S.S v MEC for Health (35/2019) [2023] ZAECMHC 8 (28 February 2023)

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[2023] ZAECMHC 8
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S.S v MEC for Health (35/2019) [2023] ZAECMHC 8 (28 February 2023)

SAFLII
Note:
Certain
personal/private details of parties or witnesses have been
redacted from this document in compliance with the law
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SAFLII
Policy
IN
THE HIGH COURT OF SOUTH AFRICA
(EASTERN
CAPE DIVISION, MTHATHA)
Case
No: 35/2019
In
the matter between
S[...]
S[...]

Plaintiff
And
MEC
FOR HEALTH

Defendant
JUDGMENT
PAKATI
J
INTRODUCTION
[1]
The plaintiff is Ms SS, a woman who claims damages against the
defendant, the MEC
for Health, in her name and representative
capacity as mother and natural guardian of the child, hereinafter
referred to as ES,
which arose out of the alleged negligence
committed by the defendant’s employees that resulted in brain
damage suffered by
ES while she was admitted at Zithulele Hospital,
on 11 March 2014. The defendant defended the action.
[2]
When the trial started on 26 January 2021, the parties agreed to
separate the special
plea of prescription as far as the plaintiff’s
claim in her personal capacity is concerned, as well as
quantum
from the plaintiff’s claim in her representative capacity. I
made the joint application as an order of court.
THE
ISSUES
[3]
The issues for determination are whether the defendant’s
employees were negligent
in the management and monitoring of the
plaintiff’s labour and the subsequent delivery of ES on any of
the grounds pleaded
by the plaintiff in her amended particulars of
claim, dated 07 September 2020. The issue further is whether or not
such negligence
caused ES to develop cerebral palsy as a consequence
of a hypoxic-ischaemic event at birth.
THE
PLEADINGS
[4]
Regarding negligence, the following was pleaded in paragraph 13 of
the amended particulars
of claim:
“
13. The defendant
was negligent in one, or more of the following respects:
13.1 At Mqanduli
Community Health Care Centre, she failed to:
13.1.1 permanently,
alternatively temporarily employ the services of suitably qualified
and experienced nursing practitioners who
understood the adverse
consequences of use of phenytoin 300mg, Degranol 200mg BD by pregna4t
women; and
13.1.2 train the
employees on the adverse consequences of phenytoin 300mg, Degranol
200mg BD by pregnant women.
13.2 At the hospital, she
failed to:
13.2.1 permanently,
alternatively temporarily employ the services of a suitably qualified
and experienced medical practitioners
who would be available and able
to examine, manage and/or give appropriate advice in respect of the
plaintiff’s labour and
to perform a caesarean section if and
when required to;
13.2.2 ensure that at
least one medical practitioner was in attendance at the hospital at
all the material times relevant hereto;
13.2.3 permanently,
alternatively temporarily employ the services of a suitably qualified
and experienced nursing staff who would
be able to properly assess,
monitor and/or manage the plaintiff’s labour;
13.2.4 ensure that the
hospital was suitably, adequately and/or properly equipped to enable
the timeous and proper performance of
a caesarean section if and when
required by the plaintiff;
13.2.5 take any or all
reasonable steps to ensure proper, timeous and professional
assessment of patients, their monitoring and
management of labour and
transfer of patients to other suitable hospitals and/or medical
facility indicated, required and/or requested;
and
13.2.6 prevent [E] from
suffering cerebral damage at birth and the consequences thereof when,
by the exercise of reasonable care,
skill and diligence, he could and
should have done so.”
[5]
In paragraph 4 of the plea to the plaintiff’s amended
particulars of claim, the defendant
pleaded thus:
“
4. 4.1 The
defendant denies all allegations of negligence and/or breach of legal
duty on the part of the defendant.
4.2 In amplification the
defendant pleads as more fully set out below.
4.2.1 The plaintiff
presented at Mqanduli Community Health Centre at approximately 14h05
where she was assessed at 14h30 and found
to be in labour.
14.2.2The plaintiff was a
known epileptic.
4.2.3 The plaintiff was
referred to the Hospital for management.
4.2.4 The plaintiff and
foetus were monitored on an ongoing basis and in accordance with
applicable prescripts, which monitoring
included continuous
cardiotocography (“CTG”). The tracings of the CTG, while
not re-assuring at some time, showed good
recovery and variability in
between.
4.2.5 [E] was born
through vaginal delivery at approximately 20h55.
4.2.6 [E]’s Agpar
score at birth were recorded as 5/10 at 1 minute and 6/10 at 5
minutes.
4.2.7 [E] suffered
intra-uterine growth restriction (“IUGR”) which was not
(and could not be) detected during the plaintiff’s
pregnancy as
she booked only on 11 February 2014 – only four weeks before
she went into labour and delivered [E] on 11 March
2014 – and
therefore too late.
4.2.8 [E] was born with a
tight nuchal cord around the neck after the plaintiff’s first
stage of her labour had progressed
rapidly to full dilatation in just
40 minutes.
4.2.9 [E]’s IUGR
primed her for birth hypoxia and the rapid progression of the
plaintiff’s labour from 3 cm to fully
dilated contributed to
the tightening of [E]’s nuchal cord at a time when it was too
late to detect, intervene and prevent
the resultant progression of
hypoxia immediately before her delivery.
4.3 Alternatively to
paragraph 4.1 above, and in the event of the above Honourable Court
finding that the medical staff and staff
providing related services
at Zithulele Hospital negligently and wrongfully breached their
duties in one or more of the respects
alleged in the amended
particulars of claim, or at all, the defendant denies that such
negligence and/or breach contributed to,
or was a cause of, the
outcomes alleged and/or any damages which the plaintiff may prove she
or [E] has suffered and accordingly
denies the contents of paragraphs
7 to 15 of the amended particulars of claim.”
[6]
For the plaintiff to succeed and hold the defendant liable for
damages, she must prove
on a balance of probabilities, causal
connection between the defendant’s negligent acts or omission
relied upon and the harm
suffered.
[1]
In
Minister
of Safety and Security v Van Duivenboden 2002 (6) SA 431 (SCA)
[2]
Nugent
JA remarked:
“
[12]
Negligence, as it is understood in our law, is not inherently
unlawful - it is unlawful, and thus actionable, only if it occurs
in
circumstances that the law recognises as making it unlawful. Where
the negligence manifests itself in a positive act that causes

physical harm it is presumed to be unlawful, but that is not so in
the case of a negligent omission. A negligent omission is unlawful

only if it occurs in circumstances that the law regards as sufficient
to give rise to a legal duty to avoid negligently causing
harm.
It is important to keep that concept quite separate from the concept
of fault. Where the law recognises the existence
of a legal duty it
does not follow that an omission will necessarily attract liability -
it will attract liability only if the
omission was also culpable as
determined by the application of the separate test that has
consistently been applied by this
court in
Kruger
v Coetzee
, namely whether a
reasonable person in the position of the defendant would not only
have foreseen the harm but would also
have acted to avert it.
While the enquiry as to the existence or otherwise of a legal duty
might be conceptually anterior to
the question of fault (for the
very enquiry is whether fault is capable of being legally
recognised), nevertheless, in order to
avoid conflating these two
separate elements of liability, it might often be helpful to assume
that the omission was negligent
when asking whether, as a matter of
legal policy, the omission ought to be actionable.
”
[7]
The plaintiff testified in her case. Four expert witnesses also
testified. Dr Constant
Ndjapa, a gynaecologist and obstetrician and
Dr Yatish Kara, an expert paediatrician, testified on behalf of the
plaintiff. The
defendant called Dr Thandi Nothanduxolo Mtsi, a
gynaecologist and obstetrician, and Professor Cooper, an expert
paediatrician and
neonatologist, to testify. Drs Ndjapa and Mtsi
compiled joint minutes, dated 11 March 2020 and 25 January 2021. Dr
Kara and Prof
Cooper also compiled a joint minute, dated 15 August
2019. The radiologists, Professor J Lotz, for the plaintiff, and Dr J
Swartzberg,
on behalf of the defendant, prepared a joint minute
dated, 10 December 2019, in an attempt to present to court the
imaging features
of the Magnetic Resonance Image (“MRI”)
brain scan and advance a diagnosis for the described pattern.
[8]
Various medico-legal reports of the above experts formed part of the
evidence. The
maternity case records, inclusive of fluid and feeding
charts, Zithulele Maternity Ward progress notes, Zithulele Hospital
prescription
charts, post-delivery discharge from Zithulele
maternity, Road to Health Card, Zithulele laboratory reports and
cardiotocography
(“CTG”) scans were also part of the
evidence. The applicable maternity guidelines were the Guidelines for
Maternity
Care in South Africa, 2007 3
rd
edition.
[9]
It is undisputed that according to the antenatal records only two
antenatal visits
appear, the first being on 11 February 2014 and the
second, on 11 March 2014. The experts agreed that the plaintiff was
primigravida
and was on treatment for epilepsy. It is also
common cause that on 11 March 2014 she was given antibiotics for
vaginal discharge.
The gestation period was estimated to be 36 weeks,
presentation was cephalic and the head was 3/5 above the symphysis
pubis. The
foetal heart rate (“FHR”) was recorded as 121,
with mild contractions and membrane not felt. She was referred to
Zithulele
Hospital as she was a known epileptic.
THE
EVIDENCE OF SS (THE PLAINTIFF’S CASE)
[10]
The plaintiff was born on 05 December 1992 in Macosa, in the district
of Mqanduli. She was 28
years old when she testified. In November
2013, she went to Mqanduli Clinic to collect her treatment for
epilepsy and because she
missed her periods she also reported same to
the nurse. She did not know the date of her last menstrual periods.
She also did not
recall the date of her visit to the clinic. At the
clinic, urine sample was taken from her and tested. However, the
results were
inconclusive, whereupon blood was drawn and she was told
to collect results in a month’s time. In December 2013, she
again
visited the Mqanduli Clinic and was told that “
I was
at the beginning of the six months, sixth month [of] my pregnancy.
”
The nurse checked the status and progress of her pregnancy and she
had a review date in January 2014, for antenatal care.
She was
further informed that there was nothing wrong with her and the baby.
[11]
According to the plaintiff, her medical and antenatal cards were kept
at the clinic. Only numbers
were issued to her. She was expected to
give the said numbers to the nurses in order to locate her cards when
visiting the clinic.
In January 2014, she returned to Mqanduli Clinic
for an antenatal review. During that visit, she was told that her
medical and
antenatal cards were missing. However, she was subjected
to antenatal procedures and given a review date in February 2014. In
February
2014, she went to Mpunzana Clinic because she was unhappy
with the fact that her cards could not be found at Mqanduli Clinic.
She
thought that the nurses in Mqanduli Clinic were negligent in
handling same. At Mpunzana Clinic she was asked if she had previously

attended another clinic. In response, she told them that she had been
to Mqanduli Clinic. She explained to the nurses that at Mqanduli

