Funda v MEC for the Department of Health, Eastern Cape (307/2018) [2021] ZAECBHC 16 (14 September 2021)

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[2021] ZAECBHC 16
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Funda v MEC for the Department of Health, Eastern Cape (307/2018) [2021] ZAECBHC 16 (14 September 2021)

IN
THE HIGH COURT OF SOUTH AFRICA
(EASTERN
CAPE LOCAL DIVISION, BHISHO)
CASE NO: 307/2018
Date Heard: 27/05/2021
Date

Delivered: 14/09/2021
In
the matter between
PHUMZA
FUNDA obo LINGOMSO
FUNDA                                                                   Plaintiff
And
THE
MEMBER OF THE EXECUTIVE COUNCIL FOR THE
Defendant
DEPARTMENT OF HEALTH – EASTERN CAPE
JUDGMENT
SMITH
J:
Introduction
[1]
The
plaintiff claims damages in her personal and representative
capacities as the mother and natural guardian of Lingomso Funda,
a
male infant born on 8 February 2016 at the All Saints Memorial
Hospital, Stutterheim, by means of normal vaginal delivery.
[2]
The
plaintiff’s claim is founded upon the alleged negligence of the
medical or nursing staff of the hospital, which allegedly
caused the
child to suffer a hypoxic ischaemic brain injury during birth,
resulting in cerebral palsy.
[3]
The
issue that falls for decision at this stage is only the liability of
the defendant and consequently whether, on a balance of

probabilities, negligence of the staff during the intrapartum period
caused the brain injury and the eventual cerebral palsy.
[4]
Apart
from the plaintiff herself, Dr Kara (paediatrician); Prof Davies
(paediatric neurologist), Dr Chimusoro (obstetrician and

gynaecologist); Prof Andronikou (paediatric neuro radiologist) and Dr
Pearce (paediatric neurologist), were called to testify on
her
behalf. The defendant called nursing sister Nonkolisko Elsie Dilla;
Dr Ntshokota; Dr Koll (obstetrician and gynaecologist)
and Prof
Rothberg (paediatric neonatologist) testify on her behalf. Mr J.
Wessels SC and Mr P. Uys appeared for the plaintiff and
Ms G.M.
Goedhart SC and Ms H Cassim appeared for the defendant.
The pleadings
[5]
The
plaintiff pleaded that the foetus suffered a hypoxic ischaemic brain
injury during the intrapartum period, and more particularly
while
under medical care at the hospital. The brain injury allegedly
resulted from substandard care by the doctors or staff who
failed or
neglected correctly to assess or monitor the maternal and foetal
condition during birth, and to act appropriately on
such assessment
or monitoring. She furthermore averred that appropriate assessment or
monitoring would probably have confirmed
foetal distress and the
necessity to intervene through either intrauterine resuscitation or
caesarean section.
[6]
The
defendant in her plea denied that the hospital staff were negligent
or that their negligence caused or contributed to Lingomso’s

cerebral palsy. She averred furthermore that the plaintiff arrived at
the hospital at approximately 09h00 on 8 February 2016, when
she was
entered into the maternity register. She was then admitted to the
labour ward and examined at approximately 09h20. She
had told the
nursing staff that she had gone into labour at 14h00, alternatively
16h00, on 7 February 2016. The plaintiff and the
foetus were
monitored at hourly intervals from 09h20. The foetal heart rate fell
within normal limits at all material times. Lingomso
was born at
12h50 on 8 February 2016, with Apgar scores of 9/10 and 10/10. The
plaintiff and Lingomso were discharged 9 February
2016.
The extent of the
injury
[7]
Before
I commence with a summary of the evidence, and in order to provide
proper context for the scientific hypotheses and conclusions
advanced
by the parties’ respective experts, it will perhaps be helpful
if I explain the agreed nature, extent and mechanisms
of Lingomso’s
brain injury.
[8]
The
experts agreed that the injury was caused by hypoxia and ischaemia,
resulting in a mixed (partial prolonged and acute profound)
brain
injury with features in keeping with hypoglycaemia. The injury
occurred over a period of hours.
[9]
The
MRI study depicts a mixed pattern of brain injury (partial prolonged
and acute profound) with injuries to the deep grey nuclei

(pulvinars), white matter, watershed and main arterial areas at the
peri-sylvian region and specific features of ulegyria, typically

associates with hypoxia and ischaemia.
[10]
The
mechanism of this injury was described as follows by the experts:
(a)
the
foetal compensatory mechanisms protect the foetal brain against
hypoxia and ischaemia by mopping up the acids generated in the
tissue
to correct the deficits. When the hypoxia and ischaemia persist, the
body moves to the next phase, being redistribution
of blood flow from
the less vital organs (for instance the skin) to preserve blood flow
to the brain. With progression of this
phase, blood will be shunted
away from the metabolic active parts of the brain to the deep nuclei
to sustain the vital organs of
life, resulting in the outer areas of
the brain developing a so-called watershed infarct;
(b)
this is described as a
partial prolonged hypoxic ischaemic injury, where the deeper areas of
the brain remain preserved. This injury
will manifest through foetal
heartrate, abnormalities, coinciding with uterine contractions;
(c)
an acute profound injury
involves necrosis of the deeper brain structures and may either occur
through a sudden catastrophic or
sentinel event (for instance cord
prolapse or uterine rupture) or more commonly through multiple
partial prolonged episodes with
eventual cumulative effect resulting
in an acute profound injury. This can result in a mixed partial
prolonged and acute profound
type of brain injury. Once again, the
injury manifest through foetal heartrate abnormalities, coinciding
with contractions; and
(d)
while isolated heartrate
measurements merely confirm foetal heartrate,  foetal heartrate
assessment timed to contractions,
informs of foetal well-being,
particularly when associated with deceleration.
The Maternity Care
Records
[11]
The records contain the following entries:
a.
The first stage of labour
started at 16:00 the day before the birth, lasting some 20 hours 20
minutes. The second stage occupied
30 minutes and the third stage 5
minutes;
b.
The membranes were
ruptured at 12h50 and the child delivered at 12h50, but the partogram
records that the membranes were ruptured
at 12h20;
c.
The monitoring of the
labour, the birth, the postpartum management of the plaintiff and
neonate was done by Sr. Dilla at 12h52;
d.
The cord was normal, the
membranes and placenta complete and normal with 3 vessels in the cord
and a placental weight of 520 g;
e.
No retro-placental clots
were present and no histology required and no sentinel event was
recorded;
f.
The neonate was delivered
in a healthy and satisfactory condition with recorded Apgars of 9/10
and 10/10 and received in the ward
at 12h50;
g.
The discharge summary
recorded that feeding options were discussed and initiated
successfully with exclusive breastfeeding to be
conducted on demand;
h.
The plaintiff took the
child to the clinic on 10 February 2016 due to twitching or fitting.
The child was examined by a nurse and
doctor, prescribed medicine,
and discharged home; and
i.
Eventually the child was
diagnosed with developmental delays and cerebral palsy.
Evidence on behalf of
the plaintiff
[12]
The plaintiff testified that when she learned of her pregnancy,
she immediately commenced antenatal care and had four
monthly
antenatal assessments prior to birth.  She was diagnosed with
HIV during the pregnancy.
[13]
By 7 February 2016, she developed back pain, and later she
experienced abdominal pains, which subsided. The next morning
the
labour pains were severe and an ambulance was called. She was
prepared for hospital, where she arrived after 7am. There a nurse

