived from the general rule that
witnesses must speak only to that which was directly
observed by
them.’ Opinion is admissible if it is relevant. Relevance is in
turn determined by the issues in the matter.
If the opinion can
assist the court in determining an issue, it has probative value,
otherwise it is superfluous. Expert opinion
evidence is received when
the issues require special skill and knowledge to draw the right
inferences from the facts stated by
the witnesses.
[60]
The Full Bench of the Eastern Cape in
J
Afrikander
discuss several types of conflicts in expert evidence that may
present itself in any given case.
[10]
The first is a conflict with regard to the assumed facts. Expert
opinion must have a factual basis. The facts upon which an expert
opinion is based must be proved by admissible evidence. A second
conflict in the expert opinion may lie in the analysis of the
established facts and the inferences drawn therefrom by the opposing
witnesses. The cogency of the expert opinion depends on its
consistency with proven facts and on the reasoning by which the
conclusion is reached. The source for the evaluation of this evidence
for its cogency and reliability are (i) the reasons that have been
provided by the expert for the position adopted by him/her;
(ii)
whether that reasoning has a logical basis when measured against the
established facts; and (iii) the probabilities raised
on the facts of
the matter. It means that the opinion must be logical in its own
context, that is, it must accord with, and be
consistent with all the
established facts, and must not postulate facts which have not been
proved.
[61]
The inferences drawn from the facts must be sound. The logic of the
opinion must be consistent,
and the reasoning adopted in arriving at
the conclusion in question must accord with what the accepted
standards of methodology
are in the relevant discipline. The
reasoning will be illogical or irrational and consequently
unreliable, if (i) it is based on
a misinterpretation of the facts;
(ii) it is speculative, or internally contradictory or inconsistent
to be unreliable; (iii) if
the opinion is based on a standard of
conduct that is higher or lower than what has been found to be the
acceptable standard; (iv)
if the methodology employed by the expert
witness is flawed. What flows from this is that the mere fact that an
expert opinion
is unchallenged, does not necessarily mean that it
must be accepted. However, if that evidence is based on sound grounds
and is
supported by the facts, there exists no reason not to accept
it.
[62]
Other considerations relevant in this context are (i) the
qualifications and the experience of
the expert witnesses with regard
to the issue he or she is asked to express an opinion on; (ii)
support by authoritative, peer-reviewed
literature; (iii) the measure
of equivocality with which the opinion is expressed; (iv) the quality
of the investigation done by
the expert; (v) and the presence or
absence of impartiality or a lack of objectivity. What is ultimately
required is a critical
evaluation of the reasoning on which the
opinion is based, rather than considerations of credibility. Should
it not be possible
to resolve a conflict in the expert opinion
presented to the court in this manner, that is, when the two opposing
opinions are
both found to be sound and reasonable, the position of
the overall burden of proof will inevitably determine which party
must fail.
It is worth emphasising that the onus as a determining
factor “
can only arise if the tribunal finds the evidence
pro and con so evenly balanced that it can come to no such
conclusion. Then the
onus will determine the matter. But if the
tribunal, after hearing and weighing the evidence, comes to a
determinate conclusion,
the onus has nothing to do with it, and need
not be further considered
.”
[63]
The third type of conflict, which may arise in expert evidence is
that of competing theories
of a purely scientific nature. The choice
between two conflicting theories is informed primarily by the extent
to which the theory
is regarded as being established and has gained
general acceptance within the specific scientific community in the
particular discipline
to which it belongs. Whether or not a theory
has been sufficiently established must be measured against
considerations such as
whether it can, and has been tested; whether
it is the product of reliable principles and methods that have been
reliably applied
to the facts of the case; and whether it has been
subjected to peer review and publication.
[64]
Fourthly, a conflict may also arise in the context of what the
accepted standard of conduct of
a medical professional is in certain
circumstances. Typically, medical negligence cases deal with the
situation where an injury
is alleged to be in complete discord with
the recognised therapeutic objective and techniques of the operation
or treatment involved.
Expert opinion, in this context, is aimed at
determining whether the conduct of a professional person in a
particular field accords
with what is regarded as a sound practice in
that field. Again, the method adopted is to evaluate opinion evidence
with the view
of establishing the extent to which the opinions
advanced are founded on logical reasoning.