Clinic they lost her cards. A new antenatal card was opened for her
with instructions that she should keep it and produce it at
a clinic
or hospital when in labour. Thereafter, she was subjected to
antenatal procedures and given a review date in March 2014.
Again,
during this visit, she was told that there was nothing wrong with her
or the baby. She could not remember the date that
she went to
Mpunzana Clinic for the first time. She only remembered that it was
in February 2014.
[12]
On 11 March 2014, the plaintiff returned to Mpunzana Clinic at
approximately 07h00 in the morning
for an antenatal review. She also
reported that she had been experiencing lower back pains since 06h00
that morning. However, she
was treated for vaginal discharge which
was noted and given treatment.  She returned home. While at
home, the lower back pains
persisted. She informed her mother who
suggested that they go to Mqanduli Clinic, which they did. The
plaintiff estimated that
she and her mother left home at about 10h00
in the morning and arrived at the clinic at approximately 11h00.
After examination,
the nurses established that she was in labour.
Considering that she was epileptic, she was referred to Zithulele
Hospital for a
doctor to manage her labour. She waited for an
ambulance that was going to transport her to Zithulele Hospital,
which ultimately
arrived and they left.
[13]
As they travelled to Zithulele Hospital, the progress of her labour
was not monitored. She was
told to lie on her back throughout the
journey. She was uncertain as to what time the ambulance arrived at
Zithulele Hospital but
estimated that it was approximately at 14h00.
She thought that they travelled for about an hour. The plaintiff was
in the company
of her mother and ambulance staff when they proceeded
to Zithulele Hospital. Upon arrival at the hospital, she was wheeled
by a
wheelchair to the maternity ward, registered and admitted. A
nurse who first interacted with her commented that she did not appear

to be in labour and asked her to urinate.  After that, the nurse
told her to climb on a bed, which she did. She inserted a
finger in
her vagina and made no comment. She then left at around 15h00. She
again interacted with another nurse at approximately
17h00 who placed
a belt like a computer (CTG) on her stomach and said nothing to her.
He/she thereafter left. The same nurse interacted
with her again at
approximately 18h00. He/she looked at the computer and wrote
something down and thereafter left. At around 19h00
the same nurse
returned, looked at the computer, recorded something down and left.
At about 20h00, she felt pains and shouted for
help and a nurse
approached her. When the nurse was at the door, she commented that
“
the baby’s head was coming out”
. One nurse
pressed on her abdomen and the other cut her, and the doctor arrived.
The baby was then delivered.
[14]
The baby did not cry at birth. The doctor took her to a separate room
and placed her in ‘
something like a box’ made out of
something like a glass’
(incubator), as the plaintiff put
it. Some oxygen was placed in her nose with some tubes. The plaintiff
did not breastfeed her.
She was given a mug and a syringe. She
expressed breast milk into the mug, sucked it with the syringe from
the mug and placed it
in the tubes in order to feed the baby. The
baby was given to her after five days and she was asked to breastfeed
her.
[15]
After some time, the baby could not crawl, walk or speak. She also
could not attend school. She
can do nothing on her own.
THE
MATERNITY CASE RECORDS
[16]
According to the maternity records, the initial assessment was at
14h30, and the plaintiff was
3cm dilated, pelvis adequate, head 3/5,
contractions < 20 seconds, FHR normal and 36 weeks on palpation.
At 17h20 bradycardia
was noted, meaning that the FHR had dropped up
to 100 beats per minute. There was no progress in labour. The
plaintiff was put
in left lateral position, and oxygen was given via
mask and ringers lactate running well, PV was done, and she was still
3cm dilated.
Contractions were moderate to strong. The doctor was
informed about the problem at 18h45. The doctor indicated that there
was no
problem, the nursing staff should continue with the
then-current management. He/she did not come to assess the plaintiff.
[17]
The next assessment was at 19h00 and three decelerations were noted
despite the then-current
management. The doctor was informed of the
plaintiff’s condition. At the time, the plaintiff was still on
continuous CTG,
oxygen and ringers lactate and lying in left lateral
position. The FHR dropped again to 100 beats per minute. The doctor
was again
called but did not come.
[18]
At 19h05 Dr Glaze recorded that the plaintiff was “
primigravida,
39 weeks by dates, 3 cm dilated, and good strong contractions.
Concern re late decels on CTG but CTG with toco looks
to show just
early decels with good recovery and good variability in between.
Several also witnessed - decels to 100bpm but good
recovery to 140.
Plan – left lateral position + oxygen- keep on CTG and monitor
closely. If not progressing or late decels,
call Dr.”
[19]
At 20h00 the progress of labour was good. Regarding the foetal
condition, the “
CTG was observed to be still up and down
”.
The overall assessment was that the progress went very quickly from
3cm to full dilatation in 40 minutes. There was no
urge to bear down.
At 20h50 the plaintiff was fully dilated and delivered a flat and
floppy baby with a cord tight around the neck
twice at 20h55, with
Agpar score of 5/10 and 6/10. Resuscitation and head cooling were
done. The baby had a seizure witnessed by
the plaintiff. However, her
condition improved. She was kept in high care in IV fluids as feeding
per mouth was not initiated.
The placenta was normal. It appeared
that the baby was premature, delivered at 36 weeks in keeping with
the birth weight of 2.5kg.
[20]
On 17 August 2018, ES was subjected to a MRI scan which proved that
the MRI study showed a mixed
pattern of prolonged partial
(peripheral) and acute profound (central) hypoxic-ischemic injury of
the brain in a chronic stage
of evolution. The acute profound injury
was dominant and global white matter loss was severe. There were no
findings of congenital
abnormalities or genetic disorders or
inflammatory brain disease. Prof Lotz and Dr Swartzberg compiled a
joint minute dated 18
and 25 November 2019, in which they agreed as
follows:
“
20.1 The study
shows a mixed pattern of prolonged partial (peripheral) and acute
profound (central) hypoxic ischemic injury;
20.2 The findings of the
MRI suggest that genetic or metabolic disorders are unlikely causes
of brain injury;
20.3 Inflammatory or
infective causes are unlikely as causes of the child’s brain
damage; and
20.4 A review of the
clinical and obstetrical records by appropriate specialists in the
field of neonatology and obstetrics to be
essential in determining
the cause and probable timing of the hypoxic ischemic injury.”
[21]
The expert witnesses who testified on behalf of the parties agreed
with the findings of the radiologists.
However, what the radiologists
did not say is the timing of the brain injury. In their view, a
review of clinical and obstetrical
records by neonatologists and
obstetricians was essential to determine the cause and probable
timing of the hypoxic-ischemic injury,
as stated above. Commenting on
the radiological report, Dr Ndjapa stated that perinatal asphyxia,
more appropriately known as hypoxic
(lack of oxygen) ischemic (lack
of blood flow) encephalopathy (brain damage) (HIE), is characterised
by clinical and laboratory
abnormalities with evidence of acute or
sub-acute brain injury due to asphyxia. He stated further that the
cause of this condition
was systemic hypoxemia and/or reduced
cerebral blood flow. He contended that birth asphyxia causes 840,000
or 23% of all neonatal
deaths worldwide. Dr Kara confirmed that the
probable cause of cerebral palsy was the prolonged partial and acute
profound hypoxic-ischaemic
insult. The experts agreed with the
radiological report, hence there arose no need for the radiologists
to testify. The evidence
by the experts shows that the insult
probably occurred during labour and not ante or post-natally.
[22]
Dr Ndjapa testified that in compiling his medico-legal report he had
regard to information from
the history of events narrated to him by
the plaintiff, available information in the maternity case records, a
perusal of reports
made available to him by the plaintiff’s
attorney of record, Mr Dayimani, a trial bundle containing NICE
guideline on epilepsies
diagnosis and management (2012) as well as
ACOG guidelines for perinatal care, 7
th
edition. The
purpose of the report was to establish whether the hospital staff was
negligent in managing and monitoring the plaintiff’s
labour and
if so, whether such negligence caused ES’ injury and resultant
cerebral palsy. His commentary would be confined
to his area of
expertise namely, pregnancy, labour and delivery with special
reference to the guidelines as well as other literature
and reviews
in order to assist in establishing whether birth asphyxia and
cerebral palsy could be attributable to antiepileptic
drugs used
during pregnancy and if there was any association between labour
monitoring, FHR abnormalities, delay in delivery time,
hypoxia, birth
asphyxia and cerebral palsy.
[23]
Dr Ndjapa opined that at 14h30 the parthogram of the clinical record
showed that the plaintiff,
who was at the time 3cm dilated, was
transferred from the latent phase of labour to the active phase, on
to the alert line. At
17h20, when there was no progress of labour,
the parthogram was not plotted. He asserted that, had the nursing
staff plotted the
parthogram, they would have noted that the
plaintiff had crossed the action line with the FHR rate abnormalities
present and immediate
action needed to be taken by delivering the
baby by the fastest route possible. This would have been by caesarean
section. The
next entry on the parthogram was at 20h50 while the
clinic card showed that she was fully dilated at 20h00, showing
incoherence
in the records. This suggested that five minutes later
she delivered ES with Agpars of 5/10 and 6/10, if the parthogram
entry is
accepted. What is clear is that from 3cm dilatation at 14h30
up to delivery at 20h55 it took at least six hours of no monitoring

