S.M v MEC for Health, Eastern Cape (25/2018) [2023] ZAECBHC 18 (27 July 2023)

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[2023] ZAECBHC 18
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S.M v MEC for Health, Eastern Cape (25/2018) [2023] ZAECBHC 18 (27 July 2023)

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IN THE HIGH COURT OF
SOUTH AFRICA
[EASTERN CAPE
DIVISION: BHISHO]
CASE NO. 25/2018
In
the matter between:
S[…]
M[…]
Applicant
and
MEC
FOR HEALTH, EASTERN CAPE
Respondent
JUDGMENT
JOLWANA J:
Background.
[1] Plaintiff instituted
action proceedings claiming delictual damages in her personal
capacity and in a representative capacity
as mother and natural
guardian of A, a girl born on 31 December 2015.  The claim is
founded on the allegation that A was born
with foetal distress,
hypoxic ischemic encephalopathy (HIE), and superadded hypoglycaemia
giving rise to spastic quadriplegic cerebral
palsy and developmental
delay.  The plaintiff’s case is that these birth defects
of A were as a result of the negligence
of the defendant’s
employees and further that that negligence caused the above mentioned
birth defects.  The plaintiff
claims that as a result of the
aforesaid negligence of the defendant’s employees during the
delivery process of A, she has
suffered damages estimated at about
R31 789 970.00.  The defendant denies that its
employees were negligent in the
management of the delivery of A.
The defendant further pleads that in any event and to the extent that
it may be found that
its employees were negligent, such negligence
did not cause the alleged birth defects. Therefore it was not
responsible for the
birth defects and therefore the damages that the
plaintiff has allegedly suffered.
[2] The facts which are
substantially undisputed are briefly the following.  On or about
31 December 2015 plaintiff attended
at Maphuzi Clinic (the clinic) as
a result of the onset of labour having started feeling labour pains
at about 02:00 am that morning.
She was examined at the clinic
and referred to Zithulele Hospital (the hospital) where she was
admitted at approximately 09h00.
She was, shortly thereafter,
examined by the nurses.  At various times during the day after
her admission she was attended
to by the nursing staff and medical
practitioners in that hospital.  Ultimately, she gave birth to A
at or about 17:10 on
31 December 2015 through assisted vaginal
extraction.  Plaintiff allegies that while under treatment,
supervision and care
of the aforesaid defendant’s employees, A
was born with the birth defects referred to above.
The pleadings.
[3] Some of the
plaintiff’s pleaded case on which the damages claim is founded
are stated briefly hereunder.  The plaintiff
has pleaded that
the defendant’s employees’ treatment, care and management
of her labour was inadequate in all or some
of the following
respects.  They failed to monitor A’s foetal heart rate
(FHR) timeously.  They failed to monitor
the plaintiff’s
blood pressure timeously.  There was no regular monitoring of
the plaintiff and her foetus.  They
failed to diagnose or
determine the onset of foetal distress, hypoxia and/or hypoxic
ischemic encephalopathy and/or superadded
hypoglycaemia.  As a
result, they failed to provide adequate treatment to the plaintiff
and her foetus in order to prevent
the development of foetal distress
and HIE.  Ultimately, during the delivery process or immediately
thereafter they failed
to diagnose that the foetus had suffered from
hypoxia and HIE and superadded hypoglycaemia.  As a result, they
failed to implement
appropriate treatment protocols.
[4] Plaintiff alleges
that the defendant’s employees failed to provide adequate care
with the necessary skill and diligence
as could be reasonably
expected of medical practitioners and nursing staff involved.
In acting in the manner aforesaid or
in failing to act as could be
reasonably expected of them, the defendant’s employees acted
negligently.  The defendant
is therefore vicariously liable for
the negligent conduct of its employees.  This is because when
plaintiff presented herself
at the hospital on 31 December 2015 an
oral, alternatively tacit agreement for the adequate rendering of
medical services to her
came into being.  The express or implied
terms, alternatively the tacit terms of such agreement were that the
defendant would
provide all medical services to her at its facilities
during the delivery of A.  The said services included the
provision
of all medical, surgical, nursing, monitoring, advisory,
supervision, care and midwifery services to her during the delivery
process
of A.
[5] The defendant’s
plea is in denial of any aspect of negligence which is alleged by the
plaintiff.  The defendant further
denies that to the extent that
some or all of its employees may have acted negligently, that such
negligence was causally connected
to A’s birth defects.
Furthermore, the defendant pleads that there is a strong probability
that the birth defects of
A were as a result of or were caused by an
underlying genetic problem in her family rather than negligence on
the part of its medical
practitioners and nursing staff who attended
to her during labour.  Negligence is therefore denied in part
because, A’s
condition is atypical to cerebral palsy as it is
progressive.  Her neonatal encephalopathy is not in keeping with
an intrapartum
ischemic injury as the onset of her seizures was long
after A’s first day of life.  The plaintiff has a poor
pregnancy
history.  On the basis of inter alia, the above,
negligence and causation are denied.  Consequently, liability to
the
plaintiff and her child, A, is denied.
The evidence.
[6] The plaintiff herself
was the only factual witness for her case.  Her evidence was
that she was born on 1[…] A[…]
1999 and she was
unemployed.  She went to school up to grade 9 at which grade she
dropped out.  She testified that her
second child, A was born on
31 December 2015.  Her first child was born on 19 September 2014
when she was 15 years of age.
She was at home at the time of
the delivery of her first child and an ambulance was called to no
avail.  She ended up delivering
the baby at home in the morning
between 8:00 am and 9:00 am.  She was assisted in the delivery
process by her grandmother
and her neighbours.  That baby was a
baby boy.  He was not alive when he was born.
[7] In 2015 she fell
pregnant again and gave birth on 31 December 2015 to a baby girl A,
the child concerned in this case.
Before A was born, she
attended the antenatal clinic and she was examined.  She visited
the antenatal clinic four times before
the labour date.  On the
31 December 2015 she started feeling labour pains at about 2:00 am in
the early hours of the morning.
Her aunts called an ambulance
which did not arrive.  She eventually took a taxi to the
clinic.  At the clinic she was
examined vaginally but not much
was done and she was told that she was being transferred to
hospital.  Indeed, she was taken
to hospital where she was
attended to at about 09:00 in the morning.
[8] At the hospital she
was again examined vaginally.  An object that looked like a
funnel was also pressed against her to
examine the heart beat of the
unborn baby.  The nurses would listen to this instrument.
She was thereafter told to walk
around the passage.  At about
11:00 am or 12:00 am, water erupted and she was taken to a bed.
After she was put on a
bed she was tied with a certain belt around
her stomach and was examined.  She was not told anything.
At some point
the belt was removed and a finger was inserted in her
vagina and then she was told to push.  She pushed but at some
point
she lost her strength.  She was assisted to deliver the
baby which she delivered at about 17:00.  She did not see the

baby which was not screaming or crying.  The baby was taken away
and she was told that she was being taken to theatre to be
sutured.
She only saw the child at about six or seven that same day when the
child was brought to her.
[9] She was told to
breastfeed the baby.  She tried but the baby could not suck. She
was advised to press her breast to get
the milk into a mug.  The
baby was not able to latch.  She expressed the milk into a mug
and cup fed the baby.
The cup feeding must have taken about a
week.  The baby started having seizures about two or three days
after birth.
The child remained with her in hospital until she
was discharged on 11 January 2016.  At the time she was
discharged the baby
was able to breastfeed.  She was never told
that there was anything wrong with the baby.
[10] When the baby was
four months old she noticed that her eyes were squinting.  When
the baby was ten months old she could
not lean or crawl.  She
had been taking the child regularly to the clinic for immunisation.
She testified that up to
the time she gave evidence, the child was
developing well.  However, she could not talk or eat properly on
her own.  She
never had epileptic fits after she was discharged
from hospital.  On 29 July 2018 she had another baby.  On
this occasion
she went to hospital at 08:00 in the morning and the
baby was born at 12:00 midday.  This baby was a stillborn.
[11] The plaintiff
testified under cross-examination.  Her evidence was that she
had fallen pregnant three times and that the
child, A was the second
born of the three pregnancies.  The child who was born on 29
July 2018 was a baby boy and was a still
born.  The first child
was also a boy and was born at home on 19 September 2014.  She
attended antenatal clinic before
that child was born.  She used
a clinic card in which the antenatal visits were recorded.  She
could not recall how many
times she visited the clinic for the
monitoring of her pregnancy but she only went to the clinic when she
was eight months pregnant
in respect of the third child.  With
respect to A she went to the clinic three times before the delivery
date.  She confirmed
that she went to the clinic on 17 August
2015, on 17 September 2015 and on 24 November 2015.  It was put
to her that according
to the hospital notes, A was sucking well on
the 01 January 2016.  She disputed that.  With regard to
the seizures which
she had testified that they had happened on the
second or third day, she conceded that she may have been wrong when
she was referred
to hospital notes which indicated that seizures only
occurred for the first time on the fourth day.
[12] When it was pointed
out with reference to the hospital notes that she had difficulty
breastfeeding the baby and that on the
01 January 2016 at about
18:00, A was sucking well, she insisted that the baby could not feed
on her own as a result of which she
had to express milk into a cup.
She however, confirmed being trained by the hospital nurses on how to
breastfeed the child.
She explained that at the time she was
given instructions on breastfeeding, the baby would be with her but
she could not suck.
She could only put her mouth on the breast
nipples.  After the plaintiff’s evidence, no other factual
witness was called
for the plaintiff.  All the other witnesses
were expert witnesses specialising in various areas as will become
apparent from
their evidence.
The plaintiff’s
expert witnesses.
[13] The first expert
witness called by the plaintiff was professor van Toorn.  He
testified that he is a paediatric neurologist
at Stellenbosch
University and Tygerberg Hospital.  He explained that his area
of expertise is anything that has to do with
the brain, the foetal
brain, the neonatal brain, and the infant brain.  He has been
practising as a child neurologist for
no less than 15 years.  He
treats epilepsy, cerebral palsy and any condition that affects the
brain.  He explained that
hypoxia ischemia is simply lack of
oxygen, lack of blood to the brain.  He was called in this case
to opine on the cause and
timing of the child’s brain injury.
He testified that based on the consideration of all the evidence that
was at his
disposal, his opinion was that A suffered a hypoxic injury
of a mixed acute profound and prolonged partial variety occurring in

the brain of term maturity.  He timed the global insult to have
occurred during the labour process.
[14] He also did a
neurological examination of the child.  This examination
revealed that A has dyskinetic cerebral palsy.
This means that
the child has a movement disorder with reasonable mobility.  The
injury in this child was confined to the
middle part of the brain
that is responsible for movement.  He testified that A was born
in a compromised state which indicates
that there were problems in
the womb and that is indicative of foetal distress.  He further
testified that the hospital records
reflecting that the baby was
sucking after birth cannot be a correct reflection of what happened
for the simple reason that absent
a suck neflex there can be no
sucking.  This baby was born flat but recovered after a bag mask
ventilation and stimulation,
there was lethargic behaviour which is a
subnormal level of consciousness and excessive sleeping.  All of
that was not normal.
There was a weak grasp reflex.  The
suck reflex was not poor, it was absent.
[15] Dr Murray was the
plaintiff’s obstetrician and gynaecologist expert witness.
She testified that the plaintiff was
on early active labour on
arrival at hospital and she was 5cm dilated.  She testified that
according to the Guidelines for
Maternity Care in South Africa, 2007
(the guidelines), when a mother is in active labour the mother’s
blood pressure and
her heart are monitored hourly, her temperature,
four hourly and her urine is measured two hourly.  The foetal
heart rate
(FHR) should be measured every 30 minutes during and after
contraction.  The liquor should be observed every two hours.

Contraction should be monitored hourly and caput moulding must be
assessed two hourly.  All of this type of monitoring is
for low
risk pregnancies.  The outcomes of the monitoring should be
plotted on a partogram from the time a patient presents
in labour to
the end so that the labour in its entirety is correctly documented.
[16] Dr Murray testified
about the entries in the hospital records as follows.  The first
entry in the hospital records is
at 09:00.  She then said that
based on this, no entries were made in the partogram until some two
hours later when she arrived
at the hospital as she had been at the
clinic at 06:50.  At that time her cervix was 5cm dilated.
The FHR was recorded
as being 135 beats per minute (bpm) and no
decelerations were noted.  She testified that the plaintiff had
been at 5cm of
dilation for some two hours by 09:00 with no change.
She had arrived at the [clinic] at 6:50 which means it was some two
hours by 09:00 with no progress.
[17] The next assessment
was at 10:00 with no change and at 10:30 the (FHR) was recorded as
normal with mild and moderate contractions.
Dr Murray testified
that had the plotting been done correctly, it would have been
realized that there was poor labour progress
which required
reasonable management including assessing the mother to check if she
was well, preferably by a doctor.  This
would have been to check
if she was not exhausted or dehydrated and that there was no
obstruction or disproportion to ensure that
the foetus was not too
big for birth.  The foetal well-being needed to be assessed or
monitored by CTG to ensure that the
foetus was well and stable for
the labour to continue and assessing the contractions to see if they
were enough.  Depending
on what was found, a plan would be made
including breaking the mother’s waters, assist labour progress,
doing a caesarean
section, giving oxytocin or doing what she called,
watchful waiting which is cautiously allowing more time.  She
explained
that according to the guidelines labour progress which has
crossed action line is indicative of a need for CTG monitoring.

Because no capturing in the first plot was done, the slow progress
was never recognised. Therefore, at 09:00 already there was
a problem
which was not picked up or noticed.
[18] The next assessment
was at 12:00 at which time the FHR was recorded as being 160 bpm
before contraction and 140 bpm after contraction.
There were no
decelerations or no slowing of the heart rate.  The membranes
were intact, the water not having broken.
The cervix was 7cm
dilated with the head being three fifths above the brim and
contractions were moderate.  Therefore, at
12:00 plaintiff had
made some improvement in the labour progress but it was still
unsatisfactory progress.  The partogram
indicated that the heart
rate before contraction was 160 bpm which was borderline high as the
normal heart rate is between 110
and 160 bpm.  So there was a
marked increase in the heart rate.  After contraction the heart
rate fell to 140.
When a heart rate falls after contraction,
that is, by definition a deceleration which is indicative of foetal
hypoxia or a foetus
in distress.  So this was suggestive of an
abnormal FHR at 12:00.  Therefore, the foetus should have been
carefully monitored
by CTG so that if there were signs of distress,
resuscitation would be done or even a caesarean section if things did
not improve.
However, the abnormality was not recognised.
[19] The next review was
at 14:00.  However, the FHR was not assessed as there was no
recording of the FHR at this time for
some two hours since 12:00.
The cervix was noted to be 5cm dilated with strong contractions.
There appears to have
been a regression in dilation.  The best
that she could posit was not that there had been a regression as that
does not really
happen, but that there was no progress in labour from
the earlier 5cm and therefore progress was abnormally slow.
Therefore,
a caesarian section should have been performed at 14:00.
But because there was no cognisance of the slow progress, no plans

were made to remedy the situation.  There was no documented
heart rate for two hours despite the abnormality shown by the

previous plotting.  This is important because even if the
patient was low risk, there should have been assessments of the

foetal condition every 30 minutes which did not happen.  This
was therefore a substandard care of a very severe degree.
[20] At 15:00 the cervix
was 7cm dilated.  This was not much better but again the FHR was
not recorded and there were strong
contractions.  There was also
an indication of a prescription for syntocinon.  Syntocinon
stimulates the uterus thus
increasing the strength and frequency of
contractions.  This drug could not be used if there were signs
of foetal distress
or obstructed labour as it can cause foetal
distress and uterine hyperstimulation by causing too many
contractions.  The most
common complication of syntocinon is
uterine hyperstimulation or tachysystole.  Hyperstimulation is
by definition having more
than five contractions in ten minutes.
This means there is not enough rest between contractions for the
foetus to maintain
oxygen levels.  Therefore, continuous foetal
monitoring by CTG is imperative.  At 15:00 there was no record
of the foetal
condition since 14:00.  The possibility of
syntocinon infusion with no CTG monitoring would constitute
substandard care of
a severe degree.  When there is CTG
monitoring, its readings should be recorded in the notes showing
heart rates, accelerations,
decelerations, variability and all the
things that one would read from the CTG.
[21] This ensures that a
record of everything that happened is kept because CTGs do fade or
even get lost or are misplaced.
In this case, the partogram was
not plotted in four hours which means there was no foetal monitoring
and when it is plotted it
shows a baseline of 170/140 bpm.  This
shows that the FHR was definitely higher and that the foetus had
tachycardia.
At this point the cervix was fully dilated at
about 16:00 with the head being right into the cervix and there were
no signs of
obstruction.  At full dilation she was now in the
second stage of labour.  At this stage strong contractions are
frequent
making it a potentially dangerous stage of labour.  The
guidelines say that the FHR should be oscillated every five minutes

whereas in the first stage of labour it is done every 30 minutes.
Therefore, monitoring must be increased to pick up any
foetal
distress timeously and act on it.  In this case the baseline
heart rate was 170 and there were decelerations according
to the
partogram.  It seems that foetal distress was going on between
12:00 and 16:00 as the baseline had gone up from 160
at 12:00 to 170
at 16:00.  However, the FHR is written as 150 to 155 in the
assessments which is contrary to what appears
in the partogram.
[22] Dr Murray explained
that there was substantial improvement in the progress of labour in
the last hour of labour which she attributed
to syntocinon infusion.
With that kind of progress, the plan to let her bear down was
correct.  However, in light of
a long labour and foetal
distress, there should have been very careful monitoring during the
second stage to make sure that there
was no foetal distress and to
quickly intervene if necessary.  The next note was at 16:30
under assessment no. 5 in which
it was noted that the patient had
been pushing for 30 minutes with a plan to inform the medical
officer.  The FHR was 150-155
bpm and the medical officer was
informed for a second opinion as the patient had been pushing for 35
minutes.
[23] Dr Murray further
testified that in 2019 while attending this trail she received the
original CTG tracings that were not readable
because they had faded
with some areas being readable.  This was the last hour of the
CTG tracings that were slightly clearer
and she could read the FHR
and the contraction pattern.  She took some pictures so as to
expand the CTG tracings on her cellphone
to enable her to see them
more clearly.  However, the trial was postponed and she
understood that the postponement was to
enable her and Dr Koll to
examine the CTGs together and do another joint minute.  Dr Koll
felt that the quality of the CTGs
was too poor and he was therefore
not prepared to comment on them.  Following the availability of
those CTGs she compiled
an addendum to her initial report with the
latter having been compiled also without some two pages of the
records that were missing.
[24] These included
assessment no.1 which was completed at 09:00.  It reflected that
the labour progress was good with maternal
vitals being normal.
The FHR was 135 – 140 bmp on a CTG and the plan was to monitor
the labour progress and the patient
was to be seen by a medical
officer.  Dr Murray testified that as a matter of fact the
patient was not progressing well.
The nurses had failed to take
note of the fact that at 06:50 at the clinic she had been at 5cm of
dilation already.  Assessment
no.2 was done at 12:00 which
indicated that the progress of labour was good and the FHR was
136-151 bpm.  Vaginal examination
was done and the recording is
that the cervix was 7cm dilated with no show on the glove.  At
14:00 the assessment recorded
poor labour progress with the cervix
still at 7cm dilated.  The heart rate was 140 – 150 bpm
and the plan was to inform
the doctor about the poor progress who
ordered syntocinon noting that it should be started if the CTG was
reactive.
[25] She summarised the
labour progress as follows based on the completed hospital notes.
At 06:50 the patient was at the
clinic and she was 5cm dilated.
At 09:00 she was at hospital where the first assessment records the
cervix at 5cm dilated
with a FHR of 135 – 140 with a plan to do
a CTG monitoring and for her to be seen by a doctor.  There is
no note of
a doctor seeing her.  At 10:00 the partogram reflects
a cervix that was 5cm dilated and the heart rate was reflected as 135

bpm with no decelerations.  At 10:30 the heart rate was 130 bpm
with no decelerations.  At 12:00 the partogram shows
a 7cm
dilation and a FHR of 160 before a contraction and 140 after
contraction with no decelerations.  She pointed out that
this
was a contradiction.  Assessment no.2 at 12:00 reflects a FHR of
136 to 151 bpm.  Therefore, the two entries both
at 12:00 are
different.  The partogram suggests decelerations but assessment
no.2 says something else and the heart rates
are different.  At
14:00 the partogram shows 5cm dilation with no regard to the heart
rate.  However, according to assessment
3, the dilation was
7cm.  Therefore, there was a discrepancy in the state of the
cervix.  There was no evidence of a
reactive CTG at 14:00.
The CTG of that time is unreadable.
[26] At 15:00 the
partogram shows 7cm dilation but the heart rate is not recorded.
The doctor’s note shows a dilation
of 7cm at 15:00 but no
mention is made of the heart rate.  The doctor ordered
syntocinon to be administered if the CTG was
reactive.
Unfortunately, at 15:00 the CTG is unreadable and no recording of its
reading at 15:00.  At 16:00 the partogram
says the cervix was
fully dilated with two strong contractions in 10 minutes.  For
the most part it stays under the 110 beats
per minute.  She
explained that at about 16:20 it goes up to 140 but immediately falls
down to 85.  It then goes up to
145 or 150 and then falls down
to another deceleration of 90.  So from two to three minutes
past four the FHR fell into a
sustained bradycardia, falling as low
as 60 bpm for at least 5 minutes after which there is a pattern of
recurrence probably late
decelerations which failed to stabilise at a
normal baseline.  This means there was very little recovery.
[27] At about 16:06 there
was a prolonged deceleration of about four to five minutes and
ongoing recurrent decelerations.
For 20 minutes the FHR was
severely abnormal with a pathological CTG tracing.  This was
indicative of severe foetal hypoxia
and probable acidosis at this
time.  The second abnormality on the CTG was in respect of the
contractions at 16:05 and 16:15.
There were eleven
contractions in 10 minutes.  So there were as little as 15
seconds between contractions at times meaning
there was no rest.
There was one contraction immediately after another contraction.
This was severe tachysystole which
means too many contractions which
caused a pattern of severe distress.  In those circumstances
assessment no.5 ought to have
reflected a foetal condition of severe
distress or some indication that the foetus was in trouble.
However, it appears that
it was not noted as it is not recorded
anywhere.  It appears that save for the notes on the partogram,
nobody realized the
abnormality in the heart rate.
[28] Then at 17:00 there
is a delivery with vacuum extraction sheet indicating that the doctor
did vacuum extraction at 17:00.
She pointed out that it was
correct for the vacuum extraction to be done which in any event
needed to be done much earlier.
The doctor noted that at 17:00
the heart rate was initially good but then there was tachycardia.
The indication that the
heart rate was initially good was misleading
because for an hour prior to the vacuum extraction there was no
indication of the
heart rate being good.  Perhaps the heart
recovered to a tachycardia but still the severe decelerations were
not recognised.
Another discrepancy is that the time of birth
was reflected as 17:10 in some places and 17:34 in others.
Whichever the correct
delivery time was, what becomes clear is that
for at least an hour prior to delivery there was a pattern of severe
distress which
was not acknowledged anywhere in the hospital notes.
[29] Had the partogram
been plotted correctly including while the patient was still at the
clinic at 06:50 am the progress of labour
would have crossed the
action line by 13:00.  This would have necessitated an
assessment by a doctor and some intervention,
be it allowing more
time, rupturing membranes, oxytocin infusion or performing a
caesarean section. Despite the progress of labour
crossing the action
line at 13:00 intervention in the form of oxytocin was only taken at
15:00.  Oxytocin intervention depended
on a good foetal
condition.  However, at 12:00 the partogram and the records do
not correlate.  The partogram was suggestive
of decelerations
whereas the records were indicating a normal heart rate.
Unfortunately, the CTG is unreadable to ascertain
what the situation
was at 12:00.  Even at 16:00 there is a discrepancy between the
partogram and the notes.  The partogram
indicates foetal
distress in the form of tachycardia and late decelerations and the
records indicate a normal baseline heart rate.
The CTG tracings
from 16:00 are readable and they confirm severe foetal distress.
Clearly the indication of a normal
heart rate was misleading.
This means that at that time what was recorded in the partogram was
correct.  This suggests
that the partogram at 12:00 might be
correct in which case there were decelerations from as early as
12:00.  She then testified
that there was a complete failure to
recognise the tachysystone and the foetal distress.  This
resulted in the foetus being
left in utero for a further hour and
probably it was during this time that the hypoxic injury was
sustained.  This is illustrative
of a severally substandard and
dangerous obstetric care in a high risk labour.
[30] It was put to her
under cross-examination that according to Dr Koll and his
understanding of the notes there never was a time
when there was an
indication for a caesarean section as there was adequate progress.
She testified that she disagreed with
that because labour progress
was inadequate for the following reasons.  The patient arrived
at 06:50 being 5cm dilated [at
the clinic] and five hours later at
12:00 she had made only 2cm of progress.  She then referred to
the guidelines where it
is stated that “poor progress in the
active phase of labour:  There is poor progress and the cervix
dilates at a rate
of less than 1cm per hour in the active phase”.
Therefore, if she was 5cm at 06:50 and was 7cm at 12:00 she had only

made 2cm of progress in five hours.  Therefore, according to the
guidelines there was poor progress.  There were also
multiple
discrepancies in the records between what was recorded in the
partogram and what was written in the assessments which
would lead to
the inevitable confusion about the foetal condition.
[31] The next defendant’s
witness was Dr Gericke.  He testified that he is a registered
specialist paediatrician and
a specialist medical geneticist.
He had an interview with the plaintiff and did a clinical genetic
examination of the child,
A.  His interview with the plaintiff
did not reveal any information that raised any issue of concern.
He testified that
on 19 November 2019 he saw the child who had a
global neurodevelopmental delay with dyskinetic cerebral palsy.
There were
no external features present which would indicate the
possible existence of an underlying clinical genetic disorder or
chromosome
disorder.  He saw the imaging report of professor
Andronikou which was done on 19 June 2018.  The scan essentially
indicated
two main things.  Firstly, it was a mixed type injury,
a profound type of brain injury.  There was also the possibility

of other conditions.  He explained that genetic conditions are
inherited conditions.  They can include all kinds of genetic

syndromes or structural brain disorders.  On the other hand
genetic metabolic diseases are biochemical processes gone wrong
in
the body which are inheritable and which can mimic cerebral palsy.
He then discussed his addendum report which he compiled
after he had
received the results of blood tests that were done to exclude certain
conditions.  His conclusion was that there
was no genetic
predisposition which had been clinically indicated.  Before Dr
Gericke could be cross-examined it transpired
that there was some
engagement between the parties’ genetic experts for purposes of
concluding a joint minute.  This
necessitated the
cross-examination of Dr Gericke to be put in abeyance.
[32] In the meantime
professor van Toorn was called.  Plaintiff’s counsel
brought to the court’s attention that
professor van Toorn, the
plaintiff’s paediatric expert witness had filed a supplementary
report which dealt with a report
filed by professor Rothberg, the
defendant’s counter-part.  In dealing with professor
Rothberg’s report he touched
on an number of issues like
macrocephaly and the significance of apgar scores both of which he
said on their own they were not
decisive of anything.  He
testified that the foetus was exposed to a lack of oxygen for
prolonged periods, possibly hours.
This, he said was with
reference to professor Adronikou’s report which talked about
prolonged partial brain injury to the
middle part of the brain.
So there was a pattern of prolonged partial lack of oxygen for an
hour or even longer which was
severe and sustained which culminated
in the injury where the central structures of the brain were
compromised.  As a result,
there were many signs of severe
neurological compromise like the baby being born flat, needing
resuscitation, lethargy, not sucking,
difficulty to arise and
neonatal seizures.  He felt that the apgar scores as they appear
on the records were assisted because
of the bag mask ventilation that
was performed.  There were signs of significant compromise with
the baby staying in hospital
for 11 days whereas healthy normal
babies get discharged within the next day or so after a vacuum
delivery.  He was of the
opinion that the use of bag mask
ventilation was indicative of secondary and not primary apnoea.
The importance of secondary
apnoea which led to bag mask ventilation
was that the foetus stopped breathing while inside the mother, in
other words the baby
was deprived of oxygen during the labour
process.
[33] He then went on to
discuss the lethargy, grasp reflex and lack of sucking.  He
explained that encephalopathy implies a
child with a depressed brain.
In this case there was no evidence of serial neurological examination
on days two and three which
made it difficult to assess the severity
of the encephalopathy.  Absence of the suck reflex was a sign of
a moderate neonatal
encephalopathy so was the lethargy.  On day
four the speech therapist could not wake up the child.  He was
of the opinion
that all these taken together were signs of a mild
evolving to a moderate degree of encephalopathy.  He agreed with
professor
Rothberg’s view that hypoxic ischemic encephalopathy
usually results in seizures within the first three days of life.

However, there were no notes or very little notes on days two and
three in the life of this baby.  He then postulated that

diagnosing seizures in the context of hypoxic ischemic encephalopathy
can be challenging and are often underdiagnosed.
[34]
He then referred to Volpe
[1]
who
says that even medical staff may have difficulty in diagnosing
epileptic seizures at an early age because of the subtle nature
of
the seizures in young babies which manifest in things like blinking,
lip smacking, tonic seizures where the baby goes stiff
or subtle
jerks to myotonic seizures.  It may well have been tonic
seizures when the baby was arching backwards or having
episodes of
intermittent extension.  These may have been manifestations of a
compromised brain or neonatal seizures.
There was also no blood
sugar documentation in the critical first three days of life.
He explained that the brain injury
pattern of a prolonged partial
nature as professor Andronikou reported was consistent with low blood
sugar levels resulting in
injury in the thalamus area of the brain.
He explained that intra-cranial haemorrhage as a cause of neonatal
seizures could
be discarded as there was no evidence of any
inter-cranial bleeds.  Similarly, hyperbilirubinemia which is
brain injury that
occurs when a baby is very jaundiced shortly after
birth could also be discarded as a cause of this child’s brain
injury.
[35] The next witness
called by the plaintiff was professor Smith.  He testified that
he is the head of the neonatal intensive
care and neonatal care at
Tygerberg Children’s Hospital.  He testified that in his
view this baby was born with in secondary
apnoea because she was born
flat with no efforts of breathing which led to manual breathing
support.  This would be in keeping
with the bradycardia that the
baby probably had and the low apgar scores underscore this point
although appear to have been changed
from 1 to 2.  He testified
that in terms of the guidelines, the baby’s care, following a
successful resuscitation should
have been escalated to a higher level
of care.  This did not happen.  With reference to the
hospital records where at
07:30 on 01 January 2016 the note read that
the baby was crying, poor latching, was hungry.  He understood
this to mean that
the doctor regarded the inability to latch and
crying as being hungry.  He considered the crying to be
attributable to irritability.
There was cerebral irritation.
There is no record showing vital observations performed between the
31 December 2015 and the
4 January 2016 other than recording body
temperatures and pulse rate.  Blood sugar level which should
have been checked and
maintained was not checked.  Blood sugar
level was checked for the first time late on the 4 January 2016.
There should
have been frequent assessment of fluid balance which was
not done.  Renal failure exclusion was never done.  The
serum
phosphate and calcium level was only done on the 4 January
2016.
[36] The baby required
good observation in the first hours after the delivery.  It is
that observation that may lead to the
infant case being escalated.
These are also necessary to prevent secondary insults to the foetal
brain.  This is also
done by checking blood sugar level as the
most basic bedside investigation to diagnose hypoglycaemia.  If
you detect them
you institute treatment to prevent another drop and
maintain stable levels of blood sugar.  It was also not
sufficient to
simply say the baby is sucking well, they should have
recorded how long did the sucking take place.  He testified that
the
speech therapist saw the baby at 15:30 on the 4 January 2016.
Her report indicates a clear level of depressed consciousness.

She reported on an abnormal oral mouth and tongue movements.
The baby was difficult to wake and recommended a syringe feeding.