registered her and conducted an internal examination, assessing the
foetal heartbeat with a funnel like object. The nurse then
told her
to wait for a doctor.
[14]
When the doctor eventually arrived, he conducted an internal
examination, assessed the foetal heartbeat with a funnel
like object,
“spoke about centimetres” and advised her that she would
be taken to another ward. There the nurse instructed
her to lie on a
bed and breathe in and out. The nurse then left her alone and told
her to call her if the pain became more severe.
[15] She
called the nurse once or twice when the pains were very severe. The
nurse then exerted fundal pressure on the upper
part of her stomach,
ordering her to push. This eventually resulted in her giving birth.
[16] The
baby did not cry and the nurse had to hold him upside down and pat
him on the back. He, however, still did not cry.
The nurse did not
assess the child but wrapped him in a blanket and placed him next to
her. She was thereafter sutured, stepped
down onto a wheelchair, and
the child placed on her lap. They were then both taken to the ward.
[17] The
ward sister instructed her to breastfeed the child, but he could not
latch onto the breast. The sister then brought
the plaintiff milk in
a cup and instructed her to cup-feed the child, which she managed to
do. Thereafter the child slept for approximately
one hour. He cried a
bit after he had woken up,. They then both slept until the next day
when they were given some cards and discharged
without being
examined.
[18] The
child was cup-fed at home. He, however, developed seizures the next
day and was taken to the Mtanyana Clinic, where
she was given a
letter for hospital  referral.
[19] At
the hospital a doctor examined the child, gave him Panado Syrup (it
is common cause that it was probably Phenobarbitone)
and thereafter
send them home. The child again suffered seizures on the 10
th
,
which subsided the following day. She later returned the child to the
clinic on a regular basis.
[20] She
first realised that something was wrong with the child at
approximately  10 months of age when he could not sit,
speak or
hold onto anything. He is currently still unable to do anything for
himself. He only sleeps and can neither sit, stand
or talk.
[21] During
cross-examination, Ms Goedhart put to the plaintiff that Sr Dilla
first assessed her after admission at 09h20.
She further put to the
plaintiff that the hospital records state that sister Dilla had
assisted her at 09h20, 10h20, 11h20 and
12h20. She was assessed by a
doctor at 09h30. The assessments were conducted by cardiotocography
(CTG). The plaintiff, however,
maintained that she was assessed only
once by Sr Dilla and a doctor, and that no belt was placed over her
abdomen at any time.
[22] Ms
Goedhardt also put to the plaintiff that Sr Dilla would testify that
she made certain entries on the Maternity Care
Records (MCR) after
the document had been requested by the plaintiff’s attorneys.
She, however, made those notes contemporaneously
on the day, but had
failed to record it. She thus admitted that she had altered the
hospital records after birth, but would maintain
that she had merely
recorded what she had done on the day.
[23]
It was also put to the plaintiff that Sr Dilla had examined the child
to tick all the boxes and that the references to 12h50
is a mistake,
as she would have done so after birth. The child looked well upon
discharge and was feeding.
[24] The
plaintiff, however, maintained that the ward sister had instructed
her to breastfeed, but the child was cup fed with
formula due to
failure to latch. Bottle-feeding commenced only after a month. She
also maintained that the seizures commenced only
on the morning of
the 10th and continued thereafter.
[25] Doctor
Kara, a paediatric expert, testified that upon examining Lingomso he
had found the child to be micro-cephalic,
with probable mixed type of
cerebral palsy, GMFCS V, spasticity, dyskinesia, abnormal movements,
abnormal tone, limited communicative
ability and epilepsy. The child
also presented with myoclonic movements (which are random sudden
jerks) and no dysmorphic features
or neurocutaneous lesion. He had
poor swallow reflexes, low central tone and variable peripheral tone.
He does not suffer from
a progressive disorder.
[26] He
had regard to the need for the stimulation at birth, the reported
history of poor sucking reflex and the convulsions
on 10 February
2020. His testimony that moderate encephalopathy was present based on
the moderate seizures was not disputed. He
concluded that the
convulsions were probably the result of intrapartum hypoxia and that
the child should have been admitted to
hospital. He testified
furthermore that the plaintiff’s history and the antenatal
record exclude any antenatal or pre-conceptual
risk factors for
cerebral palsy, aside from HIV.
[27] The
MRI indicates that the injury did not occur prior to 36 weeks
gestation and HIV could likely be excluded as the cause
of his
cerebral palsy. HIV positive mothers do have approximately 50%
increased risk of delivering a baby with encephalopathy after
birth.
HIV does not cause the injury itself, but it makes the foetus more
susceptible to hypoxia.
[28] The
child had normal anthropometrical features upon birth, in keeping
with a baby of term gestation and there is no reason
to suspect
growth restriction or growth asymmetry. This conclusion and the
mother’s report in respect of foetal movement
upon admission to
hospital, make it less likely that there was any antenatal insult to
the foetal brain.
[29] The
normal head size at birth with microcephaly postnatally, suggests
that the a perinatal insult affected normal foetal
brain growth after
birth. The foetal condition seemed to be good when the mother was
assessed at the hospital at 09h00 on 8
th
February 2016
(based on history and assessment) and when the mother was assessed by
the nurse and the doctor.
[30] He
said the mother’s description of the baby not being able to
suck, the presence of the weak cry, cup feeding and
early discharge,
are concerning, as feeds needs to be established prior to discharge.
These factors are compatible with neonatal
and encephalopathy in the
first day of life. The convulsions occurred within 2 days after birth
and the baby had a poor history
of sucking. These factors point to
encephalopathy in the first days of life. It appears that the staff
did not detect it, or even
ignored it when brought to their
attention. The convulsions necessitated immediate hospital admission
and discharging the neonate
was thus unjustified.
[31]
He excluded other possible causes of neonatal and encephalopathy at
birth, namely, congenital normalities, metabolic illness
or syndrome,
history of progressive neurological deterioration, or that the child
initially reached milestones but subsequently
fell behind in respect
of such milestones.
[32] Regarding
the timing of the injury, Dr Kara testified that there is little
evidence to support an antenatal insult. The
convulsions on day two
is more likely to be the result of brain injury during birth.
Hypoglycaemia was probably the result of poor
feeding due to
encephalopathy and possibly caused the convulsions. The most common
cause of encephalopathy is hypoxic ischaemic
insults, with the
highest risk of such occurring during labour. The most common cause
of convulsions in the first three days of
life in a term infant is
hypoxic ischaemic encephalopathy (HIE).
[33] In
his view, although the Apgar score was normal and there is no record
of resuscitation at birth, the factors that point
to the probability
that the encephalopathy was due to a intrapartum result are;
encephalopathy, the results of the MIR and the
presence of dyskinetic
cerebral palsy.
[34] According
to him, the probability is 80% that the injury to the brain occurred
during labour. In addition, the MIR scan
confirms hypoglycaemia,
which is linked to intrapartum hypoxic ischaemia. Hypoxia and
ischaemia depletes stores of glucose that
is used to produce energy
to sustain cellular activity. In addition, the child had postnatal
microcephaly with no evidence of antenatal
or postnatal injury. He
also had overt neurological symptoms of poor feeding and crying,
convulsions in the first 36 to 48 hours
of life, with no record of
assessment prior to discharge.
[35] In
his view the following factors favour the probability that the
encephalopathy resulted from intrapartum injury; the
undoubted
presence of encephalopathy; the MIR scan confirming hypoxic ischaemic
injury (with mixed pattern of prolonged partial
and acute profound),
favouring the probability that the injury occurred during the labour
(noting reasonable exclusion of other
causes of encephalopathy); the
presence of dyskenetic cerebral palsy; and features of acute profound
HIE.
[36] A
history of encephalopathy after birth makes it an 80% probably that
the injury occurred during labour. A further factor
is the MIR
features of hypoglycaemia and a link between neonatal hypoglycaemia
intrapartum HIE. The depletion of glucose caused
by hypoxic ischaemic
injury means that there is not sufficient stores of glucose left to
sustain the high metabolic activity and
high demand for energy which
occurs after birth. A compromised baby with poor feeding and poor
perfusion may not provide adequate
glucose to the brain to prevent
cellular injury, resulting in a neonatal hypoglycaemic brain injury.
[37] During
cross-examination Dr Kara maintained that there is no history of
maternal infections, intrauterine growth restriction
or HIV related
encephalopathy. He thus rated the possibility of antenatal brain
insult as less than 10 percent.
[38]
He stated that there is an 80% chance of intrapartum hypoxic
ischaemic injury evidenced by dyskenetic cerebral palsy and an
MIR
picture of basal ganglia and thalamus brain injury. He also said that
CTG’s are sensitive but nonspecific, and CTG deceleration,