as the parthogram has no recordings between 14h30 and delivery at
20h55. This, according to Dr Ndjapa, suggested that the baby
was
exposed to hypoxia over a long period of time and further foetal
abnormalities were missed or unattended resulting into negligence
and
substandard care of over at least four hours. He was also critical of
the CTGs, especially at 18h20 which showed that there
was a late
deceleration, which position changed at 18h50 when the FHR
abnormality became worse and yet no action was taken. At
20h10 the
CTG continued to be non-reassuring. He asserted that there were
neither records to show that the plaintiff was given
hexoprenaline 10
mg to delay labour, nor was she prepared for immediate caesarean
section. He asserted further that the plaintiff’s
condition of
having prolapse, was a high risk considering that she was pregnant.
[24]
According to the Guidelines, in the active phase the FHR must be
checked every 30 minutes and
the patient assessed every two hours and
that information be recorded on the parthogram. In this case, from
14h30 the plaintiff
was only assessed at 17h20, approximately three
hours later. Dr Ndjapa said: “
The staff that was examining
the patient noticed that the patient was not progressing. It is
evident that because the patient crossed
the action line it is a true
reflection that the patient was not progressing, and we know that
there was foetal bradycardia, meaning
that the heartbeat was
abnormal…There was no plotting at 17h20 because you plotted,
you will notice that there is a labour
problem.”
According
to him, failure to plot on the graph was against the Guidelines. That
is because ‘
with a graphic representation, it is very easy
to pick up that something is wrong.
’
[25]
After the doctor was notified at 18h45 that the foetal heartbeat was
dropping, he/she came at
19h05 to assess the plaintiff. Again, the
graph does not show plotting at 19h05 either by the doctor or nurse,
Dr Ndjapa stated.
Instead, what appears from the maternity case
record at 18h45 is the following: “
Dr informed about the
problem – No problem, should continue with the current
management.”
According to Dr Ndjapa, at that stage, there
was a problem with foetal bradycardia and no progress in labour. He
contended that
at this stage, it was imperative that the doctor on
call come and examine the plaintiff personally as it appeared that
the nurses
examined the plaintiff and noticed that there was a
problem. He contended further that although there was a problem at
17h20, the
labour was allowed to progress until 18:45, approximately
more than an hour later.
[26]
Dr Ndjapa interpreted the CTGs which consisted of numbers 127, 128
and 129 as the first CTGs,
the second, 130, 131, and 132, and the
third, 139, 140 and 141. He remarked that there were CTG’s
around 18h12, 47 seconds
until about 20h00, and none between 14h30 to
17h20. There was nothing before 127 and a part starting before 128
was cut and he
did not know what actually happened there, which made
it difficult for him to comment. Some pages had no continuity
especially
from 133 to 138. The defendant accepted that the CTG’s
were incomplete. As custodians of the documents, the defendant led
no
evidence explaining whether a diligent search for the missing
portions was done, when it was done and by whom or that the
whereabouts
of the missing ones were determined.
[27]
Dr Ndjapa explained different types of decelerations namely, early,
late and variable. He defined
early deceleration as a drop of the FHR
below the normal range. A CTG is used to monitor labour and indicates
what kind of deceleration
takes place at a particular time.
Management of labour depends on it. Dr Ndjapa said that foetal
monitoring includes monitoring
the maternal condition as the mother
is examined regarding contractions. Concerning foetal monitoring, he
referred to the Guidelines
where the following is recorded:
“
FETAL MONITORING
For low risk labour,
listen to the fetal heart with a stethoscope or hand-held Doppler
instrument every 30 minutes, before, during
and after contractions.
Cardiotocography (CTG) is
used for high risk labour only, and should be available in hospitals.
CTG machines are however in short
supply.
All CTG tracings must be
kept safely in the mother’s file. After CTG interpretation,
write a note in the file with a comment
on the CTG, so that a record
is available even if the CTG tracing is lost
.”
Emphasis added
[28]
Dr Ndjapa explained further that a normal CTG does not have
decelerations but good beat-to-beat
variability. The normal FHR is
between 110 and 160 beats per minute: anything above 160 beats per
minute is tachycardia, and anything
below 110 beats per minute is
bradycardia. Dr Ndjapa stated that a deceleration is timed with a
contraction to decide whether it
is early or late. To do this, the
baseline of the CTG must first be identified. Then it must be
determined by looking at the peak
of a contraction as well as that of
a deceleration to see which one comes first. Therefore, every drop of
the FHR below the baseline
is a deceleration and should be monitored
by the medical staff concerned even when it is not bradycardic. That
is so because under
normal circumstances there should be no
deceleration. Dr Ndjapa explained further that if the peak of a
deceleration comes after
the peak of a contraction, then that
deceleration is late. The opposite is early deceleration which is
usually not problematic.
[29]
Concerning CTG 127, 128 and 129, Dr Ndjapa testified that it had a
baseline of 120 beats per
minute. In this CTG, he opined that several
decelerations dropped below 120 beats per minute which meant that the
FHR was dropping.
Some of the decelerations took time to recover,
although some had a quick recovery. He opined further that the
decelerations started
much earlier and then moved to the baseline.
Amongst others, he identified another deceleration, which he referred
to as U-shaped,
whose recovery took time. The decelerations were not
only late but also pathological. He also identified contractions and
late
decelerations in CTG 128.
[30]
In CTG numbers, 130 – 132, Dr Ndjapa identified about four late
decelerations with poor
variability and testified that the baseline
was 130 beats per minute. What complicated these decelerations is
that they were problems
related to FHR variability. It was not just
late decelerations, but the variability appeared to be reduced, which
meant that the
baby was no longer recovering well like before, as
late decelerations continued. That is because once there were many
components
in the abnormal heart rate condition, the CTG became
‘
somewhat pathological
.’ It then became difficult
for the baby to keep up with the recovering process because foetal
oxygenation kept becoming impaired.
That was hypoxic and the baby
developed acidosis. Dr Ndjapa contended that the condition of the
baby continued to deteriorate.
The clinical records showed that this
CTG was classified as “
up and down
”.  He
contended further that this classification meant nothing to an
obstetrician ‘
as there is no such thing as up and down’
in a CTG. He said: “
It either shows that you are
managing labour ward but you do not know what you are actually
talking about. …[U]p and down
is not in a language of the
obstetrician.”
He asserted that in the circumstances, a
wrong decision could be taken because the person making that kind of
entry, was not sure
of what was going on. He asserted further that
the baby was fine only when the CTG was normal otherwise when
abnormal, a diagnosis
should have been made and appropriate treatment
given. This CTG was abnormal, and the foetal heart condition remained
non-reassuring.
According to Dr Ndjapa, this CTG, unlike the first
one, showed that the foetus had a reduced capacity to recover, and it
was like
a person who had been subjected to choking for a prolonged
period of time. Only when a CTG is normal, can it be said that the
foetus
is fine. If it is not, an investigation to determine the cause
of the abnormality, should be done and appropriate treatment must

follow.
[31]
Regarding the third CTG, Dr Ndjapa testified that the recording
showed that the baby was trying
to compensate but there was decreased
variability and signs of increased hypoxia. There was almost no
zigzag like the previous
one.
[32]
When Dr Ndjapa was asked as to the appropriate treatment that had to
follow after bradycardia
and no progress in labour was noted, he said
that, that condition was quite serious.  The doctor was expected
to act immediately
by coming and assessing the plaintiff’s and
the foetus’ condition and make his/her findings. In that manner
the doctor
would have had a clear understanding of what was happening
in relation to the baby and mother.  The plaintiff had strong
contractions.
The intervention that was done when bradycardia was
first noted was proper but was meant as a temporary measure to buy
time to
prepare to deliver the mother by the fastest route possible.
Considering that the plaintiff was not fully dilated and still far

from delivery, it would have been impossible to have a vaginal
delivery. Therefore, the only option would have been a caesarean

section. That is because there were warning signs of foetal distress
and the FHR did not return to normal after intrauterine
resuscitation.
[33]
When it was put to him that ES was primed for foetal distress due to
the tight nuchal cord twice
around the neck and the rapid progress of
labour, as well as the outcome, he said that when labour is monitored
and tachsystole
develops, tocolysis should be given to the patient to
reduce that tachsystole as it is an abnormal condition, otherwise it
is negligent
not to.
[34]
Regarding a condition called Intrauterine Growth Restriction
(“IUGR”), Dr Ndjapa
asserted that such a condition might
afflict a foetus. He admitted that during labour a growth-restricted
foetus also preserves
oxygen supplies for the vital parts of the
brain. However, he disputed that it would be impossible to detect
growth abnormalities
between the period 11 February 2014 and 11 March
2014 when the plaintiff visited Mpunzana Clinic for antenatal care.
According
to him, if the antenatal graph was properly plotted on the
first visit based on the information given by the plaintiff, the
abnormality
would have been picked up and acted upon. Dr Ndjapa also
admitted that the entry by Dr Glaze at 19h05 showed that there was a
sign
of late decelerations. Dr Ndjapa was concerned about the
interpretation of the CTG by Dr Glaze saying it was not only wrong
but
he/she ignored the late decelerations that were brought into
his/her attention. There were also further decelerations after he/she

had seen the plaintiff. Dr Ndjapa remarked that a patient cannot be
put on a CTG and be given oxygen. According to him, good recovery
of
the heart rate should be maintained. When there are still
decelerations, there can be no good recovery.
[35]
In paragraph 9.5 of his report filed on 20 February 2020, Dr Ndjapa
stated:
“
9.5 Fetal
condition was inappropriately monitored suggesting that the fetus may
have been exposed to hypoxia over a period of time,
long enough to
cause cerebral damage and resulting in cerebral palsy. The outcome at
delivery (poor apgars score, the need for
resuscitation and admission
to ICU, seizures in the first 24 hours) suggest that the damaging
event may have occurred during intrapartum
period. There is no
evidence that the damaging event may have occurred in the antenatal
or the postpartum period, even though the
patient was a known
epileptic there is no evidence to suggest that her epileptic
treatment was attributable to baby [ES’s]
birth asphyxia and
cerebral palsy, the damaging event may have occurred during labour
and delivery.”
[36]
Dr Ndjapa testified that for his conclusions, he relied on the
Guidelines for Maternity Care,
in South Africa, 2007 edition the
Guidelines which stipulate that when there is foetal distress and
delivery is imminent
,
meaning that the cervix is fully
dilated, the baby must be delivered immediately by vacuum extraction,
if necessary. Forceps can
also be used. If vaginal delivery is not
imminent, meaning the cervix is not fully dilated, as in the present
case, the mother
must be given hexoprenaline 10 micrograms IV to
delay the labour and prepare for immediate caesarean section. The
mother should
urgently be transferred from a community health centre
to hospital.
In casu
, the plaintiff was already in the
hospital. In this regard, Dr Ndjapa testified that according to the
hospital records, the plaintiff
was far from full dilatation (3 cm
dilated) and there was no record that she was given hexoprenaline 10
micrograms IV or prepared
for an immediate caesarean section. He
asserted that monitoring and management of the plaintiff’s
labour was not according
to the Guidelines.
THE
EVIDENCE OF DR KARA
[37]
Dr Kara’s mandate was to conduct a medico-legal assessment of
ES and advise on the causal
connection between the delivery and
subsequent neurological outcome, that is, the probability of
intrapartum asphyxia being the
causal factor. As sources of
information, he used the history from the plaintiff, medical records,
road to health card, obstetric
and neonatal records and an MRI scan
by Prof Lotz and Dr Swartzberg, in order to compile his report dated,
13 November 2018. After
examining ES, he concluded that she has
cerebral palsy called Dyskinetic Cerebral Palsy, a type of injury
that is ‘
highly specific for injury occurring during
labour
’. She has no functional use of the hands, severe
expressive and receptive impairment and microcephaly (small head).
She appeared
to be able to see and hear and has no history of
epilepsy.
[38]
Dr Kara gathered from the antenatal records that the plaintiff had no
risk factors except a history
of epilepsy. The antenatal records
showed that her first antenatal visit was on 11 February 2014,
although she told him that she
visited the clinic before that date.
There was also a comment that she booked late. In February 2014, it
was estimated that she
was 32 weeks’ gestation. A month later,
she was estimated to be 36 weeks’ gestation. It appeared that
there was no
concern about the foetal condition because she was
epileptic and therefore was a high-risk pregnancy and that her
delivery should
be managed in a hospital, which was done.
[39]
Regarding decelerations, Dr Kara explained that a variable
deceleration is a little more suspicious
of foetal compromise. He
contended that late decelerations are an ominous and highly
suspicious sign that there are concerns about
the foetal condition,
and that foetal compromise is highly suspicious. However, the
attending doctor looked at the CTG and said
the decelerations were
not late but early, with good recovery. According to Dr Kara, this
should have been a concern to the doctor
as the FHR was dropping to
about 100 beats per minute, hence he was called.  He confirmed
Dr Ndjapa’s evidence that
referring to the CTG as ‘
up
and down’,
is not a medical comment. Dr Kara remarked that
the plaintiff’s progress from 3cm dilated to full dilatation in
40 minutes
was very rapid and concerning. He stated that considering
that late decelerations were picked up by the CTG from 17h20, as well

as the comment that the CTG was up and down, clearly showed that the
doctor observed the condition of the plaintiff and the foetus.