The speech therapist reported on many other problems she observed at
that stage.  He testified that the baby going on occasional

extensions were in his view, typical tonic posturing or tonic
seizures.  Therefore, seizures were there but not recognised
as
such.  The report of the speech therapist indicated that she
also noticed that the baby was jaundiced.
[37] He testified that
the baby had a mild encephalopathy which is ascribed to intra-partum
asphyxia which therefore is hypoxic
ischemic encephalopathy.  He
and professor Rothberg agreed that it was initially stage 1
encephalopathy which evolved to stage
2.  The baby must
therefore have deteriorated at some point before she was seen by the
speech therapist on the 4 January 2016
at 15:30. The difficulties in
waking up the baby indicated deterioration in the level of
consciousness which the attending staff
did not pick up until the
neurological challenges with the baby were highlighted by the speech
therapist.  It was from this
point that care was escalated.
They could not have picked up the deterioration in the neurological
status of the baby as
they did not perform proper assessments.
He then referred to the doctor’s note referring to brain
swelling which he
said was in keeping with intrapartum sustained
asphyxia because brain swelling developed three to five days after
the insult which
is what happened in this case.  The baby
exhibited the typical case of an early onset of neonatal
encephalopathy of a moderate
degree probably due to intra-partum
sustained hypoxic ischemic injury.  He and professor Rothberg
agreed that there was no
infection that contributed as a cause to the
outcome of the baby and the development of neuro disability.  He
explained that
there was no way of explaining the compromised baby at
birth and the subsequent neurological compromise besides intrapartum
asphyxia.
[38] Professor Smith
further testified that he and professor Rothberg, the neonatologist
of the defendant entered into an amended
joint minute in which there
was agreement on the following issues.  They agreed that the
baby developed and presented with
mild hypoxic schemic encephalopathy
between birth and around 16:29 on 3 January 2016.  The baby
would not have qualified for
therapeutic hypothermia or cooling
during the first six hours of life.  The foetus suffered
intrapartum hypoxic ischemia.
The baby’s neurological
condition, the encephalopathy worsened around the 4 January 2016.
The MRI report of professor
Andronikou described features consistent
with combined partial prolonged and acute profound hypoxic ischemic
injury.  However,
the report also indicated that the MRI pattern
may be seen with toxic, metabolic and post infectious causes.
The infection
as a probable causal factor in the aetiology of the
baby’s encephalopathy has reasonably been excluded.
[39] There were also
disagreements between himself and professor Rothberg.  They
disagreed on the interpretation of the baby’s
head
circumference at birth and its implications to this matter.
Whether or not there was a macrocephaly, that is a large
head or
megalocephalic head.  He was of the view that there are no
independent head circumference values for the new borns
in South
Africa.  Some ethnic groups have large head circumference than
others.  He testified that the ratio of the head
circumference
over the weight of the baby at birth was 0.01 which was normal and
therefore proportional.  His conclusion was
that it was unlikely
or improbable that the baby suffers from megalocephaly or
macrocephally.  In any event subsequent metabolic
and genetic
investigations found no associated causal aetiological factors.
He went on to say that professor Andronikou made
no finding of
congenital anomalies of the brain or anatomical abnormalities.
[40] He disagreed that
after the evening on day 1 the neonate was well except for the
problem with latching.  His view was
that the recommended
systematic observations were not done, there was no neurological
assessment performed at 22:34, there was
poor latching and the baby
being hungry.  At 07:30 the next norming the records showed that
the baby was crying, there was
poor latching and she was hungry.
He was of the view that this condition of the baby was attributed to
hunger, mistakenly.
There was cerebral irritation and the baby
was unable to latch properly and suck due to the encephalopathy.
Therefore, the
nurse’s note at 17:10 on 01 January 2016 was not
in keeping with a baby who was sucking well as there were repeated
references
by the doctor at 22:34 the previous evening to the baby’s
inability to suck hence there was cup feeding reference at 07:30
on
the 01 January 2016 in the morning, cup feeding on 16:33 on 02
January 2016 and at 03:35 on 03 January 2016.  This taken
with
the evidence of the mother it was likely that there was inability to
latch and suck.  He was of the view that there were
very poor
observations and assessments.
[41] He explained that
progressive HIE signs were there but were only picked up for the
first time on the 04 January 2016.
They both agreed that there
was mild hypoxic ischemic encephalopathy but in his view on the 4
January 2016 it was of moderate degree.
He referred to the plan
to perform hemugluco test (HGI) blood sugar level which was not done
and he described that as being substandard.
There was no record
that blood sugar level was checked before the 4 January 2016.
New borns who suffer intrapartum asphyxia
are prone to develop early
neonatal hypoglycaemia and hypoglycaemia is an independent brain
injury factor.  There is a significant
overlap between brain
injury patterns of hypoxic ischemic nature and patterns related to
neonatal hypoglycaemia.  Therefore,
a contributory role for
hypoglycaemia cannot be excluded.
[42] Professor Smith
further testified that looking at a photocopy of the CTG trace, a
pathological foetal condition was present
around 16:00, a grossly
pathologic trace was in keeping with foetal hypoxia and acidosis.
There were excessive uterine contractions
per time interval.
The nurse’s note that before birth there had been no foetal
distress was in contradiction with the
recording of the doctor who
performed the vacuum extraction around17:05 to 17:10 who recorded
that the FHR was initially good then
tachycardia.  There were
also entries in the partogram showing foetal tachycardia before
contractions at 16h00.  The
baby was diagnosed with hypoxic
ischemic encephalopathy as the reason for her neonatal
encephalopathy.  HIE is usually preceeded
by foetal distress
during labour manifesting with detectable abnormal heart rate as it
occurred in this case.  He and professor
Rothberg disagreed on
whether expedited delivery or intrapartum obstetric management would
have avoided the neurodisability.
He was of the view that
substandard intrapartum obstetric care directly contributed to the
child’s neurological disability
and that timeous expedited
delivery would have avoided the outcome.  Furthermore, had
proper neonatal care been done the possibility
of aggravating factors
such as hypoglycaemia contributing to the outcome would have been
avoided.  Professor Rothberg agreed
that in the absence of the
family history in this case there would likely have been little to
argue other than the presence and/or
severity of foetal distress.
[43]
Dr Gericke, the plaintiff’s geneticist was called to continue
with his evidence on the basis that a joint minute had
since been
entered into between himself and the defendant’s geneticist,
professor Christianson since his previous evidence.
Dr Gericke
testified that when considering a need for genome wide testing or
other exome sequencing, according to a paper
published in 2019 on
genetic mimics of cerebral palsy
[2]
,
there are eleven indications that must be present for genetic and
metabolic conditions in a patient presenting with symptoms of

cerebral palsy.  He said that because none of these indications
were present in this child, further whole exome sequencing
or genome
wide sequencing was not indicated.
[44] Dr Genicke testified
under cross-examination.  He testified that there are five
levels of motor disability according to
the GMFCS classification and
he considered the child in this case to have a level 4.  He
explained that stage 4 would mean
the child can move with some
assistance but would probably require to be carried or moved around
with some form of support like
a wheelchair.  He explained that
the classification system uses a scale from one which is the least
disabled to five which
is the most disabled.  He said that GMFCS
stands for Gross Motor Function Classification System.  This
child was at GMFCS
4 cerebral palsy which indicates a severe level of
motor muscle disability.  He examined the child on 19 November
2019 and
he based his opinion on the examination that he conducted on
that day and his assessment was that the child was at GMFCS 4 level.
[45] He was then referred
to various reports by other experts.  He was referred to a
report by professor van Toorn dated 26
November 2018 in which he
concluded that the child was GMFCS1.  In his report professor
van Toorn explains that at GMFCS 1
the child can floor sit with both
hands free to manipulate objects, movements in and out of floor
sitting and standing up performed
without adult assistance.
These children walk as a preferred method of mobility without the
need for any assistive mobility
device. He agreed that the above
description was not of a patient with a cerebral palsy that is at
GMFCS 4.  He explained
that he would not differ with professor
van Toorn.  He therefore, did not know why on that particular
day, the child appeared
to be in the condition which led him to
classify her as level 4.  Dr Gericke was then referred to the
report of Dr Freda van
Rensburg which was dated in November 2019 the
same month as his report in which Dr Freda van Rensburg concluded
that the child
was totally mobile without any help.  He conceded
that there was a huge difference in these two assessments.  He
said
that he could not explain why on that day that he saw the child
he got the impression that she was at level 4.  He then said

that he deferred to paediatric neurologists and was prepared to
accept that the child was actually at level 1.  He then said

that the court could disregard his conclusions with regard to the
level of disability of the child.
[46] Dr Gericke was then
referred to his report where he said that the child has a history of
early convulsions occurring shortly
after birth or in the first week
neonatally.  He testified that he also concluded that the child
had a standard 3 neonatal
encephalopathy but said that was based on
his assessment of the child being GMFCS level 4.  He now
accepted that the child
was GMFCS level 1.  He explained that
neonatal encephalopathy is graded 1, 2 and 3 with 3 being the most
severe form of neonatal
encephalopathy usually characterised by the
presence of convulsions, disturbed consciousness and the presence of
neurological features.
It was put to Dr Gericke that some of
the information in his report like the baby having been hospitalized
for three weeks or longer
did not refer to the baby in this matter.
He then said that he was accepting that some of the information from
two separate
patients may have been included in the bundle he was
working on.  He explained that information from two different
patients
was entered into the historical findings in his report in
this matter.  He, however, maintained that the clinical genetic
findings and conclusions were correct and were applicable to the
child in this matter.
[47]
He testified with reference to the report of professor Andronikou
which says that the pattern of injury in this patient can
also be
seen with toxic, metabolic and post infectious causes.  He
confirmed that because of the non-progressive evolutionary
cause of
neurological feature in this child, if the toxic, metabolic and post
infectious causes were present, there would have
been a loss of
previously acquired skill.  This is because cerebral palsy is
static.  He therefore concluded that there
was no variation in
the features of this child and therefore genetic testing was not
indicated.  The question is, is there
a recurring genetic
problem or is there a possibility of a recurring mechanical problem
during labour.  Therefore, before
consideration is given to
genetic causes, one must consider a possibility of prolonged second
stage of labour associated with obstructed
labour and a relatively
large baby in a smaller sized mother.  There are specific
indications which he mentioned before, for
genome wide sequencing or
whole exome sequencing.  None of those eleven indicators are
relevant to this child.  His first
concern even before getting
into a genetic disorder was the obviously very short mother with
likely insufficient pelvis known as
cephalopelvic disproportion or
CPD for a normal delivery.  The second consideration in the
indication for a genetic test is
the absence of an incriminating
birth history which the obstetricians have indicated was a prolonged
second stage and foetal distress
before delivery.  Lastly, the
baby was delivered with a neonatal encephalopathy.  He found
nothing in the examination
of the child that would indicate a need
for further testing.  The results from Centogene
[3]
were negative.
[48] Dr Gericke was
cross-examined on the defendant’s case about genetic testing.
He started by explaining that a rather extensive
genetic testing has
already been done and it excluded a large amount of candidate genetic
disorders.  The next genetic testing
would be genome wide
sequencing (GWS).  The problem with it is that its clinical
utility could be for about five percent of
individuals with cerebral
palsy.  The information that is then generated from GWS creates
a large amount of variants of unknown
significance which may have no
bearing on the problem at hand.  If a variant of unknown
significance is found it requires
protein structural analysis to
elucidate its relevance.  Therefore, the fact that Centogene
says further investigations are
necessary or many be helpful, is a
comment that laboratories make routinely if an answer has not been
found.  But in a clinical
setting one would not go for GWS after
a large number of specific biochemical and genetic structural
disorder which could be relevant
to the patient’s problem have
been exhaustively excluded.
[49] It was put to him
that the plaintiff has had four pregnancies.  Two of those were
boys and they died, the first one reportedly
after birth and the
second one a stillborn.  There are two girls, the child A and
the last girl child.  Both suffered
seizures days after birth.
He confirmed that of the eleven indications for genetic testing at
least one of them must be there.
With regard to the family
history of the four children, there is no clinical information about
the problems the other children
suffered from.  In order to
establish that there is a causal contribution of a genetic factor to
a cerebral palsy outcome,
there must be a direct pathway that can be
inferred from the genetic abnormality to a cerebral palsy.  In
this case there
were obstetric problems with the delivery which were
an excluding factor for genetic testing.
[50] The other witness
for the plaintiff was professor John Anthony.  He testified that
he is a qualified gynaecologist, a
registered subspecialist in
maternal and foetal medicine and the head of maternal foetal medicine
unit at Groote Schuur Hospital.
He was a nominated South
African representative in a multinational panel of experts which
produced a paper on intrapartum FHR monitoring
on behalf of the
International Federation of Obstetricians and Gynaecologist which was
published in 2015.  He testified that
the occurrence of labour
for the foetus represents possibly the single most dangerous time in
pregnancy.  The baby on average
needs about 2 to 3 minutes
between contractions to allow the choriodecidual space to fill with
fresh blood.  If anything is
done to increase the frequency of
the uterine contractions by giving the mother oxytocin or
prostalglandins, the time between contractions
during which the body
can extract more oxygen as the uterus relaxes is reduced.  This
may increase the risk of the baby becoming
hypoxic and acidotic
during the course of the labour.  In addition, there are other
things that happen physiologically like
when the mother goes into the
second stage of labour.  This is when the cervix is fully
dilated and the birth process actually
begins as the baby begins to
descend through the birth canal.  In those situations, the
mother has a desire to push or bear
down.  This pushing
increases the pressure inside the uterus.  The injunction that
comes from the international and national
guidelines is that during
the second stage of labour, the foetal well being needs to be
assessed, not every half an hour as it
is during active labour but
every five minutes or after every second contraction.  This is
because during this period the
foetus is vulnerable.
[51] He then testified
that he and Dr Koll agreed on the facts recorded in the clinical
records.  Some of those facts were
that her last menstrual
period had been on 13 April 2015 and therefore her due date would
have been on 18 January 2016.  However,
she went into labour on
31 December 2015.  She therefore delivered just over 37 weeks
gestation which is term.  Her examination
was normal.  At
151cm tall her height would not arouse any particular obstetric
concern.  It is at less than 150cm where
she could be regarded
as particularly short.  All her vital signs were normal.
Her body max index was normal.
As a result the only issue of
concern was the child who died.  Routine investigations were
performed and were all normal and
the screening test for HIV was
negative.  There was no problem during the antenatal period.
The plaintiff then presented
at the clinic just before 07:00 in the
morning on 31 December 2015.  She complained of abdominal pain.
On vaginal examination
her cervix was 5cm dilated.  The FHR
which they listened to at the clinic was 124-126 bpm and contractions
were palpable.
The plan was to refer to hospital.
[52] The plaintiff then
arrived at hospital at 09:00 in the morning.  It was noted that
she had been referred from the clinic
and that she had been
experiencing pain for seven hours which was from 2 o’clock in
the morning.  Her cervix was still
5cm dilated.  The FHR
was recorded as 135-140 bpm.  It was indicated that the heart
rate was derived from a CTG.
It was evident that they did not
have any concern about the foetal well-being at 9:00 and they were
happy with the CTG.
[53] The next assessment
was at 12:00 midday.  At that time the cervix was 7cm dilated.
The attending staff felt that
the progress of labour was good.
They wrote a FHR of 136 to 151 bpm.  At 12:50 the notes
indicated that her membranes
ruptured spontaneously and that the
liquor was clear.  The FHR was recorded as 136 to 150.  At
14:00 the cervix and the
vaginal examination were done and she was
still 7cm dilated.  The nurses noted that the progress of labour
was poor and the
FHR at that stage was 145-150 bpm.  These
findings were discussed with the doctor on call who ordered the
administration of
syntocinon and said that if the CTG was reactive it
could be started.  In terms of the guidelines the administration
of syntocinon
requires an assessment of the foetal well-being before
it is infused.  This is because it can cause an increase in the
frequency
of uterine contractions and can lead directly to foetal
distress.  At 15:00 another examination was done and the cervix
was
found to be still 7cm dilated.  Now over a period of three
hours from 12:00 the cervix was still 7cm dilated.  An
assessment
was made that the plaintiff had crossed the action line
and the oxytocin was prescribed and a catheter was to be inserted and
the
management was to proceed provided the CTG was reactive.
[54] A patient can spend
up to 8 eight hours in the latent phase of labour without much sign
of cervical change and no rapid cervical
dilation without there being
any problem.  Once the patient is in the active phase of labour
it is expected to progress at
a recognisably rapid rate.  So
there are two lines drawn at an angle on the partogram.  The
first line is the alert line.
This line exemplifies a cervical
dilation taking place at a rate of 1cm per hour.  The second
line which is drawn parallel
is called the action line.  If a
woman in labour gets into the active phase of labour and starts out
in alert line but then
falters during labour and the rate of cervical
dilation does not take place at 1cm per hour and it crosses that
action line, that
indicates that there may be a problem requiring
further assessment.   So the people who assessed her at
15:00 decided
that she had crossed the action line and decided to
augment the contractions by prescribing oxytocin.  At 16:00 she
was having
very strong contractions.  When she was examined she
was now fully dilated and she had an urge to bear down.  The
notes
say that the FHR was 150 to 155 and the CTG was reactive.
[55] A reactive CTG is a
term used to imply that the CTG tracing is normal.  The plan of
the nursing staff was to get ready
for delivery and to let the mother
push.  At 16:30 they called the medical officer and said the
plaintiff had been pushing
for 35 minutes and the baby had not yet
been delivered.  They wrote down that the FHR was 150 to 158.
Then at about
17:00 the medical officer had arrived and proceeded to
deliver the baby using vacuum extraction.  A woman in her second
pregnancy
delivering vaginally for the second time, from the time she
starts bearing down should deliver within 30 minutes.
Therefore,
under those circumstances it would have been correct to
say the second stage was prolonged and therefore consideration of an
instrumental
delivery was correct.  Also if foetal distress had
been diagnosed, it too would have been valid indication for an
instrumental
delivery.  The vacuum extraction seemed to go
without any complications and it took two pulls and it lasted five
minutes and
the baby was delivered vaginally.
[56] The partogram was
incorrectly plotted in the latent phase and began at 09:00.  The
06:50 examination at clinic was not
entered where it should have been
which was in active labour part of the partogram.  The first
examination at the clinic when
the patient was 5cm dilated ought to
have been considered as active labour and considered as being the
first plot on the active
phase labour part of the partogram.
The first indication that the patient had crossed the action line
would have been at
12 o’clock.  However, on the partogram
that diagnosis was not made until 15H00, some three hours later.
Any patient
who is not progressing in labour needs to be assessed
carefully and the reason for the slow progress needs to be found.
In
first phase of labour where slow progress is found, a deliberate
examination must be done to make sure that there are no signs of

cephalopelvic disproportion (CPD).  A parous woman with a slow
progress should lead to immediate, very critical assessment
of the
labour to look for signs of disproportion and in such circumstances
oxytocin should only be prescribed after such examination.
This
is also stated in the guidelines.
[57] The heart rates that
were charted in the active phase of labour reflect ‘o’s
and ‘t’s.  These
refer to the heart rate before and
after contractions.  The FHR on the partogram was only recorded
at 12:00 and then again
at 16:00.  The requirement is that
during active labour the heart rate must be observed before and after
contractions every
half an hour.  If the partogram began at
09:00 there should have been observations at 09:00, 09:30, 10:00,
10:30, 11:00, 11:30,
12:00 when it took place, 12:30, 13:00, 13:30,
14:00, 14:30, 15:00, 15:30 and 16:00 when it took place.  So the
number of
observations was clearly not according to the prescription
that exists for patients who are in spontaneous and even completely
normal labour.
[58] Professor Anthony
explained that CTG tracings are divided into three categories.
One is normal, the second category is
called suspicious and the third
category is called pathological.  If the tracing falls into a
pathological category, there
is a high probability that the baby is
hypoxic and acidotic.  In this case the CTG was pathological.
There was a very
prolonged FHR deceleration beginning shortly after
16:00 which lasted for more than three to five minutes.  That on
its own
was so abnormal that the tracing was pathological with a high
probability that the foetus was hypoxic or acidotic.  There are

three main situations that may arise leading to a hypoxic
environment.  It is the uterine contractions.  If this is
followed by the mother pushing, there is even less blood flowing into
the choriodecidual space and the baby is in further trouble
in terms
of oxygen supply.  Then a further problem is when oxytocin is
administered thus making uterine contraction more frequent
than it
should.  What should then happen in that situation is that the
foetus should be taken out of the hypoxic environment
through
instrumental delivery.  Oxytocin should be stopped and the
mother should be stopped from pushing.
[59] At the time of the
pathological tracing there should have been an immediate action to
correct reversible causes of intrauterine
hypoxia followed by
expedited delivery.  The contractions are stopped by means of
tocolytic drugs that relax the uterus.
The CTG tracings show
many contractions which may have been aggravated by the mother being
encouraged to push when she was in the
second stage of labour.
Both the use of oxytocin and the maternal bearing down efforts should
have been stopped pending further
assessment and to allow restoration
of foetal oxygenation by means of intrauterine resuscitation prior to
expedited delivery.
There are tocolytic drugs, putting the
mother on her side to optimise perfusion of the uterus and also to
give her face mask oxygen.
Those are the components of
intrauterine resuscitation.  He testified that seemingly the
pathological tracing was not recognised
as a result of which the
necessary intervention did not take place.  This was substandard
care which was directly linked to
an increased likelihood of an
adverse outcome.
[60] Tachysystole, is too
many contractions or more than five contractions per 10 minutes.
The decision to allow the mother
to push in the face of the
pathological tracing was substandard care which would have increased
the risk of hypoxia.  The
requirement is also not just to
auscultate the FHR before and after contractions and to plot on the
partogram.  There has
to be the process of interpreting what is
found.  It is not good enough to do a CTG if it is not
interpreted.  The fact
that the CTG is running is in and of
itself insufficient for monitoring foetal wellbeing.  There was
no adequate interpretation
and the mother was allowed to push.
He said that to describe a FHR that varied between 170 and 140 bpm at
16:00 as being
normal or reactive was beyond belief.  The
uterine tracings showed tachysystole, severe recurrent decelerations
and a pathological
tracing.  The nurses called the doctor after
35 minutes of bearing down without any recognition of abnormality,
and no attempt
was made to curtail uterine contractions and no
intrauterine resuscitation was done.
[61] Professor Anthony
talked about inherent difficulties associated with monitoring the
condition of the foetus during the second
stage of labour and the
danger of interpreting badly faded tracings, a postulation of Dr
Koll.  He said that decelerations
happen during the second stage
of labour but of importance is that they should not persist after the
contraction.  If they
persist after the contraction they are
more consistent with a diagnosis of hypoxia than compression as the
head moulds through
the birth canal.  The nursing staff were
required to listen to the heart rate after contraction.  If they
hear a slow
heart rate after the contraction they will notice if
there are decelerations.  He agreed with Dr Koll about the
danger of
interpreting badly faded tracings.  However, the fact
that the tracing is faded does not mean it is always going to be
impossible
to discern anything from it.  He said if one looked
carefully at pages 39 and 40 of bundle 1G using a good light you will
be able to make out the FHR pattern and the contraction pattern.
[62] On the issue of what
is called loss of contact, Dr Koll said that in the second stage of
labour the patient is often moving
about in pain, causing loss of
contact between the probe and the foetal heart which may affect the
tracing.  While that is
true during labour the mother
hyperventilates which may cause loss of focus on the FHR as she
pushes which may disrupt the tracing
to some extent, that does not
validate what one can see and it does not make the tracings
completely uninterpretable.  He
then dealt with Dr Koll’s
statement that during the second stage of labour the foetus will
often experience periods of hypoxia
resulting in abnormal FHR
patterns that would be quite alarming if found during the first
stage.  Professor Anthony said if
there is evidence of hypoxia
no matter how it occurs, there is an obligation to act by
resuscitating the baby and expediting delivery.
On variability
he said this is where the baseline wiggles about before there is
acceleration or deceleration in the heart rate.
When it does
not wiggle about as it should, when it is a flat line, that is
usually consistent with a diagnosis of hypoxia.
The diagnosis
of hypoxia is based a several issues like, what is the baseline,
variability, are there decelerations and what is
their nature, are
there accelerations present.  All of those are components of an
assessment of the trace and variability
on its own does not define a
pathological tracing.  He therefore disagreed with Dr Koll that
because the tracing is faded
it is very difficult to make out
variability in the first two minutes and therefore you cannot tell if
the baby is in trouble or
not.  What is clear on this tracing is
that there is a very prolonged deceleration that begins shortly after
16:00 and that,
more than anything else, is an indication of a
pathological tracing.
[63] About the partogram,
professor Anthony explained that the partogram is divided into two
sections.  The first 3
rd
of the graph is the latent
phase of labour which is when the cervix is less than 3cm dilated.
The active phase of labour
on the right hand side of the graph where
there are two parallel lines drawn running from 3cm to 10cm dilation
at a given rate
of 1cm per hour.  At the active phase, labour is
expected to progress at a predictable rate.  If the deviation
goes beyond
the second line which is called the action line, there
must be some investigation to ascertain why the labour is progressing
slowly.
The partogram was incorrectly annotated for two
reasons.  First the examination at about 07:00 in the morning
where she was
5cm dilated which was evidence of second stage of
labour should be the starting point on the graph or on the alert line
and that
should have been plotted.  The starting point
determines the plots that follow to the hourly time intervals.
At 09:00
the plaintiff was still at 5cm dilated which would have been
a plot on the action line.  The next examination at 12:00 showed

evidence of progress from 5cm to 7cm which was a change of 2cm over
three hours.
[64] This was slow
progress and it ought to have been evident at 12:00.  The error
was not to start with the first finding
at the clinic.  Second,
the hospital examination at 09:00 was incorrectly plotted in the
latent phase part of the graph whereas
it should have been plotted on
the alert line as the beginning point.  All of this led to the
delayed progress of labour being
identified later than it should have
been.  By 12:00 it should have been evident that the action line
had been crossed warranting
further investigating.  The
requirement in the guideline is that there should be a critical
evaluation of slow progress in
labour to exclude CPD and foetal
distress.  Either of those events would require an emergency
delivery by caesarean section.
If neither of those clinical
diagnosis is evident, the labour can be allowed to continue.
Other interventions can be considered
like oxytocin.  There was
an indication for an intervention by means of caesarean section
delivery as early as 12:00.
However, the baby was delivered
some five hours later after 17:00.  The ongoing slow progress
together with the evidence of
foetal compromise strengthened the
intervention indications.  Intervention indication was also
evident at 15:00.
[65] He testified that
according to the guidelines a woman who shows slow progress in active
labour, must have foetal distress excluded.
In this case the
doctor initially did not evaluate the plaintiff at 14:00 before
issuing instructions for the use of oxytocin.
She was unaware
that they needed to exclude foetal distress as is clearly indicated
by her indication that CTG should be done first.
The fact that
the doctor examined the patient at 15:00, indicated that oxytocin
should be administered and the putting up of the
Ringer’s
Lactate at that particular time would have been done in order to
administer oxytocin intravenously.  Oxytocin
is known to be
associated with the risk of uterine tachysystole or too many
contractions.  That is why it should be used with
great caution
in multiparas after excluding CPD and there must be no evidence of
foetal distress and CTG monitoring should be used
where possible.
In this case oxytocin was prescribed to a parous patient which is
only done in exceptional cases.  As
a result, tachysystole
became evident.  Professor Anthony testified that he disagreed
with Dr Koll on his view that oxytocin
was ordered with due
precautions in this case.  He said due precautions are those
prescribed by the guidelines which is the
exclusion of CPD and the
exclusion of foetal distress prior to commencing with the drug and
then the monitoring that was required
after the drug was started.
[66] Dr Koll said there
is no evidence that oxytocin was administered.  Professor
Anthony dealt with Dr Koll’s argument
by saying this ignores
the circumstantial evidence of a slow labour progress, the doctor’s
assessment at 15:00 and the instruction
to administer oxytocin, the
establishment of the intravenous fluid entry through Ringer’s
Lactate and finally the more than
five contractions per 10 minutes
interval which is the evidence of tachysystole which is associated
with the use of oxytocin.
In addition, the mother was
encouraged to push which made things worse for the baby which was
also substandard care.  He said
that there was evidence of
abnormal FHR patterns from 12:00 onwards.  The labour was
augmented with oxytocin without proper
assessment.  The second
stage of labour was prolonged with maternal bearing down efforts
despite evidence of hypoxia.
The baby was then delivered in
need of resuscitation and developed seizures during the neonatal
period which then led to a diagnosis
of hypoxic ischemic injury.
Finally, the neuroradiological images were found to be consistent
with the possibility of intrapartum
hypoxic ischemic injury.
His conclusion was that the adverse outcome was therefore consistent
with intrapartum hypoxia which
was avoidable with proper standard of
intrapartum care.  The delivery took place at 17:10 whereas
there were several times
where intervention was indicated well before
the actual delivery.
[67] Professor Anthony
was cross-examined at length.  It was pointed out to him that
when the plaintiff gave birth on 31 December
2015 she was 16 years
old and that in 2014 she gave birth to a child that died soon after
birth.  He accepted both of these
facts.  He also accepted
plaintiff’s evidence that suggested that after the rupture of
her membranes which was at 11:00
she was put on a CTG which was
subsequently removed before she was told to push which would have
been at 16:00 when she was fully
dilated.  He also pointed out
that the CTG was started with the result that the tracings started at
16:02 which coincides
with the time at which she was pushing.
He testified that even if there was a CTG running before 16:00 his
issue was that
the FHR before and after contractions should have been
appropriately evaluated with a provision for electronic FHR
monitoring as
well as the correct interpretation of the tracings.
[68] He explained that
there is a difference between performing an observation and
incorrectly interpreting it.  There seems
to have been a problem
of recording a FHR before and after contractions from about 12:00.
Secondly, at the onset of the second
stage of labour at 16:00, the
nursing staff wrote in their notes that the tracing was reactive when
it was probably pathological
which also points to misinterpretation.
For instance, at 16:00 there were strong contractions and the
plaintiff was fully
dilated with an urge to bear down.  The FHR
was said to have been 150 to 155 and the CTG reactive.  The plan
was to get
ready for delivery and to let the mother bear down.
If all of that is considered together with the CTG that was running
at
that time which was probably pathological, it shows that the
nursing staff did not understand the foetal circumstances because
they misinterpreted the FHR condition.  He said that if one goes
back to 12:00 the partogram shows O at 160 and X sitting at
140 which
is a deceleration.  This means the FHR was slower after the
contraction.  By definition, a deceleration is
a reduction of
FHR of 15 bpm lasting for at least 15 seconds.  If auscultation
monitoring is used, the slowing of FHR after
a contraction merits
further investigation to ascertain that the baby is well.
[69] He agreed that it is
in the nature of CTGs to fade after some time and he agreed that in
this case the available CTG tracings
have faded.  He testified
that he inked the faded CTG tracings so that they could become more
visible.  He said that
he used a good light and a magnifying
glass to discern the components of the tracing to determine the
overall pattern and used
a rollerball pen to mark the tracing to get
an overall picture.  There was quite clearly decelerations from
16:00 onwards
which were discernible.  He then referred to the
guidelines where they deal with foetal monitoring.  There the
guidelines
say after a CTG interpretation, write a note about the
findings in the woman’s notes so that a record of the CTG is
still
available even if the CTG tracing is lost.  He bemoaned
the fact that in this case there are faded tracings and no comment

from the clinical staff on the tracings.
[70] It was put to him
that his enhanced CTG showed a very dire situation.  He
explained that the correct term was a pathological
tracing which is
associated with a high risk or high probably of foetal hypoxia and
acidosis.  If the tracing is pathological,
it is likely that the
baby is hypoxic and acidotic.  However, insult precedes injury
and it is the severity and the duration
of the insult that will
determine the likelihood of the injury.  He explained that one
cannot look at a pathological tracing
and predict the onset of
injury.  Where the baby is inadequately oxygenated there is a
need to intervene to reverse any underlying
hypoxia and to expedite
delivery as soon as possible.  He testified that from the
beginning of the pathological tracing there
are decelerations with no
discermible recovery.  There was evidence of a high probability
of hypoxia towards the end of the
labour which is evident from the
tracings.  The child was born flat and required resuscitation.
All of this was consistent
with a diagnosis of intrapartum hypoxia in
the delivery room.
[71] From 12:00 onwards
there was demonstrably slow progress of labour and beyond the action
line.  At that point there should
have already been a
consideration of the fact that the labour progress was too slow for a
parous labour.  He concluded his
evidence by saying that it
beggars belief that any trained person in any form of midwifery
obstetric care could have looked at
those tracings, faint as they
are, and thought that they were reactive.  They were highly
abnormal tracings and ought to have
been recognised as such.
Proceeding during the second stage of labour with an oxytocin
infusion running with the mother bearing
down for half an hour
without any consideration for the foetal wellbeing was substandard
care.
The defendant’s
factual witnesses.
[72] The defendant’s
first witness was sister Mbada who was called to testify as a witness
of fact.  She testified that
on 31 December 2015 she was on duty
at the labour ward at the hospital.  She was taken through the
hospital records starting
with an entry made at the clinic at 06:50
before the plaintiff was transferred to hospital.  She testified
that the plaintiff
arrived at the clinic at 06:50. On examination she
was found to be 5cm dilated.  The first entry at the hospital
was at 09:00
which was not done by her.  She testified that her
first assessment was assessment no.3 which was at 12:50 by which time
the
plaintiff had a spontaneous rapture of the membrane with clear
liquor being observed and the FHR ranged between 136 to 150 bpm.

She used a CTG machine to determine the FHR.  She noted that the
progress of labour was slow at 14:00.  This was because
the
cervical dilation was 7cm whereas it should have been 9cm.
Therefore, she remained 7cm dilated for two hours as she was
7cm even
at 12:00.  Her plan was to advise the doctor about the poor
progress of labour and she did that telephonically.
[73] At 15:00 the doctor
made a note.  The patient was still at 7cm dilated and the
liquor was clear.  The head was 3
to 4 fifth above the brim.
The plan was to administer syntocinon if the CTG was reactive.
Once the doctor has
ordered syntocinon she also completes a form
indicating how syntocinon administration is to be done.  That
form is then clipped
to the front of the patient’s file.
When it is actually being administered she would tick on that form
indicating that
she has started the infusion according to the amounts
and intervals pre-determined.  But if the patient delivers,
further
infusion is discontinued and there would be a note saying
infusion stopped.  In this case the form was not ticked at all.