[65]
What is evident from the aforegoing is that the evaluation of expert
opinion in determining its
probative value and the considerations
relevant thereto, are determined by the nature of the conflict in the
opinion, and the context
provided by all the evidence and the issues
which the court is asked to determine. In general, it is important to
bear in mind
that it is ultimately the task of the court to determine
the probative valued of expert evidence placed before it and to make
its
own finding with regards to the issues raised. Faced with a
conflict in the expert testimony of the opposing parties, the court
is required to justify its preference for one opinion over another by
a careful and critical evaluation thereof. Further, the primary
function of an expert witness is to guide the court to a correct
decision on questions, which fall within that expert’s field.
To that extent, the expert witness has a duty to provide the court
with abstract or general knowledge concerning his or her discipline,
and the criteria necessary to enable the court to form its own
independent judgment by the application of the criteria to the facts
proved in evidence. Accordingly, the mere “
pitting
of one hypothesis against another does not constitute the discharge
of the functions of an expert.
”
Finally, it is not the function of the court to develop its own
theory or thesis and to introduce on its own accord evidence
that is
otherwise founded on special knowledge and skill.
Ex
hypothesi
,
such evidence is outside the learning of the court. The function of
the court is restricted to deciding a matter on the evidence,
or
accepting or rejecting the proffered expert evidence.
[11]
[66]
There is a general obligation placed upon the parties on cross
examination of witnesses, including
experts, to put the parties’
case to the witness being cross examined. The reason for this is to
allow the witness to deal
with the evidence where he differs with
such evidence. In this regard,
Small
v Smith
[12]
and
President
of the Republic of South Africa v SARU
[13]
support the position taken by this court. Expert witnesses should
provide independent assistance to the court by way of objective,
unbiased opinions. An expert witness is not required to assume the
role of a legal practitioner or that of the court. An expert
witness
must state facts or assumption upon which his or her opinion is
based. The expert must not omit to consider the material
facts that
should detract from his concluded opinion. It is not expected of the
court to simply accept the opinions of experts.
The expert evidence
must be logical and his or her conclusions must be reached with
knowledge of all the facts.
[67]
In
Schneider
NO and Others v AA and Another
[14]
Davis J discusses the duties of an expert with reference to some
authorities, whereafter he makes the statement, with which I agree:
“
In short,
an expert comes to court to give the court the benefit of his or her
expertise. Agreed, an expert is called by a particular
party,
presumably because the conclusion of the expert, using his or her
expertise, is in favour of the line of argument of the
particular
party. But that does not absolve the expert from providing the court
with as objective and unbiased an opinion, based
on his or her
expertise, as possible. An expert is not a hired gun who dispenses
his or her expertise for the purposes of a particular
case. An expert
does not assume the role of an advocate, nor gives evidence which
goes beyond the logic which is dictated by the
scientific knowledge
which that expert claims to possess.”
[68]
In
Michael
and Another v Linksfield Park Clinic (Pty) Ltd & Another
[15]
the court had the following to say when considering expert evidence:
“
This
essential difference between the scientific and the judicial measure
of proof was aptly highlighted by the House of Lords in
the Scottish
case of Dingley v The Chief Constable, Strathclude Police 200 SC (HL)
77 and the warning given at 89D-E that:
‘
(O)ne
cannot entirely discount the risk that by immersing himself in every
detail and by looking deeply into the minds of the experts,
a Judge
may be seduced into a position where he applies to the expert
evidence the standards which the expert himself will apply
to the
question whether a particular thesis has been proved or disproved –
instead of assessing, as a Judge must do, where
the balance of
probabilities lies on a review of the whole of the evidence.”
Analysis and Findings
[69]
I am obliged to assess and evaluate the entire evidence. However, I
am troubled by the fact that
the blood test results from Ampath
Laboratories and other tests were submitted with no corroborating
evidence. The Centogene report,
which in my view, is central to the
defendant’s case, was submitted with no corroborating evidence.
The Centogene report
called for further tests and information. This
was not entirely done. The Centogene report had called for further
investigation
in order to confirm their findings. The family history
had shown no genetic conditions. This court has not been told why it
should
prefer the Centogene laboratory report over other reports. For
that reason I will consider these reports in light of all the
evidence
and to the extent that they provide admissible evidence. I
raise the issue of the Centogene report and the report from Ampath
Laboratories
because they give contradictory results. Centogene
Laboratory suggests the genetic diagnosis of autosomal dominant
Aicardi-Goutieres
syndrome 1 is possible and that the genetic
diagnosis of autosomal dominant Tuberous sclerosis type 2 is
possible. The other reports
contain no such findings. These
contradictions were not explained nor was evidence from laboratories
led during the trial. The
plaintiff’s experts had excluded the
presence of AGS.