However, the records of the summary of labour made no comment about
foetal distress. The parthogram which commenced at approximately

19h00 recorded a normal FHR at 19h00, 19h30 and 20h00, different from
what the CTGs showed
.
Concerning was the observation that the
baby was flat, floppy and had a tight cord around the neck twice, as
well as that the placenta
looked healthy, but there was no comment
about foetal distress or that the placenta looked healthy. Regarding
the neonatal record,
Dr Kara found it strange that the initial
examination noted that the baby had caput, no respiratory, distress,
normal tone, weak
and absent primitive reflexes, and normal cry.
According to Dr Kara, this is unusual to have weak reflexes, and
normal cry, a normal
tone and no respiratory signs in a baby that had
been resuscitated. He mentioned that the discordance between what the
records
said, and interventions done to the baby, was a means of
minimising injury to foetuses.
[40]
Dr Kara explained that when a foetus is in the mother’s womb it
gets its oxygen from the
mother
via
the umbilical cord and
passes it through the placenta. When the uterus contracts it cuts the
blood supply to the foetus and that
gives relative oxygen deficit to
the foetus. When the baby has compensatory mechanisms to cope with
the short period of lack of
oxygen and when the contraction stops,
the oxygen flows back into the baby. The baby will be fine because
that period of reperfusion
restores the oxygen supply to the baby and
protects it for the next contraction when the oxygen is going to be
reduced.  This
is a normal consequence of labour.
[41]
In abnormal labour, there is an accumulative deficit in the oxygen
supply to the baby with each
contraction. For instance, if the foetus
has 100% oxygen before the contraction and the oxygen is stopped
during a contraction,
the oxygen saturation drops to 50%. The oxygen
gets restored to the foetus. Before the next contraction, the foetus
would have
saved 95%, which would not be 100% anymore. When next is a
prolonged contraction and the period for oxygen to be restored after

the contraction is shorter for example, 90%, this means that over
many contractions there is an accumulative deficit of oxygen
supply
to the foetus. The foetus will compensate by shutting down blood and
oxygen supply to non-critical organs like, the lungs,
liver, kidneys
etc. Eventually, as the oxygen deficit becomes more and more it
affects the oxygen supply to the heart and the heart
will then stop
pumping. That is what manifests by foetal heart tracings because the
foetal heart tracings record that the heartbeat
during a contraction
starts dropping and that is a sign that there is foetal compromise.
That is the reason why the foetal heart
should be monitored during
labour.
[42]
Dr Kara continued that as the foetal heart compromise increases, it
affects the blood supply
to the brain. If this is a gradual process,
the brain compensates for this by shutting down the oxygen and blood
supply to the
non-critical areas of the brain and preserving oxygen
and diverting that blood and oxygen to areas of the brain necessary
to maintain
life, like areas of thought, movement, function etc. As
that compensation fails further because of continued hypoxic
ischemia,
only then will there be damage to those high-functioning
areas of the brain. He explained further that the first area of the
brain
that gets damaged in ongoing persistent hypoxia, is the
cerebral cortex and the term of the injury is called Watershed
Hypoxic-Ischaemic
Injury. When that compensatory mechanism fails,
that injury extends to the deep nucleus of the brain called the Basal
Ganglia and
Thalamus and then there will be what is called a pattern
of injury, which ES had due to a long-standing process of hypoxia.
[43]
Dr Kara observed that the maternity and neonatal notes were
disorganised. He explained that Hypoxic-Ischaemic
Injury is what
happens to the brain and also means the effect of the injury. He
added: “
If you have to take HI Encephalopathy and brain
injury in term or near term babies the most common period for that
injury to occur
is immediately before, during or immediately or soon
after labour. …If they assessed the foetal condition to be
normal on
admission to the hospital or clinic to the best of their
ability, of course, they assessed that they were of the opinion that
the
foetal condition was normal. That means that it is highly
unlikely that there was brain injury immediately prior to her
presentation
at the hospital or clinic. She presented at the hospital
at 14h00 and so it is highly unlikely that an injury occurred at
09h00
or 10h00 that morning.”
[44]
Regarding the definition of long-standing injury, Dr Kara opined that
it varies from one and
a half to two hours, maybe three. In others,
it may be five or six hours. He asserted that one cannot say that in
each baby a prolonged
injury occurs over a short or long period of
time, it is unknown but it can be said that it does occur over hours.
[45]
Concerning the MRI scan, Dr Kara stated that ES was born with a
cerebral palsy and there is an
80% probability that the injury was
due to hypoxic ischemia because she had a specific type called
Dyskinetic Cerebral Palsy which
is very commonly associated with
hypoxia. That is what the attending doctor who managed the plaintiff
at birth, thought, which
was confirmed by the MRI scan. He testified
that taking that together with the condition of the child at birth,
it makes it highly
probable that this injury occurred during labour.
That is so because when the plaintiff was admitted there were no
concerns over
the foetal condition until 17h20 when the CTG was
abnormal. That is the time when the foetus was not in optimal
condition.
[46]
During cross-examination, Dr Kara disagreed with the opinion that
being growth restricted on
its own causes hypoxic injury during a
normal labour. According to him, it is a factor that makes it more
likely. He agreed that
the labour process is hypoxic and that is why
monitoring is important in order to work out what is normal and
abnormal and in an
increased risk, an intervention would be made.
Even though he was uncertain about the gestational age of the baby,
he opined that
in the last four weeks of the plaintiff’s
pregnancy, foetal growth seemed to have progressed normally which
does not accord
with a growth-restricted foetus.
[47]
Dr Kara compiled a joint minute with Prof Cooper, on 15 August 2020.
Dr Kara concluded that both
components of the hypoxic-ischaemic
injury occurred in the labour, as indicated earlier. Prof Cooper
agreed that the acute profound
component of the injury probably
occurred in labour during the last 45 minutes prior to delivery.
Regarding the partial prolonged
component of the hypoxic ischaemic
brain injury, Prof Cooper’s opinion was that in view of the
significant asymmetrical intrauterine
growth restriction and poor
antenatal attendance with lack of information regarding foetal
well-being during the last four weeks
of pregnancy, the chance of the
partial prolonged component occurring prior to labour, is
substantial. There was no basis for this
opinion as no factual
evidence was led to support it. About Prof Cooper’s opinion
that the partial prolonged injury could
have occurred prior to
labour, Dr Kara stated that this is possible. However, he stated that
there is little reason to support
this possibility. He mentioned that
the initial assessment in labour indicated no concern over the foetal
condition. He contended
that asymmetrical growth restriction
increases the risk of intrapartum asphyxia but is not an
independently significant risk factor
for antenatal asphyxia.
[48]
Regarding prematurity, Dr Kara and Prof Cooper agreed that this might
increase the risk of intrapartum
hypoxia ischaemia but would not be
the cause of brain injury. With appropriate foetal monitoring, the
increased risk of brain injury
in labour due to prematurity, could be
anticipated.
[49]
When it was put to him that the measurements of the baby at birth
pointed more to it being born
at term than 36 weeks, Dr Kara
disagreed. He intimated that when the plaintiff visited the clinic on
11 March 2014, no plotting
as to the measurements of the baby were
made showing whether the baby was growing or not and so it could not
be said that it was
34 weeks as written in the graph. That is because
there was nothing to validate this opinion. Therefore, no one could
say with
certainty what the gestation period of the plaintiff’s
baby was. The plaintiff did not know when she had her last menstrual

periods. Dr Kara did not necessarily accept that the pregnancy was
carried to 40 weeks’ gestation. He stated that if it were,
the
baby would have been growth restricted. He therefore did not give an
opinion on the gestation period as it was unknown. He
gave a scenario
that if the baby was 38 to 40 weeks, then the baby was asymmetrically
growth restricted, which is usually on the
basis of late placental
insufficiency. He accepted that when the plaintiff visited the clinic
for the first time the gestation
period was estimated at 32 weeks and
36 at delivery. He said that if the plaintiff was 36 weeks at
delivery, the weight of 2.5kg
is on the 50
th
centile, the
length of 49 cm is below the 90
th
centile and the head
size of 34 cm is on the 90
th
centile. According to him,
this is not supportive of IUGR.
[50]
Dr Kara testified that it was highly unlikely that the plaintiff’s
epilepsy or her treatment
caused ES’s cerebral palsy as there
was no evidence to support this. He stated that a concern of sepsis
was highly unlikely
to result in brain injury considering the poor
management of labour. The MRI scan features are not reflective of an
injury pattern
of infection.
[51]
Regarding sepsis, Dr Kara asserted that the records do not show
evidence of sepsis although there
was a comment about sepsis in the
records. He asserted further that a concern of sepsis is highly
unlikely to result in brain injury
considering the poor management of
the labour. He added that the MRI scan features were also not
reflective of an injury pattern
of infection.
THE
DEFENDANT’S CASE
THE
EVIDENCE OF DR MTSI
[52]
Dr Mtsi compiled an undated report using the instruction letter from
Janilite Medico-Legal, summons,
hospital records, Medico-Legal
reports of Dr Mugerwa-Sekawabe, a gynaecologist, Dr Kara, MRI report
by radiologists, protocols
and literature. She testified that the
clinical notes showed that the plaintiff was a late booker. That is
because she booked at
Mpunzana Clinic on 11 February 2014 for the
first time and went into labour on 11 March 2014. Dr Mtsi confirmed
Dr Ndjapa’s
evidence that the antenatal graph was not plotted
on 11 February 2014, when she presented to the clinic at 32 weeks of
gestation.
She substantiated this by saying that according to the
protocol, when a patient is seen for the first time, nurses should
start
with SF measurements showing how big the foetus is.  That
was important to monitor the growth of the foetus. However, she said