This means that syntocinon infusion was never started.  With
reference to the partogram she explained that at 16:00 on the
row
meant for decelerations there is a C symbol.  That symbol stands
for clear liquor.  Putting that C symbol there was
an error.
That symbol should have been written below I even though I should not
be there anymore.  That I stands for
intact membranes.
Where there is an I there should be C instead indicating membranes
draining clear liquor as the membranes
had ruptured.  The O at
12:00 stands for FHR before contraction and X is for the FHR after
contraction.  The O at 160
and X at 140 mean that the FHR before
contraction was 160 and after contraction it was 140.  The early
deceleration goes down
in a V shape after contraction and is expected
to go back to the base line.  The heart is not beating in the
same way it was
before contraction as the contractions have exerted
pressure on it and the oxygen supply is curtailed.  The X would
depict
an early deceleration.  The X and O at 16:00 would mean
the same thing.
[74] At 14:00 the
progress of labour was poor.  At 10:00 until 10:30 the
contractions as depicted on the partogram were lighter
at less than
20 seconds per 10 minutes.  Then the contractions improved to 20
to 40 seconds per 10 minutes and finally the
contractions became
serious at 40 seconds per 10 minutes.  All that is reflected in
the manner in which the partogram is shaded.
The middle segment
of the partogram is between 11:00 and 14:00.  The contractions
were improving slightly.  They were
now above 20 to 40 seconds
per 10 minutes.  Then at 14:00 contractions became stronger.
At 15:15 contractions were strong
and therefore the likehood is that
she did not start administering syntocinon as that is what syntocinon
would have been intended
to achieve.  If it had been
administered, on the relevant block in the partogram where there is
medication IV fluid, syntocinon
would have been written and the time
it was administered.  At 16:00 the patient was fully dilated and
therefore, syntocinon
would not have been administered to a fully
dilated patient.  The baby was delivered, according to the
partogram notes, at
17:34 by vacuum extraction.  That entry
relating to time was when the entry was made.  The entry on
comments and complications
where it refers to prolonged second stage
means that 20 to 30 minutes passed before the baby was delivered.
At 16:00 she
was fully dilated at 10cm which means she was on the
second stage.  The baby was born flat with an apgar score of 6/7
and
7/10 at 1 minute after birth and then at 5 minutes after birth.
She explained that bag mask ventilation was used to give the
baby
oxygen as resuscitation as a result of which the baby recovered.
There would have been stimulation and then bag mask
ventilation.
There was a haematoma caused by vacuum extraction.  The child
was lethargic and the grasp reflex was absent.
[75] She then testified
under cross-examination.  She confirmed that the guidelines
require that there be a clinical record
of everything that is done
and to ensure that all clinical records are complete and accurate as
regards the information they contain.
She confirmed that she
was at all times aware of her record keeping responsibilities as
provided for in the guidelines.  She
testified that she was
trained on how to complete a partogram and how to interprete it
during her training.  She confirmed
that there is poor labour
progress if the cervix dilates at a rate of less than 1cm per hour in
the active phase and crosses the
partogram alert line.  She
further confirmed that the second stage of labour is prolonged if
delivery has not occurred after
after 30 minutes of pushing in a
multipara and that the plaintiff was a multipara.  She confirmed
that if the patient is already
in hospital and crosses the action
line, action is mandatory and therefore there must be syntocinon
infusion or a caesarean section.
She confirmed that she had no
independent recollection of what happened to the plaintiff and relied
on what was written in the
maternity case records for her evidence.
[76] She testified that
the plaintiff would have been in the active phase at 06:50 that
morning because at that time she was 5cm
dilated.  She confirmed
that in this case the partogram was only started at 10:00 with the
dilation being 5cm at the time
and therefore it was not correctly
completed.  She confirmed that she did not pay attention to the
fact that the partogram
was started incorrectly when she took over at
12:00.  She testified that the notes or entries on the partogram
are all hers
save for the ones at 15:00 which were made by Dr
Cilliers.  At 14:00 she recorded that the dilation was 5cm
according to her
partogram entry but that was incorrect because in
her clinical notes she had noted it to be 7cm which was a mistake on
her part
as the patient was actually 7cm dilated at 14:00.  She
confirmed that from 12:00 when she took over monitoring the plaintiff

until she gave birth at about just after 17:00, five hours had
passed.  She testified that it was not possible that from 12:00

she checked the plaintiff once as the partogram seemed to suggest.
She might have forgotten to record on the partogram everything
she
did.
[77] Her first assessment
was at 14:00 according to the assessment notes.  However, she
did make an assessment at 12:50 and
made entries not on assessment
no.3 but on the clinical notes.  The necessity to write on the
clinical notes was caused by
the change with water breaking which she
regarded as a remark as against an assessment even though she did
assess the patient at
12:50. She also did not record that in the
partogram because there was no space and she had already indicated in
the partogram
that the membranes were intact.   She
accepted that she ought to have recorded the FHR on the partogram and
she made
a mistake in not doing that.  She also accepted that
the time at 12:50 was over written as well as the date.  She
testified
that she does her assessments two hourly in the same way
she does with the partogram.  She denied that the entry she made
at 12:50 in the clinical notes was made later than that time.
She wrote it as a remark on the clinical notes and not as assessment

no.3 and the partogram because two hours had not yet elapsed.
[78] She confirmed that
according to the assessment at 12:00 it was done by her colleague,
sister Bingwa but according to the partogram
entry the 12:00
assessment was done by herself.  Her explanation for this
discrepancy was that sister Bingwa was a newly appointed
nurse for
whom it was not easy to remember to make entries both in the
assessment and the partogram.  She then had to fill
the gap.
She testified that all she recorded at 14:00 was that the FHR was 145
to 150 bpm.  There was no indication
of contractions that would
have been observed on the CTG.  There were no decelerations
recorded and there was no indication
whether the CTG was normal or
suspicious.  There were therefore no notes of what the CTG
showed.  She insisted that there
was a CTG that was running as
the contractions were not normal and the labour progress was also not
normal but she could not remember
whether she was in fact on a
running CTG at 14:00 but procedurally that should have been the
case.  She confirmed that according
to the guidelines the FHR in
the active phase should be assessed half hourly.  She said she
was not sure if the FHR was assessed
every half an hour as it should
have been the case.
[79] She confirmed that
from what is recorded on the partogram, from about 11:00 up to the
end, there were only two contractions
per 10 minutes.  She
confirmed that at 16:00 the heart rate was 170 and after the
contraction it was 140.  There was
a non-reassuring FHR at 12:00
and at 16:00 and nothing was recorded in between.  She accepted
that under decelerations in
the partogram she recorded C which was
completely wrong as C should refer to clear liquor.  Under
decelerations she put an
I which stands for intact membranes.
She explained that this was because she panicked as she tends to when
dealing with a
young woman.  She confirmed that there should
have been entries of membranes rupturing and clear liquor draining
from 12:50
and that they were not there until 16:00 when a completely
wrong entry was made.
[80] She confirmed that
at 06:50 the plaintiff was 5cm dilated and at 09:00 she was still 5cm
dilated and therefore for two hours
there was no further dilation as
normally there should be 1cm dilation per hour.  Therefore, at
09:00 already there was poor
progress.  The next assessment was
at 12:00 by which time she should be 8cm dilated as normally over
three hours as from 09:00
to 12:00 there should be 3cm dilation.
At 12:00 she was 7cm and at 12:50 when membranes ruptured she should
have been at
8cm.  She accepted that she did not check the
cervix for dilation at 12:50. She explained that this was because two
hours
had not yet lapsed.  At 14:00 when she did the next
assessment the plaintiff was still 7cm and therefore for two hours
there
was no further dilation which called for action.  She
informed the doctor who prescribed syntocinon but to be administered

only if CTG was reactive.  She accepted that she should have
made a note of what the CTG showed as instructed by the doctor
at
14:00.  She generally did what the doctor ordered.  She
insisted that it was not possible that she did not start the
CTG but
could not remember the events of that day but she did not do the
syntocinon.
[81] She accepted that
the only reason for not starting the syntocinon administration would
have been if the CTG was not reactive.
She later changed to say
that the condition of the patient could have changed which would
result in her not administering syntocinon
even if the CTG was
reactive.  It was put to her that the instructions from the
doctor was at 14:00.  It would take her
30 minutes for her to
observe the CTG.  This means by 14:30 there should have been a
note saying the CTG was reactive or not
reactive.  If it was
reactive syntocinon would start according to the doctor’s
orders.  She accepted these postulations.
She testified
that she would not have ignored doctor’s orders.  The
reason she did not start the syntocinon was not
because the CTG was
not reactive.  The possibility was that contractions would have
changed from that time to 16:00 and therefore
there would be no need
to administer syntocinon when what it was sought to achieve was
happening.
[82] She confirmed that
the frequency of contractions did not increase from 10:00 to 14:00
when she got the instructions from the
doctors.  However, she
testified that there was a great change because the contractions were
stronger.  At 16:00 the
dilation changed which is why she did
not carry out the doctor’s orders.  The frequency of
contractions was not improving
but the contractions were intense.
From 14:30 to 15:00 the doctor arrived and made a note at 15:00 and
recorded her findings.
Her notes indicate that the dilation was
still 7cm, which is what it was at 14:00 and at 12:00.  It was
then put to her that
if the CTG was running the doctor would not have
told her to check if CTG was reactive before syntocinon infusion and
catheter
insertion.  Sister Mbada testified that she was unable
to confirm that the CTG was not running.
[83] Sister Mbada was
then referred to the guidelines where they deal with partogram alert
and action lines.  The mandatory
action is the transfer to
hospital, the oxytocin infusion at the hospital or a caesarean
section.  The doctor indicated that
the plaintiff had crossed
the action line and decided that syntocinon infusion must be done.
The syntocinon infusion would
be done through a drip in which it is
injected in a fluid called Ringer’s Lactate.  Sister Mbada
confirmed all of these
propositions put to her.  It was further
put to her that at 15:00 when the doctor made entries on the
partogram she did not
indicate what the FHR was at that time.
Therefore, if the CTG was running continuously the doctor would have
written the
heart rate at 15:00 and would have indicated if there
were any decelerations.  She maintained that she did not
administer
the syntocinon.  In that regard she relied on the
fact that if she had administered it she would have ticked the
syntocinon
infusion document indicating the infusion rates as well as
the times.  Secondly she would not have done the infusion
because
of the increased intensity of the contractions.
[84] She confirmed that
the Ringers Lactate was the way in which the syntocinon infusion was
to be done.  It was put to her
that she did administer
syntocinon as instructed.  Her evidence in this regard was that
according to her recollection she
did not do it if her memory was
correct.  However, she confirmed that she had no memory of this
particular case and relied
on the maternity case records.  She
also confirmed that she would not have ignored the doctor’s
orders.  However,
as an independent nurse she can ignore the
doctor’s instructions if the situation changed.  The
intensity of the contractions
improved and the patient was
experiencing some birth pains.  On this latter issue she relied
on the shading of the partogram
on the contractions portion from
14:30. It was pointed out to her that the doctor examined the patient
at 15:00 by which time she
would have been aware of the contractions
before 15:00.  She agreed that the frequency of the contractions
did not change.
It was put to her that even the intensity of
the contractions was the same at 15:00 as it was at 14:00.  Her
evidence in this
regard was that the patient was experiencing strong
contractions even though their frequency had not improved.  She
was therefore
satisfied as a midwife with an independent function.
She therefore exercised her discretion and overruled the
doctor.
[85] She confirmed that
on 31 December 2015 she was still a registered nurse and not a
midwife and that she did her midwifery qualification
in 2018.
She was trained in interpreting CTGs and how to complete a
partogram.  It was put to her that she recorded
a heart rate of
170 before contractions and 140 after contraction which is different
to what she recorded in her assessment no.4
of the hospital records
where see indicated that the CTG was reactive.  Her explanation
for this discrepancy was that when
the patient pushes the heart rate
picture changes.  She confirmed that at that stage she was not
pushing yet, she merely had
an urge to bear down.  She then said
that the urge to bear down has got a way of causing the heart rate to
change.  She
confirmed that the heart rate in assessment number
4 which was 150 to 155 bpm was different to what she wrote on the
partogram.
Her explanation for the discrepancy was that when
she wrote an assessment based on a running CTG, by the time she wrote
on the
partogram there would be a change.  It was then put to
her that if that was the case she would have seen on the CTG that the

heart rate was non-reactive as it would have changed to 170 before
contraction which is tachycardia and abnormal as it is higher
than
160 and then after contraction it was 140.
[86] At this stage of the
cross-examination sister Mbada went on a tangent about her experience
of delivering babies which she said
in some cases she would think
that the child would not be alive because the patient had become
uncontrollable with the baby also
pushing out on its own especially
when the baby is in the perineum.  But such babies would come
out perfect and crying vigoriously.
Therefore, at this stage of
birth, the second stage especially when the baby is in the perineum
the CTG may be grossly abnormal
but the baby comes out alive and
crying.  She agreed that her partogram entry at 16:00 showed a
heart rate that was not normal.
She accepted that what she
recorded in the partogram indicated a late deceleration.
However, what she wrote was a C not an
L.  The C related to
clear liquor.  If she had seen a late deceleration she would
have recorded it with an L. She insisted
that her entry was not an L
but a C even though the heart rate was 170 and 140 before and after
contraction.  She agreed that
the block on which she wrote C is
meant for deceleration which is either E/V/L/N and there is no C that
is applicable.  However,
her intention was to write C not an L.
She later accepted that she should have written an L for late
deceleration.
She accepted that she therefore could not have
written that the CTG was reassuring.  It was put to her that at
16:00 there
were two contractions per 10 minutes.  She accepted
that it was an abnormal CTG.  It was put to her that the CTG
showed
at least 8 contractions per 10 minutes.  She accepted
that such a CTG would lead to a suspicion of foetal distress which is

when the FHR is abnormally high or abnormally low.
[87] The next witness for
the defendant was Dr Linde.  Her evidence was that on 31
December 2015 she was stationed in the maternity
ward as the medical
officer in charge.  The patient had been seen at the clinic at
06:50 and was referred to hospital where
she was attended to from
09:00.  She had been in labour since 02:00 am and she was 5cm
dilated.  The plaintiff’s
second assessment was at 12:00
and her 3
rd
assessment was at 14:00.  During all
these three assessment she was not involved.  An entry was made
at 12:50 that there
was a spontaneous rupture of membranes.  The
third assessment at 14:00 which was done by sister Mbada indicated
that there
was no progress since the last assessment at 12:00.
The 3
rd
assessment which was at 14:00 was done on time in
that a patient has to be examined every two hours.  She was 7cm
dilated
with the cervix still thick or the presenting part or head
was still high up or above the pelvic brim.  All of these were
indicative of poor labour progress.
[88] The plan was to
inform the doctor about the poor progress.  At 15:00 she
recorded her own assessment which she had done.
According to
the partogram the patient had crossed the action line which was also
indicative of poor progress.  The CTG would
have been reactive
because the plan was based on its remaining reactive which was the
syntocinon infusion to augment the labour.
She would also be
put on a catheter in order to empty the bladder to remove any
obstruction.  In the absence of risk on allowing
labour to
continue it would be allowed to continue.  In that case it would
not be necessary to immediately perform a caesarean
section.
Finally, part of the plan was that the doctor would be called if
there were any problems.  She confirmed that
she did not make a
note that in fact the CTG was reactive at the time.  However, if
there was any evidence of a non-reactive
CTG or any decelerations of
the heart rate she would have been concerned about the foetal
distress.  She plotted her dilation
finding of 7cm.
[89] She personally put
up a drip to give fluid to support the patient in poor progress to
prevent dehydration so she connected
her to the drip which was
Ringers Lactate.  The syntocinon administration infusion is done
by first ensuring that the CTG
tracing does not reflect a worrying
FHR to exclude any sign of foetal distress.  If there were signs
of foetal distress, the
syntocinon administration is
contraindicated.  It would only be started based on a reactive
CTG.  Every woman in labour
has their own oxytocin but sometimes
to augment labour an artificial oxytocin called syntocinon is used if
the contractions are
either too weak or too uncoordinated.  At
Zithulele Hospital they had a specific prescription sheet that was
used which indicated
the rate it was to be given as well as the
time.  Where the patient is a grand multi-gravida, meaning she
had had many pregnancies
and labours before, it would be risky to
augment her labour.  The second thing would be to check that the
progress of labour
had been plotted at least 2 hourly on the
partogram.  Thirdly the foetal heart rate is monitored through a
CTG while syntocinon
is being infused and if continuous CTG
monitoring is not done or possible, syntocinon infusion cannot be
started.  If the
CTG shows too many contractions or any foetal
distress, syntocinon should be stopped immediately as it can be
stopped at any point
if it is unsafe to continue with it.  This
would be the case if there is an overstimulated uterus which is five
or more contractions
per ten minutes which would reflect on the CTG.
Also if FHR is becoming too fast or showing signs of decelerations or
any
signs of foetal distress syntocinon should be stopped
immediately.
[90] She testified that
the prescription itself does not confirm administration.  There
does not seem to be confirmation that
it was in fact given.
Medication that has been given is documented.  When the Ringer’s
Lactate was put up the
syntocinon administration did not start.
If it had been administered there would have been a tick on the
infusion chart.
The patient was fully dilated at 16:00 and
depending on the situation one could keep it running even if she was
fully dilated.
She testified that it was unclear if syntocinon
was actually administered or not.  However, it was unlikely that
it was given
as there was nothing to document its administration.
There was no note of the syntocinon in the partogram or in any of the

following assessments.  There was no time at which she was
concerned about the welfare of the foetus.  A consideration
to
augmenting the contractions through syntocinon would be given if
there are no other risk factors and an emergency caesarean
section is
not needed.  The bladder is most commonly the biggest reason for
the slow progress and if membranes are not raptured
one would need to
rapture it which normally causes labour to happen quickly.  On
CPD or cephalopelvic disproportion her evidence
was that this would
mean that the head is not able to pass through the pelvis.
[91] Under
cross-examination Dr Linde testified that by the end of 2015 she
would have had about six to eight months experience
in the maternity
ward.  She appreciated the importance of making a note of
everything she did as provided for in the maternity
guidelines.
It is provided that a note should be written about the findings of a
CTG monitoring process so that a record
of the CTG is still available
even if the CTG tracing is lost.  She confirmed that she found
the plaintiff to have crossed
the action line when she assessed her
at 15:00 indicating poor labour progress.  A normal labour
should progress at 1cm dilation
per hour and in this case it was much
slower.  In that case where action line is crossed, if there is
no foetal distress that
action could be syntocinon infusion but if
there is foetal distress the action is a caesarean section.  But
things like emptying
the bladder or even rupturing the membranes are
some of the actions that could be performed when the action line is
crossed.
In this case membranes had already raptured at 12:50
and while the bladder was still full it was unlikely to be the reason
for
the poor progress but she had the catheter put in to empty it so
as to rule it out.
[92] When she saw the
partogram and noticed the poor labour progress she determined that
there was a need for syntocinon infusion
to make contractions
frequent and to make the labour progress quickly.  She noted
that the patient was 7cm dilated with clear
liquor and the head was 3
to 4cm above the brim which was still very high up.  She agreed
that no FHR was noted and that FHR
should be monitored every 30
minutes by auscultation or CTG monitoring.  She confirmed that
she did not make a note of what
the FHR was on the partogram.
The plan was to start syntocinon and to put a catheter and to allow
labour to progress and
to call the doctor if there were problems.
CTG was to be checked before syntocinon infusion and the
catheter insertion.
She admitted that it was possible that if
she had seen the CTG she would have written a note thereof.
[93] She admitted that
she had a duty to make notes of the conditions she found from the
examination.  Any mistake with syntocinon
infusion may cause
foetal distress with bad outcomes for the baby.  The guidelines
do provide that there must be no evidence
of foetal distress before
syntocinon infusion and that it must be used with great caution in
multiparas and after the CPD would
have been excluded.  It was
then put to her that if there had been a CTG running she would have
written what the FHR was and
what the contractions were.  She
testified that while a CTG finding was a central finding practically
it would be almost impossible
to make the note that she did without
having seen a CTG.  She understood her note in that regard to
mean that if the CTG remained
reactive the syntocinon and catheter
could be done.  She agreed that the latest heart rate recorded
on the partogram closer
to 15:00 was at 14:00 which was an hour
before.  She therefore, agreed that from 14:00 there was no
record of a reactive CTG
but she denied that there was no CTG
monitoring.  As for putting up Ringer’s Lactate her
evidence was that it could
have been in preparation for syntocinon.
But it is also used very often in prolonged labour where the patient
would not have
been eating or drinking.  It was common to run
fluids for such patients and therefore denied that the sole purpose
of putting
up Ringer’s Lactate was to administer oxytocin.
If after putting the catheter on and the CTG remained reactive and
the progress was still poor the intention was for the nurse to inject
the syntocinon into the Ringer’s Lactate fluid.
[94] She confirmed that
nurses and midwives would not start a medication without prescription
from the doctors.  But they could
increase or discontinue it or
lower it depending on the contractions.  They could not refuse
to administer it if it was prescribed.
But if the patient’s
labour progressed before the infusion started they may not administer
it.  For instance, when a
catheter is put in sometimes things
change unexpectedly.  In that situation a midwife could decide
what to do if syntocinon
was no longer needed.
[95] She agreed that if
the progress of labour crosses the two-hour action line it is
required that syntocinon infusion should be
started if there is no
CPD and no evidence of foetal distress.  She was satisfied that
there was no foetal distress and there
was no indication of CPD.
She was therefore required to start syntocinon infusion and
preparations for it were done.
However, it was very difficult
for her to say it was actually infused as there were no notes to
support that conclusion.
Her intention after her assessment at
the time was that the patient could benefit from syntocinon
augmentation.  She agreed
that a properly drawn partogram should
look like exhibit 1G drawn by professor Anthony and therefore the
partogram for this patient
was incorrectly drawn.  Therefore,
the labour in this matter was severelly delayed and the contractions
were inadequate.
Inadequate contractions call for syntocinon
augmentation.  There was no indication or entry of syntocinon
infusion or that
it should be stopped.  It was put to her that
at 16:00 there were two contractions per 10 minutes and she was 10 cm
dilated
and if syntocinon was infused it had to be continued until
birth.  She agreed that there was no note indicating a change
that
would have made syntocinon infusion unnecessary but there were a
few missing links to syntocinon administration because of the absence

of ticks for it.  But there was missing information both for and
against the possibility of syntocinon administration.
[96] If there was
tachysystole from 16:00 until the CTG was discontinued about half an
hour later, which indicates going from very
poor contractions to
tachysystole, that would point strongly that syntocinon had been
administered.  She testified that tachysystole
would be when the
contractions were happening too frequently and too quickly which
causes a problem for the oxygen supply to the
baby.  But that
could happen during labour even without syntocinon.  The effect
of syntocinon would be to increase the
frequency and strength of
contractions.  But contractions can increase both in frequency
and strength on their own without
syntocinon administration.
[97] Dr Cilliers
testified that she was on duty at Zithulele Hospital on 31 December
2015 where she had been a grade 2 clinical
medical officer since
2013.  She was asked to come and assist with the vacuum
extraction delivery.  The process started
at 17:05 and was
completed at 17:10. She had been asked to come and assist by the
first on call, Dr Phillips saying there was a
delayed second stage
labour.  The CTG was reassuring, the assessment of the pelvis
was normal, the patient was a 16 year old
grav-2 para zero with a
second stage delayed labour.  Dr Phillips was a junior doctor
doing his community service having been
at the hospital for six
months.  So it was her responsibility to assess the situation as
a senior doctor and confirm if vacuum
extraction was the correct
procedure.  She did all the examinations and she was satisfied
that the case was a good case and
a learning opportunity for Dr
Phillips to be skilled.  When she arrived in the ward the
patient was on a running CTG and there
was Dr Phillips who would have
been called by the midwife.  In that setting there were two
patients, the mother and the baby.
She needed to determine the
wellbeing of both patients.  One of the pre-requirements for a
vacuum extraction is to look at
the foetal wellbeing.  This is
necessary to assess if the baby is well enough to go through the
process of vacuum delivery.
This is done through a running CTG
where the assessment is whether the CTG is normal, suspicious or
pathological.  The baby
has to have enough reserve to go through
a vacuum normal vaginal delivery from a reading of CTG tracings.  The
notes she made
on the day indicated that initially the CTG was good
which means it was reassuring and then tachycardia.  Foetal
tachycardia
meant that there was a stressful situation but it was not
a pathological one.  A pathological one would be bradycardia, a
very low FHR which is the concerning one and if that was the case she
would have made a different assessment.
[98] Her assessment was
that the foetal well-being was good and she excluded foetal distress
so that she could carry on.  She
checked the cervical dilation
and the mother was fully dilated.  She had with her the maternal
records including the assessment
notes which had been recorded at
various times.  She was then referred to the maternal notes
which indicated that the baby
was born a bit flat but recovered after
bag mask ventilation and had a heamatoma caused by the vacuum cup.
She testified
that in the first minute after birth while doing apgar
scores and assessing the foetal wellbeing, if there is a need to help
the
baby breathe more, to supply more oxygen you first start with
stimulation and then move towards bag mask ventilation.  That

led to a good recovery and the five minutes’ assessment showed
the baby to be no longer blue but pink which means that the
baby was
well oxygenated and breathing better.  She did the bag mask
ventilation herself.  She was on duty during that
whole weekend
but at some point on 31 December 2015 she handed over to Dr Mans who
saw the baby at about 22:00.  She only
saw the baby again on 3
January 2016 which was the last time she saw the baby.  She made
a note that the baby was breast feeding.
She noted the need for
counselling with the grandmother to provide breast feeding support.
There was also a note for a speech
therapist and dietician
intervention to support the mother with the baby’s breast
feeding.  The baby was still cup feeding,
with no active
breastfeeding.  The plan was to help the mother to do
breastfeeding before she was discharged by establishing
good
breastfeeding practices.  The note on speech therapy and
dietician intervention reflected that the baby was only cup
feeding
and needed assessment by a speech therapist.  This was a
multidisciplinary approach to deal with the cup feeding situation
so
that dietician and speech therapist would come and help in
establishing breastfeeding.
[99]
Under cross-examination she confirmed that for respiration she gave
the baby an apgar score of 1. She confirmed that the record
did not
reflect that the baby was crying.  She put the baby on nasal
prong oxygen and after she was happy with her breathing
she went to
the theatre to deal with the 3
rd
degree tear the mother had sustained.  At
18:30 the bay was still on nasal prong oxygen.  It was put to
her that an hour
and a half after birth the baby was not yet normal.
She testified that if she was concerned about the baby’s
neonatal
outcome she would have admitted her to the neonatal high
care unit and put up an IV line and not to initiate breastfeeding.

She would have written good notes for monitoring for an extensive
plan.  Her assessment was that the baby was well enough.

The apgar score of 7 at 5 minutes was a good apgar score according to
the guidelines and was not concerning.  She testified
that every
baby that is born is resuscitated to stimulate it and this is done
within 30 seconds of birth and therefore resuscitation
is not
indicative of a bad outcome.  She however, agreed that an apgar
score taken on a resuscitated baby is an assisted score.
[100] If she had been
worried, she would have admitted the baby to the high care unit for a
higher level of monitoring.  If
she had time she could sit next
to the baby, take off the nasal prongs and make sure that the baby
was 100% off oxygen and do a
non-assisted apgar score.  On the
baby being born flat and lethargic an hour and a half later, the baby
still receiving oxygen
according to the nurse her evidence was that
that changes everything significantly but according to her notes she
was convinced
that the baby was okay which was why she did not admit
her to high care.  When it was put to her if she accepted that
the
baby was not okay, she testified that she would accept that.
She was referred to grasp reflex which was weak and another
fundamental finding that the suck reflex which was absent meaning the
baby could not latch or feed from the breast.
Even at
22:34 a note was made by the doctor about poor latching which would
be a consequence of an absent reflex.  She testified
that there
were two components to poor latching.  It also involves not just
the baby but the mother as well in getting the
baby to breastfeed but
she could not comment much as she was not there at that stage.
[101] Dr Cilliers
testified that when she first arrived to attend to the patient there
was foetal tachycardia which meant that the
baby still had reserves.
The CTG that she saw that was running was normal and there was a good
response from the baby’s
heart rate during that time.  All
of that told her that the baby was well.  When the baby was
born, the apgar score was
6 and 7 and 10 later which was a very good
outcome for a delivery.  A diagnosis of a poor foetal outcome is
made if the apgar
score is less than 3 according to the guidelines.
On that basis she could not have picked up that there was ischemia.

The Standard Treatment Guidelines of Paediatrics of 2017 say if the
one minute apqar score is less than three and the five minute
apgar
score is six or less, that is a poor outcome which is more suggestive
of a diagnosis of HIE.  When she assessed the
baby, none of that
criteria was met.  She testified that according to her notes
when she arrived, the CTG was initially good
and then tachycardia.
She testified that while she did not have a recollection of what the
CTG showed, she did write in her
own handwriting that it was
initially good but then tachycardia which was when she made the note
on the vacuum delivery.
She therefore presumed that the CTG was
running at the time because that is what usually happens.  She
would not have made
such a comment or note if she was not reading
from a CTG.  The notes are made retrospectively.  If there
was a pathological
CTG she would not have proceeded without assessing
other emergency measures to take to get the baby out as soon as
possible.
[102] The tachycardia was
at about 17:00 although she could not tell exactly when it started
because they work on the presumption
that the CTG trace would be
available.  Some of the indications for a safe vacuum delivery
are that the head of the baby must
be in the perineum which means the
head must be down at the base of the pelvis.  The mother must be
10cm dilated and if the
baby’s delivery is delayed then the
vacuum or ventouse delivery can be done when all those clinical signs
are indicated.
Consideration is given to the fastest way of
getting the baby out.  She testified that tachycardia is a heart
rate of about
160 or higher.  But if it is more than 160 for an
extended period of time, that is more concerning.  When it is
above
160 it is non-reassuring.  If it is non-reassuring you
must consider it in detail to see what other features are there on
the CTG.  Those would be things like variability and the
contraction pattern.  These help determine if the CTG is in fact

reactive or nonreactive.  She admitted that she did not do any
of those further investigations.  She was satisfied that
the
condition of the baby and the mother was such that a ventouse
delivery could be done relatively safely.  She admitted
not
writing her other observations but said if there was a problem she
would have written it down along the lines that the CTG
is
pathological with poor beat to beat variability.  So when there
was foetal tachycardia, that was indicative of a suspicious
CTG trace
as against a pathological one.
[102] A suspicious trace
has a low probability of hypoxia.  Her noting foetal tachycardia
means there was sufficient reserve,
a suspicious CTG but the baby
could be delivered normally.  If there was poor beat to beat
variability or if she was worried
about prolonged decelerations she
would not have allowed a junior doctor who has never done vacuum
extraction by himself to do
it on a pathological CTG.  She would
have gotten the baby out herself as the most experienced clinician
there.  She agreed
that to assess whether a CTG is suspicious or
pathological it has to run for a certain period of time.  At one
time a CTG
may be suspicious at other times it may be normal and yet
at others it may be pathological.  There was no obstruction for
the baby to come out.  She did not do an episiotomy because they
did not think that it was an obstructed labour.  They
do it if
they think that the perineum is too tight and will not stretch and
they rarely do it as they do it only in extreme cases.
She
denied that the third degree tear was caused by the head of the baby
being big relative to the vaginal opening.  She testified
that
she did not think that that was a problem at all as there was no
moulding, no caput and no oedema.  The vaginal examination
done
before the baby was born was not indicative of an oedema.  The
cause of the third degree tear in her view was because
Dr Phillips
was not skilled enough to do a vacuum extraction without causing a
tear.
[103] The vacuum
extraction was very easy in that there were only two pulls.  It
started at 17:05 and by 17:10 it was completed
which was 5 minutes
later.  She confirmed that the first stage was delayed.
She testified that if there is a delayed
first stage of labour you
intervene but that does not mean the baby is hypoxic.  If there
was foetal distress the syntocinon
augmentation would not have been
considered.  A caesarean section would instead have been
considered.  This was not an
abnormal labour at all.  She
agreed that according to the guidelines there was poor progress in
the active stage of labour.
She testified that from 16:00 to
17:00 which was an hour she progressed from 7 to 10 cm dilation.
Two hours for delayed second
stage of labour is allowed according to
the guidelines.  When she arrived and saw poor progress she
could see that there was
intervention and it worked and there was a
good CTG.  She wanted to get the baby out as soon as possible as
she did not want
to wait for the two permissible hours.
She remembered a vigorously crying baby following a very good vacuum
extraction
performed by one of her junior colleagues whose outcome
was good because the baby was crying.
[104] It was put to her
that taking everything together from poor progress going into the
second stage, the poor respiration on
which she acted correctly, she
should have had a high suspicion that there could have been foetal
distress.  She testified
that excluding the apgar score of 10
out of 10 at 10 minutes given by sister Mbada, still on apgar score
of 6 and 7 out of 10 and
a crying baby was very good.  An apgar
score of 7 out of 10 at 5 minutes was good but if it was less there
would be a worry
of an acute incident of hypoxia in which case an IV
Line is put up and the baby is kept at nil per 02 and it is admitted
to high
care unit.  She testified that without taking anything
away from Dr Mans, if she came back from theatre and there was a
problem
and concern she would have picked it up at 18:30 and would
have made extensive notes at 18:30 saying the baby is not doing well,

maybe she missed a foetal distress.  Instead the note she made
was that the baby needed to start breastfeeding and was hungry.