especially late deceleration, is highly predictive of foetal
compromise.
[39] Hypoglycaemia
is probably a consequence of the cerebral injury that affected
feeding, raised cerebral metabolism, increased
glucose consumption,
depleted the baby’s glucose stores and caused a hypoglycaemic
brain injury. As a result, the injury
as such was not the cause of
the brain injury.
[40]  In
the reply to questions put to him by the court, he testified that
seizures make it more probable had the injury
occurred intrapartum.
He also said that despite some inconsistency in the records, the
cerebral palsy was due to an intrapartum
hypoxic ischaemic injury
supported by the postnatal microcephaly and lack of evidence of
antenatal or postnatal injury.
[41] Professor
Andronikou testified that the injury occurred over many hours and
that an extensive portion and important parts
of the brain are
involved. These include severe damage to the motor and sensory cortex
(which allows a child to function). The
internal capsules, which
controls movement and the deep nulclei involved in the thalamus is
also severely affected. A large portion
of the brain, which includes
the peri-sylvian, posterior watershed and the occipital areas are
also damaged,
[42] Professor
Davis testified that the child fits criteria for neonatal
encephalopathy based on hypoxia and ischaemia with
a Sarnat Grade 2
moderate encephalopathy, and as a result hypoxia and ischaemia should
be considered as a cause of the cerebral
palsy.  He said that
term babies born in depressed conditions in lower and middle income
countries, usually result from intrapartum
hypoxia or birth asphyxia.
Reperfusion injury (the tissue damage caused when blood supply
returns to tissue) is part of the main
hypoxic ischaemic injury.
Multiple potential causal pathways can cause cerebral palsy in term
infants. A broader perspective is
necessary before attributing
neonatal encephalopathy to an intrapartum event. It thus calls for a
comprehensive multi-dimensional
assessment of neonatal status and all
potential contributing factors, including maternal medical history,
obstetric antecedents,
intrapartum factors and placental pathology.
[43]
He explained that there are a number of compensatory mechanisms
available to a foetus, and the basic mechanisms of the
hypoxic
ischaemic injury or hypoxic ischaemic encephalopathy are:
(a)
the so-call buffer stage
where, because of hypoxia ischaemia to tissues, the tissues generate
acids. The body then buffers or mop
up these acids, attempting to
correct the deficit. This is a stage where there is not likely to be
neurological damaged to the
foetus. However, if the hypoxia ischaemia
persists, then the next phase occurs, which is redistribution of
blood-flow in the foetus,
when blood is then divided from so-called
less vital organs, like the skin, to the brain to try to preserve
blood flow to the brain
in order to preserve life in the brain stem
itself;
(b)
the blood is diverted from
the cerebral cortex (outer regions of the brain) to the central
areas, resulting in deprivation of oxygenated
blood to these areas
with infarction or cell necrosis, (i.e. partial, prolonged hypoxic
ischaemic damage);
(c)
watershed infarcts occur
during uterine contractions and can be repeated over a lengthy period
(even several days), and these partial
prolonged insults manifest
through foetal heartrate abnormalities, particularly during uterine
contractions;
(d)
acute profound injuries
involve necrosis in deeper brain structures and present either as a
sudden catastrophic or sentinel event
(i.e. cord prolapse or uterine
rupture) or a build-up process of multiple partial prolonged episodes
with the final episode resulting
in a cumulative effect, which
results in turn in a mixed acute profound and partial prolonged
picture;
(e)
partial prolonged insults
manifest through changes in foetal heartrate and foetal condition,
and appropriate intervention can successfully
be instituted through
expedited delivery; and
(f)
generally a foetus will
suffer brief hypoxic bouts during labour, which are normally well
tolerated during the first buffer stage.
Continuation beyond the
buffer stage results in partial prolonged or watershed injury, and
eventual acute profound injury.
[44]
He questioned the quality of foetal monitoring during the later phase
of labour when the plaintiff presented to hospital, and
was of the
opinion that foetal distress was either missed or overlooked. In his
view, had the plaintiff been given reasonable intrapartum
obstetric
care and the delivery expedited, the hypoxic ischaemic asphyxia
injury of a combined partial prolonged and acute profound
nature,
neonatal encephalopathy and consequential cerebral palsy, would
probably have been prevented.
[45] During
cross-examination Prof Davis maintained that the seizures at 48 hours
of life indicate moderate to serious encephalopathy.
He said that
seizures are often delayed in HIE. In his opinion, the injury most
probably occurred during the intrapartum stage
and most probably
resulted from substandard intrapartum obstetric care.
[46]
He said that intrapartum hypoxia is the most probable causal factor
of neonatal encephalopathy, and substandard intrapartum
obstetric
care the predictable and preventable causal factors. In his opinion
reasonable intrapartum obstetric care and expedited
delivery would
probably have prevented the hypoxic ischemic injury, neonatal
encephalopathy and subsequent cerebral palsy.
[47] Doctor
Chimusoro, a paediatric specialist, testified that having had regard
to the hospital records, he was of the view
that the foetal heartrate
assessments were only done hourly instead of every 30 minutes, as
required by the guidelines. In his
view the partogram was obviously
not completed contemporaneously, but probably after the event.
[48] The
CD 4 count (a test for a type of white blood cell that helps the body
to prevent infections) and the viral load was
not recorded. There is
a difference in the management of mothers with or without suppressed
viral load. No serious ailments were
noted, and the treatment
prescribed for HIV seemed adequate.
[49]  In
his view the normal and anthropometrical medical features reasonably
exclude intrauterine growth restriction.
[50] He
said that the delay in assessment from 09h20 constitute substandard
care. The intensity of contractions increased as
the labour
progressed. The foetus should therefore have been more closely
monitored during the second stage of labour when the
contractions
became stronger, and the staff had to ensure that those strong
contractions did not result in hypoxia. In his opinion,
this is why
the foetus had to be monitored every half hour during active phase of
labour and after second contraction in the second
stage (10cm
dilatation). He criticised the records for not referring to the
maternal and foetal condition and the progress of labour
itself, and
the staff for not recording the foetal heartrate every half hour.
[51] In
his view, the recorded foetal heartrate was probably recorded
ex
post facto
. It is highly unlikely that the foetal heartrate would
be similar before and after contractions. Proper auscultation in
terms of
the guidelines entails foetal heartrate assessment before
and after contractions. Decelerations would have been identified
through
proper auscultation, and could have been attended to through
intrauterine resuscitation, intravenous fluids and medication to
relax
the uterus and contractions. Other possible causes of distress
could have been identified and excluded. In his view, the partogram