[70]
There is no controversy about the report of Dr Mugerwa-Sekawabe. The
entire report has been accepted
by the defendant. In such
circumstances, I therefore accept that the findings and opinions of
Dr Mugerwa-Sekawabe are common cause.
Briefly, Dr Mugerwa-Sekawabe
mentioned some critical findings which I do repeat below.
[71]
Dr Mugerwa-Sekawabe finds that the management of the labour, both at
the clinic and hospital,
was of a substandard nature because -
71.1 MSL is an
indication for CTG monitoring (this is monitoring by a
cardiotocograph machine). Even in the absence of a CTG, the
FHR ought
to have been checked with handheld Doppler instrument every 30
minutes before, during and after contractions. This did
not happen.
71.2 The baby
aspirated meconium during the delivery. It would appear that the
baby’s airways were not cleared of MSL as provided
in the
protocols.
71.3 The
non-monitoring of the FHR probably resulted in abnormalities of the
FHR which accompany foetal acidosis going undetected.
This resulted
in the newborn being born with low APGAR scores – one of the
signs of hypoxic ischemic insult.
71.4 The
intrapartum management of the unit was flawed.
71.5 If the
monitoring had been proper “
it would have been possible to
detect those unfavourable factors which have necessitated
interventions. The failure to undertake
these observations, in line
with accepted standards – and also not instituting measures of
clearing the baby’s airways
of the meconium fluid at delivery
so as to mitigate against meconium aspiration – amounted not
only to substandard care but
was also a breach of the duty of care.”
71.6 In all
probability, Dr Mugerwa-Sekawabe concluded that pointers to
intrapartum hypoxia went unnoticed, leading the foetus to
suffer from
a hypoxic ischemic injury.
[72]
The defendant did not challenge the report of Dr Mugerwa-Sekawabe and
instead, his findings were
admitted in the pre-trial minutes. I
cannot fault the report by Dr Mugerwa-Sekawabe. Accordingly, I accept
the evidence of Dr Mugerwa-Sekawabe.
[73]
Dr Mugerwa-Sekawabe relied upon the direct evidence of the plaintiff.
The medical staff had a
duty to record the treatment that was
accorded to the plaintiff. The defendant’s employees were
obliged to keep punctilious
clinic and hospital notes pertaining to
the plaintiff’s treatment. I agree with the submissions of Mr
Van der Walt, counsel
for the plaintiff in this regard. The missing
hospital records remains questionable. In my view, the defendant’s
employees
had breached their legal duty to maintain official hospital
records. In such circumstances, the plaintiff’s evidence as
summarised
in the report of Dr Mugerwa-Sekawabe should prevail.
[74]
In
Lungile
Ntsele v MEC for Health, Gauteng Provincial Government
[16]
it is said:
“
(46)
Logic and common sense dictates that the plaintiff’s labour and
A’s subsequent birth endured for a longer period
of time than
the few minutes suggested by the plaintiff under cross-examination.
It is unfair and unjust for the defendant’s
counsel without any
cogent evidence from the defendant’s employees regarding the
treatment accorded to the plaintiff or any
reasonable explanation
tendered by the defendant’s employees regarding the
disappearance of the plaintiff’s clinic
and hospital records,
to expect the plaintiff to be precise and specific about the
treatment accorded her at the clinic and hospital
whilst under
anaesthesia.
(115)
There is a legal duty on the nurses at the clinic, the doctor
and
nurses at the hospital to record the treatment accorded to the
plaintiff and Ayanda. The defendant’s employees were obliged
to
and must have made and kept punctilious clinic and hospital notes
pertaining to the plaintiff’s treatment.
(116)
The clinic and hospital notes are missing from the plaintiff’s
and A’s files. There is a duty on the clinic and hospital
record custodian staff in terms of
sections 13
and
17
of the
National
Health Act No 61 of 2003
to safeguard the plaintiff’s and A’s
clinic and hospital records.