At 19:00 the baby was with the mother in the labour ward which is a
low risk ward so the baby was not in a high care unit.
She did
not know why there was poor latching which Dr Mans noted.  The
cardiovascular system was good, good respiration, the
spine was
normal and neurologically the baby was fine.
[105] It was put to her
that when she saw the baby at 18:30 it was not well and that she
missed clear signs like absent suck reflex
which leads to poor
latching.  There were clear signs of encephalopathy which she
missed as a result of which she should have
referred the baby to a
higher facility or ICU and not return it to her mother.  She
disagreed with all of that proposition.
[106] The last witness of
fact for the defendant was Dr Mans.  He testified that on 31
December 2015 at night he was the doctor
on duty.  His shift
started at 19:00 and went through the night until 08:00 the following
morning.  During that period,
he was the only doctor on duty.
Emergency cases are highlighted during the handover.  On the 31
December 2015 no specific
problem was mentioned that he could
recall.  He saw the baby on 31 December 2015 as part of his
normal duties.  This
baby was not a patient that was highlighted
during the handover.  The post-neonates are generally well and
low risk and are
therefore easy to attend to.  The doctor would
see one patient, rush to emergency and back to the ward to do the
next patient.
With respect to this patient his note was done at
22:34. This means that he would have been busy with other duties
before doing
the post-neonates round.  Before he made the note
at 22:34 he would first have spoken to the patients.  He noted
that
the baby was hungry and there was poor latching and also wrote,
cardio-vascular system to look at the heart and pulses.  He
did
the respiratory examination and he was not worried.  He checked
the spine and also did a neurological examination.
[107] He saw both the
baby and the mother at the same time and noted that the mother had no
clue on how to breastfeed.  He
would have asked the mother to
breastfeed while standing next to her and could see that she was not
able to position the baby comfortably
to latch on to the nipple.
The plan was to review the baby on discharge.  This meant that
at that point there was nothing
of concern to him about the baby who
was essentially lodging until the mother was counselled and her
perineum wound was dealt with.
His reference to cardio-vascular
system review was because the baby was crying.  He has done
informal training in breastfeeding
and was aware that there were many
people who struggle with connecting the baby well to the breast.
His assessment based
on the notes was that the baby looked ready and
willing and wanting to feed but was not being positioned optimally
for breastfeeding.
The mother needed to be taught on how to do
it.  His expectation was that his colleagues who would come
after him would see
the notes and do the necessary instead of
processing the patient routinely.  The next morning at 07:30 on
01 January 2016
he noted that the baby was crying and there was poor
latching and was hungry.  By that he meant that the baby wanted
to feed
but the connection between the baby and the mother’s
breast which is called latching was not good.  The plan was to
cup feed and then breast feed.  They had a situation of a
feeding difficulty in a baby that appeared to be able to feed and
a
feeding connection or latching that was not good.
[108] He saw the baby
again on the 04 January 2016 at 10:19.   He noted that the
baby was not breastfeeding properly after
looking at the feeding
which he presumed to be a contributing factor to the baby being
slightly yellow meaning the serum bilirubin
levels was slightly high.
The plan was for a dietician and speech therapist interventions
which is a multi-disciplinary approach.
Breastfeeding
counselling was normally done by the dietician and the speech
therapist at Zithulele Hospital.  The plan was
also for the
total serum bilirubin levels to be confirmed through the necessary
test.  He saw the baby again on 04 January
2016 at 16:22 after
being called by a nurse reporting that the baby was fitting.  At
that point the baby appeared yellow and
his note therefore referred
to jaundice.  It seemed to him that there had been a
deterioration because the baby was fine for
the first three days and
then had fits all of a sudden.  He then questioned or queried
HIE as he did not know what could have
led to the insult in the brain
leading to seizures.  He then made a plan to look into the
situation and manage it in line
with their set protocol and
operational management book. He made further notes at 18:21 as he
spent time with this baby trying
to understand the situation.
The next note was on 05 January 2016 at 07:39 and it indicated that
there were no further seizures
since the previous day at 21:26.
His issue was that there seemed to have been a shift from the
earlier picture from
birth as depicted in the notes.  He made
further notes on 05 January 2016 at 14:45 when he did a ward round.
He made
a note referring the baby to the occupational therapist.
As he was the doctor in the labour ward that week he saw the child

again on 06 January 2016 and the whole patient management process
continued and his notes ended.
[109] His evidence under
cross-examination was that when he starts his round he would speak to
the nurses to hear about problems.
He would then go to the
labour ward and speak to all the mothers after which he would speak
to each mother individually.
He speaks to the mother while
examining the baby.  Then he would go to the file and look at
the delivery time and apgar scores.
He saw Dr Cilliers’
notes including the fact that the baby was on nasal prongs for
oxygen.  He testified that when he
saw the baby it was not on
nasal prongs.  He agreed that there is reason to believe that
there may be a risk of hypoglycaemia
as the glucose level may be
depleted after a baby has suffered hypoxic ischemic injury.  He
added that there was no recorded
risks of hypoglycaemia.  He
testified that they have high regard for abnormal findings that are
reported and the procedure
is that if a nurse makes an abnormal
finding the doctor must be informed immediately.  It was put to
him that because of time
limitations he did not consider the
condition of the baby after birth properly.  He testified that
he examined the baby and
he felt that the baby could latch.  He
had examined the baby twice and there was no scalp trauma.  The
nurse’s
note on a haematoma must have been a thumb suck.
[110] If there was an
issue of a suck reflex that was absent, he would have been called
immediately.  He was referred to the
notes of a speech therapist
regarding an absent rooting reflex and suckling difficulties the baby
had and its sleeplessness made
on 04 January 2016.  He insisted
that any suggestion that his initial assessment was incorrect was
denied by him.  He
said that the baby was clearly crying and
active and moving all the time during the first two days and
therefore his initial assessment
was not incorrect.  He
testified that his recorded notes showed that he watched the baby
breastfeeding.  When he made
reference to poor latching it meant
that he saw the baby moving to the breast on 31 January 2015 at
22:34.   On 01 January
2016 at 07:30 there was another note
on latching and the baby being hungry.  That was indicative of
an active baby wanting
to latch.  In the morning on 04 January
2016 the baby was not breastfeeding nicely which meant that he saw
that the baby’s
breastfeeding was not happening nicely.
There was no comment on 4 January 2016 on his notes about the level
of consciousness
of the baby.  He agreed that feeding
difficulties are common in cases of HIE and they are typical features
of hypoxic ischemic
injury. He then said that while poor feeding and
lethargy are associated with HIE, his starting point was the mother’s
inability
to breastfeed the baby.  Once that is addressed they
then look at other features.  Where the baby is crying, moving
well
and active, an association is not normally made with HIE.
He agreed that this baby had HIE and did end up having sucking
problems.  But at the point of his examination of the baby there
was no HIE concern as the baby did not have the classic features.
The defendant’s
expert witnesses.
[111] The first expert
witness called by the defendant was Dr Koll.  He is a semi
retired specialist obstetrician and gynaecologist.
He compiled
a report and also did joint minutes with Dr Murray and with professor
Anthony.  Based on the information that
they had at the time he
and Dr Murray concluded a joint minute accepting that syntocinon had
been prescribed and administered on
the plaintiff.  He testified
that antenatal assessment of a foetus can only indicate that the baby
is alive and measuring
fundal height only indicates that the baby is
growing.  There is no way of making a neurological assessment of
the baby.
Therefore, an injury or abnormality, be it congenital
or genetical that was present in the womb prior to the onset of
labour, routine
antenatal care would not have picked it up.
Radiologists can time it to the peripartum area, in other words late
antenatal
to some time after birth.  That is why he and
professor Anthony agreed in a joint minute that there was nothing
detectable
antenatally that could have affected the outcome.
[112] In other words the
antenatal course progressed fairly uneventfully.  He was
referred to Dr Murray’s comment in
their joint minute in which
she said that the foetus had several significant labour related risk
factors for hypoxic brain injury.
Those were the prolonged
labour, the oxytocin infusion, the substandard foetal monitoring
especially during oxytocin administration
and the fact that the
second stage of labour was complicated, needing instrumental
delivery.  The minute indicated that he
did not disagree with
those postulations.  He explained that there is a difference
between risk and cause.  There were
discrepancies in the
assessment of the cervical dilation.  The doctor assessed the
patient when she perceived that the patient
had crossed the action
line.  In the absence of disproportion, she decided to augment
the labour.  The labour progressed
rapidly after augmentation
thus justifying the decision of the doctor.  There was CTG
monitoring as evidenced by the recording
of FHR ranging between
different figures.  That can only be done on a CTG.  One
can also see a range on a handheld doppler.
At 16:00 the CTG is
reflected as reactive and at 16:00 the FHR was 150-158.  His
view was that for a large portion of the
labour process the patient
was on a continuous CTG although the detail when she was on it and
when she was off it is unknown.
[113] He testified that
there are things that should have been filled in on the partogram
which were not and therefore it does not
document the full picture.
The definition of tachysystole is more than five contractions in a
ten minute period.  That
indicates that the uterus is being
overstimulated which, as professor Anthony illustrated, may lead to
progressive hypoxia threat
as labour progresses as a result of
relative lack of oxygen.  Therefore, tachysystole needs to be
managed on a fairly urgent
basis.  The CTG monitors only two
things, the heart rate by giving a tracing of a heart rate of the
foetus.  That has
four elements; variability, the beat to beat
variability which suggest a healthy baby.  Then there are
decelerations where
you get early decelerations, variable
decelerations and late decelerations.  Early decelerations are a
mirror image of a contraction.
Variable decelerations are not
related to contractions and late decelerations occur regularly after
a contraction.  The one
looks for the presence of
accelerations.  You look for baseline variability, presence of
decelerations and accelerations.
If accelerations are present,
that is a very good sign of foetal well-being.  That is the
cardio part of the CTG.  The
tocograph simply measures the
surface tension on the mother’s skin.  While the CTG gives
a very good representation
of contractions, it is not so good during
the second stage because of the mother pushing and changing
positions.
[114] While writing notes
in a busy labour ward is very important, however, he was of the
opinion that the primary responsibility
of a clinician is to care for
patients as one cannot sacrifice care of a patient in order to write
comprehensive notes.  He
agreed with professor Anthony that a
random measurement of the foetal heart does not tell anyone
anything.  The assessment
at 12:00 indicated foetal movement and
the plaintiff was 7cm dilated.  So from 10:00 until 12:00 the
progress was adequate.
The next assessment was due to 14:00 at
which time the cervix remained 7cm dilated.  The FHR was 145-150
bpm. The head was
high and the plan was to inform the doctor about
poor progress.  The doctor ordered syntocinon with an
instruction that if
CTG was reactive it could be started.
[115] At 15:00 Dr Linde
made a note which also noted that the patient had crossed the action
line and ordered syntocinon, a catheter
and that CTG was to be
checked if it was reactive before those things were dore.
Syntocinon was to be administered in half
an hour if the CTG was
reactive.  At 16:00 the patient was fully dilated.  He and
professor Anthony were in total agreement
that oxytocin is a
dangerous drug which is to be used with extreme caution especially in
a multipara.   So if sister
Mbada felt that something had
changed and decided not to administer it, that was a commendable
decision if something had changed.
In that case it would not
have been wrong for sister Mbada not to follow the doctor’s
orders and not administer it when it
would have been inappropriate to
administer it.  At 16:00 when the second stage started there was
no caput and no moulding
so the pelvic assessment was adequate and
therefore there was no evidence of CPD.  Up until 16:00 he could
not find fault
with the actual management of the labour.  What
can be faulted was note keeping.
[116] In assessing poor
progress of labour CPD must be excluded as a first step and foetal
distress.  If foetal distress or
CPD are present, then caesarean
section must be done.  Any other intervention is not
acceptable.  The main determinants
of CPD are caput and
moulding.  Prior to doing vacuum delivery, pelvic assessment
must be done and if the pelvis is contracted
then a caesarean section
might be a better option.  In this case both moulding and caput
were excluded.  Assessment no.4
at 16:00 in respect of the FHR
was 150 which was indicative of a reactive CTG.  30 minutes
thereafter there was an assessment
by the sister and the patient had
been bearing down for 30 minutes and the doctor was informed at
16:30. The delivery was completed
by vacuum extraction at 17:10.
[117] The guidelines do
provide that if the patient has been pushing for 30 minutes, the
diagnosis of a prolonged second stage labour
can be made.  He
testified that he and professor Anthony are in agreement that hypoxic
stress on the baby gets progressively
worse.  So if this baby
was under progressive hypoxic stress and the CTG was reactive at
16:00 then it would be highly unlikely
that there was evidence of
foetal distress prior to 16:00.  In light of the fact that in
labour hypoxia is a progressively
increasing risk, the risk at 16:00
would have been more than the risk at 15:30.  He had huge
reservations in commenting on
a ghost of CTG that he could not see as
he said in the joint minutes.  He was therefore not prepared to
say that there was
evidence of foetal distress or that there was no
evidence of foetal distress as he was unable to read the faded CTGs.
[118] His evidence when
he was cross-examined was that he could find no fault with the
management of the labour based on the maternity
case records.
However, he would agree that the record keeping was faulty as there
were some discrepancies.
His view was that the fact
that hypoxic stress on a baby gets worse until it is delivered and
the recorded normal FHR shortly before
delivery would indicate that
there was no evidence of foetal distress and therefore no indication
that intervention should have
been sooner.  He saw the CTGs that
were put on the screen by Dr Murray and heard her evidence.  He
also heard the evidence
of professor Anthony who used the pictures Dr
Murray had photographed, of the same CTGs to draw a clear line of
what the CTG’s
showed.  He would not comment on those CTGs
for the reason that they both hold the opinion they do based on what
they could
see.  He was of the view that what you cannot see is
much more important than what you can see.
[119] Where there are two
tracings intermingling, one cannot see clearly where one comes down
and where another one goes up.
Therefore, he could not comment
on foetal distress.  His view was that the tracings were
unreadable.  He testified that
the tracings that professor
Anthony drew were suggestive of a severely distressed foetus.
The tracings he drew were in the
early part of the second stage of
labour almost an hour before the baby was born.  If the baby was
subjected to that degree
of hypoxic stress for an hour the baby would
have been severely compromised at birth.  His field of expertise
ends at the
apgar scores and with the apgar scores for this baby he
would not have been concerned as an obstetrician. His understanding
of
an assisted apgar score is if a baby is on a ventilator and the
ventilator is breathing for the baby or the baby is on continuous
bag
mask ventilation at five minutes.  But if the baby needed a
little bit of oxygen and by five minutes the baby is breathing

spontaneously on nothing more than a nasal prong oxygen that did not
represent an assisted apgar score but he would defer to the

neonatologist.
[120] With regard to his
minute with professor Anthony, Dr Koll testified that they agreed
that the active phase of labour should
have been diagnosed at the
clinic at 06:50. They agreed that the prescribed frequency of
maternal and foetal observations were
not recorded.  With regard
to the intrapartum foetal monitoring and the decelerations on the
partogram, abnormal variability
is over 25 bpm or less than 5, so
normal variability is 5 to 25 bpm.  Therefore, a range of 136 to
151 would indicate the
normal range of variability.  He
testified that the evidence of the plaintiff was that she was on CTG
monitor from the time
of ruptured membranes.  He agreed that
there should have been re-evaluation of the tracing at 12:30 and
there is no record
that it was done.  That is substandard record
keeping.  In terms of the guidelines there should have been
re-evaluation
of the condition of the foetus every half an hour even
for a normal labour, never mind a patient who is on a CTG.  He,
however,
said that if the court accepted that professor Anthony has
given a correct depiction of that tracing then it was a very
pathological
tracing and immediate action was required.
[121] He added that the
nurses continued with the labour.  They had a running CTG
tracing that they could see and they were
experienced and were not
concerned.  He emphasised that only if the court accepted the
hand drawn tracing of Prof Anthony,
then that would represent a
pathological tracing and therefore immediate action was required.
He testified that his experience
indicated that looking at a CTG in
the second stage of labour is extremely difficult.  The only way
is by actually putting
the hand in the abdomen, feeling the
contractions and listening to the foetal heart with a transducer.
When one looks at
the tracing for that time afterwards you cannot
make head or tail of it.  However, the tracing would be almost
unreadable
on a large number of occasions.  Therefore, he
disagreed with the proposition that a CTG is accurate in the second
stage of
labour and easier to interpret than listening and feeling.
[122] On the original CTG
the tocograph was clearer than the cardio portion.  The cardio
portion was completely unreadable.
The original tocograph was
faint but he would not dispute its enhancement but disagreed very
strongly with the enhancement of the
cardio.  As far as the
contraction pattern is concerned, it could be uterine contraction or
it could be anterior abdominal
wall.  It is unusual to get that
number of contractions in that sort of pattern lasting for that short
period of time in a
tachysystole.  A tachysystole is more
commonly longer contractions.  Such patterns are normally caused
by patients pushing
uncontrollably.  The ideal is to try and
coach the mothers and encourage them to push with contractions to
create an expulsive
force with all the available powers, the uterus,
the abdominal wall muscles and if you are doing a forceps or vacuum
delivery,
all these forces must act together to get the expulsive
force.  However, sometimes mothers just lose it, they lose
control
in the second stage of labour and start pushing
uncontrollably, unrelated to the contractions.  He therefore
felt that the
picture in this case looked like a case of a mother
pushing uncontrollably.
[123] He confirmed that
the second stage of labour was delayed and when there is a delayed
second stage action should be taken.
He was of the view that
there was no evidence of substandard care but there was undoubtedly
substandard care in the record keeping
of observations.  He was
of the view that at the time that syntocinon was prescribed, it was
indicated.  That time was
at 15:00 when it was prescribed but
there is no evidence that it was administered.  If there was a
change the nurse could
decide not to administer it.  It was put
to him that there were strong contractions, in other words,
contractions that were
longer than 40 seconds in duration and there
were two of those every 10 minutes.  He confirmed that that
started at 14:00
and it was recorded until 17:00.  There was
nothing in the partogram to indicate a change that would allow the
nurse not to
follow the doctor’s orders.  He confirmed
that on the records there was nothing that indicated any change.
It
was put to him that according to the guidelines the second stage
is prolonged if the foetal head has not descended onto the pelvic

floor after two hours of full dilatation or if delivery has not
occurred after 30 minutes of pushing in a multipara woman.

Using this criteria, the patient was fully dilated at 16:00 and
therefore a prolonged second stage should have been diagnosed at

16:30. He agreed with this observation in his minute with professor
Anthony.
[124] It was put to him
that if one looks at the tocograph and accept that it is correct,
what is depicted there is what the nurse
would have seen.  The
nurse would not have been able to distinguish between deviations
caused by contractions or by the mother
pushing.  Seeing the
pattern of deviations, she should call the doctor immediately if the
mother did not stop bearing down.
He testified that the first
step would be to try and talk the mother down and if that did not
work and she was worried about foetal
distress as excessive pushing
is not a problem unless it is associated with foetal distress.
Therefore, if she was happy
with the foetus and indeed there is an
indication that at 16:00 and at 16:30 there was no concern about the
well-being of the foetus.
Furthermore, the tracing that the
nurses were seeing at 16:00 and 16:30 was not the tracing drawn by
professor Anthony, it was
a tracing that was just from the machine at
that moment.  They were seeing a tracing that himself, professor
Anthony and Dr
Murray were in agreement were capable of
interpreting.  Seeing that tracing they were not concerned about
foetal distress.
When it was put to Dr Koll that the nurses,
seeing abnormal deviation pattern on the tocograph should have been
concerned and that
the partogram indicated that at 16:00 the FHR was
170.  His response was that the CTG drawn by professor Anthony
showed a
single spike lasting just a few seconds up to 170 which
would not constitute tachycardia.
[125] He went on to
explain that on the baby being hypoxic, hypoxia is a normal event
during the second stage of labour.  The
determinant was whether
that hypoxia was severe enough to cause injury especially because
hypoxic stress gets worse and worse.
If the baby was born and
the brain injury had occurred at the time of birth, then it would
have been severally hypoxic at the time
of birth and this baby was
clearly not.  He went on to say that even with normal deliveries
babies are often born with mild
hypoxia that responds very rapidly to
resuscitation.  This happened even at an elective caesarean
section where a small resuscitation
is sometimes required.  This
would be because it is not just intrapartum hypoxia that is at play
but also the transition of
the baby from intra uterine to the extra
uterine life which is a difficult transition for which often the
babies need a little
help.  As an obstetrician if one accepted
the tracing drawn by professor Anthony, it would be very suggestive
of intrapartum
hypoxia.  As hypoxic stress gets progressively
worse, the said tracing was done at least 40 minutes before the baby
was actually
born.  Therefore, if hypoxic stress had continued
for that period of time he would have expected the baby to be born in
a
severely hypoxic state and would have required significant
resuscitation.
[126] Dr Janse van
Rensburg who compiled a joint minute with professor van Toorn first
testified about her initial report.
She testified that she had
consultation with the plaintiff who told her that in 2018 her third
baby was delivered following a normal
pregnancy that was for a full
term of nine months.  During the first pregnancy, when she went
into labour she stopped feeling
foetal movements and the same thing
happened during her third pregnancy in the process of giving birth
while in hospital.
Her first baby had already died at birth and
the same applied to the third baby.  It transpired at some point
that both the
first and third babies who both died were males.
With regard to A she testified that she was fully mobile without any
help
and she therefore classified her as being GMFCS 1 in her
report.  She and professor van Toorn also agreed with each other
on this in their joint minute.  They also agreed that she had a
dyskinetic type of celebral palsy functioning at level 1 with
severe
global developmental delay.  She was asked about Volpe’s
criteria for neonatal encephalopathy that would implicate
the
intrapartum period.
[127]
She testified that according to Volpe
[4]
the neurological syndrome that accompanies serious peripartum hypoxic
ischemic injury is the prototype for neonatal HIE.
In
considering the nature and timing of hypoxia-eschemia as the etiology
of neonatal HIE, three features are considered to be important:
1.
The evidence of foetal distress and of foetal risk for
hypoxia-ischemia, for instance foetal heartrate abnormalities,
sentinel
event, foetal acidemia; 2 the need for resuscitation and or
low apgar scrores; 3, an overt neonatal neurological syndrome in the

first hours or day of life.  She testified that neonatal
encephalopathy is divided according to mild, moderate or severe
degrees.  A had mild neonatal encephalopathy after her birth
until the 4 January 2016.  It is only when she suddenly
deteriorated on 4 January 2016 that the question of a change to
moderate neonatal encephalopathy came into discussion.  She

testified that if one takes these criteria and apply them to A, the
people who did the delivery did not think there was foetal
distress
and/or foetal risk for hypoxia-ischemia.  There was a need for
resuscitation.  Therefore, criteria number 2
was met and
criteria number 3, she did have a mild neonatal encephalopathy but
definitely there was no moderate to severe neonatal
encephalopathy.
[128] When A deteriorated
on 4 January 2016, her HIE score was still 6 out of 22.  That
means her score of 6 out of 22 would
fall in the mild category.
But if there were seizures that may have turned into the moderate
neonatal encephalopathy.
Contrary to what is usually seen in
severe hypoxic-ischemic encephalopathy that leads to brain injury,
A’s level of consciousness
was normal despite not feeding and
then suddenly deteriorated on 04 January 2016.  The evolution
according to Volpe, of the
overt, neurological syndrome, hypoxic
ischemic encephalopathy is the first 12 hours, 12 to 24 hours, and
then from between 24 and
72 hours and then beyond 72 hours.  So
contrary to what is usually seen, this case is not a typical case of
neonatal encephalopathy.
[129] Professor
Andronikou who compiled the MRI report described the injury that he
had seen on the MRI as one that could possibly
fit in with
hypoxic-ischemic brain injury but that other causes such as
metabolic, infective and toxic causes would need to be
excluded.
Metabolic causes also include genetic causes. He did not mention
supper added hypoglycaemia.  She testified
that as neorologists,
they start with the history.  In the case of A, there appears to
have been no concerns during the pregnancy.
The factual
witnesses did not detect foetal distress.  She was born flat and
needed resuscitation but her level of consciousness
improved
immediately.  She did have a problem with feeding and then there
is a debate about how much of it could be attributed
to her and how
much to her mother.  At most she would have scored a mild
neonatal encephalophathy.  Although children
with HIE can
improve and then deteriorate, she did not show that progressive
deterioration over the next hours and days until the
4 January 2016
when she started having seizures.  At that point her HIE score
was done and it was 6 but she was clearly ill.
She had
difficult to control epileptic seizures which had to be treated with
two drugs.  After that her development has been
slow.  Her
biggest problem when she saw her was that she had cognitive
impairment and not her motor function which was level
1.
[130] A had atypical
history in the neonatal, perinatal period and peripartum period.
This is a very unusual neonatal encephalopathy.
Her situation
taken as a whole does not sound like the usual post hypoxic-ischemic
cerebral palsy that is normally seen.
The features in the MRI
scan are atypical and the reporting radiologists mentioned that other
conditions would need to be excluded.
Professor van Toorn and
herself then agreed that metabolic and genetic testing needed to be
done.  Indeed, shallow testing
was done but further testing was
unfortunately prohibited.  When one looks at the family history
as a whole, there are four
children and the mother said she had the
same partner.  He was not open to being examined.  There
were two boys who then
died and the history indicates that they may
have died during the labour process.  A has a neurological
condition.  Then
the youngest daughter had a normal birth or at
least her apgar scores were normal.  Out of the blue she had a
seizure which
was investigated and no cause was found.  She did
not have any other signs of neonatal encephalopathy.  Not only
was
the examination of the fourth child prohibited but also a request
to do further genetic testing on the blood of A that had already
been
sent overseas was prohibited and that blood was ordered to be
destroyed.
[131] With all these
uncertainties it is not known what further examination and chromosome
studies would have revealed but it looks
like there is a genetic
disorder in this family.  It looks like the two male children
were exceptionally vulnerable and they
died during the process of
being born.  Then there is A with her condition and then there
is the fourth child.  Both
girls did not have the same clinical
picture but A had a neonatal encephalopathy level 1 from her birth on
31 December 2015 until
the 4 January 2016.  The fourth baby was
normal until two days after delivery.  Both of them developed
epilepsy.
There is therefore a need to exclude epileptic
encephalopathy and X-linked genetic disorders and there is a need to
exclude genetic
conditions that would interfere with delivery of
energy.  It appears that during the normal asphyxia process of
birth, the
children who were normally grown up with no evidence of
intrauterine growth restriction, but the moment they suffered
asphyxia
and the stress of the asphyxia, they just decompensate it
and the males died.  They were stillborn and A was born in a
flat
state.  There was therefore a need to look at the genes
that would generate energy and the genes that code for membrane
stability
which would be the genes that are affected in the epileptic
encephalopathies.
[132]
During cross-examination Dr van Rensburg was referred to an article
by Bhorat
[5]
in which the
writers say that clinical features that should prompt evaluation for
genetic metabolic conditions in a patient presenting
with symptoms of
cerebral palsy are an absent history of any perinatal risk factors
for brain injury.  It was then put to
her that genetic testing
or metabolic testing should be considered in cases where you do not
have a history for brain injury and
that abnormal or a pathological
FHR would be a perinatal risk factor for brain injury.  Her
evidence was that one cannot take
the absence of one single factor
and conclude that there should be no genetic testing.  It cannot
be said that because there
is an abnormal CTG there should be no
genetic testing.  She was asked if the court were to accept the
evidence of Dr Murray
and professor Anthony regarding the features of
the CTG, her opinion would change and she would therefore accept that
A had an
intrapartum hypoxic ischemic injury.  She testified
that as a neurologist she still had difficulties with the doctors
being
there and not seeing any evidence of foetal distress.
Furthermore, there was the retrospective finding based on a very poor

CTG in circumstances in which the CTG may be affected by other things
that are not distinguishable from how it would read in respect
of
foetal distress.
[133] It was put to Dr
van Ransburg that seizure activity might have taken place but missed
because for the first three days in
hospital there was skeleton staff
with relatively fewer observations of the child and the child was
lodging with its mother and
not at nursey.  Her evidence in that
regard was that while it was possible that some clinical seizures
could have been missed,
most of the seizures occur within 6 to 12
hours of delivery if it was hypoxic ischemic in nature.  During
that period Dr Mans
was still on duty where he popped in again to see
the mother and the child.  If there were any severe or prolonged
seizures,
there would have been a change in the level of
consciousness of the baby and there was no evidence of that.  It
was further
put to Dr van Ransburg that clinical features that should
prompt the evaluation for genetic and metabolic conditions were not
present
in A.  She disagreed with that postulation saying that
clinical means history and examination.  Any parent who has lost

two children before birth should in any case be genetically
investigated.  Then there is a child with a disability and
another
one who had seizures in the neonatal period.  A family
history is clinical evidence which is prominent in this case.

With regard to the absence of the history of any perinatal risk
factors for brain injury which would be absence of a risk factor
like
intrapartum asphyxia, as the question was put to her, she testified
that it cannot be said that there were no perinatal risk
factors in
light of the family history.  The terrible obstetric history was
a huge perinatal risk factor which professor van
Toorn agreed should
be regarded as a distal factor.
[134]
The defendant’s next witness was professor Rothberg who
together with professor Smith did a joint minute as neonatologists.