that it would not have made a difference because, on 11 March 2014,
the baby was delivered. When it was put to her that Dr Ndjapa
was
adamant that proper plotting, even at that late stage would have been
of assistance, she agreed. However, she asserted that
to monitor the
growth of a foetus, several antenatal visits are required
.
For
instance, if in this case there were two or more visits plotted, that
would have established a pattern. One spot on the graph
and an
attempt to do a second one would not assist because there would have
been one spot. On 11 March 2014, the graph was also
not plotted at
the Mpunzana clinic. Dr Mtsi opined that the plaintiff did not
present at the clinic due to labour pains and the
graph should also
have been plotted because that could have given an impression of poor
growth. She opined further that failure
to plot was therefore wrong.
[53]
Dr Mtsi stated that although on the morning of 11 March 2014,
the plaintiff was not in labour, had the nursing
staff plotted the
antenatal graph, they would have been able to suspect that there may
have been intrauterine growth retardation.
She later changed and said
that ‘
the graph is useful if there were a number of
antenatal visits, two visits will not help that’s why I’m
trying to indicate
to you an error for instance already that is done
in the first and the second visit.
’
[54]
It was difficult for Dr Mtsi to interpret the medical records
suggesting bradycardia at 17h20,
on 11 March 2014, saying that no
indication of the duration of the condition was given. According to
her, ‘
it was absolutely unclear’
. She said that
before defining bradycardia, she would have to see the CTG that
showed bradycardia at 17h20 and could not assume
that it was more or
less than ten minutes because she did not know. She therefore
admitted that the onset of bradycardia was unknown.
That is because
between 15h00 and 17h00 there was no account as far as the foetal and
maternal well-being was concerned. Dr Mtsi
stated that the ones who
managed the plaintiff’s labour ought to have been alive to the
fact that they were dealing with
a distressing foetus, the onset of
which was unknown to them. The unknown was a cause for vigilance in
the management of labour.
She asserted that the cause of foetal
distress was not investigated. However, she maintained that when
bradycardia was established,
the defendant’s employees acted
appropriately.
[55]
Dr Mtsi confirmed that once bradycardia is picked up, the cause and
why it happens should be
investigated in order to determine what
intervention to make. Then it should be ascertained whether or not
the condition responds
to the correction and correct it if it does.
She admitted that the investigation of the cause of bradycardia is
also important
as it tells the clinician that he/she must determine
the timing of the delivery, the objective of which is to avoid
prolonged foetal
hypoxia. This confirms Dr Ndjapa’s evidence.
She contended that a caesarean section is indicated when there is
foetal tachycardia,
bradycardia, the reduced variability and late
decelerations, at the same time. She contended further that it does
not happen in
obstetrics that when only one parameter is diagnosed
then a caesarean section is done.  She later altered her version
when
I asked her questions to clarify certain aspects of her evidence
and agreed that bradycardia is the opposite of tachycardia and
that
these two cannot coexist at the same time but might exist in quick
succession.
[56]
Regarding CTGs, Dr Mtsi stated that the quality of those that she
worked on, were very poor for
proper analysis. She stated further
that there was an element of guess work which was unacceptable for
CTGs. She had to use a lot
of imagination, an incorrect way of
interpreting CTGs. She contended that the fact that there was a lot
of interference with the
CTGs, they were not the typical CTGs that
were supposed to be interpreted, especially in the management of a
patient that ended
up being unwell. She found it very difficult to
give proper evidence due to the poor quality of almost all the CTGs.
She suggested
that either the doctor or nurses who saw the monitor
and the CTGs progressing in front of them, had an advantage, compared
to her.
Otherwise, she had to speculate as she was struggling to
interpret the same, which was unfair on both sides.
[57]
Dr Mtsi opined that a normal CTG does not necessarily mean that there
should absolutely be no
decelerations, thereby disagreeing with Dr
Ndjapa about his classification of a normal CTG. According to her,
once there is a repetition
of decelerations, the CTG falls into
category 2, which is suspicious or category 3, pathological. She
contended that before a caesarean
section is done, a suspicious CTG
should be observed for a long time and seen to be worsening. That is
so because a suspicious
CTG, in most cases, is not an indication for
an immediate caesarean section. According to her, decelerations are
an indication
that there could be a problem or something worse than
or equally as bad as decelerations, beat-to-beat variability. When
assessing
a CTG, attention is not only given to decelerations but
variability is also as important. About reduced variability, she
stated
that one would have to ‘
go back and investigate what
treatment was the patient on and was she on something that is
paralysing the central nervous system
.’ Concerning CTG 127,
128 and 129, she identified no evidence of reduced variability and
stated that same did not qualify
as category 3 (pathological) CTG.
She identified a slight variable deceleration in-between beat-to-beat
variability and according
to her, that was normal.
[58]
It was difficult for Dr Mtsi to accurately assess the lateness of the
decelerations or variable
ones. She lamented the poor state in which
the CTGs were. She disagreed that the late decelerations identified
by Dr Ndjapa in
the first CTG, were indeed late. She said that it
‘
does not show any reduced variability in the first place.
’
Instead, she identified contractions which she described as those
that could not really be used to assess whether or not
the
decelerations, she identified, were early or late. She identified one
deceleration that she said would have raised questions
in terms of
its nature, length and time it took to recover. She noticed, however,
that throughout that deceleration, beat-to-beat
variability was still
very normal such that there was a good response which showed a
healthy baby. That is because a baby that
has decelerated, would not
respond with a good beat-to-beat variability. In her reading of the
CTG, there was no compensation that
had to be done by the foetus. She
stated that she would have been extremely worried if the foetus’
recovery had gone up to
160 or down to about below 100, which is 80
because then that would have been an indication of severe bradycardia
and tachycardia.
[59]
During re-examination, Dr Mtsi testified about degrees of foetal
distress and that not every
early sign of foetal distress requires
intervention by way of a caesarean section. However, she accepted
that foetal distress develops
over time and may move from less to
severe.
[60]
During cross-examination, Dr Mtsi identified a variety of
decelerations in the first CTG, which
she said were not late but had
good beat-to-beat variability. She added that in this CTG she could
find an area of interference
with the accuracy of the CTG. She
thought that, that could have been caused by the maternal pulse rate
that was picked up as it
is known to cause decelerations. It was
difficult for her to interpret another deceleration that she
identified in the second CTG.
It was further difficult for her to
comment on the third and fourth decelerations. In all, she identified
four decelerations and
could only interpret one. Regarding the second
CTG she identified five decelerations which she could not interpret
and one which
she classified as early.
[61]
Dr Mtsi conceded during cross-examination that at 19h05 Dr Glaze
issued an instruction that the
plaintiff be closely monitored, which
was not done. She accepted that this was not in keeping with the
doctor’s instructions.
She further conceded that the fact that
no one could account for the foetal condition and the plaintiff’s
progress from the
time the doctor gave instructions in terms of her
dilatation, was a problem and constituted substandard care. When she
was asked
to reconcile the fact that in her reports she said there
was no substandard care, she said: “
I do not know how to
respond to that
.” She conceded further that the CTG at
20h00 showed a situation that had deteriorated and at that time,
nothing could be
done by way of caesarean section to save the baby as
that was not the onset of the problem, thereby confirming the
evidence of
Dr Ndjapa. She later deviated and stated: “…
I
think we are both guessing sir because I do not know, and I am unable
then to say that that was the onset of labour or not the
onset.”
However, she agreed with Dr Ndjapa that the CTGs remained suspicious
and were not normal.
[62]
When Dr Mtsi was asked whether a caesarean section would be
appropriate if the CTG was suspicious,
she referred to the suggested
management by Figo Consensus Guidelines on Intrapartum Fetal
Monitoring (referred to in the trial
as the FIGO document) as well as
her experience, were that when one has got a suspicious trace, one
gives it enough time and action
to correct reversible causes, if
identified. She added: “…
[E]nough time is if you see
severe deterioration from these CTGs then you know that no I’m
not going to continue here but
a suspicious CTG is highly unlikely to
result in hypoxia or acidosis in the fetus so you’ve got time
to assess, re-assess
and re-assess so action to correct a reversible
cause had been continuing…”
[63]
Concerning the nuchal cord around the foetus’ neck twice, Dr
Mtsi explained that the baby’s
head was 3/5 up as late as
twenty hours and suddenly dropped to 1/5 in 40 minutes according to
the nurses’ description. She
thought that the sudden drop with
the tight cord would subject the baby to a tightening cord and cause
a little bit more lack of
oxygen. She added that a cord may be two
times around the neck at delivery without causing much damage but in
the circumstances
that she described, it would cause more danger. She
did not think that the nuchal cord was tight at all stages. She
admitted that
if the nuchal cord was tight around the neck twice, the
nurses could have picked that up that there was something wrong with
the
FHR if they monitored it. In her opinion, only after the
plaintiff became fully dilated did the head drop rapidly and it is
when
the problem was exaggerated. She confirmed that her proposition
was speculative.
[64]
During cross-examination, Dr Mtsi agreed that had those who managed
the plaintiff’s labour
decided to perform a caesarean section
at 19h30, they would have had enough opportunity to deliver the baby,
given the fact that
the actual delivery was at 20h55.
[65]
When Mr Bodlani put to her that intrauterine growth restriction is a
risk factor but did not
cause the condition, Dr Mtsi could not
answer. However, she conceded that not every baby born growth
restricted has cerebral palsy.
She conceded further that a growth
restricted baby has problems coping with labour and would indicate
with a depressed heart rate,
except that in certain circumstances
they respond more aggressively.
[66]
When she was asked about the possibility of chorioamnionitis
(inflammation or infection), Dr
Mtsi testified that there was no
evidence or diagnosis of chorioamnionitis but vaginal discharge. The
placenta was not examined.
She quoted from page 281 of an article
called the South African Medical Journal which states: “
Placental
mediated disease can result in hypoxia or foetal priming for hypoxia
with some degree of IUGR present when labour starts.”
However, she conceded that there was no confirmed case of placental
insufficiency, in the instant case. She confirmed further that
the
clinical finding was that the placenta was normal.
[67]
Dr Mtsi confirmed that according to the clinical notes, ES was born
distressed and was resuscitated
at birth and given oxygen and put in
a box immediately after birth. She was assisted to breathe.
[68]
Dr Mtsi compiled a joint minute with Dr Ndjapa dated 11 March 2020.
The importance of this joint
minute were the following concessions
made by Dr Mtsi that:
68.1 There was no
plotting onto the antenatal graph, the growth chart was completely
blank and it was unknown on which centile the
pregnancy growth was;
68.2 The parthogram on