entries between 10h50 and 12h50 and contractions were drawn in one
movement and raise suspicion.
[52] The
staff had to assess the foetal heartrate before and after
contractions. This is done to determine whether the foetal
heartrate
recovers after the contraction. Should foetal distress occur,
intrauterine resuscitation should be conducted, which includes

putting the patient on the left side, administration of fluids,
oxygen and medication to relax the uterus to stop contractions,
and
determining whether there are other reasons for foetal distress, like
a cord prolapse.
[53] He
testified that in his opinion the foetal heartrate should have been
charted at every second contraction or every five
minutes during the
second stage of labour. The records show that monitoring was not done
effectively. Consequently, the substandard
intrapartum care missed a
hypoxic event. He also criticised the staff for not recording the CTG
findings, even in the absence of
tracing paper.
[54] During
cross-examination, he explained the distinction between HIV and HIE
types of encephalopathy, and said there was
no evidence of optimistic
infections. He also commented on the specific substandard care,
stating that the condition of the foetus
should have been assessed
through auscultation when plaintiff was bearing down.
[55] He
criticised the record keeping , explaining that the method of
recordal casts doubt on whether it was truly done.
[56] In
addition, he maintained that the intrapartum monitoring was
substandard and had missed a hypoxic event. In his view,
the foetal
condition was apparently normal upon admission and the injury
therefore probably occurred during birth at the hospital.
In his
opinion, the Apgar scores are probably incorrect and contradicted by
neonatal encephalopathy and the true condition of the
child.
[57] In
response to a question put to him by the court, doctor Chimusoro
explained that if the hypoxic event had occurred prior
to the
admission it would have showed in an abnormal foetal heartrate
pattern. Because the heartrate was normal on admission, the
hypoxic
event could only have taken place after admission. If the foetal
heartrate pattern is normal at admission, then it means
that there
has not been any brain insult, because the brain regulates the way
the heart beats and how the variation in the heart
changes. If the
damage had occurred before she was taken to the hospital, it would
have been evident from the foetal heartrate
at the time of admission.
[58] In
his view a hypoxic event with recovery, without any intrauterine
resuscitation, is highly unlikely. It is also obstetrically
unlikely
that whatever insult was causing the baby to be hypoxic would
spontaneously correct. Thus, he excluded antenatal brain
injury due
to normal heartrate patterns upon and immediately after admission. He
said that the intrapartum monitoring was clearly
substandard and had
missed obvious foetal distress.
[59] Doctor
Pearce testified that she had assessed the child clinically and found
him to be micro-cephalic, which is indicative
of lack of brain
growth, with no other conditions mimicking cerebral palsy. Her
clinical findings correlate exactly with the MRI
features of the
child. The history obtained from the plaintiff fits the criteria for
a Grade 2 neonatal encephalopathy, resulting
from intrapartum hypoxia
and ischaemia.
[60]
She excluded other possible and probable causes for NE II, like
infection, congenital brain abnormalities, substance
abuse and
medication. She had also considered and excluded other probable
causes for cerebral palsy including:
(a)
intrauterine growth
restriction, as the anthropological measurements were normal for
gestation; and
(b)
intracranial haemorrhage
(which is also excluded on MRI), inborn errors of metabolism and
genetic causes.
[61] In
her opinion, the child has a mixed type of cerebral palsy,
predominantly dystonic with superimposed left hemiplegia.
He is
classified as GMFCS V (which is the worst level of impairment for
cerebral palsy; MACSV (manual ability classification scale);
and
CFCSV (communication function classification scale).
[62] She
said that the MRI, the history obtained and the clinical records
support the child’s diagnoses. His condition
is most likely the
result of peripartum hypoxia, as founded upon assessment of
antenatal, intrapartum and post-natal possible causes
of the
encephalopathy and outcome. HIV probably played no role in the
outcome as the plaintiff was at stage 1 of HIV, with an unknown
CD 4
count and no indications of maternal infection, illness or
intrauterine growth restriction.
[63] She
testified that hypoxic ischaemic injury is divided into primary and
latent energy failure, with the primary failure
being the initial
insult. During the latent phase, the child seems to recover, but the
reperfusion of blood can result in a reperfusion
injury. It is
possible that the child may be born in the latent phase of injury,
with resultant decompensation resulting in neurological
damage.
[64]
The neonatal seizures were a significant concern. The child had to be
fully examined and admitted. The seizures had probably
exacerbated
the brain injury in an already fragile infant and contributed to his
condition.
Evidence on behalf of
the defendant
[65] Sister
Dilla is a registered nurse and has been employed at the hospital
since 2012. She testified that she managed the
labour and birth and
completed the MCR and made certain corrections thereto. An auxiliary
nurse made a single time entry.
[66]
She first assessed the plaintiff at about 09h20, when she did a
vaginal examination and monitored the foetal heart rate by
CTG. The
foetal heartrate remained in the normal range between 110 – 160
beats per minute. The labour had progress well,
no foetal distress
was present, there was no resuscitation required after birth, and the
child was generally well.
[67] In
regard to the initiation of breastfeeding, she testified that she had
put the child on the mother’s breast and
he immediately started
to suck her fist. The mother also tried to make him breastfeed when
she was busy suturing her. Feeding was
discussed and initiated
successfully, with the plaintiff reporting no problems.
[68] She
disputed the plaintiff’s assertions that she only assessed her
once on the day of the birth; that the child
did not cry upon birth
(stating that in the absence of crying she would have cut the cord
and called for help to resuscitate the
baby); and that the child did
not suck from the breast, stating that the child showed intention by
sucking his fist while she was
drying and weighing him.
[69] During
cross-examination Sister Dilla testified that the maternity ward
averages five births per day.
[70] She
received general training on the guidelines for maternity care during
her diploma studies, specialist training on
CTG during her advanced
midwife course (March 2016, which was after the birth of the child),
but no training on the neurology of
neonates.
[71] She
had no independent recollection of the birth, and was wholly
dependant on the MCR in reconstructing it. She described
the birth as
just a normal birth “like thousands of others”.
[72]  She
confirmed that proper recordkeeping assists others to ascertain the
condition of the unit (mother and child)
during birth; identifies
assessments which were not done; CTG interpretation and result should
be recorded to provide lost tracking;
and that all tracings should be
retained and stored. She also conceded that monitoring of the foetal
condition during birth identifies
and avoids foetal distress.
[73] She
said that the hospital did not have CTG paper on the day. She
therefore assessed the foetal condition and heartrate
on the screen
of the CTG machine, supplemented by abdominal palpatation to
determine contractions. She used fetoscope auscultation
to supplement
CTG assessments.
[74] She,
however, later on stated that she used the fetoscope during the first
assessment and then continued with CTG assessment.
She claimed CTG
assessments were used from 09h20 for 30 minutes at a time. She forgot
to note the CTG assessment or record the
findings, but recorded the
heartbeat in her partograph.
[75] She
said that foetal distress is associated with decelerations not
continuing after contraction or either bradycardia
or tachycardia.
Short-term foetal heartrate variability and late decelerations are
indicative of a good foetal condition. When
she was asked whether a
healthy foetus also shows decelerations with contractions, she
responded that “it can if there is
contractions”.
[76] Mr
Wessels put to her that she has a limited understanding of what the
CTG shows, even after her training on CTG. According
to doctor Koll
the interpretation of a CTG is difficult and requires training. By
the time she claimed to have used the CTG, she
had not yet received
the training. Dr Koll testified that without paper one cannot assess
the relationship between the contractions
and the foetal heartbeat.
[77] During
cross-examination Sr Dilla was also confronted with the
ex post
facto
amendments to the original records. She maintained that she
completed the records on the day of the birth.
[78]  She
testified that the entry “urine NAD” was noted when she
assessed the patient. However, it was clear
from the record that this
was written in afterwards. She also said that certain new entries
were not made by her when it is clear
from the record that the
handwriting was similar and probably hers.
[79]
She was also unable to explain another entry namely, “Sister
Tswago receiving the neonate” and the discrepancy
with the
original document.
[80] When
it was put to her that alterations were made by her to validate the
contents and contemporaneous nature of the records,
she responded
that she had no access to the record after discharge and there should
only be one record for each birth.
[81]
She was also confronted with various errors and mistakes in the
record, inter alia:
(a)
the
time and date which were not entered in the correct blocks.
Commencement of labour pains was initially recorded as 14h00, but