He testified that the clinical information in this case was that
there were four pregnancies.  Two males who died and two
females
who had seizures and one progressed to cerebral palsy.  He
explained that a phenotype is what a person, the individual
looks
like and the genotype is what the genetic pattern would look like
when one investigates it.  In this case there is a
picture of
babies that appear to have grown well during pregnancy and then have
different outcomes with the boys dying, either
immediately
postnatally or before birth.  The females survive with variable
expression.  He said that this is a genetic
picture that needed
to be further investigated.  He referred to ACOG, the American
College of Obstetric Gynaecology and the
AAP, the American Academy of
Paediatrics task group on the study of encephalopathy and cerebral
palsy
[6]
. Therein the writers
say:
“
To
determine the likelihood that an acute hypoxic-ischemia event that
occurred within close temporal proximity to labour and delivery

contributed to a neonatal encephalopathy, it is recommended that a
comprehensive multidimensional assessment be performed of neonatal

status and all potential contributing factors, including maternal
medical history, obstetric antecedents, intrapartum factors
(including heart rate monitoring results and issues relating to
delivery) and placental pathology.”
[135] In this case a
multidimensional assessment would obviously include the family
history and the obstetric antecedents.
He testified that
essentially the plaintiff’s case was that the proximal risk
factors led to the neonatal encephalopathy
and cerebral palsy.
He said that there are proximal risk factors and distal risk
factors.  The proximal risk factor
which is close to the
intrapartum period is said to be the sole problem in this case which
caused the neonatal encephalopathy.
This was said to be,
according to professor Smith, an obstetric problem which is pathway
A.  Pathway B talks about distal
risk factors.  Distal
means far away from the time of delivery whereas proximal risk factor
would be closer to the time of
delivery.  A family history would
be a distal risk factor.  An antepartum distal risk factor would
be something like
if the mother develops hypertension during
pregnancy, diabetes or HIV.  The question in this case is
whether there was a proximal
risk factor, the intrapartum asphyxia.
He explained that the delivery itself is a high risk situation.
[136] He testified that
in his joint minute with professor Smith, the latter was arguing
pathway A whereas he argued pathway B.
He was making a case for
genetic investigation.  He referred to professor Andronikou’s
report.  He said the genetic
investigation was not sufficiently
done.  He said professor Andronikou had opened the door and was
in fact recommending genetic
investigation where he says “the
patient requires evaluation by a paediatric neurologist and may have
to undergo testing
for metabolic disorders.”  He then
referred to what professor Smith says in his joint minute:
“
Neonatal
hypoglycaemia may injure the thalamic pulvinar.  The pulvinar is
injured in the present matter.  The thalamic
pulvinar has been
highlighted as a distinguishing factor when determining whether the
HIE injury was compounded by neonatal brain
injury related to
hypoglycaemia.”
[137] Professor Rothberg
further testified that there are typical occipital changes as well.
In his opinion with regard to
professor Andronikou’s report,
the changes were not obvious and had the changes of hypoglycaemia
been obvious, then professor
Andronikou would not have just included
it in the list of metabolic disorders but would have been specific
about the hypoglycaemic
changes being present.
[138] Professor Rothberg
continued with his evidence explaining his argument for genetic
testing.  He referred to the plaintiff’s
literature bundle
in an article written by Cowen et al 4 published in 2003 which he
said is frequently referenced in the discussion
of whether an injury
was intrapartum or antepartum.  He said at page 261 the authors
say:
“
Our
data do not exclude the possibility that antenatal factors could
initiate a causal pathway for perinatal brain injury and that
they,
possibly together with genetic predispositions to hypoxic-ischemic
injury, might make some infants more susceptible than
others to the
stressors of labour and delivery.”
[139] He testified that
in his joint minute with professor Smith they are in agreement
regarding the following.  The baby developed
and presented with
mild hypoxic ischemic encephalopathy between birth and around 16:29
on 3 January 2016.  They agreed that
at 16:29 was the first time
that the bilirubin results indicated an abnormality.  Dr Mans
did the bilirubin at that time.
[140] They agreed that
the foetus suffered intrapartum hypoxic ischemia.  However,
professor Smith goes for pathway A and it
means that it is the result
of the insult during the management of labour.  On the other
hand, he testified that he could
not exclude additional asphyxia as a
result of obstetric management but he agreed that there was
intrapartum hypoxia ischemia.
They also agreed that the
neurological condition (encephalopathy) worsened around 4 January
2016.  Suddenly there was fitting
and that changed the condition
at 16:00 on the 4 January 2016 which was some 95 hours after birth.
He explained that professor
Andronikou’s report was equivocal
with “may” being highlighted.  They also agreed on
cerebral palsy based
on the joint minute of the paediatric
neurologists as they both did not see the child.
[141] He testified that
24 hours after birth there is a note that the baby was sucking well.
Under those circumstances admission
to a high care unit or ICU for
intensive care monitoring would have been inappropriate and there
were no features of a progressive
HIE.  The clinical progression
between days one and five was not compatible with the progressive
HIE. Consequently, other
causes for the encephalopathy as manifested
by the seizures must be considered.  Professor Smith is of the
opinion that substandard
intrapartum obstetric care directly
contributed to the child’s neurological disability and that
timeous expedited delivery
would have avoided the outcome.
Furthermore, had proper neonatal care been afforded to the baby, the
possibility of aggravating
factors occurring and contributing to the
outcome such as hypoglycaemia would have been avoided altogether.
[142] Professor Rothberg
testified that in the absence of the family history in this case
there would likely have been little to
argue other than the presence
or severity of foetal distress.  However, the family history
cannot be ignored.  Significant
factors include four
pregnancies.  Two males died late in pregnancy or shortly after
birth.  A female presented with
HIE and subsequently developed
cerebral palsy and global developmental delay.  A second female
is reported to have had seizures
on the first or second day of life.
This pattern of males being affected while females are less so
affected, fits with recognised
modes of inheritance, X-linked or
mitochondrial disorder.  The onset of seizures was late for a
progressive HIE, therefore
other causes for the late neonatal
encephalopathy should be sought.  He concluded his main evidence
by saying that the distal
risk factor or the genetic factor plus a
proximal risk factor of asphyxia would have led to neonatal
encephalopathy.  The
final outcome was cerebral palsy related to
a combination of factors.  It is not clear that expedited
delivery would have
altered the outcome.
[143] Professor Rothberg
then testified under cross-examination.  He said that indeed it
was his evidence that the foetus suffered
intrapartum
hypoxia-ischemia.  However, he was of the view that the
intrapartum hypoxia-ischemia may have underlying mechanisms.
In
pathway A it is postulated that the intrapartum asphyxia was largely
the result of what happened during the intrapartum phase
which would
be an obstetric issue.  On the other hand in pathway B which is
what he postulates, the intrapartum asphyxia was
also related or
alternatively related to the normal asphyxia process as has been
described very well by professor Anthony that
every baby suffers
asphyxia.  In a situation of a primed foetus, that intrapartum
asphyxia, that normal asphyxia may become
pathological.
Therefore, he was only in agreement that there was intrapartum
asphyxia.  While he accepted that the normal
asphyxia does not
result in HIE, A was not a normal baby, it was a primed baby in which
the labour may trigger the pathology.
He was aware that the
neonatologists are in agreement that at birth there was neonatal
encephalopathy which was the result of intrapartum
hypoxia-ischemia
which was assessed as mild HIE and he agreed with that.
According to Volpe the sequence of events is that
following the
hypoxic-ischemic insult and a brief period of apparent improvement
between 24 and 72 hours of age, the level of consciousness

deteriorates in neonates whose HIE is progressing.  After 72
hours, the stupor continues and abnormal sucking, swallowing
and
tongue movements prevent feeding.  In A’s case the problem
was only poor latching.
[144] There was no
deterioration in the level of consciousness between that time.
Both the notes and the evidence refer to
poor latching rather than
poor sucking.  In this case those who were observing the baby
did not observe progressive signs
of encephalopathy until 80 hours
and more.  Professor Smith agreed that in 24 to 72 hours there
is progression in most cases.
The evidence is that Dr Cilliers
examined the baby at 18:30.  At about 22:00 which was about five
to six hours after birth,
Dr Mans examined the baby and that was a
systematic examination in which he looked specifically at the
neurological status of the
baby and he found the baby to be normal.
After that the notes refer to poor latching.  Dr Cilliers
indicated positively
on breastfeeding and said an assessment was
necessary to assist with the feeding and then the note says sucking
well.  On
the issue of a long weekend and understaffing that was
mentioned, the evidence of Dr Mans was that there was a daily visit
to ensure
that the babies that could go home were able to go home
with their mothers.  Professor Rothberg testified that he agreed
that
there was no daily systematic investigation.  However, he
was of the opinion that a baby with a progressive encephalopathy
and
becoming more and more stuporous would be obvious to the nursing
staff who are constantly cup feeding the baby.  Nurses
were cup
feeding the baby and the baby was able to feed.  All of that is
not a picture of a progressive encephalopathy with
a progressive
stupor.
[145] He accepted that
subtle seizures may be missed.  However, seizures occur in
concert will other signs such as progressive
deterioration in level
of consciousness.  It is impossible that if A was undergoing
progressive encephalopathy with interference
with the level of
consciousness, level of conscious tone etc, the nurses would not be
commenting about that.  The comments
of the speech therapist
were about 94 hours of age which was well after 72 hours on 4 January
2016 at 15:30. The baby was not comatose
or stuporous before 72
hours.  Something happened which was why Dr Mans asked, “why
now?”.  It is apparent
that the child had been normal up
until well into day 4 and suddenly there was a problem.  He was
of the view that the cause
of the late onset of seizures might be
bilirubin toxicity.  The child was not manifesting signs of
progressive HIE until the
point when she was assessed by the speech
therapist who made the observations she did.  With regard to
professor Andronikou
raising the red flag of possible metabolic
genetic conditions, he testified that conditions such as canavan
disease, krabbe disease
and wilsons disease are genetic conditions
and those were examples of genetic conditions that he referred to.
In light of
the family history, the child required an evaluation.
What professor Andonikou said was that the picture is not specific
for hypoxic-ischemic injury and therefore there should also be a
genetic evaluation or investigation.
[146] The last witness
called by the defendant was professor Christianson who had been
called as a subspecialist in genetics.
He testified that he
prepared a joint minute with Dr Gericke.  At some point in their
interactions as geneticists engaged
in the matter they became aware
of the fourth child who also had neonatal seizures.  Dr Gericke
suggested that a Whole Exome
Sequencing (WES) be done in those
circumstances with specific emphasis on cerebral palsy and epileptic
encephalopathy.
[147] Based on the
documentation that was available and A’s clinical features he
stated that he did not think that the first
four days of A’s
life were consistent with neonatal encephalopathy 2 or 3 or overt
neonatal neurological syndrome.
He therefore suggested that a
neonatologist should be consulted.  Then he became aware of the
third pregnancy outcome and
then the fourth pregnancy.  The
fourth child had been delivered apparently well until she fitted on
the second day of life.
He then recommended that the fourth
pregnancy needed to be assessed by an obstetrician.
Furthermore, the baby as well as
other members of the family needed
to be medically evaluated by a paediatric neurologist and a medical
geneticist.  He was
of the view that if indicated, the fourth
child should also have an MRI.  If it became necessary,
depending on what the MRI
showed, a medical genetic testing would
then be considered.
[148]
He then testified about a report from Centogene in respect of A.
He described the test that had been done as a deep
analysis of a
narrow field of metabolic disorders.  It is the same type of
testing that would be done in WES and WGS but it
is confined to a
specific number of disorders.  On this test there were no
metabolic disorders that were diagnosed.
There may be other
rare conditions that were not tested for but on the Centogene panel
for metabolic disorders the results were
negative.  Centogene
recommended WES as the next step.  While he was considering and
working on a WGS being done by Centogene,
a letter was received from
plaintiff’s attorneys prohibiting any further genetic testing
and prohibiting even the use of
the blood sample that was already
with Centogene
[7]
.
[149] He testified that
when the said letter was received Centogene had some blood of A that
was left and therefore there was no
need for a further drawing of a
blood sample.  However, it may have become necessary to draw
blood from the mother and father
but in respect of A the further
testing could have been done with the blood sample Centogene already
had.  He testified that
metabolic disorder genetic testing had
been done.  He explained that basically genetic testing is a
process in which one can
test for a particular gene.  The next
test is for a panel of genes which cover a particular group of
problems.  There
is then WES which covers up to 80% of genes
that code for proteins needed to run the body.  Finally, you
have the WGS which
covers everything covered by WES plus many genes
known in the genome.  There are many problem causing genes but
the WGS will
look at the genes and if an abnormality is found it will
be pointed out.  He added that increasingly more problem causing
genes are being found and if one of them is found, it has to be
related to the phenotype of the particular individual to see if
it is
relevant.
[150] He testified that
his interpretation of professor Andronikou’s MRI report on A
was that there were four possible causes
for A’s condition.  It
was hypoxic ischemic injury of a combined acute profound and
partial-prolonged, toxic causes
and metabolic causes.  Those
would include canavan disease, krabbe disease and wilson disease as
well as post infectious causes.
He explained that professor
Andronikou did not have a clinical picture.  Therefore, in light
of A’s clinical phenotype
and the significant family history
including the 3
rd
and 4
th
children, a genetic
etiology other than a chromosomal imbalance which was largely
excluded by the Cento LCV or a metabolic disorder
largely excluded by
Cento metabolic testing must be added to the list of possible
causes.  He disagreed with Dr Gericke who
said that A had no
genetic predisposition.
[151] Under
cross-examination professor Christianson testified that both
professor van Toorn and Dr van Rensburg confirmed that
A had mild
dystonic cerebral palsy and he accepted that.  He also accepted
professor Rothberg’s opinion that she had
HIE grade 1.  On
day four after the seizures, the child developed neonatal
encephalopathy grade 2 with seizures which was
not typical of
neonatal neurological syndrome as described by Volpe.  He
explained that there was a difference between what
professor Rothberg
and professor Smith said when they suggested that the primary
etiology of A’s injury was hypoxic ischemic
in origin.
His understanding was that professor Andronikou said the features on
A’s brain may be due to hypoxic ischemic
injury of a combined
acute-profound and partial prolonged nature meaning it was possible.
However, the pattern of injury
in A can also be seen in toxic,
metabolic and post infectious causes.  This means that it may
not be hypoxic ischemic of acute
profound and partial prolonged.
It may be due to a toxic cause, or a metabolic cause or post
infectious cause.  He therefore
did not consider professor
Andronikou’s report to mean that hypoxic ischemic injury was
the primary cause.  After becoming
aware of the third and fourth
child he decided to add into the list of possible causes, the genetic
causes.
[152] Professor
Christianson was referred to a report of the defendant’s
radiologist, Dr Schwartzberg in which he inter alia
opined that the
features in the MRI scan in A are consistent with hypoxic ischemic
encephalopathy due to perinatal ischemia.
Professor van Toorn
also compiled a report in which he agreed with professor Andronikou
that the abnormalities seen in the MRI
scan were those of chronic
evolution of a global insult due to hypoxic ischemic injury of a
mixed acute-profound and prolonged
partial variety occurring in a
brain of term maturity.  In his evidence professor van Toorn
also pointed out that the two
radiologists, professor Andronikou for
the plaintiff and Dr Schwartzberg for the defendant concurred that
the pattern of injury
is that of hypoxic ischemia.  While he
agreed that Dr Schwartzberg made the findings that he did and
professor van Toorn made
the statements attributed to him, he pointed
out that professor Andronikou made it clear that the injury pattern
“may”
and bolded the word “may” which was
critical in reading his report.  But he accepted that Dr
Schwartzberg’s
opinion was that it was hypoxic ischemic injury
of a partial prolonged and acute profound type.  Therefore,
there were significant
differences between the statements of the two
radiologists.  Professor Andronikou and Dr Schwartzberg differed
and there was
no joint minute between them and both of them were not
called to testify.
[153] It was put to him
that toxic and post infectious causes that professor Andronikou also
referred to have been excluded and
he agreed that they have been
excluded.  That leaves hypoxic ischemia and metabolic causes and
he added a third which is genetic
disorders or congenital disorders.
Metabolic testing largely excluded metabolic causes.  He
explained that as a geneticist
and in light of the additional
information and the family history and having known that A had
congenital macrocephally and the
fourth child who also had some
issues, he was of the view that genetic testing needed to be
explored.  He agreed that save
for hypoxic ischemic injury all
the possible causes that professor Andronikou mentioned have been
excluded but he considered genetic
testing to be necessary.  He
disagreed that evidence of foetal distress and a difficult labour
would militate against doing
further genetic testing.  He said
he accepted that A has cerebral palsy and that both Dr van Rensburg
and professor van Toorn
say she has mild dystonic dyskinetic cerebral
palsy.  It was put to him that the neonatologists, professor
Smith and professor
Rothberg have agreed in their joint minute that
the foetus suffered intraparturn ischemia and they are the correct
specialists
to make the diagnosis.
[154] He testified that
he had decided that the Cento-LCV test be done and professor
Andronikou had decided that the Cento metabolic
test be done so that
metabolic causes could be excluded.  The Cento-LCV test was done
to deal with his clinical diagnosis
of macrocephaly.  However,
the Cento-LCV test did not detect macrocephally.  He was looking
at the macrocephally as part
of the phenotype but when the discovery
of the 3
rd
and 4
th
children was made he had to
evaluate the situation because it revealed a significant family
history.  There were neonatal
seizures in both A and the fourth
child and all of this required further testing like WES or WGS.
That is how he got to write
to Centogene asking them for their
suggestions.  The LCV test which did not show congenital
macrocephaly was the baseline
test.  There are many other tests
that could be done including WES and WGS.
[155] Professor
Christianson was asked with reference to Dr van Rensburg who stated
in her report that A had dyskinetic cerebral
palsy as well as a
moderate degree of neonatal encephalopathy.  He said that on his
part he did not feel that the child had
cerebral palsy but deferred
to a paediatric neurologist.  He deferred to an obstetrician.
The issue of the fourth child
became a relevant factor when on day
two of her life, she developed seizures with no obvious reason when
she had apparently been
normal, having been born with normal apgar
scores and had been breastfeeding.  There were no questions of
hypoxic ischemic
encephalopathy in the first hours or day of life.
According to Volpe in the first hours or day of life there was no
overt
neonatal neurological syndrome.
Negligence.
[156] Some of the facts
about what happened on 31 December 2015 are largely common cause or
cannot be disputed, at least not cogently.
The plaintiff was at
a local clinic at 06:50 having started feeling labour pains at about
02:00 am that morning.  The clinic
decided to send her to
hospital for the management of the labour after a vaginal examination
had been done and the cervical dilation
had been assessed.  She
was found to be 5cm dilated at the clinic.  She arrived at
Zithulele Hospital at 09h00 at which
time the first entry in the
partogram was made.  Her cervical dilation was assessed and it
was found that she was still 5cm
dilated.  There appeared to be
no concern about the foetal condition.  Perhaps it is important
to note that at this time
there had been no progress in her dilation
as she had been assessed as being 5cm dilated at 06:50 at the
clinic.  Therefore,
by 09h00 it had been two hours with no
progress in dilation.  At 12:00 another assessment was done.
At this time the
heart rate was 160 bpm which according to Dr Murray,
was borderline high as the normal heart FHR is between 110 and 160
bpm.
In Dr Murray’s opinion regard, being had to the
plaintiff’s first child who was born at home as a still born,
this
slow labour progress was concerning.  She testified that
according to the partogram at 14:00 there was no cognisance taken
of
the slow labour progress and consequently no plans were made to
remedy it.  There was no documented heart rate for two
hours
from the last plotting at 12:00 which had shown abnormality.
There should have been plotting at least every 30 minutes
and this
did not happen.
[157] It was also common
cause that there was poor recording of the monitoring which therefore
meant that the observations that
were done were not always recorded
to see the heart rate, accelerations, decelerations and variability
at different times.
What would have been observed from the CTG
should have been recorded in the notes and the partogram.
According to Dr Murray,
the partogram showed that no monitoring was
done for four hours from 12:00 to 16:00.  When the plotting was
done on the partogram
the FHR baseline was 170 bpm at 16:00 and it
dropped to 140.  This means that the FHR baseline was higher and
therefore there
was tachycardia.  The FHR was two high and then
there was slowing after contraction, a pattern similar to 12:00 where
it had
been at 160 bpm.  Dr Murray was of the opinion that on
the reading of the partogram, it appears that foetal distress was on

going between 12:00 and 16:00 as shown by the baseline FHR having
gone up from 160 to 170.  The recording of the FHR of 150
to 155
in the notes does not agree with what appears in the partogram.
[158] According to Dr
Murray the report of professor Andronikou refers to acute profound
and partial prolonged brain injuries.
This means that he found
evidence of brain injury that occurred suddenly and evidence of brain
injury that would have occurred
over a long period of time.  The
evidence of brain injury over many hours was in keeping with what
appears in the notes where
the first recording of foetal distress was
based on decelerations on the partogram was at 12:00 but the baby was
only delivered
at about 17:00.  The five hour period was enough
period for the baby to sustain brain injury as the baby would have
been struggling
to maintain normal oxygen levels for five hours while
in distress.  That made the foetus more vulnerable to injury so
that
even the normal birth process might have been the last straw
which the baby could not cope with.
[159] Based on the
maternity case records, Dr Murray summarised her evidence on the
active phase of labour.  I must again point
out that most of
this evidence is common cause, having been gleaned from the maternity
case records.  At 12:00 the partogram
suggested decelerations
but assessment no.2 does not and the recorded FHRs are different.
At 14:00, according to the partogram,
the cervix was 5cm dilated with
no recorded FHR.  However, according to assessment no.3, the
cervix was 7cm dilated which
showed a discrepancy regarding the
cervix.  At 15:00 the cervix was 7cm dilated but there was no
recording of the heart rate.
At 15:00 an order was given for
syntocinon infusion but there is no record of a reactive CTG at
15:00.  At 16:00 the cervix
was fully dilated according to the
partogram with two strong contractions in 10 minutes.  The FHR
was 170 bpm before contraction
and 140 after a contraction with late
decelerations.  However, according to assessment no.4 at 16:00,
the cervix was 10cm
dilated with strong contractions with a FHR of
150-155 bpm with a reactive CTG.  Therefore, what was on the
partogram and
the assessment notes were completely different.
[160] She also testified
about the faded CTG tracings which she had taken pictures of with her
cellphone and enhanced them to improve
their legibility.  The
admissibility of such evidence to which the defendant objected very
strongly with the defendant’s
expert refusing to have regard to
the faded CTGs saying he could not read them is being questioned and
objected to.  I will
deal with this issue pointedly later in
this judgment.  Dr Murray further testified that if the
partogram had been plotted
correctly, the labour progress would have
crossed the action line at 13:00 indicating a need for a doctor to
make an assessment
and decide on the required intervention.
This could have been allowing more time, rapturing the membranes
which, in any event,
had ruptured spontaneously at 12:50, giving
oxytocin or performing a caesarean section.
[161] Her opinion was
that there were several significant labour related risk factors for
hypoxic brain injury.  These were
the prolonged labour, the use
of oxytocin, substandard foetal monitoring especially during oxytocin
administration and the complicated
second stage of labour which
necessitated instrumental delivery.  With regard to whether or
not the oxytocin was administered,
she was of the firm opinion that
it was administered.  She based her opinion in this regard on
the contraction pattern which
showed hyperstimulation.  There
should also have been a nursing note explaining why it was not given
as the doctor had ordered
it, if it had not been given.  If the
pre-requisites for it were met, which were a reactive CTG and a
catheter, logic dictates
that it would have been given as the doctor
had ordered it.  If it was not given it could only be because
the CTG was not
reactive meaning the FHR was not normal.
[162] She testified that
at 12:00 there was an indication for a caesarean section as there was
a delayed labour progress.
At 14:00 the labour progress
continued to be poor and therefore due consideration should have been
given to performing a caesarean
section.  In this case the
cervix was dilated at 5cm at 06:50 and was 7cm at 12:00.
Therefore, the plaintiff had progressed
only 2cm in five hours.
By definition labour progress was poor.  There was substandard
care in her opinion in the failure
to timeously diagnose failure to
progress, the failure to plot the partogram accurately which led to
the failure to diagnose the
poor labour progress, the failure to
react to probable foetal distress from as early as 12:00, the failure
to react to foetal distress
at about 16:10, and the probability that
oxytocin was given in an unmonitored manner.  That would have
led to severe uterine
tachysystole which was also unrecognised with
the foetal distress that came with it.  All of this happened to
a patient who
was a high risk as she had already lost another baby.
The contraction pattern of 10 to 11 contractions in 10 minutes
suggested
the use of a uterine stimulant and tachysystole was in
keeping with the use of syntocinon.  It was contended on behalf
of
the plaintiff that the essence of Dr Murray’s evidence was
not disputed by any of the defendant’s witnesses.
[163] Professor Anthony
testified that the hospital notes started at 09:00 and that entry was
incorrectly plotted on the latent
phase part of the partogram graph.
A patient who is not progressing in labour needs to be carefully
assessed and the reason
for the slow progress needs to be found.
In a parous woman the diagnosis of the slow progress should lead to
the critical
assessment of the labour to look for signs of pelvic
disproportion.  In such circumstances oxytocin should only be
prescribed
with great caution after such examination.  The FHR
on the partogram was recorded only at 12:00 and at 16:00.  The
expectation
is that during the active labour phase, the observation
of the FHR should be done before and after contraction every half an
hour.
Therefore, the number of observations were clearly not
according to the prescripts even for patients who are completely
normal.
The foetal well-being was inadequately assessed.
At 12:00 it was the first time in which the partogram was correctly
plotted
before and after contractions as it is shown by the different
heart rates before and after contractions.  From 12:00 onwards

the FHRs were slower after each contraction compared to the baseline
rates.  The difference in the observed FHRs is significant
and
should have led to the suspicion of foetal hypoxia.  This should
have led to the introduction of continuous CTG monitoring
with
re-evaluation of the tracing every 30 minutes.
[164] There does not
appear to have been a consideration of foetal hypoxia or foetal
distress as a possibility.  At no stage
did anybody take
cognisance of the fact that the baby might be hypoxic which was
substandard care.  At 12:00 the disparity
between the pre and
post contraction heart rate was observed but the significance thereof
was not taken into cognisance by the
attending staff.  The
plaintiff reached full dilation at 16:00 with the nursing staff still
recording a large disparity between
pre and post contraction rates.
The CTG tracing at this time was pathological even though it is not
known for how long that tracing
was pathological.  What is known
and discernible is that that tracing was abnormal from the
beginning.  The tracing he
received was faint but he examined it
with a good light and a magnifying glass and used a felt pen to
highlight the tracings. He
was able to make out a discernible
tracing.  He enhanced it by tracing what was available in order
to determine the pattern
of the abnormality.  The tracing begins
at 16:00 and for the first two minutes it shows a baseline of about
145 bpm followed
by a FHR tracing that decelerates progressively down
to sometimes as low as 55 bpm.  When it reverses the baseline
heart rate
is 145 bpm.  Once it gets back up to the baseline
there is a brief period of tachycardia which means a heart beating
very,
very faint going up to about 170 bpm.
[165] This is followed by
a decline with further decelerations being evident for the rest of
the tracing.  There were repetitive
decelerations until the
tracing ended at about 16:25 and the baby was delivered at 17:10. He
could see nine contractions which
is tachysystole.  With such
frequent contractions there was not enough relaxation time between
them for the baby to get more
oxygen to maintain normal metabolism.
That tachysystole is a recognised complication of an oxytocin
infusion.  Its evidence
in the tracing starts from 16:00 to the
end of the tracing.  If the tracing falls into a pathological
category there is a
high probability that the baby is hypoxic and
acidotic.  When there is foetal distress especially in the
second stage of labour
oxytocin must be stopped. The mother must stop
pushing and the contractions must be stopped and intrauterine foetal
resuscitation
must be done.  Tocolytic drugs should have been
used to relax the foetus.  Both the contractions that were being
augmented
by the use of oxytocin infusion and the maternal bearing
down effort should have been stopped to allow restoration of foetal
oxygenation
through intrauterine resuscitation prior to the expedited
delivery.  According to the available hospital records the
pathological
tracing was not recognised and the necessary
interventions did not take place.  That was substandard care
which was directly
linked to an increased likelihood of an adverse
outcome.  More than 5 contractions in 10 minutes constitute
tachysystole.
The decision to allow the mother to push in the
face of a pathological tracing was substandard care which would have
increased
the likelihood of foetal hypoxia.
[166] The patient
remained at 7cm of dilation for three hours up to 15:00.  At
12:00 disproportion and foetal distress should
have been considered
and critically evaluated. Not doing it was substandard care.  By
14:00 the progress of labour was non-existent
for the preceding two
hours and there is no recording of the FHR charted on the partogram
despite a previous abnormal finding.
There should have been an
intervention by means of caesarean delivery as early as midday as
there was an indication for it.
However, the baby was delivered
after 17:00, some five hours later.  The indication for
caesarean delivery at 14:00 was shown
by the ongoing failure to show
adequate progress of labour.  The same indication existed at
15:00.  The failure to correctly
complete the partogram led to
the late recognition of slow labour progress.
[167] In the partogram
only two contractions per 10 minutes were recorded throughout the
entire course of the labour.  On the
available CTG tracings
there were quite clearly numerous contractions every 10 minutes and
not two per 10 minutes as depicted in
the partogram.  The
problem of the FHR from 12:00 went unrecognised by the nurses.
The decision to use oxytocin should
have followed a very careful
assessment of the labour which did not happen.  Foetal distress
was not excluded before the introduction
of oxytocin.  It was
prescribed for a parous patient.  The foetal distress went
unrecognised and no intervention took
place.  On the contrary,
the mother was encouraged to push and she was given oxytocin.
Encouraging her to push and the
use of oxytocin were contra-indicated
because of the pathological tracing.  All of that was
substandard care.
[168] There was a period
of 5
1/2
hours during which there was evidence that the
baby was trying to compensate by slowing her FHR after contractions
because it was
becoming hypoxic.  It was likely that there was a
gradual worsening hypoximia.  In addition to that, oxytocin was
introduced
and the mother was encouraged to bear down in the second
stage of labour which more than likely led to the sudden
intensification
of the hypoxic stress as evidenced in the
pathological tracing.  The neuroradiological diagnosis provided
by professor Andronikou
was that of acute profound hypoxic injury and
partial prolonged injury to the foetal brain.  That is
consistent with what
appears to have happened during the course of
this labour.  The apgar score of 7 at 5 minutes did not
necessarily exclude
the possibility of acidosis.  As an
obstetrician, his view was that there was evidence of foetal
distress.  The baby
needed some support at the time of delivery
as the neurological syndrome took place.  The prerequisites for
a diagnosis of
neonatal encephalopathy due to intrapartum asphyxia
are present in this case with no obvious explanation.
[169] His conclusions
were that this was an uncomplicated pregnancy.  The mother went
into spontaneous labour at term.
The problem arose with the
management of the labour which was characterised by substandard care
in a number of respects.
The FHR monitoring was infrequent and
incorrectly interpreted or at times not interpreted at all during the
first stage of labour.
There was inadequate monitoring of the
active phase of labour which included the inadequate use of the
partogram.  Oxytocin
was used without a proper prior assessment
to exclude disproportion and without excluding the possibility of
foetal distress.
The second stage of labour was not adequately
managed.  It was allowed to continue despite the fact that the
tracing was abnormal
and the mother was allowed to push.  The
oxytocin was allowed to continue.  His final conclusion was that
“
the adverse outcome was consistent with intrapartum hypoxia
which would have been avoidable with a proper standard of intrapartum

care leading to delivery at several points where intervention might
have been indicated well before the actual delivery at 17:10.
”
[170] Sister Mbada’s
evidence on negligence was that she attended to the plaintiff’s
labour.  She testified that
the order for syntocinon meant that
it should be given 30 minutes after a reactive CTG.  If it is
administered a drip is inserted
with a catheter also applied.
The syntocinon is added into the drip.  The prescription from
the doctor for syntocinon
was made at 15:00.  At that time the
plaintiff was still 7cm dilated.  The instruction was that the
CTG must be reactive
before the syntocinon was infused and the
catheter was applied.  When infusion is started a tick is made
every time it is
infused.  She confirmed that if there are
changes in the intensity and frequency of the contractions syntocinon
is not started.
If infusions continue a tick is made on the
prescription form.  If it is discontinued she would write
“infusion stopped.”
Because there were no ticks it
meant that syntocinon infusion was never started at all.  She
did not have a recollection of
what happened on that day and for her
evidence she relied on the maternity case records.
[171] She took over
monitoring the plaintiff at 12:00 and at the time she did not realize
that the partogram was started incorrectly.
She confirmed that
the completion of the partogram is essential in the management of the
labour.  She confirmed that she made
a mistake on the partogram
at 14:00 when she recorded 5cm dilation whereas in the clinical notes
she recorded 7cm.  She accepted
that it was a mistake on a very
important aspect of the monitoring of the labour.  She accepted
that the CTG drawn by professor
Anthony and shown to her was abnormal
with at least 8 contractions per 10 minutes at 16:00.  However,
nowhere in assessments
no.4 or 5 did she indicate that she suspected
foetal distress.  At no stage did she suspect that the foetus
was in distress
and that action should be taken to remove the stress
or to do an emergency extraction or a caesarean section.  The
second
stage in this case was prolonged but she did not write the
time when the plaintiff was fully dilated.  She did not accept
that the fact that dilation improved from 7cm at 15:00 to 10cm at
16:00 which was 3cm in one hour was way faster than the norm and

indicative of oxytocin having been administered.
[172] Dr Linde’s
evidence was that she made an entry on the partogram at 15:00 when
she performed a PV examination on the
plaintiff.   She
assessed the cervix to be 7cm dilated and the head of the baby was
three to four fifths above the pelvic
brim.  At this time the
plaintiff had crossed the action line on the partogram.  She put
her on a drip with Ringers Lactate
and inserted a catheter.  If
there were signs of foetal distress syntocinon would not be
administered.  Ringers Lactate
is used to infuse syntocinon.
The prescription did not confirm that syntocinon was administered.
There would be a tick
if it was administered.  She was therefore
uncertain that syntocinon was administered.
[173] Under
cross-examination she testified that when she saw that there was poor
progress in labour her decision was to prescribe
syntocinon.
When she made the entry and the assessment of the plaintiff, she did
not record the FHR on the partogram.
There was no evidence on
the partogram of FHR at about 15:00.  There was no evidence of a
reactive CTG or a satisfactory FHR
for at least an hour before her
entries and syntocinon instruction.   She said that Ringers
Lactate could have been put
up for rehydration and not only for
syntocinon administration.  She intended to have syntocinon
administered.  When she
assessed the plaintiff she was satisfied
that there was no foetal distress and there was no indication of
CPD.  The partogram
was incorrectly plotted.  The progress
of labour was even slower than she appreciated and that by all
accounts the labour
was severely delayed.  The contractions were
inadequate from 14:00 which would necessitate the augmentation of the
labour
with syntocinon.  At 16:00 and assuming that it was
administered, there was no indication for it to be stopped.  The
entry at 14:00 was probably falsified as she only gave instruction
for syntocinon at 15:00.  There was nothing in the records
to
indicate that sister Mbada had any reason to believe that there had
been a change in the circumstances which rendered the administration