page 12 of the clinical record suggested that at 14h30 the plaintiff
was 3cm dilated with head level 3/5
above the pelvis membrane still
intact having moderate contractions and was transferred from the
latent phase of labour on to the
alert line of the labour graph,
suggesting that she had entered the active phase of labour as seen on
the parthogram;
68.3 At 17h20 the
parthogram was not plotted. It was evident that if the nursing staff
had plotted it with the information as required,
they would have
noted that the plaintiff had crossed the action line and having in
mind, on record that FHR’s abnormalities
were present, it was
necessary that immediate action be taken by delivering the baby by
the fastest route and this would have been
by caesarean section and
avoid unnecessary delay and further intrauterine exposure to foetal
hypoxia;
68.4 The parthogram was
empty, no records between 14h30 until the time of delivery. The only
CTG suggesting foetal monitoring at
any point available for comment
were those that were performed between 18h00 and 18h30 and these were
also non-reassuring therefore
not only suggesting a substandard care
during labour, but also suggesting that the baby may have been
exposed to intrauterine hypoxia
over a long period of time, long
enough to have to result in birth asphyxia and cerebral palsy.
Further to that, the doctor was
informed about the patient not
progressing and the CTG abnormalities but did not come to assess the
plaintiff personally. The parthogram
was poorly filled leading to
poor decision making;
68.5 At 20h50 the
plaintiff was fully dilated while in the clinical record it was said
that the plaintiff was fully dilated at 20h00
suggesting an
incoherence in the records. Nevertheless, it appeared that five
minutes later she delivered ES at 20h50 with Agpars
of 5/10 and 6/10
who did not cry at birth and also had a tight cord around the neck,
twice;
68.6 Perinatal asphyxia,
also known as hypoxic ischemic encephalopathy (lack of oxygen),
ischemic (lack of blood flow) and encephalopathy
(brain damage) was
characterised by clinical and laboratory abnormalities with evidence
of acute or sub-acute brain injury due
to asphyxia. The primary
causes of this condition were systemic hypoxemia and/or reduced
cerebral blood flow;
68.7 Perinatal morbidity
associated with hypoxic ischemic encephalopathy could occur in the
antepartum, intrapartum or postpartum
period. In many cases this
reflected inadequacies in the antenatal care, the decision making as
well as poor intrapartum and immediate
postpartum care. The quality
and timing of antenatal care with delivery plan as well as an
appropriate intrapartum obstetric care
was key in preventing
perinatal morbidity such as birth asphyxia and cerebral palsy;
68.8 There was
substandard care on the labour monitoring and management of the
plaintiff. There was delay in taking action when
the FHR rate was
noted to be bradycardic. As a result of inappropriate recording and
plotting on the labour graph, the hospital
staff failed to diagnose
labour dystocia and therefor failed to take action when it was
necessary to do so;
68.9 ES was born a
premature. She did not cry at delivery and required resuscitation,
had cooling and apparently seizure witnessed
by the plaintiff was
assessed by the paediatrician as cerebral palsy dominantly
dyskinetic. Antenatal causation including infective
causes as well as
infant factors had been excluded as the probable cause attributable
to ES’s cerebral palsy by both paediatricians
and the MRI
report from the radiologists suggesting that the damaging factor most
probably occurred during labour and delivery.
Dr Mtsi added: “
I
agree that
probably
the insult occurred during
labour but I do not have information regarding the exclusion of risk
factors like prematurity, infection
and epilepsy. My conclusion on
that is that I will leave it to the multidisciplinary team to decide
on that issue.”
(Her emphasis added)
Dr Mtsi further agreed
with Dr Ndjapa that:
68.10 The foetal
condition was inappropriately monitored suggesting that the foetus
might have been exposed to hypoxia over a period
of time, long enough
to cause cerebral damage and resulting in cerebral palsy. The outcome
at delivery (poor agpar score, the need
for resuscitation and
admission to ICU, seizures in the first 24 hours) suggested that the
damaging event might have occurred during
the intrapartum period.
There was no evidence to suggest that the damaging event may have
occurred in the antenatal or postpartum
period even though the
plaintiff was a known epileptic there was no scientific evidence to
suggest that ES’s cerebral palsy
might have been attributable
to her epileptic treatment; and
68.11. The poor outcome
of ES might have been prevented had proper obstetric care been
provided by Zithulele Hospital staff to the
plaintiff and delivery of
ES, expedited. Dr Mtsi again added: “
I agree that
it
may
have been prevented but again we need a
multidisciplinary team to determine the causation.
”
(Her emphasis added)
[69]
In another joint minute compiled by Drs Mtsi and Ndjapa dated, 25
January 2021, unsigned by Dr
Mtsi, she made a turnaround regarding
her position, especially after receiving information she claimed she
did not have when she
signed the joint minute dated, 11 March 2020.
She said that she did not have all the information as well as CTGs
and was therefore
unable to make a proper assessment. Strangely, she
conceded that as an expert, she has a responsibility to be
independent when
expressing an opinion, equip herself with all the
relevant information before preparing a medico-legal report and
comment on a
joint minute. By appending her signature to the joint
minute, she was communicating that she knew what the case was all
about as
she had all the relevant information at her disposal and
that the contents of the joint minute were a true reflexion of her
understanding
of the case she was dealing with. She further conceded
that, that was the position when she committed to the report that she
prepared
preceding the time she entered into the joint minute.
THE
EVIDENCE OF PROF COOPER
[70]
According to Prof Cooper, a neonatologist and head of the department
of paediatrics, ES was growth
restricted. That is because she was a
size below the 10
th
percentile of babies her age, at the
time of birth. He regarded ES as a 39 to 40 weeks’ gestation,
hence he concluded that
the birth parameters of ES were asymmetrical
intrauterine growth restriction which was usually on the basis of
late placental insufficiency.
About late booking for antenatal
visits, he said:
“…
I think
once booking is as late as she did, the only thing one really has got
to rely on is her recollection of the last menstrual
period. Which I
think Dr Kara and I quite agree, may or may not be accurate. But it
makes it extremely difficult to assess intrauterine
growth
restriction because you really need to be following a pregnancy over
months, not over weeks, in order to pick that up. So
in terms of
picking up growth restriction and a whole range of other problems,
this would be compromised, severely compromised.”
[71]
Prof Cooper asserted that to get a good reasonable idea of the
gestational period, a mother has
to attend an antenatal clinic at
least before 20 weeks of gestation because even sonar cannot give an
accurate estimation of gestational
age. He asserted further that it
would be virtually impossible for the attending staff to detect IUGR
as the plaintiff was a late
booker.
[72]
Commenting on the MRI scan, Prof Cooper stated that the partial
prolonged injury sometimes occurs
over at least an hour or hours or
even days while acute profound occurs in just over 45 minutes. He
asserted that during a contraction
there is a compromise in
oxygenation, nutrients and blood flow across the placenta. This is
called an episode of partial hypoxia
because a contraction lasts
about 30 to 45 seconds. During this period there are usually enough
reserves in each cell as each cell
has an emergency supply of glucose
which is sugar and energy. In some cases, this may occur before
labour when there are episodes
of poor perfusion particularly in the
face in the context of IUGR or placental insufficiency. This pattern
of brain injury will
occur over at least an hour or many hours or
sometimes even days.
[73]
Prof Cooper, however, stated that in acute profound hypoxic-ischemic
injury where there is sudden
severe cut-off, an almost complete
cut-off of blood flow to the brain, the compensatory mechanism cannot
function. The whole brain
gets affected and the damage may start
occurring within ten minutes if it carries on for more than 45
minutes and the baby will
not survive because the central parts of
the brain are the most active. They will be severely affected. At
times, the partial prolonged
injury may have started and as time
progresses, it goes into a complete shutdown in perfusion of the
brain and that is when one
gets the mixed pattern of both partial
prolonged and acute profound.
[74]
Regarding CTGs, Prof Cooper remarked that it was the domain of
obstetricians to interpret and
act upon what they observe. In his
report dated 01 June 2020, he concluded:
“
5. [ES] suffered
both a partial prolonged and acute profound hypoxic ischaemic brain
injury during the peripartum period around
term gestation. The
partial prolonged component of the injury could have occurred prior
to labour in view of the fact that she
had significant intrauterine
growth restriction, but may also have occurred during labour. The
acute profound component of the
injury probably occurred during the
45-minute period prior to delivery. Expert obstetric opinion is
needed to determine whether
there were any signs of fetal distress
and whether brain injury was avoidable.”
[75]
Prof Cooper contended that the acute profound component of the injury
must have occurred anywhere
between 10 and 45 minutes, may be even 50
prior to delivery. He conceded that there was neither recognised
sentinel event nor comment
made at birth, that the baby was growth
restricted. He conceded further that in order to put a baby on a
particular centile, gestation
in weeks should be known. At their
disposal, they had an assessment of the symphysis fundal height that
was said to be 32 weeks,
four weeks before delivery and last
menstrual periods that gave the gestation of 40 weeks. After looking
at the parameters, he
found that 36 weeks’ gestation period was
highly unlikely and that the strong probability was that they were
looking at a
term baby of 39 to 40 weeks. He confirmed that there was
no evidence of placental insufficiency as the placenta was not
examined.
[76]
It is important to note that the defendant did not lead direct
evidence as far as the clinical
and hospital records were concerned
although both parties made extensive reference to same during the
leading of evidence. Koen
J in
NH
v MEC for Health
KZN,
[3]
had the following to say regarding medical records:
“
[8]
Statements in the medical records that are favourable to the
Defendant are hearsay where
the author thereof was not called to
testify, and hence not admissible
[4]
.
…No application was made for the admission thereof in evidence
in terms of section 3 of the Evidence Law Amendment Act
1998, but
even if there was, it would be unlikely to have succeeded as there
was no evidence that the author thereof was no longer
available to
give that evidence….
[9]
Recordings favourable to the Plaintiff’s case in establishing
negligence and
liability generally, and accordingly damaging to the
Defendant’s case, made as part of the records kept by the
Defendant’s
servants, are however on a different footing. They
constitute admissions by the servants of the Defendant made in the
ordinary
course of discharging their duties, which are binding
against the Defendant.
[5]
The
Defendant’s staff are obliged to make these statements by
recording the medical position as it unfolds in the records.
They
have an obligation to speak on behalf of the Defendant and dispute
what is recorded, if indeed incorrect.”
[77]
W
ith
the above information in mind,
I
have to accept the medical records favourable to the plaintiff, as
admitted by the defendant. I also have to keep in mind that
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/she
is bound to employ reasonable skill and care as provided for by Innes
CJ in
Van
Wyk v Lewis.
[6]
Importantly,
the medical records show no record before bradycardia was noted at
17h20 after the plaintiff was admitted at Zithulele
Hospital on 11
March 2014. This means that for about two hours there was no
monitoring of either the plaintiff’s or the foetus’