eventually amended to 16h00, being the correct time of onset of
severe labour pains;
(b)
recording
the contractions as being moderate, but plotting the same as weak on
the partogram. She admitted the plotting was delayed
by other work
and waiting for the doctor to complete his examination of the
plaintiff;
(c)
the
plaintiff did not have mild contractions at 10h20 and the
contractions were plotted continuously when the birth book was
returned
to her from the doctor. She denied continues plotting of the
strong contractions plotted at 11h20;
(d)
the
foetal condition was not recorded at 10h20 as observations were done
hourly and not half hourly in terms of the protocol;
(e)
the
recorded foetal heartrates at 11h20 (140 and 134 bpm) constituted a
foetal heartrate deceleration after a contraction;
(f)
the
“summary of labour” entry on full dilatation was only
recorded approximately 30 minutes after the delivery and care
of the
plaintiff and the child and scratched over when she re-calculated the
duration of the birth;
(g)
she
initially gave evidence that the time of onset of labour was obtained
from the plaintiff after birth, then, that this time was
obtained at
09h20 but recorded after birth, and finally that the time was changed
after she again asked the plaintiff regarding
her commencement of
labour pains;
(h)
changes
in the time of birth from 12h30 to 12h20 was attributed to a mistake
or misprint occurring after calculating the duration
of birth until
full dilatation. She denied that the entry of bearing down at 12h25
fits better with full dilatation at 12h20 then
12h30;
(i)
she
admitted that the records were not recorded contemporaneously, but
after she cared for the mother and child and resulted in
inaccurate
times being noted;
(j)
discrepancy
on the time of rupture of the membranes, namely 12h50 as opposed to
12h20 in the partogram, resulted from her attending
to and confusing
patients and findings and relying on her memory exclusively;
(k)
she
did not listen to the foetal heartrate after every second contraction
during the second stage of labour, but conducted continuously
CTG;
(l)
generally
and on the day she did not apply dedicated Apgar scoring, but instead
made a general assessment while handling the child
and recorded same
after the assessment of the neonate and summary of labour forms;
(m) the “First Examination
of the Neonate” form was completed after admission of the
mother and child to the post-natal
ward and after attending to other
births and routine issues in respect of the child.  She relied
on her memory and confused
the gender of the child as this was not
recorded contemporaneously;
(n)
she
could not explain the meaning of tests to be conducted to determine
moro-reflex or muscle tone, referring thereto as features
of the
skin. She was also unable to distinguish hypotonic from hypertonic,
also referring thereto as features of the skin; and
(o)
the
entry relating to Sr Tshwago at 12h15 confirms that the latter had
examined the child.
[82]
Although she disputed that the child was cup fed, she
eventually stated that she had seen the child being breastfed.
She
also said that she had remained with the neonate and the plaintiff
for up to 40 minutes after birth.
[83] Doctor
Koll is a practicing gynaecologist and obstetrician. He testified
that despite the late antenatal presentation,
foetal wellbeing could
be determined through assessment of the height of fundus, foetal
heart assessment, observing the maternal
wellbeing and the standard
observations conducted during antenatal visits. The birth
anthropometrical measurements indicated no
evidence of prematurity or
post-dated birth and gestational age is not a factor in this case.
[84] He
said that it is very difficult to estimate the onset of active labour
and there is no significance in the time of onset
of the
contractions. The most important time to assess foetal heartrate it
is before and after a contraction to exclude a very
late
deceleration. Hospital staff are trained to assess and identify
decelerations.
[85] He
conceded that the foetal heartrate was not monitored half hourly and
that this constitute substandard care. A CTG machine
measures
beat-to-beat foetal heartrate and the numbers on the LED screen would
change constantly. After CTG interpretation the
findings should be
written down to provide for lost CTG tracings. The CTG has four
critical findings, but requires paper to be
running to determine
those. He said that Sr Dilla was apparently using the machine more as
a labour saving device.
[86] For
practical purposes foetal heartrate is all that is available to
determine foetal wellbeing. If a foetus becomes hypoxic,
the
receptors in the cardiovascular system respond by slowing the
heartrate to reduce oxygen usage. Decelerations, which start
and end
with contractions on its own, has no clinical significance. Late
decelerations start after the apex of the contraction
and recovers
after the recovery of the contraction, and are suggestive of hypoxia.
Variable decelerations are more difficult to
interpret and tend to
drop sharper and recover quicker.
[87] He
said that variable decelerations are divided into typical and
atypical decelerations, with atypical variable decelerations
having a
shoulder on either side, maintaining variability through the
deceleration (the beat-to-beat variability continues through
the
deceleration) and typically last longer than a minute. In the absence
of shouldering or it lasting longer than a minute, there
is a loss of
variability through the deceleration, which is referred to as a
typical variable deceleration.
[88] Reduction
in foetal heartrate recorded on the partogram at 11h20 (140 beats per
minute/134 beats per minute) is variability.
Deceleration has a
reduction of more than 50 beats per minute or produce a change in
baseline of more than 6 to 15 beats per minute.
More severe
reductions exceed 25 beats per minute, which is considered excessive.
The patterns of variability and decelerations
are completely
different.
[89] There
is no practical way of recording the foetal heartrate during the
second stage of the active phase of labour as the
midwife attending
to the birth, is gloved and sterile. The midwife, however, listens to
the foetal heartrate with her hand held
Doppler on mother’s
abdomen, but only with some difficulty.
[90] Recordings
of foetal heartrate are only done subsequently in the summary of
labour and identified through the presence
of foetal distress. He
said that he has never seen a recorded foetal heartrate during this
phase of labour being made on a partogram.
[91] Assessment
of cervical dilatation is subjective and dependent upon the
impression of the assessor. The strength of contractions
is measured
in conjunction with the progress of labour. If the labour is not
progressing then powers (the strength of uterine contractions),
the
passenger (the foetus), the presenting part (the part of the baby
that leads the way through the birth canal), and the progress
of
labour, have to be assessed. If the labour is progressing at an
acceptable rate, then the strength of the contractions are
irrelevant, being deemed adequate and the progress of labour
acceptable.
[92]
Although he chose not to comment on the accuracy of the MCR, stating
that a forensic expert would be required, he ventured
that labour
progressed well to normal vaginal delivery of “a live male
infant, the weight and the Apgars are recorded”.
Foetal
distress is very unlikely, as the foetal heartrate recordings
remained normal. His opinion and report were based on contemporaneous