of syntocinon unnecessary.  If there was tachysystole it would
be on overwhelming indication that syntocinon was administered.
[174] Dr Koll’s
evidence was that he is a semi-retired obstetrician and
gynaecologist.  He agreed with Dr Murray that
there were several
significant labour related risk factors for hypoxic brain injury.
These were the prolonged labour, the
oxytocin infusion, substandard
foetal monitoring especially during oxytocin infusion and the second
stage of labour was complicated
leading to instrumental delivery.
However, there was a difference between risk and cause.  The
definition of tachysystole
is more than 5 contractions in a 10
minutes period.  That indicates that the uterus was being
overstimulated.  If contractions
were too frequent with no
sufficient gap in between the contractions the baby is in a greater
threat of having hypoxia.  For
that reason tachysystole has to
be managed on a fairly urgent basis.  He was not prepared to
comment on the CTGs or that there
was evidence of foetal distress as
he simply was unable to read those CTGs.  He was of the opinion
that if the baby was subjected
to that degree of hypoxic stress as
depicted in those CTGs for an hour before birth, she would have been
severely compromised at
birth.  The baby was clearly not
severely compromised.  He agreed that tachysystole would
increase the risk of an abnormal
heart rate and increased hypoxic
stress on a foetus but it does not always lead to a problem.  He
agreed that whether there
is a contraction putting stress on the baby
or whether there is bearing down putting stress on the baby or both,
the fact of the
matter was that there should not be more than 5
contractions per 10 minutes as that would increase the risk of
hypoxia.
Plaintiff’s
submissions on negligence and causation.
[175] The following
submissions on negligence were made on the basis of which it was
argued on behalf of the plaintiff that the
defendant was negligent in
the care of the plaintiff when she delivered A.  It was
submitted that sister Mbada’s evidence
was that she did not
have a clear understanding of the completion of the partogram and
made mistakes in the completion of the records.
She did not
make notes of everything that happened to the plaintiff during labour
and did not make notes of what the CTG traces
showed at any stage.
As there was delayed labour progress, action was mandatory in terms
of the guidelines whether it was
administering oxytocin or
performance of a caesarean section.  She was not allowed to
override the doctor’s orders regarding
the syntocinon infusion
unless there was a clear change in the circumstances of the
plaintiff.  If she did not comply with
the doctor’s orders
to infuse oxytocin she should make notes and there was no note made.
There were no circumstances
recorded that allowed her to ignore the
doctor’s orders.  She accepted that the CTG drawing by
professor Anthony was
the CTG belonging to the plaintiff and A. It
showed foetal distress.  She never thought that the baby was in
distress.
On the basis of all her evidence, it was submitted on
behalf of the plaintiff that sister Mbada contradicted herself.
She
admitted not doing the monitoring of the mother and foetus as
required.
[176] About the evidence
of professor Anthony and Dr Murray it was submitted that they are
both recognised experts in the field
of obstetrics.  Professor
Anthony is a worldwide renowned expert and a South African
representative in FIGO, the worldwide
body setting standards for
foetal monitoring.  Both professor Anthony and Dr Murray can
read and interpret CTGs.  It
was submitted that Dr Murray showed
a photograph of the original CTG on a screen in court.  It was
never suggested to her
in cross-examination that what she showed as
the heart rate and contractions on screen with her cursor did not
appear clearly on
the CTG tracings.  That CTG was clearly
pathological and contractions were clearly abnormal and both the
pathological heart
rate and grossly abnormal contractions could be
seen on the screen in court when she testified.  Professor
Anthony had enhanced
the same CTG tracings and confirmed that they
were pathological and the contractions were in excess of what normal
contractions
should look like.  Therefore, they deprived the
foetus of the rest time to oxygenate properly.
[177] It was submitted
that Dr Koll indicated in the joint minute that he could not see what
was on that CTG.  However, when
he testified his evidence was
that he could not see the cardio portion (heart rate) section of the
CTG but could see the tocograph
(contraction) section.  Even
though he could not see the cardio portion he then said that one
could not interpret the CTG
during the second stage because the
mother would be pushing.  On this basis, it was submitted on
behalf of the plaintiff that
Dr Koll was not an objective witness.
He suggested that the contraction pattern was not clear and normal
because the mother
was pushing.  Professor Anthony and Dr Murray
explained why Dr Koll was wrong and what the effect of pushing would
show which
would be the jaggedness of the lines which was not the
case.  Dr Koll’s evidence was that the tocograph showed
the mother
pushing uncontrollably.  It was submitted that it was
irrelevant whether the pattern in the tocograph was produced by
contractions
or pushing as it remained dangerous to the baby and the
nursing staff observing uncontrolled pushing should record it and
call
a doctor which sister Mbada did not do.
[178] Professor van
Toorn, a paediatric neurologist, testified on causation.
Submissions were made with regard to his evidence
on causation.
His evidence was that he assessed the hospital records in this case.
He testified that MRI scans do not
time the injury.  Therefore,
an MRI scan cannot tell when the injury happened, whether it was
within hours or days but it
can tell what the cause of the injury
was.  In order to time a brain injury a comprehensive approach
was required.  This
would entail looking at the risk factors
that could cause brain injury.  You look at things like the
onset of labour and the
period before birth.  You look at the
growth of the baby, the head circumference, whether there was
meconium stained liquor,
whether the mother had diabetes.
During the intrapartum period and during the process of labour, risk
factors are things
like whether the labour was prolonged and whether
it was properly monitored and whether there were bleeds etc.
After birth
you look at what could have compromised the baby, lack of
oxygen, did the baby collapse, was there infection, was there low
blood
sugar.  All of this is a comprehensive approach to
establish causation.  He testified that FHR monitoring is vital
because
it is a sensitive way.  If the baby is in trouble, you
will pick up abnormalities in the FHR.  If a FHR monitoring is

done, you will pick up if the baby is in trouble.  This is when
there is a lack of oxygen to the brain or lack of oxygen to
the heart
as there will be abnormalities in the FHR.
[179] Professor van Toorn
made reference to the guidelines. When there is no adherence to them
there is a potential of harm and
the guidelines provide best
practices.  If there is clear evidence of foetal distress you
have to intervene.  This is
because, the longer the baby remains
in a distress environment, the higher the risk of brain injury.
What happens is that
the baby tries to compensate by shunting blood
from the heart and if the distress is too long then it decompensates
which leads
to brain injury.  He referred to the reports of the
radiologists, professor Andronikou and Dr Schwartzberg.  He
pointed
out that they both agreed that the pattern of injury on the
scan was that of hypoxia ischemia.  This means that there was
lack of oxygen and diminished blood to the brain.  If there is
lack of blood to the brain, it causes damage because brain cells

require oxygen.
[180] The radiologists
concurred that the pattern of injury is hypoxia ischemia and the
injuries were of a combined nature.
This means that there was a
prolonged partial, meaning that it happened over a long time.
During that prolonged partial period,
the brain tries to protect the
core, that middle part, because that is where critical functions
occur during respiratory rate consciousness.
If there is
diminished blood flow to the brain, blood going to the outer surface
of the brain is shunted to the inner core to try
and protect the
middle part which is crucial for life.  The scans in this case
reflect that.  There was prolonged partial
happening over hours
and at some stage the brain could not direct the blood anymore to
protect the core as there was significant
compromise.  This led
to the injury to the centre, the middle part of the brain called the
thalamus and peri-rolandic cortex.
The MRI imaging showed that
there was exposure to hypoxia and lack of oxygen for hours whereafter
the compensation probably could
not help and there was decompensation
which then led to the damage to the middle part, the core of the
brain.
[181] Professor van Toorn
also referred to a suggestion by professor Andronikou that some of
the metabolic causes had to be excluded
mentioning three conditions
that had to be excluded.  He understood professor Andronikou to
be saying that hypoxic ischemia
was the most likely diagnosis of the
brain injury but metabolic causes had to be considered.  Upon
the blood becoming acidotic
through lack of oxygen, the baby tries to
protect itself.  If hypoxia continues, you get the
cardiovascular stage.  This
is when blood is taken from organs
that are not essential like the gut, the skin and the liver and is
sent to the heart and the
brain to protect these organs.  During
those two stages there is no injury to the brain even though there is
an insult.
The third stage is when there is not enough blood
going to the brain.  The brain sends blood from the brain’s
outer
surface just to protect the core, the inner surface. Then you
get a pattern of injury where there is damage to the outer surface
of
the brain but the inner core, the middle part is not damaged.
[182] This is called
prolonged partial and it usually takes hours.  This is because
when the uterus starts to contract, it
tries to push the baby down
which diminishes blood flow to the brain.  If there are strong
contractions you listen to the
FHR every half an hour before, during
and after contractions.  If that is not done, drops in the heart
rate may be missed.
When the mother is ready to deliver which
is the second stage of labour you listen to the FHR every 5 minutes
or after every second
contraction.  The reason it is done more
frequently is because the risk is higher because during all these
contractions the
baby becomes exhausted especially if labour is
prolonged and tired and then there is collapse.  During collapse
the heart
does not pump blood anymore leading to inadequate blood
flow to all parts of the brain.  This is why there is mixed or
combined
picture in which there is prolonged partial followed by
acute profound injuries.
[183] He referred to the
report of Dr Murray in which she said that foetal distress was not
acted upon.  There was also a prolonged
second stage in which
the baby was exposed to prolonged contractions than was necessary.
Guidelines provide that if the action
line is crossed for 5 hours the
baby is being put at risk.  If a potentially dangerous drug such
as oxytocin is administered
to an exhausted baby who is exposed to
prolonged contractions thus causing the uterus to contract even
further that can potentially
harm the baby.  He testified that
even though he did not see the CTGs he had no doubt that there were
FHR changes because
of the severity of the brain injury.  When
the baby came out it was flat and needed resuscitation.  During
the first
examination it was said that the baby was lethargic.
This means that there was depressed level of consciousness.  She

was sleepy and was not able to be raised at some stage.  She was
not sucking and had no suck reflex.
[184] Professor van Toorn
referred to Dr Murray’s report which referred to decelerations
and tachycardia which means the FHR
was high.  There were hours
where there was no recording at times for two to three hours.
He testified that where cerebral
palsy was caused by genetics, it
would cause brain malformations in most cases.  The brain looks
abnormal in this case and
often where there are genetic causes of
cerebral palsy, the image is often normal.  He considers genetic
causes if a child
has cerebral palsy but the scan is normal.  In
this case with this type of injury, the pattern showed hypoxia
ischemia and
it was unlikely that there were genetic causes that made
this baby vulnerable to hypoxia ischemia.  There were none of
the
risk factors of infection of the placenta or premature labour or
the baby being growth restricted.  The antenatal period was

unremarkable.  He agreed with professor Andronikou that the
abnormalities are those of chronic evolution of a global insult
due
to hypoxic ischemic injury of mixed acute profound and prolonged
partial variety occurring in the brain of a term maturity.
This
happened during the labour process based on all the considerations
and all the available evidence.
[185] The baby has
dyskinetic cerebral palsy as Dr van Rensburg agreed and there were no
dysmorphic features and therefore genetic
testing was not indicated.
He examined the child and could find no abnormalities in the other
systems because if you have
metabolic conditions sometimes they
affect not only the brain but also the heart or the kidney or liver.
Other possible conditions
were excluded.  He was also of the
opinion that the baby’s head growth was within normal limits.
He found no congenital
brain abnormalities or metabolic
abnormalities.  This baby was critically ill and had seizures
and required multiple medicines.
However, four years later she
had no further seizures.  There was no evidence of the baby
declining or developing new neurological
symptoms.  When he
examined her, the profile he got was consistent with the child’s
damage during labour from hypoxic
ischemia, not metabolic causes.
He looked at the evidence of infection of the brain.  The CT
scan did not report that.
The radiologists did not report that
there was an infection.  Because the baby became very ill and
started having fits, the
doctors looked for infections and even
looked at the possibility of meningitis or blood infection.
Blood tests came back
negative.  The baby was well grown and the
head circumference was normal and at the onset of labour the FHR was
reported as
normal.
[186] He testified that
according to Volpe, prolonged labour is a well recognised risk
factor.  Secondly, the baby needed resuscitation
and was
reported as being flat.  Thirdly, she had neurological syndrome
within the first hours or days of life.  The
first examination
showed the baby being lethargic with no suck reflex.  The next
morning there was excessive crying, poor
feeding and on day four the
baby started having fits.  Subsequently she had to be
hospitalised for 11 days.  She needed
to be tube feed through
the nose because she was not sucking and she was unconscious.
The neonatal records support that the
baby was born in a compromised
state and required resuscitation.  That supports foetal
distress.  He testified that if
the baby had a metabolic
condition that caused seizures one would expect the baby to have had
seizures for her whole life because
metabolic problems do not
disappear.  The baby had no seizures since being discharged from
hospital.  His opinion was
that the way the child developed in
the last four years to the time he saw her was consistent with being
damaged during labour
because of hypoxic ischemia.  When there
is cerebral palsy, the lesion to the brain is static.
[187] Professor van
Toorn’s evidence on macrocephaly was that A had a cephalic
haematoma which is a bleed outside the brain
between the scalp and
the bone which could increase the head circumference.  However,
the ratio between the head circumference
and the weight is within
limits.  If there was a genetic macrocephaly, the macrocephaly
would persist.  However, that
was not the case with A as her
head circumference became normal later on.  The megalocephaly
postulated by professor Rothberg
is one of the causes of
macrocephaly.  Macrocephaly simply means an enlarged head
circumference whereas megalocephaly implies
the enlargement of the
brain.  It is a developmental disorder but the MRI imagery did
not report it and therefore it can be
discarded.  Therefore,
both macrocephaly and megalocephaly can be discarded.
[188] On apgar scores,
professor van Toorn said they should not be interpreted in isolation
as they are generally poor predictors
of outcome.  The apgar
score which was 5 at 1 minute is poor as it should be 7 or more.
Even the condition of the baby
was not in keeping with good apgar
scores.  He disagreed with Dr Koll that the baby was not
severely compromised at birth.
All the evidence including notes
from the examination of the baby and the brain scan suggest a
compromised baby.  There was
also secondary apnoea which is
indicative of a foetus that was deprived of oxygen during the labour
phase.  On day 2 or 3
there was no serial neurological
examination which made it difficult to tell how severe the
encephalopathy was.  The absence
of a suck reflex which is
considered as moderate was not normal. Lethargy is also a sign of
moderate neonatal encephalopathy. On
seizures his evidence was that
young babies do have subtle seizures in which the babies become still
or have subtle jerks or myotonic
seizures.  These seizures can
be very difficult to diagnose at an early age even for trained
medical staff.  Blood sugar
was not recorded in the critical
first three days of life and yet the baby was at risk of low blood
sugar due to the abnormal neurological
signs.  The baby’s
brain injury pattern was consistent with exposure or injury due to
low blood sugars.
[189] He and Dr van
Rensburg agreed that the baby’s brain injury was not due to
high levels of jaundice at birth. Her clinical
picture was not in
keeping with a genetic epileptic disorder as the seizures were
confined to the period of birth and there was
oxygen deprivation and
possible sugar and the baby did not have seizures later in her life.
The condition of the baby at
birth, the intrauterine environment of
the baby was not optimal because of secondary apnoea.  The suck
reflex that should
be present shortly after birth was not there at
first examination of the newborn.  This is therefore a textbook
sign of moderate
encephalopathy.  He was of the opinion that
there was a worsening of encephalopathy up until day 3 or 4 after
which there
was gradual improvement until discharge on day 11.
The absence of written notes implies poor management because note
keeping
is a vital part of management.  On day two or three
there were no vital signs recorded.  There is no evidence of
doctors
performing a neurological examination and blood sugar was not
monitored.
[190] The dietician was
concerned about the baby’s inability to suck and the speech
therapists stated that the baby could
not be woken up and had
difficulty keeping her awake and had no suck reflex.  There was
a tongue thrust and she advised against
breast feeding.  Feeding
was to be done with syringe.  The baby went into extensions
intermittently.  Prof van Toorn
said that all these were very
abnormal severe neurological signs and in his opinion they were part
of the evolution since birth.
Metabolic and genetic
investigations as recommended by professor Andronikou were done and
were negative.  These investigations
were sophisticated.
Sophisticated genetic investigations have to be targeted meaning that
the laboratory should be told what
the suspected underlying cause is
so that they know where to look.  He has experience and does
perform genetic tests with
a geneticist.  This baby had
destructive, hypoxic ischemic brain changes and there was no
neurometabolic condition that could
fit the evolution of this
picture.  He was of the view that the tests that have been done
cover any metabolic condition that
could cause compromise to
newborns.
[191] Professor Smith is
a neonatologist who has done extensive research and is a world a
claimed neonatologist with considerable
expertise in birth asphyxia
of babies.  He testified that the plaintiff’s pregnancy
was a high risk pregnancy because
the previous baby died after birth
following a home delivery.  In his opinion A’s condition
was caused by intrapartum
asphyxia for the following reasons.
The antenatal period leading up to the labour on 31 December 2015 was
unremarkable.
The maternity case records state that at 12:00
the FHR was 160 bpm.  It was therefore on the verge of
tachycardia which is
non-reassuring because a normal FHR varies
between 110 and 160 bpm.  When it reaches 160 you should keep an
eye for the non-reassuring
foetal condition.  He had seen a copy
of the CTG trace of around 16:00 which was in Dr Murray’s
report.  He can
read CTGs and that trace showed a grossly
pathological CTG implying that the foetus was hypoxic.  In other
words, there was
oxygen deficiency.  A foetus can withstand
quite severe and extended episodes of hypoxia before injury to the
brain occurs.
What is seen in the CTGs at 16:00 is a foetus
exposed to an insult of hypoxia and if that hypoxia goes
uninterrupted it will eventually
change to acidosis.  This means
that the tissues of the foetus become deficient in oxygen, cannot
operate properly and therefore
start making acid which then spills
over into circulation which affects organ function especially the
heart.
[192] When a CTG is like
that, foetal distress must be interrupted quickly to avoid injury.
In this case there were no expedited
interventions to interrupt
foetal compromise which was substandard care.  The CTG also
showed an excessive number of uterine
contractions which means the
womb was stimulated to produce the excessive contractions.  A
foetus needs about 60 to 90 seconds
to recover from a deceleration
between contractions.  His conclusion was that the foetal
distress at about 16:00 implied a
compromised foetal oxygenation
status because there was insufficient time between uterine
contractions during which the foetus
could be re-oxygenated.
Hypoxia resulting in acidosis explains the loss of variability of the
FHR during contractions.
This warranted urgent attention.
There is no record that the nursing staff recognised the pathological
CTG tracing.  Therefore
no interventions were made such as
intrapartum resuscitation and no expedited delivery was planned or
performed.  Intrapartum
resuscitation would have entailed
administering maternal oxygen, putting the plaintiff on her side, the
discontinuation of the
infusion of oxytocin and consideration being
given to administering tocolysis.  When the midwife completed
the assessment
of the newborn form she recorded that there had been
no foetal distress before birth.  This contradicts the doctor
who performed
the vacuum extraction at about 17:05-17:10 who recorded
a FHR abnormality which was initially good and then tachycardia.
Tachycardia is one of the signs of probable foetal distress.
The second stage of labour was prolonged.  At birth the
baby was
described as being born flat but recovered after bag mask ventilation
and stimulation.  She was described as lethargic
with weak grasp
reflex, and absent suck reflex.  The baby’s breathing was
inadequate for the first five minutes or more
because the apgar score
notes of 1 for breathing at 1 minute and 1 for breathing at 5
minutes.  The baby was probably born
in the state of secondary
apnoea because the baby was flat at delivery, being limp without any
efforts of breathing and then required
manual breathing support.
The one minute apgar more for the heart rate was changed to 2.
[193] Professors Smith
and Rothberg agreed that the baby suffered intrapartum asphyxia as
stated in their minute.  At 17:30
the baby was on nasal prong
oxygen.  The baby had tachycardia which is a pulse rate of more
than 160.  The baby’s
blood sugar level was not checked.
New born babies who suffer probable intrapartum asphyxia are prone to
develop early neonatal
hypoglycaemia which is an independent brain
injury factor.  Therefore, hypoglycaemia has a contributory role
for the injury.
That was substandard treatment.  The
baby’s care following a successful resuscitation should have
been escalated
to a higher level of care.  That was not done in
the first hours after birth.  The records saying that the baby
was showing
poor latching and hungry were related to irritability as
a result of developing cerebral irritation several hours later which
is
why the baby was crying.  The doctors interpreted the baby as
crying because she was hungry.  The records of inability
to
latch and crying at around 19:30 were in keeping with stage 1
encephalopathy.  The doctors recorded diagnosis of HIE at

discharge was in keeping with his assessment.
[194] The condition of
the baby after birth included cup feeding which was abnormal.
Babies who sustain intrapartum asphyxia
typically have the inability
to latch, suck and swallow properly.  If the baby did not have
good sucking and swallowing which
persisted, it is encephalopathy
that persisted and started to deteriorate at some point but was not
recognised until the speech
therapist came on the scene at about the
4 January 2016.  The speech therapist recognised that the infant
could not suck and
swallow, had abnormal tongue movements and
thrusting.  She observed that the infant had back arching
movements.  That
could be in keeping with probable tonic
seizures.   The infant was jaundiced and none of that was
recognised between
the 31 December 2015 and the 3 January 2016 by the
attending medical staff.  Professor Smith opined that until the
3 January
2016 the baby’s care was substandard as it should
have been escalated to a higher level of care than a normal nursey
after
the resuscitation.  That did not happen which was
substandard care.
[195] Blood pressure was
never checked, erecting venous fluid was not done, frequent
assessment of fluid balance, that is intake
and output was not done,
restricting fluids was not done, excluding renal failure was not
done, maintaining serum electrolytes,
calcium, magnesium and
acid-base status within a normal physiological range was never done.
Calcium was done once.
The aim of performing these vital
functions is to prevent secondary insults to the brain.  The
priority was to prevent secondary
aggravated brain injury and they
did not do that.  The baby had been stressed by hypoxia. It will
outstrip its glucose supply
and develop hypoglycaemia.  There is
no evidence that the baby’s sugar level was checked until day
4.  Hypoglycaemia
may injure the thalamic pulvinar and the MRI
scan shows injury to this part of the brain.  The fact that they
did not check
the blood level sugar during the first two or three
days was inexcusable.  On 04 January 2016 the baby’s level
of consciousness
was depressed.  The baby did not have a rooting
reflex, that is, she did not turn her head to suck.  The baby
reached
a level of 313 jaundice which means that she was developing
jaundice at least a day or two before starting to become yellow.

Yellowness is observed when it reaches a level of 120.  There is
no indication that it was picked up that she was developing
jaundice.
[196] Professor Smith’s
opinion was that regard being had to the probable seizures, abnormal
sucking pattern, level of consciousness,
inability to latch, he
concluded that at approximately 94 hours, the features were in
keeping with stage 2 neonatal encephalopathy
or a moderate degree of
encephalopathy.  The baby’s condition followed a rather
typical course of birth asphyxia leading
to an early onset neonatal
encephalopathy, namely a mild encephalopathy.  Very inadequate
or no assessments were done between
the 01 January 2016 and the 3
January 2016.  During this period, fluctuations in the baby’s
level of consciousness and
seizures were likely to develop.
That was probably missed because of inattention being paid to the
clinical condition.
The staff would not have picked up the
deterioration of the baby’s neurological status because they
did not perform proper
assessments.
[197] They did a cranial
ultrasound on 4 January 2016 and found brain oedema.  The
recorded brain swelling was in keeping with
intrapartum sustained
asphyxia because brain swelling develops three to five days after the
insult and this is exactly what happened.
The brain swelling
strongly supports an injury of hypoxic ischemia in close proximity to
the actual birth, that is labour.
Professor Smith’s
opinion was that the baby exhibited the typical course of an early
onset neonatal encephalopathy of moderate
degree.  The negative
metabolic and genetic screening results lead him to conclude that the
probable cause for the baby’s
neurological impairment is
directly related to intrapartum asphyxia.  The probability of
undiagnosed neonatal hypoglycaemia
as a contributing factor to the
patterns of injury described by professor Andronikou.
[198] Dr Gericke’s
evidence was for purposes of expressing an opinion on whether there
was a pre-existing genetic hereditary
factor which may have
contributed to an intrapartum injury or cerebral palsy and/or intra
neurodevelopmental outcome as currently
manifesting in A. He regarded
the baby’s measurements as normal growth measurements for a new
born baby.  There were
no indications of a family history, MRI
findings or clinical findings during assessment which indicated a
progressive disorder.
There were no external features which
indicated a possible existence of an underlying clinical genetic
syndrome or chromosome disorder.
He described A as having no
progressive evolutionary course of neurological features.
Hidden genetic conditions have their
own characteristic neuroimaging
findings and these are either associated with progressive metabolic
disorders, neurodegenerative
disorders or intrauterine infections
related calcifications.  The neuroimaging analysis did not
record these.  He did
not see any atypical features that were
present or indicated the need for metabolic and genetic testing.
There were no specific
clinical or radiological findings to seriously
consider infections or toxic exposures during pregnancy.
[199] Genetic evolution
needs to take into account a family pedigree, personal history of the
child, the course of the development
of the child and the findings in
a specific instance.  The targeted sequencing of several areas
of the expressing genes which
is the exome – are looking for a
number of indications which could be considered relevant in A’s
case have been found
to be negative.  The second consideration
is that the indications for genetic testing is the absence of an
incriminating birth
history.  The obstetricians have indicated
that there was a prolonged second stage and foetal distress before
delivery and
the baby was delivered with a neonatal encephalopathy.
166 genetic metabolic conditions have been excluded.
There is
no 100% end point in the extensive GWS and WES.  The
further you go the more uncertain variants you pick up whose clinical

significance is not yet known.  Therefore, there is no point
where it can be said that everything has been tested.  The

further one goes down the line, it is the law of diminishing
returns.
[200] Dr Gericke was
invited to comment on Dr van Rensburg’s opinion in which she
said that A was the sole survivor of three
pregnancies.  She
developed a moderate degree of neonatal encephalopathy and appears to
suffer from dyskinetic cerebral palsy
and associated developmental
delay in all aspects of functioning.  She appears to be
developing slowly and is still making
progress and has not shown any
degeneration or deterioration in functioning and is totally mobile
without any help.  His response
was that all of this means that
almost all genetic conditions associated with cerebral palsy can be
excluded because they are progressive
in nature and are associated
with pervasive encephalopathy whereas cerebral palsy is a static
encephalopathy.
[201] Dr Cilliers was the
second doctor on call and assisted Dr Philips in performing a vacuum
extraction.  Her evidence was
that the CTG was initially good
and then there was foetal tachycardia.  She performed a bag mask
ventilation on A at birth.
After the 31 December 2015 she next
saw A on 3 January 2016.  On her assessment on 3 January 2016 as
recorded in her notes,
the baby was breastfeeding.  Under
cross-examination Dr Cilliers conceded that she only had a vague
recollection of certain
events and did not remember all the details.
The clinical records did not indicate that the baby cried after
birth.
At 18:30 the baby was still on nasal prong oxygen.  The
baby’s apgar scores were assisted scores.  There was lack

of the latch reflex.  The apgar scores for heart rate were
altered from an initial score of 1 to 2.  On 5 January 2016
the
baby was still on a nasal gastric tube.
[202] Dr Mans was on
night duty call on 31 December 2015 and assessed the baby at 22:34.
He saw the plaintiff again on 01 January
2016 at 07:30.  On 04
January 2016 when he saw the plaintiff again, he recorded a total
serum bilirubin of 313.  He also
recorded that the baby was not
breast feeding nicely.  At 16:22 on 4 January 2016 he recorded
jaundice and c-reactive protein
zero which implies no significant
infection and inflammation.  He then questioned why there was a
deterioration and queried
hypoxic ischemic encephalopathy.  He
discussed the matter with a senior colleague Dr Gord.
Recommendations for the cranial
ultrasound and lumbar puncture were
made.  This was to make sure that the brain of the baby was
well.  At this stage
hospital records showed that the baby had
had a seizure.  At 18:21 another seizure was recorded by a
nurse.  Dr Mans
performed a cranial ultrasound which showed only
oedema.  There was no evidence of infection and bleeding based
on CSF results.
He performed an HIE score and recorded 6/[22]
on 5 January 2016.  He prescribed phenobarbitone and midazolam
for the seizures.
[203] Under
cross-examination Dr Mans conceded that he was not aware of what
happened between 01 January 2016 and the 4 January
2016 when he
returned.  He testified that when he initially assessed the baby
she was not on nasal prong oxygen but it was
normal to put a normal
baby on nasal prong oxygen.  Blood glucose level is usually
assessed after birth because the baby may
have suffered a hypoxic
ischemic injury and to assess for hypoglycaemia.  A reflex will
not just disappear and will only change
if there is an insult.
Hypoxic ischemic encephalopathy means that the baby was suffering
from hypoxia and ischemia which
was intrapartum.  He agreed that
the baby had HIE and ended up with sucking problems.  He wrote
HIE as a working diagnosis.
[204] With regard to the
defendant’s expert paediatric neurologist, Dr van Rensburg the
following submissions were made for
the plaintiff.  Her evidence
was that Professor van Toorn and herself examined the plaintiff and
A.  Her information
was the third baby was delivered in 2018 by
means of a vacuum extraction.  It was a male baby.  She and
professor van
Toorn agreed in their joint minute that A was GMFCS
level 1.  She accepted the reports of the radiologists.
She and
professor van Toorn agreed that canavan’s disease and
krabbe’s and wilson’s diseases were not applicable to A.

She regarded the plaintiff’s pregnancy outcomes history as a
very serious risk factor.  The hospital records did not
indicate
clinical seizures in A for the first 72 hours of life.  She and
professor van Toorn agreed that there was a neonatal
encephalopathy
of a moderate degree.  They agreed that there was partial
prolonged hypoxic ischemic dysfunction and that it
can cause acute
profound changes.  The lumber puncture performed on A did not
indicate a bacterial infection or meningitis.
According to her,
the HIE score performed on A was done when A was on a midazolam
infusion, which cannot be done.  She was
of the opinion that A
displayed an atypical history in the peripartum period and there was
a very unusual neonatal encephalopathy.
[205] Under
cross-examination Dr van Rensburg testified that she and professor
van Toorn agreed that there was neonatal encephalopathy
in A which
turned into moderate neonatal encephalopathy on 4 January 2016.
She had assumed that on the findings of Dr Gericke,
there was a
change in the motor symptoms of A.  During the period 1 January
2016 to 4 January 2016 there were few examinations
done on A.
On probabilities, if there was intrapartum hypoxia ischemia, then the
cerebral palsy was an etiological factor,
hypoxia during labour.
She did not know whether hypoxia was imposed upon another condition
and it was one of the possibilities.
With proper monitoring, if
there was a genetic vulnerability to hypoxia, it may be detected if
that was when the injury was suffered.
It was a possibility
that in the first three days in hospital with skeleton staff and with
relatively few observations, it is highly
likely that seizure
activity may have taken place while the child was with the
plaintiff.  There was no indication that toxic
conditions
brought about A’s condition but she was of the view that they
had not been totally excluded.  There was no
evidence to suggest
toxic conditions and there were no post-infective causes for the
child’s condition.  Metabolic conditions
have been
excluded but not all genetic conditions have been excluded.
There was no prematurity and there was no intracranial
haemorrhage.
There was no evidence of infection, stroke or kernicterus.
There was no evidence of oscillated generalized
hypotonic, prominent
ataxia, signs of peripheral neuromuscular disease, reduced or absent
reflex, sensory loss or eye movement
abnormalities.
[206] Professor Rothberg
was the defendant’s expert paediatric neonatologist.  His
evidence was that he would regard
this case as a poor pregnancy
outcome.  Genetic risk factors must be considered.  The
court must decide on the proximal
risk factor, the labour itself, the
labour stress or mismanagement.  Clinical risk factors could act
as triggers and a clinical
risk factor could be intrapartum asphyxia
for cerebral palsy where there is genetic susceptibility.  A
developed and presented
with mild hypoxic ischemic encephalopathy
between birth and around 16:29 on 3 January 2016.  This child
suffered intrapartum
hypoxic ischemia. The points of disagreement
between professor Smith and himself related to the interpretation of
the head circumference
measurement at birth and the possible
implications or relevance of the matter.  At the time of birth,
A was in primary apnoea
and the bag mask ventilation is not an
indication that the baby was in secondary apnoea.  He and
professor Smith agreed that
A had an intrapartum hypoxic ischemic
brain injury.  They agreed that at birth there was a neonatal
encephalopathy which resulted
from the intrapartum hypoxic ischemia
and was assessed as mild HIE.  He disagreed with professor Smith
that genetic causes
have been excluded particularly because a female
child born in 2020 also had a postnatal seizure.  He did not
consider A to
have an epileptic syndrome.  In his view, the
family history could not be ignored and there were significant
factors which
included four pregnancies, two males died late in
pregnancy or shortly after birth, A presented with HIE and
subsequently developed
cerebral palsy and later developmental delay.
He was of the view that one cannot confidently state that an
expedited delivery
would have avoided the ultimate neurological
disability.
[207]
Under cross-examination he conceded that A suffered intrapartum
hypoxic ischemia.  However, he believed that A was in
the
situation of a primed foetus such that normal asphyxia became
pathological.  Volpe and Wassmik
[8]
differed about the latent phase improvement.  Volpe describes 24
to 72 hours’ deterioration.  Wassmik describes
6 to 15
hours and after that several days.  There was no systematic
evaluation of A during the first three days.  Recognition
of
seizures in the new born period can be difficult because of subtle or
absent clinical manifestations.  Clinical manifestations
of
neonatal seizures may be overlooked, even by skilled observers and
neonatal seizure identification by clinical observation was

suboptimal.  He disagreed that that the progression of HIE would
be typical but agreed that there was a deterioration which
was
observed by the speech therapist and the nurse when the child
suffered a seizure.  The head circumference of A was 97
th
percentile
but he was of the view that the big head of A was significant but was
part of the phenotype and a red flag.  The
Ethiopian study would
place A at the 92
nd
percentile.
He said that absent the family history in this case there would be
little to argue other than the presence and/or
severity of foetal
distress.
[208] Professor
Christianson is qualified as a paediatrician and specialises as a
geneticist.  He testified that A had congenital
macrocephally
which is an abnormal enlargement of the head.  It is frequently
familial, meaning if one of your parents has
a large head, you may
have a large head.  In cases where it is familial it is usually
benign because the parent is normal
and the child is normal.
But it can be genetic in origin associated with metabolic disorder
and syndromes.  This is
another pointer in the phenotype of A to
a possibility of a genetic issue.  When he examined the child he
thought she was
GMFCS1.  She was not obviously dysmorphic and
had no cataracts and no neurocutaneous syndrome.  He did not
consider that
she had cerebral palsy and if she did, it was subtle
which he said must be assessed by a paediatric neurologist.  He
referred
to the report of professor Andronikou and his comments that
the features may be due to hypoxic ischemic injury of a combined
acute
profound and partial prolonged nature.  He said that the
word “may” should not be ignored.  Professor
Andronikou
stated that the pattern of injury may also be seen with
toxic metabolic and post infectious disorders.  He gave examples
of
krabbe, canavan and wilsons diseases but it is not an exclusive
list.
[209] That is why he did
the Cento metabolic tests and he considered that the child should be
seen by a paediatric neurologist and
may require testing for
metabolic disorders.  On his clinical assessment, A was born
with congenital macrocephaly.  With
regard to the fourth
pregnancy, he suggested that this pregnancy should be assessed by an
obstetrician.  The baby with other
members of the family needed
to be medically evaluated by a paediatric neurologist and a medical
geneticist.  Further medical
genetic testing on this family
needed to be considered.  He then referred to the genetic tests
that were done and said that
the Centogene metabolic test is next
generation sequencing based on copy number variation.  This is a
deep analysis but of
a narrow field, just in the field of metabolic
disorders.  The result was negative which means there were no
metabolic disorders
diagnosed on this test.  The WES can find
80% of problems but if you do a WGS you might get a 20% increased
yield of problems
or abnormal sequences.  However, it is not the
full way.
[210] Then Cento-LCV test
was done, that is a Cento metabolic test.  It is a whole genome
in next generation sequencing based
on large copy number variation
analysis.  This also produced a negative result as well.
He stated that WES should be
done but said doing WGS would even be
better as there is nothing beyond it currently.  He said if WES
comes back negative
and there is still a need for genetic
investigation you do the WGS.  He believed that the family
history, the macrocephally,
the first four days of life of the baby
not being typical of neonatal encephalopathy grade 2 or 3 makes this
case qualify for Cento
genome.  He referred to the
correspondence between professor van Toorn and Dr van Rensburg in
which it is stated that the
plaintiff’s obstetrician gave a
feedback on the fourth pregnancy which was complicated by obstructive
labour and a prolonged
second stage.  The pelvis of the mother
was reported as being insufficient and the maternal height is 1.5
metres.  A
family history of consanguinity or a sibling or other
relative with similar neurological symptoms may suggest a possibility
of
a genetic condition.
[211] The MRI scan in
respect of A was abnormal.  He did Cento metabolic and Cento-LCV
genetic testing that was limited based
on facts that were available
after he saw A.  Now there are further findings that he cannot
explain from a geneticist point
of view.  The test was not only
looking for what is known.  It was also looking to the future to
find genes that are
associated with or can cause CPs that are not yet
known.  WES is a powerful tool to identify deficiencies, the
likely cause
of genetic variants, in particular sequencing of
multiple family members, which can reduce a number of candidate gene
DNA variants
to one or two and thus lead to finality and precise
diagnosis.
[212] Under
cross-examination professor Christianson stated that A was not
dysmorphic, that is she had normal features.  There
were no
neurocutaneous lessions which means birth marks, different types of
birth marks which can be associated, and they are dysmorphic
features
because they are associated with genetic disorders and syndromes.
He accepted that she had cerebral palsy but did
not have neonatal
encephalopathy type 2 or 3.  He accepted professor Rothberg’s
opinion that she had grade 1.
His understanding was that on day
four, after seizures A developed neonatal encephalopathy grade 2 with
seizures.  That is
not typical of neonatal neurological syndrome
as described by Volpe.  He would like to see where the
neonatalogist described
hypoxia ischemia enough to cause neonatal
encephalopathy grade 1.  Professor Christianson was referred to
a minute between
professor Smith and professor Rothberg in which with
reference to the MRI report of  professor Andronikou, they say:
“
Professor
Andronikou described features consistent with combined partial
prolonged and acute profound and hypoxic ischemic injury.