”
[75]
Prof Lotz analysed the damage to the brain of E and made use of
slides in his presentation of
evidence. Prof Lotz concluded that
there was a hypoxic ischemic insult. The evidence of Prof Lotz is
consistent with the report
prepared by Dr Mugerwa-Sekawabe which had
pointed to a hypoxic ischemic injury. Prof Lotz evidence was not
meaningfully challenged
under cross-examination. I was satisfied with
the evidence of Prof Lotz. He gave logical opinions and he was clear
in his evidence.
I do accept his evidence, more so that it is in line
with the report by Dr Mugerwa-Sekawabe.
[76]
Dr Gericke was the only fully qualified genetic expert. The defendant
relied on the evidence
of Dr Keshave. The evidence of Dr Gericke was
straightforward to the effect that E does not have AGS. In supporting
his conclusion,
Dr Gericke pointed out that the variant identified in
the Centogene report means that E has a genetic result of no
functional significance
at all. That is because it is of unknown
significance and it is not diagnostic of AGS. The defendant’s
counsel, Mr Maseti,
could not challenge in a meaningful way, these
conclusions. Accordingly, I accept the evidence of Dr Gericke. It was
logical and
supported with convincing analysis of objective evidence.
[77]
Dr MacDonald was tasked to perform a CT scan and studied the MRI scan
in order to specifically
make conclusions with reference to
neuroimaging of AGS. In his explanation, he informed this court that
AGS is rare and he indicated
what is expected in a neuroimaging
diagnosis of AGS. According to Dr MacDonald, the CT and MRI scans
demonstrate none of these
features expected for AGS. There are no
calcifications, which effectively exclude AGS as a possible
diagnosis. The white matter
damage seen in the brain of E is the
typical watershed distribution, specifically sparing the temporal
lobes and there is severe
cortical thinning in the watershed region.
I accept Dr MacDonald’s evidence. It is logical and an
objective analysis of the
facts and available information.
[78]
Dr Redfern also came to the conclusion that there was no AGS. In
reaching his conclusion, he
had researched and considered the
clinical and MRI characteristics of AGS. I have no hesitation in
accepting his evidence and opinions.
I was satisfied with his
analysis and his conclusions are logical. I also do consider the fact
that there is an agreement amongst
all the experts that AGS is a rare
genetic disorder.
[79]
I have difficulties in accepting Dr Keshave’s evidence. I
highlight the following shortcomings
in his evidence:
79.1 Dr Keshave’s
evidence was speculative and incapable of throwing any doubt on the
otherwise acceptable opinion of
the plaintiff’s expert
evidence. The opinion evidence of plaintiff’s expert was based
on sound grounds and supported
by the basic facts.
79.2 I cannot
ignore the fact that Dr Keshave had called for several tests to be
conducted for as long as the first tests
were not giving his desired
outcomes. Dr Keshave had sought to qualify himself as a geneticist.
Dr Keshave had introduced new material
facts which were not contained
in his expert opinion. There was no acceptable explanation given by
him. In his expert report, Dr
Keshave never mentioned that he had a
physical possession of the MRI scans. During his oral testimony, he
created an impression
that he had possession of the MRI scans. During
cross examination by Mr van der Walt, counsel for the plaintiff, Dr
Keshave was
evasive in his answers. I was not impressed with the
explanations given by Dr Keshave for introduction of the new facts.
79.3 I cannot find
an explanation why Ampath Laboratories results should not be relied
upon, according to Dr Keshave. He sought
to testify about genetic
analysis and thereby discount the expert in the field, Dr Gericke. I
find this unacceptable. An objective
expert would give concessions
where appropriately needed in respect of experts in the field. Dr
Keshave was less convincing in
doing so.
79.4 Whilst I do
appreciate the concession given by Dr Gericke that persons like Dr
Keshave and Dr Redfern, may have some
knowledge of genetics in their
field, genetics is a specialist area. Dr Gericke is a specialist in
genetics and I therefore prefer
his opinions over those of Dr
Keshave.
79.5 For these
reasons, I find that Dr Keshave’s evidence had shortcomings and
it would not be safe for this court to
rely thereupon.
[80]
From a reading of Dr Keshave’s evidence and what he agreed to
in the joint minute with
Dr Redfern, it is evident that he was not
able to raise AGS as a cause of the injury to E, any higher than it
being a mere possibility.