records that he was applied with; as he saw them and he had no bases
to dispute or confirm those records.
[93] When
hypoxia occurs in the latter part of labour, it does not simply come
and go. During early labour it is theoretically
possible that the
baby suffers a hypoxic episode and recovers. Later in labour hypoxia
is a progressive condition, with contractions
increasing in strength
and severity. The baby is under stress of the contractions for
longer, while the head is descending, making
the last part of the
labour by far the most dangerous.
[94]
If the baby has a hypoxic episode in the latter part of labour, the
hypoxia progressively increases and is at its worst at
the time that
the baby is born, with the resultant and expected signs of hypoxia in
the baby. A hypoxic baby is expected to be
flat or atonic, lack
reflexes and will have a low heartbeat with a blue coloration.
[95] During
cross-examination, he testified that he has not delivered a baby for
more than 2 years and last worked in public
healthcare approximately
20 years ago. The institution where he works pre-dominantly does CTG
assessments and auscultation is hardly
ever conducted.
[96] He
said that he did not assess or consider placental insufficiency at
all and growth restriction played no role in this
case. Chronic
centile insufficiency probably caused no growth restriction. Any
increase in HIV related hypoxia could make the foetus
more prone to
hypoxia during the labour process. The exact pathway in respect of
cerebral palsy and HIV has not been determined,
but it is believed to
be an inflammatory process causing a placental problem with
oxygenation and hypoxia in a baby. This would
have been determinable
through foetal heartrate assessment during birth.
[97] If
the foetus suffered a hypoxic period, the hypoxia would have
progressively increased with contractions, building up
towards the
end of the birth and would probably have resulted in a decelerating
heartrate showing that the foetus is in distress.
The hypoxia would
increase and worsen as the birth progresses and would be identifiable
through foetal heartrate abnormalities.
[98] The
National Guidelines for Maternity care (the guidelines) find
application and sets a basic minimum protocol. All clinical
events
during the labour and birth need to be recorded fully and properly.
In terms of the guidelines, foetal condition should
be assessed half
hourly, before and immediately after contractions in the active phase
of labour to assess deceleration or foetal
distress. It is not
sufficient only to listen after a contraction, as the onset of the
contraction would remain unknown. Assessment
of the baseline
heartrate only is of very little of assistance.
[99] The
danger of a hypoxic ischaemic injury lies primarily in late
decelerations and not necessarily in the presence of tachycardia
or
bradycardia. A foetus with a normal heartrate between 110 and 160
beats per minutes can be in severe distress. A heartrate should
be
seen in context and not only as an isolated number.
[100] Tying
up foetal heartrate with contractions requires palpatating the
abdomen from commencement to end and recording the
foetal heartrate
in accordance with the contraction. The heartrate should be recorded
before and after the contraction and any
delay in recovering should
be determined.
[101]  He
could not confirm whether the foetal heartrate was determined before
and after a contraction in this case. When
he conducted his pre-trial
meeting with Dr Chimusoro, he accepted that the foetal heartrate was
monitored by way of auscultation
and had no information of foetal
heartrate assessment by means of CTG.
[102]
He testified that a CTG running with paper will show:
a)
variability,
which changes from beat to beat. Reduced variability can be
associated with problems on its own and if persisting,
it must be
acted upon due to possible pre-maturity, sleep, drugging or distress;
b)
baseline,
which should range between 110 and 160 bpm, with readings below 100
and above 180 being abnormal, and readings between
100/110 and
160/180 being non-reassuring;
c)
decelerations;
and
d)
acceleration,
which is a reassuring feature.
[103] He
said that hypoxic events do not necessarily confirm the presence of a
brain injury. This results from the protective
mechanisms available
to the foetus. Brain injury only occurs once the protective measures
are no longer effective.
[104] The
acute profound type of injury usually occurs right at the end of the
hypoxic event, and can present either as a single
acute profound
event or as a result of partial prolonged hypoxia, resulting in a
mixed pattern. The partial prolonged insult can
cause an acute
profound injury.
[105]  He
furthermore testified that on CTG, the foetal heartrate is shown in
relation to contractions and in the absence
of paper only certain
features can be determined, like a sudden or acute bradycardia. The
interpretation of CTG can be particularly
complex and lead to
significant disagreements. For a nurse to determine abnormality in a
CTG, she would require training in reading
of the CTG.
[106] Assessment
on the CTG without paper will only yield the same results as what is
seen in hand held Doppler, being the
heartrate at a specific point in
time. This can only be tied up to the contraction through palpatation
with the hand to determine
the relationship with the contraction,
although certain CTG’s also has a display indicating the
pressure in the uterus, which