However, professor Andronikou also indicated that the MRI pattern may
be seen with toxic metabolic and post-infectious causes.”
[213] He questioned the
way they have worded it with reference to the report.  He said
what professor Andronikou said about
the features
may
be due
to hypoxic injury of a combined acute profound and partial prolonged
nature.  He said that there was therefore a difference
between
what professors Rothberg and Smith were saying and what professor
Andronikou said which he echoed.  He did not think
that hypoxic
ischemic injury was the primary cause.  He considered that there
may be a hypoxic ischemic injury, there may
be metabolic causes,
there may be toxic causes, and there may be post-infectious causes.
After learning about the third and
fourth child, he then considered
to add into that list, genetic causes.  He was then referred to
the report of Dr van Rensburg
in which she refers to the defendant’s
radiologist, Dr Schwartzberg’s report in which the latter said
there were no
congenital abnormalities, neuronal migration disorders,
cysts, hydrocephalies, masses, haemorrhages, blood breakdown
products,
calcification, midline shift, profusion restriction.
He said from his perspective as a geneticist he saw no neuronal
migration
disorders or congenital disorders.
[214] He disagreed that
both radiologists concurred that the pattern of injury was hypoxic
ischemia arguing that professor Andronikou
used the word “may”
and therefore what Dr Schwartzberg and professor Andronikou said were
different.  He conceded
that toxic and post-infections cause
have been excluded to the extent that they could be.  Two
conditions remaining were the
hypoxic ischemia and metabolic causes.
The third condition is genetic disorders or congenital disorders.
He conceded
that in professor Andronikou’s report there were
only two conditions that remained and metabolic testing has largely
excluded
one of those two conditions.  He agreed that all the
possible causes mentioned in professor Andronikou’s report have

been excluded except for hypoxic ischemic injury.  He insisted
on the macrocephally which he said was frequently familial.
[215] He was referred to
sister Mbada’s evidence who said that she took the measurement
over the haematoma.  He said
he did not accept that the
haematoma would have been part of the measurement of the head
circumference saying that where the cup
is placed was not where you
would normally do the measurement.  Notwithstanding the evidence
of sister Mbada, he said that
the measurement could not be doubted.
The macrocephally was part of what he used to suggest that WGS should
be explored.
Notwithstanding the evidence of professors van
Toorn and Smith that the measurement was unreliable he insisted that
A had congenital
macrocephally.  However, the Cento-LCV test
targets, inter alia, macrocephally and it did not detect
macrocephally.
Submissions on
causation.
[216] It was submitted
that the defendant had pleaded a general denial and did not plead
that the agreed cerebral palsy was caused
by any specific condition.
The MRI scans were assessed by professor Andronikou, Dr Schwartberg
and professor van Toorn.
Professor van Toorn and Dr Schwartberg
stated that the scans were consistent with hypoxic injury of a
partial prolonged and acute
profound type (mixed).  Professor
Andronikou also stated that:
“
However,
the pattern of injury in this patient can also be seen with toxic,
metabolic and post-infectious causes.  Possible
metabolic
conditions that can have this appearance include Canavan disease,
Krabbe disease and Wilsons disease.  The patient
requires
evaluation by a paediatric neurologist and may have to undergo
testing for metabolic disorders to distinguish these potential

causes.”
[217] On the basis of
this statement, the plaintiff argues that nothing further was
suggested by professor Andronikou about any
further conditions that
may provide the picture seen in A’s scan.  Professor van
Toorn stated that professor Andronikou’s
primary aetiology was
hypoxic ischemic damage but other possibilities had to be excluded.
Metabolic conditions were excluded
by the Cento metabolic
(sequencing) including NGS based CNV analysis and Cento-LCV –
Whole genome NGS large copy number variation
analysis.
Metabolic conditions were also clinically excluded by professor van
Toorn, professor Smith and Dr Gericke.
Professor Christianson
conceded that genetic metabolic causes have been excluded.
Professors Smith and Rothberg agreed that
A suffered intrapartum
hypoxic ischemia which resulted in encephalopathy after birth which
progressed to stage 2 by day four with
seizure activity.
Speculation about epileptic encephalopathies are irrelevant and were
in any event excluded by professor
van Toorn and professor
Christianson conceded that.  No defendant’s expert
suggested that epileptic encephalopathies
could be the cause of A’s
brain injury.  Professor Rothberg also conceded that there is
little to argue about in this
case save for the extent and duration
of the hypoxia other than the genetic issue on which he is not an
expert.
[218] It was further
submitted on behalf of the plaintiff that when one puts everything
together, the clinical factors and the events
of the relevant period,
all fit perfectly into the picture of intrapartum hypoxia ischemia.
The factors that are considered
important by the plaintiff are the
following.  There was no adverse antenatal history.  The
foetus and the plaintiff
appeared in good condition during admission
to hospital.  There was prolonged active phase of the first
stage of labour without
normal progress, which is a risk factor for
foetal distress.  There was a deceleration recorded at 12:00
which is a serious
risk factor for foetal distress.  There was
significant substandard monitoring which is a risk factor that foetal
distress
will not be detected.  There was delayed progress of
labour which called for intervention by way of caesarean section or
administration
of syntocinon subject to careful monitoring as it is
dangerous and a risk factor for tachysystole.  There was a
seriously
pathological CTG at 16h00 with bradycardia (decelerations
below 110) and tachycardia (heart rate above 160) as well as severe
tachysystole
with up to 11 contractions in 10 minutes.  Only up
to 5 contractions are acceptable.  This is a serious risk factor
for
foetal distress and hypoxia ischemia.
[219] The second stage of
labour was delayed and again this is a risk factor for foetal
distress.  The mother was pushing in
the presence of
tachysystole during the prolonged second stage.  Once again this
is a serious risk factor of hypoxia.
The baby was born flat in
a state of secondary hypoxia, ie. not breathing and had to be
resuscitated firstly with an ambu bag and
then with nasal prongs for
at least 1
1/2
hours.  The baby had an absent suck
reflex and poor grasp reflex.  The baby had to be cup-fed for 4
days at least and
developed seizures.  An ultra sound scan
showed oedema (swelling of the brain) on day 5 which is a typical
consequence of
hypoxia ischemia.  The baby probably developed
hypoglycaemia as a result of hypoxia ischemia.  The baby’s
treatment
in hospital was suboptimal as the baby was not escalated to
a higher facility and not properly tested as she should have been
according
to professor Smith.  The mixed picture of hypoxic
ischemia would have developed over hours which is consistent with the
clinical
picture of probable distress in the foetus.  The
mechanism of damages as explained by professor van Toorn then fits in
with
brain damage of partial prolonged and acute profound type as
seen on the MRI scan.  The child has dyskinetic cerebral palsy.
[220] It was argued that
all the above factors constitute a prototype that is normally seen
for cerebral palsy caused by hypoxic
ischemic intrapartum.  All
other reasonable causes for the cerebral palsy have been excluded by
all the experts.  Only
professor Christianson was of the view
that further genetic testing (WGS) should be done on the family.
He cast doubt on
what other experts agreed upon.  For example,
he did not think that A had cerebral palsy but still referred the
issue to paediatric
neurologists who both found dyskinetic cerebral
palsy.  He did not accept that there was encephalopathy which he
should have
deferred to neonatologists as he is not an expert on that
issue.  The neonatologists did find positively that there was
encephalopathy.
Professor van Toorn and Dr van Rensburg also
agreed that there was encephalopathy.  However, professor
Christianson maintained
his denial and sought to rely on Volpe.
His refusal to concede when he should indicate his bias.
[221] He drove genetic
testing for metabolic disorders.  The results excluded genetic
metabolic causes but still he did not
accept the results and insisted
on further testing.  However, he acknowledged that further
testing may not bring about a conclusive
result as there are five
classifications of variants which may be inconclusive whose clinical
manifestations are unknown.
To arrive at a conclusive finding
will take years requiring input from various experts in medical and
genetic fields.  This
would cause unnecessary protraction to the
trial with taxpayer funded cost implications.  He did not accept
the literature
of Pearson et al which postulates that genome testing
is contraindicated in cases of a poor obstetric history which
happened in
A.  He made a diagnosis of macrocephally and was the
only expert to do so.  At the same time he concedes that
macrocephally
can be benign with a parent having a large head and the
child having a large head with no consequences.  He would not
accept
the inaccuracy of the head measurement and ignored the direct
evidence of sister Mbada that she took the measurement over the
haematoma.
The evidence of professors van Toorn and Smith was
that they doubted the correctness of the measurement.  He did
not accept
their evidence that the head must be assessed in relation
to the length and weight which is normal.
[222] He would not accept
professor Smith’s view, a world renowned neonatologist, that
his personal experience was that head
circumferences recorded in
hospital are notoriously wrong and over-assessed.  Instead he
persisted with his opinion that there
was macrocephaly even when A’s
head had proportionally reduced at 5 years.  This usually
happens when there was a hypoxic
injury and the brain does not grow
as it should.  He conceded that there was no megaloncephally
without saying how macrocephaly
would be related to the destructive
brain damaged that can be observed on the scan.  Very
significantly, the Cento-LCV test
that was done which inter alia
targets macrocephaly came back negative for it.  He still
persisted that there was macrocephaly.
All of this illustrates
his bias.  Another reason for him going beyond what professor
Andronikou suggested, the testing or
exclusion of metabolic, toxic or
infectious causes, by seeking to do further genetic testing was
because of the macrocephaly that
he diagnosed.  This is contrary
to the facts.  He made no contribution to resolving the question
whether negligence was
closely related to the cerebral palsy.
The court will assess the evidence on that question on probability,
not certainty.
[223]
In the final analysis, it was submitted on behalf of the plaintiff
that there was only one reasonable explanation for A’s
MRI
picture and that is hypoxic ischemia of a partial prolonged and acute
profound type.  The defendant does not suggest an
alternative
reason.  In
Goliath
[9]
the court said:.
“
When
an inference of negligence would be justified and to what extent
expert evidence would be necessary would no doubt depend on
the facts
of the particular case.  Questions of absolution from the
instance at the close of the plaintiff’s case aside,
a court is
not called upon to decide the issue of negligence until all of the
evidence is concluded….  Thus any such
explanation as may
be advanced by a defendant forms part of the evidential material to
be considered in deciding whether a plaintiff
has proved the
allegation that the damage was caused by the negligence of the
defendant or its servants.  Here although the
procedure
performed on Ms Goliath was under the control of the MEC’s
employees and what they did or did not do was exclusively
within
their direct knowledge, none of those employees were called to
testify.  In
Ratcliffle
v Plymouth and Torbay Health Authorily
(para 48) Lord Justice Brooke
made the point that:
‘
It
is likely to be a very rare medical negligence case in which the
defendants take the risk of calling no factual evidence, when
such
evidence is available to them, of the circumstances surrounding a
procedure which led to an unexpected outcome for a patient.
If such a
case should arise, the judge should not be diverted away from the
inference of negligence dictated by the plaintiff’s
evidence by
mere theoretical possibilities of how that outcome might have
occurred without negligence: the defendants’ hypothesis
must
have the ring of plausibility about it … .’
Lowe J appears to have
allowed himself to be diverted from the obvious inference of
negligence dictated by the evidence in this
case by virtue of his
heightened focus on the applicability of the maxim
res ipsa
loquitur
to cases based on alleged medical negligence.  He
appeared not to appreciate that:
‘
At
the end the trial, after all the evidence relied upon by either side
has been called and tested, the judge has simply to decide
whether as
a matter of inference or otherwise he concludes on the balance of
probabilities that the defendant was negligent and
that that
negligence caused the plaintiff’s injury.  That is the
long and short of it.’”
Defendant’s
submissions.
[224] In its simplest
expression the defendant’s case is that negligence is denied in
that on admission at the hospital at
09:00 on 31 December 2015,
having been referred by a clinic, the plaintiff was soon put on CTG
monitoring which was ongoing.
To the extent that some of the
activities of the continuous monitoring of the plaintiff during
labour may not have been properly
recorded, that did not translate
into a poor management of her labour which was, throughout, within
the acceptable norms and standards
especially as provided for in the
guidelines.  With regard to causation, the defendant’s
case is that in the first instance,
even if it were to be found that
the defendant was negligent, such negligence did not cause the
child’s poor outcome.
The defendant contends that in
light of the poor pregnancy history of the plaintiff, the
macrocephaly that the defendant alleges
the child suffered from
together with the possible genetic causes, the child’s
condition was not caused by the alleged poor
monitoring but by a
predisposition to a poor outcome.  This required further genetic
investigation which was prevented by
the plaintiff who refused
genetic testing despite a viable blood sample that was readily
available.
[225] For its defence,
the defendant relied on the evidence of four factual witnesses and
four expect witnesses which has largely
been referred to above. Some
of it is again referenced below in order to contextualise the
defendant’s contentions in some
respects.  The defendant
submits that the plaintiff was first seen at the clinic at 06:50 and
consequent upon being referred
to Zitulele Hopsital by the clinic,
she was attended to shortly after her arrival at 09:00 at the said
hospital where preliminary
examination was done as recorded in the
maternity case records.  Sister Mbada’s own assessment was
at 12:50 at which
stage the plaintiff had a spontaneous rapture of
the membranes and was draining clear liquor.  The FHR was
between 136 and
150 bpm and the monitoring was done using CTG.
During the next assessment at 14:00 the FHR was noted as 145 to 150
bpm.
Sister Mbada noted that the labour progress was slow.
As a result, she notified the doctor who ordered syntocinon which was

to be administered if CTG was reactive.  She understood this to
mean that the CTG would be monitored over a period of 30 minutes
to
check if its baseline was between 110 and 160 bpm and ensuring that
there were no decelerations in line with the guidelines.
Only
in those circumstances would the syntocinon infusion be done.
[226] However, syntocinon
infusion was not done because if it had been administered, the
syntocinon administration document which
is clipped in the patient’s
file is ticked each time the required amount of infusion is
administered as prescribed until
the infusion is stopped.   That
document would be signed at the start of the infusion process.
Even the stopping
of the infusion would similarly be indicated and
documented.  Based on the absence of any of these indicators,
she concluded
that it was never administered even though it had been
prescribed because the labour progressed naturally.  The
defendant
contends that the fact that labour progressed naturally was
evident from the assessment at 14:00 and the partogram.  The
contractions
as is evident on the partogram became stronger, making
it unnecessary to administer it.  At 15:15 the contractions were
serious
and strong and therefore it was unlikely that she would have
gone ahead and administered syntocinon.  Only Ringers Lactate

was administered in preparation for possible syntocinon
administration and the hydration of the patient.
[227] The submissions of
the defendant on Dr Linde’s evidence, one of its factual
witnesses was that she was on duty on 31
December 2015 and her duties
included attending at the maternity ward.  At 15:00 she made an
entry after having assessed the
plaintiff.  Consequent upon that
assessment she ordered that if the CTG was reactive the plaintiff
should be given syntocinon
to argument her labour and a catheter
should be inserted to empty her bladder to prevent labour
obstruction.  She allowed
labour to continue as there was no
risk in allowing it to progress naturally. It was not necessary to
perform an urgent caesarean
section or any other urgent
intervention.  It was further noted that she should be called if
there were any problems.
Her assessment of the foetal wellbeing
was through the CTG through which she checked for any signs of foetal
distress.  She
made partogram entries at 15:00 where she plotted
on the lower part that the dilation was 7cm.  She explained that
the Ringers
Lactate was often used in the labour ward as it contains
electrolytes and lactate.  It is a supportive fluid commonly
used
in rehydrating patients.  Therefore, it was denied that the
administration of Ringers’ Lactate was suggestive of the

syntocinon having been administered.
[228] Her evidence was
further that at Zithulele Hospital they had a prescription sheet
which indicated dosage rates for syntocinon
administration as well as
time intervals for its administration.  Therefore, its mere
prescription did not equate to its actual
administration, maintaining
that it was never administered.  The defendant argued that Dr
Linde’s evidence was that
tachysystole was not only
attributable to syntocinon infusion but does happen naturally during
labour.  Therefore, it was
denied that the occurrence of
tachysystole, even if it were to be accepted that it occurred, was
indicative of syntocinon infusion.
However, to the extent that
the tachysystole hypothesis was premised on syntocinon infusion based
on disputed CTG tracings and
further premised on disputed enhanced
CTG drawings, it was vehemently denied, it being the defendant’s
case that syntocinon
was not administered.  It was further
argued that the foetal wellbeing of the baby was based on a running
CTG even though
the recordal of the findings of the observations of
the CTG might have been suboptimal.
[229] The defendant’s
case was further based on the evidence of Dr Cilliers, one of the
defendant’s factual witnesses
who was on duty at Zithulele
Hospital on 31 December 2015 as the second doctor on call.  Her
evidence was that the vacuum
extraction began at 17:05 and was
completed at 17:10. She was called by Dr Philips to assist him in
delivering the baby.
On her arrival Dr Philips explained that
the plaintiff was 16 years old with para-zero grav2 with a delayed
second stage.
Dr Philips was a junior doctor and she decided to
upskill him by allowing him to do the vacuum extraction under her
supervision.
When she arrived the plaintiff was in labour with
CTG that was running and the midwife was also present, who presumably
called
Dr Philips.  She assessed the CTG tracings to see if it
was normal, suspicious or pathological and found it reassuring.  On

that basis she excluded foetal distress and allowed Dr Philips to
complete the vacuum extraction which was uneventful.
[230] Another factual
witness of the defendant was Dr Mans.  On 31 December 2015 he
was on duty between 19:00 on 31 December
2015 and 08:00 on 01 January
2016.  He examined the plaintiff and the baby when he did his
postnatal rounds at about 22:34.
He noted a third degree tear
on the plaintiff and found that she had no clue on how to
breastfeed.  He noticed that the baby
was hungry and there was
poor latching.  He based his view that the baby was hungry on
the fact that the baby was crying and
that babies cry a lot when they
are hungry.  His evidence was that there was nothing that
concerned him about the baby who
was basically lodging with her
mother as she had been admitted for her third degree tear.
Ordinarily babies were allowed
to go home after six hours but this
baby had to stay with her mother.  He was adamant that the child
was hungry and displayed
the primitive reflexes necessary for
breastfeeding.  However, the mother was unable to initiate
breastfeeding.  He saw
the mother and the baby again on 01
January 2016 at 07:30. He noted that the baby was hungry but could
not feed because of the
lack of feeding connection with its mother.
He proposed cup feeding to deal with the child’s nutritional
needs in light
of the mother’s inability to breastfeed the
hungry baby.
[231] He next saw the
baby on 04 January 2016 at 16:00.  There was a nurse’s
note that the baby had started fitting.
This was the first
occasion that the child started having fits.  It was argued that
this was not in keeping with a classical
case of neonatal
encephalopathy as the onset of seizure was after four days.  He
testified that at 18:21 on 4 January 2016
the nurses observed further
seizures.  It appeared that there were no further seizures on 05
January 2016 at 17:29 as there
was a note that there had been no
seizures since 21:26 the night before.  Under cross-examination
he testified that in ascribing
poor latching to the inability of the
mother to breastfeed he had not made a mistake as he had watched, as
per the notes, the mother
breastfeeding.  He never diagnosed HIE
but merely queried it.  It was argued on behalf of the defendant
that Dr Mans’
evidence supported the defendant’s
contention that the child did not display any features that were in
keeping with a typical
HIE.
[232] This brings me to
the defendant’s contentions on its expert witnesses’
evidence.  Dr Koll was the defendant’s
obstetrician and
gynaecologist.  He concluded a joint minute with Dr Murray, the
plaintiff’s obstetrician and gynaecologist.
His evidence
was that initially he and Dr Murray believed that syntocinon had been
administered.  He and Professor Anthony
did a joint minute in
which they agreed that there was nothing detectable antenatally which
could have affected the outcome in
this case.  He further
testified that there were discrepancies in the assessment of cervical
dilation.  He agreed with
Professor Anthony that in monitoring
FHR, one must listen after a contraction in that a random measurement
of the FHR does not
tell anything.  Neither he nor Professor
Anthony could explain the 5cm dilation at 14:00.  There was
another assessment
at 15:00 by Dr Linde who ordered that CTG should
be monitored and that the labour should be allowed to progress.
She had
excluded CPD and foetal distress and with the membranes
having raptured at 12:50 and draining clear liquor, she was assured
of
the foetal condition.
[233] He agreed with the
doctor who, in light of the clear liquor, ordered catheter to drain
the bladder, putting up a drip for
Ringers Lactate which was
important for rehydrating the plaintiff and ordering syntocinon which
could be infused if the CTG was
reactive.  He would not fault
the management of the labour until 16:00 which was about an hour
before delivery.  During
assessment no.4 the FHR was 150 bpm
which was reactive and reassuring of the foetal wellbeing and the
plaintiff was allowed to
bear down.  Dr Koll found that to be
reasonable.  He would not comment on the CTG tracings which he
said were unreadable
as they were illegible.  His evidence was
essentially that besides poor record keeping, his assessment of the
actual management
of the labour was that he could find no fault in
how the defendant’s staff managed the plaintiff’s labour
in that she
was kept on a continuous CTG which was reactive and there
was clear liquor which was indicative of the absence of foetal
distress.
[234] The defendant
argued its case for genetic testing on the evidence of Dr van
Rensburg, professor Rothberg and professor Christianson.
Dr van
Rensburg signed a joint minute with professor van Toorn in which they
agreed on the need for metabolic and genetic testing
following the
discovery of the information that the plaintiff had given birth in
2014 and a third one in 2018 both of which were
still born births.
They agreed that the fact that both children who were still borns
were males was an indicator for genetic
testing.  She had
classified A as GMFCS 1 which was an indicator of her motor
functionality.  She however, later discovered
that Dr Gericke
had classified A as GMFCS 4 which is severely disabled.  This
baffled her as it meant that the child’s
functioning was
fluctuating which was not in keeping with cerebral palsy.  This
was an indicator for a genetic predisposition
and not negligence or
substandard care which might have been responsible for the child’s
condition.
[235] The defendant
argued that Professor Andronikou’s report was that metabolic
and genetic causes may be responsible for
the MRI findings.
Therefore, it would be unjust to find in plaintiff’s favour as
the plaintiff actively prevented the
defendant from pursuing what it
considered to be a viable defence by her refusal to have further
genetic testing done.  The
defendant argued that it is incorrect
to distinguish metabolic disorders from genetic disorders.  This
is because metabolic
disorders including the possible ones mentioned
by professor Andronikou, are usually genetic in nature.
[236] Reference was also
made to Dr van Rensburg’s evidence that on 4 January 2016 A
qualified as having moderate encephalopathy.
According to Volpe
seizures usually start within 6 to 12 hours and before 72 hours in a
hypoxic ischemic brain injury.  In
this case there was a
deviation from that norm.  It was pointed out that the most
common pattern of deep grey matter injury
in a term infant with
cerebral palsy is the involvement of the thalamus and globus
pallidus.  One usually sees a ventrolateral
thalamic
involvement.  There can be involvement of the posterior of the
internal capsule and the posterior cart of the putamen.
But if
there is a severe injury the whole thalamus, the whole putamen
including the globus pallidus and the head of the caudete
nucleus can
be involved.
[237] It was submitted
that it is noteworthy that in plaintiff’s case the injury was
on the medial aspect of the thalamus
and the head of the caudete
nucleus.  It is not the typical basal ganglia involvement that
is seen in a full term hypoxic
ischemic brain injury.
Therefore, one cannot say what the exact cause of the injury is and
the question remains open.
It was argued that Dr van Rensburg’s
opinion was that A displayed atypical history in the peripartum
period and there was
an unusual neonatal encephalopathy.  Distal
factors needed to be considered which included the very poor
pregnancy history
which complicated the situation.  Radiological
findings were atypical of hypoxic ischemic brain injury.  Dr van
Rensburg
would not accept the suggestion that Dr Gericke made a
mistake about the child’s GMFCS level in the absence of
clinical notes
of his assessment on the day he examined the child
which he failed to produce.
[238] The defendant’s
case is also that professor Rothberg and professor Smith differed on
the pathways for cerebral palsy.
Professor Smith argued for
pathway A which is that as a result of the insult during the
management of the labour, the injury was
caused.  Professor
Rothberg on the other hand, was of the opinion that while he could
not conclude whether there was additional
asphyxia as a result of the
obstetric management, he agreed that there was intrapartum hypoxia
ischemia.  The neurological
condition (encephalopathy) worsened
around the 4 January 2016 which was after 89 hours.  He agreed
with professor Anthony
that infection has been reasonably excluded.
They agreed that their diagnosis of cerebral palsy was based on the
joint minute
of the paediatric neurologists as neither of them had
seen the child.  He was also of the view that on the child’s
assessment
at 22:34 by Dr Mans, the latter was so unconcerned about
the condition of the baby that he made a note to review the child on
discharge.
The deterioration when the seizures occurred at
16:00 and he was called and saw the child at 16:22 some 95 hours from
birth, was
atypical for a baby to deteriorate with seizures.  He
was of the view that the fact that the plaintiff had four
pregnancies,
two males dying late in pregnancy, one female with HIE
which developed into cerebral palsy and global developmental delays,
the
second female also had seizures on the second day of life were
all good indicators for genetic testing.
[239] All of these poor
pregnancy outcomes spoke of an underlying problem in the family
rather than bad obstetric management, which
also called for genetic
testing.  The onset of seizures in A was late for a progressive
HIE.  According to Volpe, other
causes for the neonatal
ancephalopathy should be sought.  Even the equivocal nature of
professor Andronikou’s report
in which hypoxia-ischemia and the
possibility of other conditions including conditions with a genetic
basis pointed to the necessity
for genetic testing.  His view
was that definitive tests have not yet been done to conclusively rule
out a genetic condition
that may have predisposed A to intrapartum
asphyxia.  On the other hand, intrapartum asphyxia may have been
an independent
factor that was superimposed on a genetic condition.
Therefore, one cannot state that expedited delivery would have
avoided
the ultimate neuro-disability.
[240] His evidence was
that pathway A looked only at intrapartum asphyxia as a result of
obstetric mismanagement.  Pathway
B is when there is a genetic
risk factor and other distal factors.  He agreed that there was
intrapartum asphyxia which may
have been related to the usual stress
of normal birth but it acted adversely in this case because the brain
had been primed by
the underlying genetic condition.  In this
case there was a problem that occurred at the time of conception in
the form of
genetic abnormality regard being had to the history of
the four affected children.  There are always elements of
hypoxia and
ischemia in every pregnancy.  In a baby that is
susceptible, that is primed, the brain may be triggered to undergo
energy
failure and present with neonatal encephalopathy and
ultimately cerebral palsy which is what would have happened in
pathway B.
[241] The last expert
witness for the defendant on which the defendant argued its case on
causation was professor Christianson.
On his evidence it was
argued that there are other genetic epilepsies which have not been
excluded by the gene sequencing by the
Cento metabolic panel.
Other panels could be tested but it was better to just do the WES or
WGS.  He added that at present
there was nothing beyond the WGS.
The evaluation of the
evidence.
[242]
The legal position and guidance on how medical evidence should be
evaluated was stated as follows in
Oppelt
[10]
by the Constitutional Court from which I quote generously:
“
The
correct approach to the evaluation of medical evidence is the one
laid down by the Supreme Court of Appeal in
Linksfield
where it held that –
‘
it
is perhaps as well to re-emphasize that the question of
reasonableness and negligence is one for the court itself to
determine
on the basis of the various, and often conflicting, expert
opinions presented.  As a rule that determination will not
involve
considerations of credibility but rather the examination of
the opinions and the analysis of their essential reasoning,
preparatory
to the court’s reaching its own conclusion on the
issues raised.
…
Although it has often
been said in South African cases that the governing test for
professional negligence is the standard of conduct
of the reasonable
practitioner in the particular professional field, that criterion is
not always itself a helpful guide to finding
the answer.
…
That being so, what is
required in the evaluation of such evidence is to determine whether
and to what extent their opinions advanced
are founded on logical
reasoning.  That is the thrust of the decision of the House of
Lords in the medical negligence case
of
Bolitho v City and Hackney
Health
Authorily
[1997] UKHL 46
;
[1998] AC 322
(H.L.C
(E.).  With the relevant
dicta
in the speech of Lord
Browne–Wilkinson we respectfully agree. Summarised, they are to
the following effect.
The court is not bound to
absolve a defendant from liability for allegedly negligent medical
treatment or diagnosis just because
evidence of expert opinion,
albeit genuinely held, is that the treatment or diagnosis in issue
accorded with sound medical practice.
The court must be
satisfied that such opinion has a logical basis, in other words that
the expert has considered comparative risks
and benefits and has
reached ‘a defensible conclusion’ (at 241G-242B).
If a body of professional opinion overlooks
an obvious risk which
could have been guarded against it will not be reasonable, even if
almost universally held (at 242H).
A defendant can properly
be held liable, despite the support of a body of professional opinion
sanctioning the conduct in issue,
if that body of opinion is not
capable of withstanding logical analysis and is therefore not
reasonable.  However, it will
very seldom be right to conclude
that views genuinely held by a competent expert are unreasonable.
The assessment of medical
risks and benefits is a matter of clinical
judgment which the court would not normally be able to make without
expert evidence
and it would be wrong to decide by a simple
preference where there are conflicting views on either side, both
capable of logical
support.  Only where expert opinion cannot be
logically supported at all will it fail to provide ‘the
benchmark by reference
to which the defendant’s conduct falls
to be assessed’ (at 243A-E).
…
This essential difference
between the scientific and the judicial measure of proof was aptly
highlighted by the House of Lords in
the Scottish case of
Dingley
v The Chief Constable, Strathclyde Police
2000 SC (HL) 77 and the
warning given at 89D-E that:
‘
[O]ne
cannot entirely discount the risk that by immersing himself in every
detail and by looking deeply into the minds of experts,
a judge may
be seduced into a position where he applies to the expert evidence
the standards which the expert himself will apply
to the question
whether a particular thesis has been proved or disproved –
instead of assessing as a judge must do, where
the balance of
probabilities lies on a review of the whole of the evidence.’”
The CTG tracings.
[243] There has been a
lot of evidence about the plaintiff having been on a running CTG for
the most part of the labour.  However,
and I might add,
regrettably, those CTG tracings have allegedly faded.  There are
also allegations that they may even have
been tampered with
deliberately in some places.  I do not think that this Court
should comment much on the tampering issue,
especially an attempt to
apportion blame for the alleged tampering, if indeed it actually
happened without any form of evidence.
It did not help that no
document expert was called to testify so that the court would be able
to certain that the CTGs were not
just damaged or had not just
faded.  They had, in those parts, been deliberately tampered
with.  I simply do not think
that this Court should be expected
to answer that question nor was it asked to make a finding on it.
It would be gravely
concerning though were it to be true as it is
laced with pure criminality and an attempt to hide the truth by the
obliteration
of evidence.  However, it appears that the CTG
tracings from about 16:00 to about 25 minutes or so thereafter were
not affected
by the alleged tampering.  They seem to have only
been affected by fading.  It was never suggested by any of the
parties
that anything else beyond fading might have happened to that
portion of the tracings.  Consequently, I intend to deal with