The suggestion that the prolonged partial
intrapartum asphyxia resulting in hypoxic ischaemic encephalopathy
after birth is consistent
with the uncontroverted evidence by Dr
Mugerwa-Sekawabe. Dr Keshave cannot undo this conclusion. The demand
for several tests to
be conducted on child E, seems to suggest that
Dr Keshave had a resolve to find anything that will explain away from
the hypoxic
ischaemic encephalopathy injury on E. At least, for the
court, some measure of certainty on what the cause of the injury
suffered
by E, was expected from Dr Keshave. Dr Keshave failed
dismally in this regard. I have my reservations about the Centogene
report.
No conclusive evidence about this report was led and that
leaves me with many questions than answers. On the other hand, the
plaintiff’s
experts presented logical opinions which is
supported by facts.
[81]
Dr Zikalala agreed with the plaintiff’s expert witnesses that
there is no calcification
on the CT scan on child E and she confirms
that the prolonged partial hypoxic ischaemic injury watershed
involvement is the hallmark
of prolonged partial hypoxic ischaemic
injury. In her evidence, Dr Zikalala testified, I quote:
“
Ms
Zikalala: I cannot exclude AGS in this case. We look for MRI
features, we did not find all of them admittedly. It is a genetic
test, a scientific test, I am not a geneticist, if the person
..[indistinct] is such then I cannot exclude it, unless the person
says something else and that is not my field of expertise. I will
leave it with the …[indistinct].
”
[82]
The above answer is less convincing when regard is had to the first
report of Dr Zikalala when
she records the following:
“
Cystic
encephalomalacia in the anterior and posterior watershed zones. In an
appropriate context, this is seen as the sequelae of
partial hypoxia
of prolonged duration in term infants. These findings need further
correlation with clinical history and findings.”
[83]
The position and views of Dr Zikalala only changed after the report
by Centogene and at the instance
of Dr Keshave’s intervention.
This is clearer when regard is had to the report prepared on 4 April
2019. In the report, Dr
Zikalala makes this statement under her
findings:
“
Cystic
encephalomalacia in the anterior and posterior watershed zones.
Differentials include metabolic conditions, infections and
hypoxic
ischaemic encephalopathy. However, correlation with clinical history,
pediatric assessment, biochemistry and genetic testing
confirmed
Aicardi-Goutieres syndrome, making the other causes less likely.”
[84]
During questioning by this court, Dr Zikalala made the following
concession:
“
Court
:
You do not have a case of AGS, but you cannot ignore the clinical
findings of other expert and you believe to them so I must look
onto
those findings. I must be looking onto those but from your
perspective as you sit here, you do not have a case. It is not
your
case that there is AGS here. That is my last clarity I want from you.
Ms Zikalala
:
What I am saying is I do not have classical features of AGS
therefore, I will look into the clinicians, the experts and the
genetic
information given by the geneticist.
”
[85]
I was not convinced by Dr Zikalala. The inconsistencies in her
evidence have not been convincingly
justified. The differences
between her initial admissions and the subsequent report after the
Centogene report, cannot be reconciled.
She admits that she is not an
expert in genetics. I have already accepted the evidence of Dr
Gericke, which I do prefer, because
of its logic and common sense
based on the admitted evidence. For these reasons, I reject the
evidence of Dr Zikalala.
Conclusion
[86]
On the whole, the evidence, in particular the report prepared by Dr
Mugerwa-Sekawabe, supports
the expert opinion that the brain injury
sustained by E and the disabilities that later followed, were the
result of prolonged
partial hypoxic ischaemia during labour as
opposed to AGS. The injury is consistent with the conduct of the
defendant’s medical
staff and nurses, allowing a severely
prolonged labour of the plaintiff to continue with no monitoring,
exposing the fetus to a
risk of hypoxic type brain injury. The
plaintiff’s experts have, in my view, objectively evaluated the
available facts, the
limited medical records and the clinical
findings logically and carefully. Both Prof Lotz and Dr MacDonald
found that it was a
hypoxic ischaemic insult of a partial prolonged
nature. The defendant’s expert, Dr Zikalala, had initially
agreed with these
observations. Dr Keshave could not dispute those
observations with certainty. He was non-committal and speculative in
his analysis.
[87]
I have been invited by the plaintiff’s counsel, Mr Van der
Walt, to consider the conduct
of Dr Keshave in this case. My
attention was drawn to the fact that the behaviour of Dr Keshave
failed to meet the basic expected
standards from an expert. The
suggestion is that he was not independent. Whilst I have reservations
about Dr Keshave’s insistence
on several tests and the
subsequent interactions with Dr Zikalala, who thereafter changed her
initial report, I do not believe
that there has been some form of
mala fides
on the part of Dr Keshave. Accordingly, I decline
to draw any adverse inference against Dr Keshave.