can be tied up to the heartrate.
[107] The
CTG has to run long enough to provide an overall picture of the
foetal heartrate in order to determine whether the
contraction and
heartrate do not correlate. But, such assessment can only be properly
conducted through a CTG machine with paper,
to confirm foetal
distress.
[108] He
said that if the court accepts that the injury occurred intrapartum
and the baby was deemed to be hypoxic at birth,
he would accept the
probability that foetal distress occurred intrapartum. However, he
does not see the condition of the baby upon
birth to be hypoxic. If
the court accepts that there was hypoxia during the labour,
culminated in a hypoxic baby being born, then
the MCR cannot be
correct.
[109] Professor
Rothberg has worked in neonatology from 1980 until 1996, and in
health policy development until 2005, whereafter
he became the Head
of the Wits School of Therapeutic Sciences. In formulating his
opinion, he had considered the original and amended
records and was
of the view that the amendments to the record made no difference to
his opinion.
[110] He
testified that it was significant that most of the plaintiff’s
labour occurred before hospital admission, when
monitoring was not
possible and the injury occurred as early as 17 hours before
delivery. Referring to the literature entitled
“
A review of
the conundrum of mild hypoxic ischemic encephalopathy”
, he
said that the child initially had hypoxic ischaemic encephalopathy
Stage 1, and he therefore disagrees with Professor Davis
that this
literature does not find application. The child’s
encephalopathy progressed to moderate on the third day, (stage
2). He
said the features of mild encephalopathy might be difficult for a
non-specialist to detect. Such a child may be hyper-alert
and not
lethargic, but may present with other problems, such as feeding
problems. The literature was written to assist with diagnoses
and
treatment of hypoxic ischemic encephalopathy in the first 6 hours of
life and to initiate cooling.
[111] Neurological
examination is subjective in nature and abnormality may be subtle and
difficult to discern. The timing of
the insult affects not only the
clinical presentation, but also the progression of the
encephalopathy. In the early hours after
a significant hypoxic
ischaemic event, the majority of new-borns do not demonstrate clear
signs of moderate or severe brain compromise.
Yet, these
abnormalities may develop in the ensuing hours to days. The time of
the insult affects the clinical presentation as
well as progression
of neonatal encephalopathy.
[112] Although
the timing of the insult is predominantly perinatal, it is not always
clearly identified and could encompass
antenatal as well as acute on
chronic compound insults. Infants who had a severe antenatal event
may recover by the time of birth
at which time the stage of
encephalopathy is perceived as mild in infants. In contrast, an
infant with a more acute insult can
have only mild abnormalities on
neurological examination in the first 6 hours of age, which can then
evolve to moderate or severe
abnormalities after the first day of
life. An insult can occur many hours before birth and can also have
different manifestations
both in and ex utero.
[113]  He
also referred to the following passages in: “
Volpe’s
Neurology of the new born”
“In the clinical setting available methods are not ideal for
the timing and duration of hypoxic ischaemic insults…
The
large majority of insults occur in the late intrauterine intrapartum
period.”
Intrapartum asphyxia and cerebral palsy - is there a link?
“There is a group of termed infants that is triaged initially
to the regular nursery without any markers of stress; these
infants
develop a syndrome of neonatal and encephalopathy with seizures in
the first 12 to 24 hours, exhibited systemic organ dysfunction,
and
have acute neuroimaging changes in the distribution that are
consistent with chronic intermittent interruption of placental
blood
flow. It is the author’s experience that this subset of infants
accounts for approximately 50% of the cases of neonatal
and
encephalopathy; this is consistent with observations that were made
by other investigators.”
[114]  Professor
Rothberg referred to the subacute intrapartum hypoxic ischaemic brain
injury referred to in the literature
and had reference to the
essentials for such injury, which include a cord PH higher than 7,
with no delivery room resuscitation
and normal Apgar scores and
presenting with encephalopathy and renal dysfunction.
[115]  He
then explained that while cord PH was not present in this case, he
postulated that one of the reasons was that
they could not test for
it in hospital. He believed that they did not feel it was indicated.
[116]  He
then said that the majority of these requirements are fulfilled in
this case and said that “it was postulated
that these infants
suffer a cerebral insult before labour and have a sufficient recovery
to exhibit an uncomplicated labour and
then develop a postnatal
encephalopathy”.
[117]
In his opinion, the child suffered an intrapartum hypoxic ischemic
event during the early intrapartum period and might have
recovered.
In this regard he referred to an article entitled: “
The
Bermuda Triangle of neonatal neurology, cerebral palsy, neonatal
encephalolpathy and intrapartum asphyxia”
and quoted the
following excerpt;
“Some children with neonatal encephalopathy will have
intrapartum asphyxia. Some children with neonatal encephalopathy and