those CTG tracings which were the only ones about which some of the
experts gave evidence.
[244] The defendant
contends that professor Anthony’s evidence based on the
enhancement of the photos of the CTGs which were
taken from the
original CTGs by Dr Murray is not established on facts and is
therefore speculative even to the extent that anything
could be made
out of them.  The defendant argues that even where clear and
legible CTGs which appear abnormal are available,
CTGs do lend
themselves to different interpretations by clinicians of the same
level of seniority and are therefore an unreliable
tool.  The
defendant rejected professor Anthony’s enhancement which it
called a drawing in circumstances in which even
a document examiner
was unable to enhance the faint or faded original CTGs which the
document examiner had been requested to do.
Therefore, the
defendant rejected any opinion based on professor Anthony’s
enhancement.  The defendant, in a nutshell,
argued, even on the
basis of those CTGs that the plaintiff has failed to prove that its
employees acted negligently when attending
to the delivery of A by
the plaintiff.  It further argued that the plaintiff also failed
to establish, on probabilities, that
any negligence as the court may
find, caused the injury in A.
[245] The issue of the
CTGs’ illegibility and the evidence of the plaintiff’s
experts both Dr Murray and professor Anthony
and indeed that of the
defendant’s obstetrician, Dr Koll and Dr van Rensburg, the
defendant’s paediatric neurologist
has made them one of the key
cogs in the assessment of the evidence in this matter.  Perhaps
it is important to state the
obvious fact that parties are poles
apart about the admissibility of the faded CTGs and their
enhancement.  Therefore, the
relevance of the evidence that was
given by the plaintiff’s expert witnesses in seeking to rely on
them to the extent that
the plaintiff contends, they prove the
existence of foetal distress and syntocinon infusion at the relevant
time is disputed.
The defendant disavows their relevance and in
fact contends that there are no CTGs to speak of as the CTGs were
unreadable due
to fading.  It is common cause that during the
hearing of this matter in the open court in Bhisho on 28 November
2019 the
original maternity case records were available in court.
Dr Murray was given access to them and saw that the original CTGs
had
faded.  However, she felt that some areas in them were readable
especially the CTG tracings from about 16:00.  She
could read
the FHR and contraction patterns on them.  She decided to take
some pictures using her cellphone so that she could
expand the
pictures for better legibility.  It is common cause that
photocopies of those pictures were made part of the court
bundles and
were included in Dr Murray’s addendum report and were dealt
with in her joint minute with Dr Koll.
[246] When she testified,
her cellphone pictures were shown in court during trial by being
projected on a screen in court when she
testified about them.
At that stage there was no objection to her evidence as far as the
admissibility of the photographs
was concerned or her evidence in
that regard.  It was never contended that she could not give
evidence based on her pictures
on the basis that her pictures were
inadmissible.  What has always been the defendant’s
contention was that the original
CTGs had faded and were consequently
unreadable and nothing could be made of them.  It was never
contended that she could
not have enhanced their visibility and
testify on the basis of what could be gleaned from them or that her
cellphone enhancement
was inadmissible.
[247] In essence the
plaintiff contends that the evidence of both Dr Murray and professor
Anthony should be assessed and weighed
together with the rest of the
evidence in this matter. This would include their evidence on the
enhanced CTG tracings and professor
Anthony’s own enhancements
which he described how he did it in his evidence.  His evidence
was that he used Dr Murray’s
photocopy, and with a felt pen,
made that copy more readable.  He also used a good light and a
magnifying glass so that he
would be able to be properly guided as he
did his enhancement with a felt pan.  The real issue is, in my
view, less about
professor Anthony’s enhancement or enhanced
CTG copy but more about Dr Murray’s photographs of the CTG
about which
she testified in court and was in fact cross-examined
with no objection.  During professor Anthony’s evidence
when he
was cross-examined, it was never suggested that his drawing
was in anyway at variance with the photograph taken by Dr Murray and

on which she led evidence in court.
[248]
With regard to all this evidence about the CTGs from 16:00 or there
about to the end and the photographs that Dr Murray made
which found
their way into the court bundle in terms of the Rules of Court, the
plaintiff relies on
Protea
Assurance
[11]
.
On that authority the plaintiff submitted that Dr Murray’s
evidence on her photographs of the CTG tracings and professor

Anthony’s enhancement thereof is admissible evidence from which
the court is entitled to draw certain inferences and conclusions
in
the normal course of its evaluation of the entire evidence.  The
court said in
Protea
Assurance
:
“
The
remarks to be found in the cases to which I have been referred and in
which the concept of a document has been considered, were
not
intended to be exhaustive expositions of what the word comprehends
and they certainly do not positively support the notion
that a
photograph cannot be regarded as a document.  See
Seccombe
and Others v Attorney – General and Others
1919 TPD 270
at 277 and
Sneech
v Hill Kaplan Scott and Partners
1981
(3) SA 332
(A) at 338.  Nor is it important, for present
purposes, to distinguish between a photograph which amounts to ‘reele
getuienis’, as Schmid calls it in Bewysreg 3
rd
ed at 341, and one which is
taken to prove the existence of that which has been photographed.
Rule 36 (4) shows, I think,
that a photograph was regarded as a
document by the framers of the Rules for reference is made in that
subrule to ‘medical
reports, hospital records, X-ray
photographs or other documentary information of a like nature’
(my emphasis).  The
use of the word ‘other’ after
the inclusion of X-ray photographs indicates, to my mind, that
photographs were regarded
by the framers of the Rules as documentary
information.  Furthermore, as was pointed out during argument,
if photographs are
not covered by the use of the word ‘documents’
in Rule 35 (1), no provision would have been made in the Rules for
discovery
in the ordinary course of photographs.  It seems most
unlikely that photographs were intended to be excluded.  The
fact
that specific provision regarding photographs in some of the
other Rules does not point to a contrary conclusion, for those
provisions
relate only to those photographs which a litigant proposes
to use at the trial, and would have remained priviledged but for the

litigant’s desire to use them at the trial.  Such
provisions do not cater, as Rule 35 (1) does, for the possibility

that the litigant’s adversary might wish to make use of a
relevant, but unpriviledged, photograph in the former’s
possession.  I conclude, therefore, that the photographs in
question are documents within the meaning of Rule 35(12) and that

respondents are entitled to inspect and copy them.”
[249] The defendant did
not make any countervailing argument on the basis of which it was
sought to suggest the basis on which Dr
Murray’s photographs of
the original CTGs should not be accepted as real evidence.  I
was not referred to any authority
on the basis of which Dr Murray’s
photographs should be deemed inadmissible or that her evidence on
them should not be assessed
together with the rest of the evidence.
As I said before, no suggestion was made that there wre any
differences between what
the defendant referred to as professor
Anthony’s drawing and Dr Murray’s photographs in a way
that sought to suggest
that professor Anthony might have either erred
or been inaccurate or came up with a document or drawing that was, in
even a minute
way, at variance with Dr Murray’s photograph or
photocopy.  What the defendant sought to do was to adopt an
obstructionist
approach to that evidence and to professor Anthony’s
enhancement and indeed refused to engage with the CTGs on the basis
that they were illegible or unreadable and in fact the defendant
submitted that there were no CTGs to speak of.
[250] Even Dr Koll’s
refusal to engage with those CTGs on the basis that they are
unreadable was difficult to understand.
He vacillated between
saying that the entire CTGs were unreadable to saying that only the
cardio portion was unreadable but
the tocograph portion was
readable.  That is how he propagated his evidence on a mother
pushing uncontrollably.  In other
words, he would not engage on
those CTGs but where engaging on them suited his views he was
prepared to give evidence on them.
His refusal to engage with
Dr Murray’s photographs, his refusal to engage with the
enhanced version or drawing by professor
Anthony and in fact his
selective refusal to have anything to do with the faded CTGs to the
extent of not dealing with Dr Murray’s
photographs on the basis
that they were made from faded original CTGs is troubling for an
expert witness.  One would have
expected him to, at the very
least, directly deal with them even if conditionally upon them being
an accurate reflection of the
actual CTG tracings.  He never
made any of the attempts that were made by his colleagues and
counterparts and fail to see
what they could see.  After all, it
is for the court to determine the admissibility of any evidence.
A witness cannot
choose not to engage with any evidence based on her
or his views of that evidence.
[251]
This approach by an expert witness is concerning as it seems to be at
variance with the duties of an expert witness in court
proceedings
which were reaffirmed recently in
MEC
for Health, Limpopo
[12]
by Molemela JA (as she then was) as follows:
“
The
functions of an expert witness were explained by this Court as
follows in
McGregor
and Another v MEC for
Health, Western Cape
:
‘…
The
functions of an expert witness are three fold.  First, where
they have themselves observed relevant facts that evidence
will be
evidence of fact and [be] admissible as such.  Second, they
provide the court with abstract or general knowledge concerning
their
discipline that is necessary to enable the court to understand the
issues arising in the litigation.  This includes
evidence of the
current state of knowledge and generally accepted practice in the
field in question.  Although such evidence
can only be given by
an expert qualified in the relevant field, it remains, at the end of
the day, essentially evidence of fact
on which the court will have to
make factual findings.  It is necessary to enable the court to
assess the validity of opinions
that they express.  Third, they
give evidence concerning their own inferences and opinions on the
issues in the case and the
grounds for drawing those inferences and
expressing those conclusions.’”
[252] Dr Koll did not
perform the functions of expert witnesses as explained above when it
comes to the CTG tracings.  His
approach was to evasively and in
some ways obstructively refuse to engage with that evidence
altogether even if subject to any
conditions and reservations as he
could have.  This unfortunately gave the impression of an expert
witness who refused to
say something that was not aligned with the
defendant’s postulations or defence as if he was in court as a
defendant’s
witness as against an expert called by the
defendant.  I think that there is a significant difference
between the two.
I accept the photograph of the CTG tracings
taken by Dr Murray and I accept the enhancement thereof by professor
Anthony being
satisfied as to how he went about doing the enhancement
to make the picture more legible which he explained in his evidence.

Therefore, the evidence of Dr Murray and that of professor Anthony on
the CTG tracings from about 16:00 will be considered as will
the rest
of the evidence to assist the court in determining what could
reasonably be concluded about the foetal condition during
that final
hour before the birth of A.  That evidence will also be factored
in in determining both the issue of negligence
and the issue of
causation and be considered together with the entire body evidence in
this matter.
The syntocinon
infusion.
[253] This brings me to
the similarly contentions issue of syntocinon infusion.  The
evidence of sister Mbada was that when
she assessed the plaintiff at
14:00 she found her to be still 7cm dilated.  This meant that
she had remained at 7cm for two
hours from 12:00 which called for
action.  She informed the doctor who prescribed syntocinon which
was to be administered
if the CTG was reactive.  She accepted
that there was no note at 14:00 which showed what the CTG tracings
reflected at that
time.  She insisted that although she could
not remember the events of that day she did not administer
syntocinon.  If
it were to be accepted that the doctor’s
instruction for syntocinon infusion was given at 14:00, it would have
to be accepted
that in line with her evidence that she would need 30
minutes to observe the CTG which would take her to 14:30.  There
was
no note at 14:30 in the same way that there was none at 14:00
indicating what the CTG tracings reflected.  Therefore, there
is
no way of knowing what the CTG showed between 12:00 and 14:30 for two
and a half hour.  There is another troubling feature
about the
defendant’s case in this regard.  Dr Linde distanced
herself in her evidence from having ordered or given
an instruction
for syntocinon at 14:00.  In fact she said that such entry in
the notes was falsified.   This says
a lot about sister
Mbada as the maternity case records, where she is concerned, are
punctuated by many things from inconsistencies,
gaps and writing over
to changing some of the original entries that she had made.
When she would have made those changes
is difficult to tell.
This is over and above the alleged tampering with certain portions of
the CTGs for which nobody has
taken responsibility.
[254] If the CTG was
reactive at 14:30 with the 30 minutes CTG observation time having
lapsed she should start syntocinon infusion.
There is no note
indicating that it was started or that it was not and the reason
therefor.  If she started it at 14:30, this
would explain the
improvement in cervical dilation at or about 15:00.  Her
evidence was that the reason she would not have
done the infusion
would not be because the CTG was not reactive.  There was a
possibility that from 14:00 and 16:00 contractions
would have changed
making it unnecessary to administer it.  Her evidence was that
contractions were stronger even though their
frequency did not
improve.  She testified that between 14:30 and 15:00 the doctor
arrived.  It is common cause that Dr
Linde made a note at 15:00
indicating that the plaintiff was still 7cm dilated.  This means
that for two hours from 12:00
to 14:00 she remained 7cm dilated.
[255] However, and
inexplicably there was no note of what the CTG showed and there was
no partogram entry by Dr Linde reflecting
the foetal well-being.
If prescription was actually made at 15:00, it was done without any
indication of the foetal well-being
in circumstances in which the CTG
was said to be running.  Her evidence that she could not have
prescribed syntocinon without
looking at the CTGs is neither based on
fact nor what she could remember in circumstances in which she
reposed a lot of confidence
on sister Mbada.  It is common cause
that Ringers Lactate was put up in preparation for syntocinon
infusion and the catheter
was inserted.  There was basically no
reason for not administering syntocinon except of course if the CTG
was non-reactive
but the partogram is silent about the CTG readings
at that time.  The proposition that despite syntocinon having
been prescribed
and all the necessary preparations for its infusion
having been made, the sudden cervical dilation improvement from 7cm
to 10cm
in one hour after the prescription was done was a mere
coincidence is difficult to understand.  So is the sudden
phenomenon
of a natural oxytocin which was not there at any time
before the prescription or at least did not have this huge and
remarkable
effect on contractions and dilation.  This would mean
that the dilation that was not happening at 1 cm per hour for 7 hours

or so, suddenly made a quantum leap of 3cm in one hour on its own.
This defies logic.
[256] The only reason
given both by sister Mbada and Dr Linde for the idea that syntocinon
was not infused despite all its indications
being met on their
evidence and preparations having been made is the fact that they did
not make notes or ticks indicating that
syntocinon was infused.
This is bewildering from both of them as they both failed to make
crucial notes about the foetal
well-being at crucial times and in
fact ignored the guidelines.  They both failed to make the
necessary partogram entries
as required by the guidelines.  In
other words, they did not at any stage show themselves as being
diligent in note keeping
or making crucial entries in the maternity
case records.  In fact Dr Linde herself gave an instruction for
syntocinon infusion
without as much as having seen the patient and
assessed her condition and that of the foetus at 14:00, if the
evidence of sister
Mbada is to be accepted in that regard.  Looking
at their evidence and that of the plaintiff’s expert witnesses,
Dr
Murray, professor van Toorn, professor Anthony and even that of Dr
Koll in which inexplicably he sought to align himself with the

defendant’s factual witnesses even on this issue, none of this
argument about syntocinon not having been administered is
sensible
let alone probable.  On probabilities syntocinon was
administered grossly negligently which resulted in the picture
that
is dipicted in the evidence of both Dr Murray and professor Anthony
about the pathological CTG tracings from about 16:00.
The
evidence, considered as a whole, clearly suggests that syntocinon
infusion was prescribed negligently.  It was also negligently

administered with no doctor being present at the time of its
administration.  This even though Dr Linde was aware about the

patient’s severely delayed labour progress which caused her to
prescribe syntocinon in the first place.  After that,
instead of
remaining with the patient to personally monitor her, she disappeared
from the scene inexplicably.  A new doctor,
Dr Philips came into
the picture who had no previous background about the foetal
condition.  He would have to rely on whatever
he would make of
the incomplete and often contradictory hospital notes which it is
common cause, were deficient in some material
respect or whatever
briefing he would get from the hapless sister Mbada.
[257] It turned out that
he could not do vacuum extraction and had to call Dr Cilliers to come
and assist.  This was for a
patient to whom time was of the
essence and these medical personnel were rather lackadaisical about
what was clearly a critical
situation of a risky labour.  This
negligence which was the theme of their handling of the plaintiff’s
labour in this
matter cannot be wished away.  Even this idea
that it made a difference that the contraction pattern of about as
much as 8
or 9 contractions in 10 minutes was caused naturally by the
mother uncontrollably pushing, a postulation of sister Mbada, Dr
Cilliers
and Dr Koll, as against syntocinon infusion is bewildering.
The fact of the matter is that the plaintiff was encouraged to
push
by sister Mbada who was clearly out of her depth, with little or no
proper consideration for the foetal well-being.
She was left on
her own devices in circumstances in which she was clearly neither
qualified nor experienced enough to understand
the gravity of the
situation.
Conclusion.
[258] The result of all
of this is that the plaintiff has, on a balance of probabilities,
proved negligence and causation as the
evidence clearly indicates.
The approach by Dr Christianson to pursue the genetic testing
hypothesis by ignoring crucial
evidence misses one very important
point.  That is that the plaintiff is not required to establish
as a scientific fact that
it was not the genetic predisposition that
led to the outcome and birth defects of A.  She was required to
prove on a balance
of probabilities that more than anything else it
was the negligent conduct of the defendant’s employees which
caused the
birth defects of A.
[259] In essence
professor Christianson appeared to have set out to do a scientific
exploration of the endless possibilities in
the hope that he will
achieve the scientific certainty that he pursued with zeal in his
quest to answer the question relating to
the unfortunate family
history of the four children born of the plaintiff allegedly from the
same partner.  This is because
all of them had some or other
misfortune.  This ignores the fact that the first child was born
at home with no form of medical
assistance whatsoever where nothing
could have been done to prevent or even monitor foetal distress.
Speculation about the
first child possibly having some form of a
genetic disorder has no factual basis.  The same applies with
the third child even
though he was born in a hospital environment.
The fact is that there is no factual basis for a conclusion that that
child
had any form of genetic malformation.  The fourth child
had epilepsy on the second day of life after what was described as

very good apgar scores.  The facts around her are not very clear
and it would be improper if not dangerous to make conclusions
about
anything relating to her in circumstances in which in the fullness of
time evidence might suggest something else.  The
second child A,
the child in this case was a victim of many things.  This is
from incompetence of the nursing staff as clearly
demonstrated by an
inability to plot a partogram meaningfully and to make meaningful
notes that are not only informative but also
complement that which is
plotted on the partogram.  In fact, that partogram was largely
ignored as was the foetal well-being
of the child.  The doctors
themselves did not give an impression of medical practitioners that
gave themselves time to ensure
that foetal well-being was not
compromised or that neonatally nothing was amiss.
[260] The fact that the
date was 31 December 2015, a new year’s eve did not help as
there was skeleton staff.  I need
not repeat what was appears to
have happened with regard to the evolution of the neurological
situation of this child.  What
is clear is that from being born
in a compromised state, her precarious situation was not appreciated
which led to it not being
adequately addressed.  In fact, this
baby appears to have been treated neonatally no differently from the
intrapartum obstetric
handling.  Her delivery was handled even
less than that of a normal as against risky pregnancy.  The
failure to appreciate
the deterioration that started from birth until
the speech therapist came into the picture and looked into her
seriously speaks
volumes.  As for Dr Mans, he appears to have
been lulled into a false sense of confidence about the status of this
baby by
how Dr Cilliers and Dr Philips who were involved in the
actual delivery would have handed her over as a normal healthy
“vigorously
crying baby” which is improbable and
farfetched.  It was a proverbial comedy of errors, to make light
of a very serious
matter.  The genetic investigation cannot be
used to blindly embark on endless scientific research of genetic
possibilities
at the expense of the facts of the shocking handling of
this delivery which led to the outcome.  I must say that
professor
Christianson’s attempt to brush everything aside in
pursuit of this genetic testing theory whose end point he could not
cogently
articulate cannot be countenanced.  I also had some
difficulties with Dr van Rensburg’s evidence at least in one
respect,
still on the genetic testing issue.  Dr Gericke
incomprehensively and shockingly allowed notes or documents of two
other patients
he was working on to get mixed up with the records in
this matter, if his explanation is anything to go by.  It was
beyond
carelessness of him to allow that to happen.
[261] However, he
explained his mistake which is still difficult to fully understand.
He then conceded that he was accepting
that A was GMFCS 1 and not 4
as he had previously testified.  On the basis of the reference
to A being GMFCS 4 by Dr Gericke,
Dr van Rensburg insisted on the
idea that A had a progressive as against static cerebral palsy.
This ignored the evidence
that in fact A’s cerebral palsy was
static as a matter of fact.  She clung on this progressive
cerebral palsy idea to
also push for genetic testing.  I could
not understand that even as I accept her discomfort which was well
placed, with Dr
Gericke’s process of examination of his
patients and how he then goes about compiling his reports.
However, none
of this should be allowed to remove focus from the
established facts and the logical process of legal reasoning as
against scientific
reasoning leading to legal as against scientific
proof.
[262]
In dealing with the factual witnesses’ evidence and the
conflicting opinions of experts in this matter, I was guided
by our
case law some of which is referred above including the recent case of
J.A.
obo D.M.A
[13]
.
In that matter Van Zyl DJP had this to say:
“
Conceptually
there are several types of conflicts in expert evidence that may
present itself in any given case.  The first
is a conflict with
regard to the assumed facts.  By reason of its very nature,
expert opinion must have a factual basis.
The facts upon which
an expert’s opinion is based must be proved by admissible
evidence.  An expert opinion based entirely
on inadmissible
evidence is itself inadmissible.  The facts may be established
by asking the expert witness in examination-in-chief
what those facts
are.  “An expert’s opinion represents his reasoned
conclusion based on certain facts or data,
which are either common
cause, or established by his own evidence or that of some other
competent witness.  Except possibly
where it is not
controverted, an expert’s bold statement of his opinion is not
of any real assistance.”
How those facts are proven
is determined by the principles of evidence and the usual methods
used for judicial fact ̶ finding
and rational decision-making.
Where the expert him or herself observed relevant facts, that
evidence will be evidence of
fact and admissible as such.  Where
the opinion seeks to take issue on the facts with the version of
direct eyewitness evidence,
credible eyewitness evidence conforms to
the probabilities, will generally take preference to the opinion of
an expert of what
the facts are.  In the final result, the
decision of what the facts are must be founded on an assessment of
the evidence as
a whole and the probabilities as they appear
therefrom.
The inferences drawn from
the facts must be sound.  The internal logic of the opinion must
be consistent, and the reasoning
adopted in arriving at the
conclusion in question must accord with what the accepted standards
of methodology are in the relevant
discipline.  The reasoning
will be illogical or irrational and consequently unreliable, if (i)
it is based on a misinterpretation
of facts; (ii) it is speculative,
or internally contradictory or inconsistent to be unreliable; (iii)
if the opinion is based on
a standard of conduct that is higher or
lower than what has been found to be the acceptable standard; (iv) if
the methodology employed
by the expert witness is flawed.  What
flows from this is that the mere fact that an expert opinion is
unchallenged does not
necessarily mean that it must be accepted.
However, if that evidence is based on sound grounds and is supported
by the facts,
there exists no reason not to accept it.”
[263] In the final
analysis the plaintiff has, on a preponderance of probabilities,
proved that the birth defects of A were caused
by the negligence of
the defendant’s employees.  Professor Andronikou’s
MRI scan report made the following finding
concerning the injury
pattern of A:
“
Bilateral,
symmetrical involvement of the para-sagittal, peri-Rolandic and
peri-trigonal deep/periventricular white matter regions
of the brain
in combination with the involvement of the thalami and caudate nuclei
may
be due to a hypoxic ischemic
injury of a combined acute-profound and partial-prolonged nature.
However, the pattern of injury
in this patient can also be seen with
toxic metabolic and post infectious causes.  Possible metabolic
conditions that can
have this appearance include Canavan disease,
crabbe disease and Wilsons disease.  The patient requires
evaluation by a paediatric
neurologist and may have to undergo
testing for metabolic disorders to distinguish these potential
causes.”
[264] I am of the view
that to a fairly reasonable extent, all the other potential causes of
the injury pattern in A have been reasonably
excluded.
Furthermore, I take the view that dispite professor Andronikou
having, in his report, used the word “
may
”, his
primary finding was that the birth defects of A were due to a hypoxic
ischemic injury of a combined acute-profound
and partial prolonged
nature.
[265] The inadequate
monitoring has, in this case, resulted in the foetal distress being
missed which was substandard care.
The lack of proper notes
that would have easily enabled the various medical staff involved in
the management of the delivery of
A to appreciate the unfavourable
environment the foetus was in largely also contributed to the foetal
distress not being appreciated
as it should have.  Perhaps even
at the risk of repetition, it is not without significance that the
plaintiff was already
in the active phase of labour as early as
06:50.  She remained at 5cm of dilation throughout until about
12:00 when she progressed
to 7cm some five hours later.  That
was a severely delayed labour progress.  There is no evidence of
any thorough going
investigation of the severe delay at any stage and
an informed decision being made one way or the other about any
necessary intervention.
In fact the evidence is that despite
the plaintiff being a risky labour, was only seen by a doctor at
about 15:00 for the very
first time.  That was some six hours
since she was seen by nurses at 09:00 who had in any event
negligently wrongly plotted
her in the latent phase of the
partogram.  There were numerous instances of substandard care
which punctuated every step of
A’s delivery process with nobody
making any serious effort, beyond a seemingly occasional glance at
the CTG when it was running.
The hospital staff’s notes
were so inadequate that they could easily confuse even the author
thereof not to mention the doctors
who seemed to have placed heavy
reliance on the clearly underqualified and clearly inexperienced
sister Mbada, if her notes are
anything to go by.  In fact she
admitted that when A was born she had not yet done midwifery yet
which she only finalised
in about 2018.  It is fair to say when
she testified in this matter she was more experienced and qualified
than in 2015 when
she was allowed to single handedly monitor the
delivery process of A and manage the plaintiff’s labour when
she was clearly
not qualified to do so.
[266] The unguided
syntocinon infusion simply made worse what was already a critical and
potentially dangerous situation.
It gets worse in that even if
sister Mbada’s and Dr Koll’s evidence were to be accepted
that the patient was pushing
uncontrollably between 16:00 and the
delivery, she did nothing to ensure that the pushing which she
encouraged the plaintiff to
do was being carefully monitored to
ensure that the foetal well-being was not thereby compromised.
It seems to me that from
sister Mbada to Dr Linde who prescribed the
syntocinon and disappeared thereafter, and indeed to Dr Cilliers, and
Dr Mans, everybody
seemed to rely on some hope for the best and not a
well informed decision based on a careful observation of the facts
and the critical
tests like sugar test results being done.  To
make the point clear that there was lack of appreciation of the fact
that the
delivery of A was in troubled waters, an admittedly
inexperienced Dr Philips was the one who had to deal with the actual
ventouse
delivery.  He had to call a senior colleague, Dr
Cilliers for assistance.  All of that added to the delay that
was already
severe and dangerous for the foetal well-being which was
never, at any stage critically assessed.  Dr Cilliers used a
risky
pregnancy to train a young and inexperienced doctor just to
upskill him when she appears not have given herself time to
critically
evaluate the hospital notes and the partogram and make the
required entries.
[267] In all these
circumstances it is clear that A suffered intrapartum asphyxia which
directly led her to suffer injuries that
caused her the damage due to
the failure of the hospital staff to adequately monitor her from the
very beginning at 09:00 all the
way to the delivery of the baby and
thereafter until day 4 of her life.  The attempt by to try to
make a clear distinction
between poor note keeping and substandard
care is difficult to understand as they even ignored the obvious
results of that poor
note keeping.  There was also substandard
care even at the neonatal stage which manifested itself in a proper
analysis of
the neurological symptomatic lack of suck reflex, poor
grasp and latch reflex and lethargy not being investigated.  The
crying
was simply and lazily attributed to hunger by Dr Mans and a
conclusion was made without properly analysing the situation.

It was then concluded that the only reason the baby was not
breastfeeding was the mother’s inability to breastfeed hence

the recommendation for breastfeeding counselling without any attempt
at excluding encephalopathy.  That too was substandard
care as
it contributed to the failure to place the baby under a higher level
of care which, in any event, should have been done
following a
resuscitation and the obviously less than normal level of
consciousness of the baby.  In the result the plaintiff
must
succeed in her claim for damages.
The result.
[268] Therefore, the
following order shall issue:
1. The defendant is held
liable to compensate the plaintiff in her personal and representative
capacities as the mother and natural
guardian of A for the damages
suffered as a result of the defendant’s breaches of the
agreement and/or legal duty to the
plaintiff and A such amount as may
be proved or agreed upon.
2. The defendant shall
pay the plaintiff’s costs of suit including the costs
occasioned by the employment of two counsel as
well as all costs of
the plaintiff’s expert witnesses.
M.S. JOLWANA
JUDGE OF THE HIGH
COURT
Appearances:
Counsel
for the plaintiff:
J
WESSELS SC WITH C. CREMEN
Instructed
by:
ENZO
MEYERS ATTORNEYS
EAST
LONDON
Counsel
for the defendant:
T.M.
NTSALUBA SC WITH S.Y. MALINGA
Instructed
by:
NORTON
ROSE FULBRIGHT SOUTH AFRICA
c/o
SMITH TABATA ATTORNEYS
EAST
LONDON
Date last
heard

: 27 October 2022
Supplementary heads filed
on    : 03 November 2022
Date
Delivered

: 27 July 2023
[1]
Volpe
J.J.: Neurology of the Newborn fifth edition page 402.
[2]
Pearson
T.S et al. Genetic Mimics of Cerebral Palsy: Movement Disorders,
Vol. 34, No.5, 2019 page 625 at page 628 where the following
are
listed:
Absent history perinatal
risk factor for brain injury, family history of sibling with similar
neurological symptoms, motor symptoms
onset after an initial period
of normal development, developmental regression, progressive
neurological symptoms, paroxysmal
motor symptoms or marked
fluctuation of motor symptoms, clinical exacerbation in the setting
of a catabolic state (e.g, febrile
illness), isolated generalized
hypotonia prominent ataxia, signs of peripheral neuromuscular
disease (reduced or absent reflexes,
sensory loss), eye movement
abnormalities (e.g., oculogyria, oculomotor apraxia, or paroxysmal
saccadix eye-head movements).
[3]
Centogene
is a laboratory based in Germany which conducted the metabolic
testing in this matter which are referenced in the evidence
[4]
Volpe
page 483.
[5]
Bhorat
I et al: Cerebral palsy and criteria implicating intrapartum hypoxia
in neonatal encephalopathy – an obstetric perspective
for the
South African setting: (2021) 111 SA MJ 3 pages 280-288.
[6]
The
American Academy of Pediatrics: Neonatal Ancephalopathy and
Neurological Outcome, Second Edition: Peadictrics Volume 133,
Number
5, May 2014:
http://pediatrics
a
appublications.org/.page e 1483.
[7]
The said letter
reads “To the extent that your client and/or Centogene may be
in possession of a portion of the blood sample,
under no
circumstances whatsoever is your client permitted to perform or
undertake any further whole exome sequencing, genome
sequencing or
any other genetic tests of any kind or nature.  In particular
there is a cluster of our client’s constitutional
rights that
would be fundamentally breached, viz, those of dignity, privacy,
freedom of security, bodily integrity etcetera.
In addition to
the constitutional rights that may be infringed your client has
already exhausted its remedy for medical examination
in terms of
Uniform Rule 36 (5).  At common law it is well established that
a person’s right to bodily integrity and
autonomy entitles him
to refuse medical treatment or assessment and subjecting a person to
unauthorized medical procedures to
which he or she has not consented
has been held to constitute invasion of privacy.”
[8]
Wassink
G et al: The Mechanisms and treatment of Asphy encephalopathy:
Volume 8 Article 40 February 2014: www.frontiersin.org.
[9]
Goliath
v MEC for Health, Eastern Cape
2015 (2) SA 97
(SCA) para 17-18
[10]
Oppelt
v Head: Health, Department of Health Provincial Administration:
Western Cape
2016 (1) SA 325
(CC);
2015 (12) BCLR 1471
(CC) para 36.
[11]
Protea
Assurance Co Ltd v Waverly Agency CC & Others
1994 (3) SA 241
(CPD) at 250 B-G.
[12]
MEC
for health, Limpopo v LWM obo D M (502/2021)
[2022] ZASCA 146
(27
October 2022) para 17.
[13]
J.A obo D.M.A. v
Member of Executive Council for Health, Eastern Cape
2022 (3) SA 473
(ECB);
[2022] 2 All SA 112
(ECB) paras 11 & 12.