[88]
I agree with the plaintiff’s submissions that there had been
inadequate monitoring during
the birth process when there would have
been danger signs such as a prolonged labour process and other signs
of distress of the
fetus. The child has been born in a compromised
position with low APGAR scores. The MRI clearly shows a hypoxic
ischaemic insult
of a partial prolonged nature. The insult must have
taken place during the intrapartum period when regard is given to the
entire
evidence and opinions of Drs Mugerwa-Sekawabe and Redfern. Dr
Gericke, a qualified geneticist, has removed any possible clinical
signs of AGS. The admitted facts in the pre-trial minute, joint
expert minutes and the common cause facts established the plaintiff’s
case on a balance of probabilities.
[89]
I find that the defendant had breached their contractual obligations
of care and thereby caused
E to suffer hypoxic ischaemic insult of a
partial prolonged nature. The net result is that the defendant is
liable to compensate
the plaintiff.
[90]
For these reasons, the plaintiff’s case must succeed on the
merits. The costs of this part
of the trial should follow the
results, and I have not been persuaded differently. The plaintiff is
entitled to the costs of the
experts that have been employed.
Order
[91]
In the result, the following order is made:
1.
The merits and quantum are hereby separated in terms of
Rule 33(4).
1
.5cm; margin-bottom: 1cm; line-height: 200%">
2.
The determination of quantum is postponed
sine die
.
3.
The defendant is held liable for the plaintiff’s agreed or
proven damages arising from the
cerebral palsy suffered by the minor
child “E”.
4.
The defendant shall pay the plaintiff’s costs relating to the
issue of
merits
, which costs shall include the employment of
two counsel, together with all reserved costs, if any, which costs
shall include:
4.1
The travelling expenses, reservation and appearance fees, if any,
together with the costs of the preparation
of their reports and
qualifying fees, if any, of the following expert witnesses:
4.1.1 Dr E
Mugerwa-Sekawabe – Specialist Obstetrician & Gynaecologist;
4.1.2 Dr A Redfern
– Senior Specialist/Paediatric Neurologist;
4.1.3 Professor J
Lotz – Professor of Radiology / Neuroradiologist;
4.1.4 Dr G Gericke
– Clinical Geneticist; and
4.1.5 Dr A
MacDonald – Professor of Radiology.
4.2
The defendant shall pay interest on the aforesaid costs at the
current prescribed legal rate of interest from
date of allocator or
agreement to date of payment thereof.
M
NOTYESI
JUDGE
OF THE HIGH COURT (ACTING)
Appearances
:
Counsel
for the plaintiff
:
Mr Van Der Walt SC
together with V Msiwa
Attorney
for the plaintiff
:
Sakhela
Incorporated
East London
Counsel
for the respondent :
A Maseti
Attorney
for the defendant :
Office of the State
Attorney
East London
[1]
2002 (6) SA 431
SCA at para [12]; LD obo AD v Member of the
Executive Council responsible for the Department of Health
[2021]
JOL 49623
(ECM) at p2
[2]
KX v Member of the Executive Council for Health, Western Cape
[2021]
JOL 51401
(WCC) at p3
[3]
Kruger v Coetzee
1966 (2) SA 428
(A) at 430E
[4]
1938 AD 379
at 392(3)
[5]
1914 AD 519
at 525, see also [K…]X[…]
supra
at p3
[6]
2000 (4) SA 735
(W) at 127
[7]
2004 (3) SA 305 (SCA)
[8]
[1939] 3 All ER 722
(HL) at 733
[9]
J Afrikander obo DMA v The MEC for Health, Eastern Cape – Full
Bench – Case No: C A & R 8/2021 at p9 para
10,
see also cases referred to in the judgment
[10]
J Afrikander
supra
at p9 – p17
[11]
See J Afrikander obo DMA
supra
at p17
[12]
1954 (3) SA 434 (SWA)
[13]
2000 (1) SA 1
(CC) at 36 [para 61 – 65]
[14]
2010 (5) SA 203
(WCC) at 211 E-J, see also
Mediclinic
Ltd v Vermeulen
2015
(1) SA 241
[15]
2001 (3) SA 1188
(SCA) at par 40
[16]
2013 (2) All SA 356
(GSJ)