well-being.
NEGLIGENCE
AND AUTHORITIES
[78]
In the instant case, the plaintiff relies on negligence and must
therefore establish it. If at
the conclusion of the case the evidence
is evenly balanced, she cannot claim a verdict, for she will not have
discharged the
onus
resting upon her.
[7]
In
Mitchell
v
Dixon
1914
AD 519
at 525 Innes ACJ said:
“
A
practitioner can only be held liable in this respect, if his
diagnosis is so palpably wrong as to prove negligence, that is to

say, if his mistake is of such a nature as to imply absence of
reasonable skill and care on his part, regard being had to the
ordinary level of skill in the profession.”
[79]
In
Kruger
V Coetzee 1966 (2) SA 428 (A)
[8]
Holmes
JA (Beyers ACJ, Van Blerk JA, Botha JA, Wessels JA concurring) held:
“
For
the purposes 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.”
[80]
In casu
,
it was undisputed that the standard of care that the defendant was
required to provide to the plaintiff and ES had to meet amongst

others, the applicable Guidelines, as alluded. The relevant provision
inter
alia,
relates to foetal distress and its management,
[9]
which states:
“
FETAL DISATRESS
This is suspected when
the following signs are observed:
·
Baseline fetal heart rate ≥ 160 beats per minute
·
Baseline fetal heart rate ≤ 110 beats per minute
·
Variability persistently ˂5 beats per minute on CTG, in
the
absence of sedating drugs
·
Late decelerations of the fetal heart rate
MANAGEMENT OF FETAL
DISTRESS
1.
Explain the problem to the mother
2.
Lie the mother in a left lateral position
3.
Give oxygen b face mask at 6 L/minute
4.
Start an intravenous infusion of Ringer-Lactate to run at 240
mL/hour
5.
Do a vaginal examination for cervical dilatation and to
exclude
cord prolapse:
-
If vaginal delivery is imminent (cervix fully dilated), deliver
immediately, by vacuum extraction if necessary
-
If vaginal delivery is not imminent, give hexoprenaline 10
micrograms IV and prepare for immediate caesarean section. Arrange
urgent
transfer from a community health care centre to hospita
l.”
Emphasis added
[81]
During the trial, it was undisputed that the plaintiff was put on a
CTG at 17h00 and there was no continuous
monitoring. That is because
according to the plaintiff, a nurse would come, look at the screen
and leave. The clinical notes showed
that intrauterine resuscitation
was done after bradycardia was noted at 17h20. The plaintiff was 3 cm
dilated at the time, which
meant that vaginal delivery was not
imminent. There was no indication that she was given hexoprenaline 10
micrograms IV and was
also not prepared for an immediate caesarean
section, as provided for in the Guidelines. During the period between
17h20 and 18h20
the plaintiff was not monitored whilst on CTG, as
stated.  No nursing staff was with her and therefore no one knew
what was
happening to her.
[82]
After the doctor was again informed of the foetal condition at 18h45,
he/she did not personally
come to assess the condition. Instead
he/she gave instructions that the then-current intervention be
continued which had been applied
since 17h20. At 19h00 decelerations
were noted about three times, despite the management. The doctor was
again informed and requested
to come and assess the plaintiff, the
FHR was still dropping and intrauterine resuscitation was
continuously applied more than
an hour later although there was
clearly no progress of labour. The plaintiff and the foetus remained
unmonitored after 19h05 after
the doctor had given an instruction to
monitor her closely. It was clear that FHR was not normal all this
time. This was common
cause between Drs Ndjapa and Mtsi that at no
stage was the CTG normal from the time bradycardia was noted and
after intrauterine
resuscitation was started. Notwithstanding this
condition, the plaintiff’s labour continued as if nothing wrong
was noted.
The fact that the foetus was suffering from hypoxia was
known by the nursing staff and the doctor, who was called at 17h20
and
18h45. According to the Guidelines, they were aware that vaginal
delivery was not imminent and they were supposed to have given
the
plaintiff hexoprenaline 10 micrograms IV and prepared for immediate
caesarean section, which they did not do. There was no
need to
transfer her to a hospital as she was in the hospital already.
Moreover, according to the Guidelines, foetal distress is
one of the
common indications for caesarean section, which was disregarded by
the defendant’s employees.
[83]
During the cross-examination of Dr Ndjapa, the
defendant did not challenge his evidence of what in his opinion,
constituted good
FHR recovery in obstetrics. It was never put to him
that what he identified as late decelerations and its
characterisation in the
first CTG, were in fact not and no reason was
advanced as to why it would not be late decelerations. It was the
case even when
he testified that the late decelerations were starting
to be pathological and that there had been no normal CTG. He that he
identified
four late decelerations and elements of poor variability
in the second CTG. This was also undisputed. The defendant did not
put
it to Dr Ndjapa that a caesarean section was indicated only when
there is bradycardia, tachycardia, reduced variability and late

decelerations, at the same time. Evidence that has not been
challenged by the defendant, stands uncontroverted and strengthens

the plaintiff’s case.
[84]
Dr Mtsi testified differently from what she stated in her
Medico-Legal report. She adapted her
evidence as the trial
progressed, as shown above.  She failed to answer pertinent
questions put to her. In my view, she did
not assist the court but
gave evidence in order to protect the defendant. Her opinion was
therefore not independent. She, however,
conceded that the management
of the plaintiff’s labour was substandard. She changed her
stance after the case for the plaintiff
had been closed. This conduct
cannot avail the defendant.
[85]
On the other hand, Prof Cooper’s theory of IUGR can also not
stand due to the fact that
the gestational period of the plaintiff
was unknown, which he conceded. This theory was intended to conclude
that the baby was
born at term, which fact is unsupported by the
evidence. That is because when the plaintiff presented at Mpunzana
Clinic on 11
February 2014 and 11 March 2014, the antenatal card was
not properly completed, as plotting was not done. Moreover, the
plaintiff
was uncertain about her last menstrual periods, as alluded.
The gestation period was therefore not established. Prof Cooper
relied
on hearsay. In
Mathebula v RAF (05967/05)
[2006] ZAGPHC 261
delivered on 08 November 2006
, Meyer JA, as he then was,
remarked:
“
An
expert is not entitled, any more than any other witness, to give
hearsay evidence as to any fact, and all facts on which the
expert
witness relies must ordinarily be established during the trial,
except those facts which the expert draws as a conclusion
by reason
of his or her expertise from other facts which have been admitted by
the other party or established by admissible evidence.”
CAUSATION
[86]
The relevant questions are: (i) what was the factual cause of the
ultimate condition of ES; and
(ii)
did the
negligence on the part of the employees of the defendant cause or
materially contribute to the brain injury suffered by
her in the
sense that the respondent, by the exercise of reasonable professional
care and skill, could have prevented it from developing.
Dr
Mtsi was long-winded in her explanations and concentrated on the
maternal rather than foetal condition. This evidence was not
led in
her evidence-in-chief.
[87]
In this regard, Nkabinde J (Moseneke DCJ, Froneman J, Jafta J and Van
der Westhuizen J concurring)
in
Lee
v Minister of Correctional Services 2013 (2) SA 144 (CC)
[10]
remarked:
“
[38]
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.”
[88]
The learned Judges continued at para [41]:
“
[41]
…[I]n the case of an omission the but-for test requires that a
hypothetical positive act be inserted in the particular
set of facts,
the so-called mental removal of the defendant’s omission. This
means that reasonable conduct of the defendant
would be inserted into
the set of facts. However, as will be shown in detail later, the rule
regarding the application of the test
in positive acts and omission
cases is not inflexible. There are cases in which the strict
application of the rule would result
in an injustice, hence a
requirement for flexibility.”
[89]
In order to apply this test one must make a hypothetical
enquiry as to what probably would
have happened but for the
wrongful conduct of the defendant. This enquiry may involve the
mental elimination of the wrongful
conduct and the substitution of a
hypothetical course of lawful conduct and the posing of the question
as to whether upon such
a hypothesis plaintiff's loss would have
ensued or not.
[11]
[90]
In the instant case, for the defendant to be held liable for the act
or omission committed by
its employees it must be proved that the
injury sustained by ES was reasonably foreseeable and the defendant’s
employees
failed to provide the level of skill and competence that
would otherwise be expected to be provided by reasonable health care
employees
in the circumstances. However, a plaintiff is not
required to establish the causal link with certainty, but only to
establish
that the wrongful conduct was probably the cause of the
loss, which calls for a sensible retrospective analysis of what would
probably
have occurred, based upon the evidence and what can be
expected to occur in the ordinary course of human affairs rather
than an
exercise in metaphysics.
[12]
[91]
Dr Ndjapa testified that the defendant’s employees delayed in
taking action at the time
when the FHR was bradycardic. Due to
inappropriate recording and plotting on the labour graph, they failed
to take action when
it was necessary. They were therefore negligent
in their treatment of the plaintiff as they failed to timeously
deliver the baby
by caesarean section. It was clear that the foetus
was in trouble at 17h20 and they unnecessarily allowed labour to
continue without
appropriate monitoring, especially between 14h30 and
18h00. That is because at 18h30 the CTG was non-reassuring and
delivery was
essential to prevent further exposure of the foetus to
hypoxia and brain damage. Dr Mtsi was of the opinion that there was
no negligence
in the management of the labour as monitoring was
appropriate and the problem was recognised rather than ignored.
However, she
conceded that an abnormal CTG was discovered.
[92]
Mr Bodlani, for the plaintiff, submitted that had there been
immediate delivery of ES after the
onset of bradycardia, in all
probability, she would not have sustained cerebral palsy. Mr
Ntsaluba, on behalf of the defendant,
argued that the management of
the plaintiff’s labour was proper and not substandard. He
stated that EL was growth restricted
and this was not and could not
have been detected during the plaintiff’s pregnancy as she only
booked on 11 February 2014,
a mere four weeks before 11 March 2014
when she went into labour. He added that EL’s IUGR primed her
for birth hypoxia and
rapid progression of labour from 3cm dilation
to full dilatation which would have contributed to the nuchal cord
around her neck
twice at a time when it was too late to detect and
intervene effectively. He submitted that the rapid progression from
the first
to the second stage of labour, and the tightening of the
nuchal cord twice around her neck, most probably caused the dominant
acute
profound of hypoxic-ischaemic brain injury which explained the
picture depicted on the MRI scan. He submitted further that even
if
the defendant’s employees could be found to have been
negligent, the causal effect of the outcome was not that of
negligence
but rather the fact that the child was primed by IUGR for
birth hypoxia and the tightening of the nuchal cord immediately
before
birth.
[93]
The plaintiff pleaded that the negligence of the employees of
the defendant in the management of her labour and delivery of [ES]

who had developed foetal heart abnormality as a consequence of foetal
deoxygenation did not properly attend to the matter (condition)
in
circumstances where it was necessary to do so. They failed to adhere
to the standard of practice of reasonable nurses and doctors
in their
respective positions to ensure that foetal deoxygenation was attended
to without delay to prevent ES’s development
of a
hypoxic-ischaemic injury.
[94]
Regarding the evaluation of credibility and reliability of expert
evidence, Wallis JA (Fourie
and Koen AJJA concurring) in
Pricewaterhouse
Coopers Incorporated and Others v National Potatoe Co-operative Ltd
and Another [2015] 2 All SA 403 (SCA)
[13]
referred to
Wightman
v Widdington (Successon de)
2013 QCCA 1187
CanLII)
where it was remarked thus:
“
Legal
principles and tools to assess credibility and reliability
[326] “Before
any weight can be given to an expert’s opinion, the facts upon
which the opinion is based must be found
to exist”
[327] “As long as
there is some admissible evidence on which the expert’s
testimony is based it cannot be ignored; but
it follows that the more
an expert relies on facts not in evidence, the weight given to his
opinion will diminish”.
[328] An opinion based on
facts not in evidence has no value for the Court.
[329] With respect to its
probative value, the testimony of an expert is considered in the same
manner as the testimony of an ordinary
witness. The Court is not
bound by the expert witness’s opinion.
[330] An expert witness’s
objectivity and the credibility of his opinions may be called into
question, namely, where he or
she:
•
accepts to
perform his or her mandate in a restricted manner;
•
presents a product
influenced as to form or content by the exigencies of litigation;
•
shows a lack of
independence or a bias;
•
has an interest in
the outcome of the litigation, either because of a relationship with
the party that retained his or her services
or otherwise;
•
advocates
the position of the party that retained his or her services; or
•
selectively
examines only the evidence that supports his or her conclusions or
accepts to examine only the evidence provided by
the party that
retained his or her services.”
[95]
In Ruto
Flour Mills v Adelson (1) 1958 (4) SA 235 (T)
[14]
Boshoff J stated that a party seeking to introduce expert evidence
must satisfy the court that the witness not only has specialist

knowledge, training, skill or experience but that he/she can, on
account of these attributes or qualities, assist the court in

deciding the issue, that he/she is an expert for the purpose for
which he/she has been called upon to express an opinion,
[15]
the witness does not or will not express an opinion on hypothetical
facts that have no bearing on the case or which cannot be reconciled

with all the other evidence in the case.
[16]
[96]
With the above in mind, I considered the various experts’
evidence on behalf of the plaintiff
in support of her claim. I also
took into account the evidence given by the defendant’s
experts. I was impressed by the evidence
of the experts who testified
on behalf of the plaintiff as they testified in their respective
fields and made conclusions founded
on sound factual and evidential
basis. Regarding the evidence on record, the evidence of Drs Ndjapa
and Kara, in their field of
expertise, leaves no doubt in my mind
that the cause of the injury to ES was a consequence of negligence on
the part of the defendant’s
employees.
[97]
The evidence of the defendant’s experts, Dr Mtsi and Prof
Cooper were not impressive as
it was unsubstantiated by the facts of
this case. Dr Mtsi could not interpret the CTGs and yet she still
expressed an opinion which
was speculative in nature and
unacceptable, which she conceded. She relied so much on literature
and not on material facts upon
which her opinion was based. Prof
Cooper’s theory of IUGR and placental insufficiency was also
not supported by the evidence.
Diemont JA in
S
v Collop 1981 (1) SA 150 (A)
[17]
stated that
although
an expert witness may refer to textbooks and a doctor to medical
treatises to refresh his/her memory, or to correct
or confirm his
opinion, such books are not evidence
per
se.
Addleson
J
[18]
remarked that when an
expert relies on passages in a text-book, it must be shown, firstly,
that he can, by reason of his own training,
affirm (at least in
principle) the correctness of the statements in that book; and,
secondly, that the work to which  he
refers is reliable in
the sense that it has been written by a person of established repute
or proved experience in that field,
which was not the case here.
[98]
Notwithstanding her misgivings, Dr Mtsi continued and interpreted the
CTGs. She asserted that
the last CTG depicted a worsening scenario
than the previous one. This CTG coincided with the onset of strong
contractions because
all along the contractions were not long and
strong. However, she agreed with Dr Ndjapa that at that stage there
could have been
quite a significant amount of activity before
delivery nothing could have been done by way of caesarean section to
salvage the
situation. Surprisingly, she confirmed that no normal CTG
was available before 20h00 and yet refused to accept that at 20h00
the
problem that had started earlier,   had deteriorated.
She confirmed the evidence of Dr Ndjapa that when the foetus was

bradycardic and there was a drop up to 100 beats per minute up to 100
beats per minute but picked up to 120 beats per minute that
was
sufficient warning that the baby’s heart beat was abnormal.
CONCLUSION
[99]
In my view, the conduct of the defendant’s employees was
negligent as it was clearly not
according to the Guidelines. They
should have foreseen the reasonable possibility of their conduct
causing harm to the foetus and
should have taken steps to guard
against such an occurrence. They failed to uphold this standard. The
cause of ES’ injury
resulted from the negligent conduct of the
defendant’s employees, acting in the course and cope of their
employment at Zithulele
Hospital in respects already stated above.
They failed to deliver the plaintiff by caesarean section due to poor
progress in labour
as at the time the plaintiff was not fully
dilated. Bradycardia was noted at 17h20 and resuscitation that was
done as an intervention
until 20h50, more than three hours later.
This fell short of the required standard. Instead, the injury was
prolonged when it was
obvious that there was no progress to the
detriment of ES who developed cerebral palsy. Had immediate delivery
of ES was done,
she would not have been injured. There was no
evidence of IUGR suggested by Dr Mtsi and Prof Cooper, as this was
not supported
by the evidence. The plaintiff’s claim has to
succeed as she has, on a balance of probabilities, successfully
proved her
case.
ORDER
[100]
In the circumstances, I issue the following order:
1.
The defendant shall pay 100% (one hundred percent) of the
plaintiff’s agreed or proven damages in her representative
capacity
for and on behalf of her minor child, ES, which damages flow
from the neurological injury sustained by ES during labour and
delivery
at Zithulele Hospital on 11 March 2014 and the resultant
cerebral palsy which she suffers from.
2.
The plaintiff’s claim in her personal capacity and
issues relating to quantum are postponed
sine die.
2. The defendant shall
pay the plaintiff’s taxed or agreed party and party costs on
the High Court Scale, such costs to include
(but not necessarily be
limited to) the following:
2.1 The costs
attendant upon the obtaining of the medico-legal reports and/or
addendum reports and/or joint minutes, if any, of
the expert
witnesses in respect of which notices in terms of Rule 36(9) of the
Rules of Court, were filed;
2.2 The qualifying and
appearance fees of the expert witnesses in respect of which notices
in terms of Rule 36(9) of the Rules of
Court, were incurred;
2.3 The reasonable and
necessary air transport and accommodation costs and expenses in
respect of expert witnesses in respect of
which notices in terms of
Rule 36(9) of the Rules of Court were filed, where such fees were
incurred; and
2.4 The reasonable
fees of 2 (two) counsel, where such services were engaged, including
the preparation of heads of argument and
running of the trial on a
virtual platform and in Court.
3. The defendant shall
pay interest on the plaintiff’s taxed or agreed costs of suit
at the prescribed statutory rate calculated
from a date (14) fourteen
days after agreement in respect thereof, or a date 14 (fourteen) days
after affixing of the Taxing Master’s
allocatur,
to date
of payment.
BM
PAKATI
JUDGE
OF THE HIGH COURT, GQEBERHA
Plaintiff’s
Counsel:

Adv A Bodlani with Adv Ntikinca
Instructed
by:

Dayimani Inc
Defendant’s
Counsel:

Adv TM Ntsaluba SC with Adv DT
Young
Instructed
by:

Norton Rose Fulbright South Africa
Attorneys
Heard
on:      26, 27,28, 29, January 2021, 01
February 2021, 03, 04, 05,06,07,10,11 May 2021, 22, 23,24,

25,28,29,30 June 2021, 01,02 July 2021, 27,28 June 2022.
Judgment
delivered:

28 February 2023
[1]
See Minister of Police v Skosana
1977 (1) SA 31
(A) and Blyth v Van
Den Heever
1980 (1) SA 191
(A).
[2]
At para [12].
[3]
(1287/2014)
[2018] ZAKZPHC 8 (4 April 2018).
[4]
See
DZ Zeffertt and AP Paizes Hoffman and Zeffertt’s the South
African Law of Evidence 4
th
ed, at 183ff.
[5]
DT
Zeffertt and AP Paizes Hoffman and Zeffertt’s the South
African Law of Evidence 4
th
ed, at 183ff.
[6]
Van
Wyk v Lewis
1924 AD 438
at 444.
[7]
Va
n
Wyk
supra
at 444.
[8]
At
430e.
[9]
At
page 55 of the 2007 Guidelines.
[10]
At
para [38]; see also International Shipping Co (Pty) v Bentley
1990
(1) SA 680
(A) at 700E-H.
[11]
International
Shipping Co (Pty) Ltd v Bentley 1990 (1) SA 680 (A).
[12]
Minister
of Safety and Security v Van Duivenboden
2002 (6) SA 431
(SCA) at
para [25].
[13]
At page 441 para [98]; see also Coopers (South Africa) (Pty) Ltd v
Deutche Gesellschaft fur Schadlingsbekampung Mbk
1976 (3) SA 352
at
370.
[14]
At 237C-D.
[15]
Goliath v Fedgen Insurance Company Ltd 1994 (2) PH F 31 E at 83.
[16]
S v Mkohle
1990 (1) SACR 95
(A) at 100d.
[17]
At
167B.
[18]
Menday
v Protea Assurance Co Ltd
1976 (1) Sa 565
(E)at 569H.