no intrapartum asphyxia will develop later CP.”
He
concluded that in this case insult occurred early intrapartum.
[118] With
reference to an article entitled “
Education and debate: a
template for defining a causal relation between acute intrapartum
events and cerebral palsy: International
consensus statement”
,
and in particular the following postulations:
“Sentinel hypoxic event: an intrapartum or intrapartum
hypoxic event can be silent. It is only when it is apparent
or
detectable that it helps define the probable timing of the event and
the determination of whether its sequelae might have been

preventable.”
He stated that there is evidence that this happened in the present
case.
[119]  And
regarding literature entitled: “
Timing of injury in the
fetus and neonate”
, he referred to the following excerpt;
“The clinical patterns…are highly supportive of the
compelling experimental evidence that injury to the brain is not
a
single ‘event’ occurring at or just after the insult, but
rather that hypoxia-ischaemia precipitates a biochemical
cascade of
events and changes in cerebral blood flow and activity, which lead to
cell death well after the initial insult (during
recovery from the
insult) … even following relatively severe insults cerebral
oxidative metabolism as measured by magnetic
resonance spectroscopy
can pass or even fully recover in the so-called ‘latent’
phase lasting, approximately 6-9 hours
before the onset of secondary
deceleration, which is marked by cell swelling, overt large
stereotypic seizure… and eventual
accumulation of
exitotoxins.”
[120] He
explained that the excitotoxins will leak out due to damage to the
cells, resulting in brain seizures due to energy
failure in the cell,
which is unable to retain integrity, resulting in cell death. The
injury might not only involve the area where
insult occurred, but may
extend beyond with the energy failure starting at the most damaged
parts of the brain and then spreading
outwards.
[121] And
referring to the article: “
Neonatal Encephalopathy and
neurological outcome, 2nd Edition (Report of the American Colleague
of Obstetricians and Gynaecologist
(ACOG)
Task Force on
Neonatal Encephalopathy”
, he referred to the following
excerpt:
“A category II foetal heartrate pattern lasting 60 minutes or
more that was identified on initial presentation with persistently

minimal presentation or absent variability and lacking acceleration
even in the absence of decelerations, is suggestive of a previously

compromised injured foetus.”
[122]  Professor
Rothberg consequently criticised Dr Chimusoro’s statement that
a child with previous hypoxic ischaemia
insult would always present
with abnormal heartrate patterns. He said that multiple children with
previous events will present
with no foetal heartrate abnormalities.
The earlier during labour the insult occurred, the more variable the
presentation of neonatal
encephalopathy.
[123] On
a question by the court as to whether his opinion that the injury
most probably occurred during the unmonitored portion
of labour is
predicated on the assumption that the MCR correctly reflect what
occurred during delivery, Prof Rothberg confirmed
that that was
indeed the case.
[124] He
said that a maximum of a third of the labour occurred while being
monitored in hospital with the balance of the labour
occurring prior
to admission. A hypoxic event could not have occurred in the late
intrauterine period without an indication of
neonatal encephalopathy.
In his opinion, recovery or adaptation may result in no signs of
foetal distress during active labour,
normal Apgar scores at one and
five minutes, no requirement for resuscitation and a normal
examination in the early post-natal
period, as was the case here.
[125] And
he gave the following explanation of the mechanism of reperfusion
injury:
a)
after
the hypoxic ischaemic injury, and when the flow is restored, the
foetus may not show signs of insult (the latent phase);
b)
during
the latent period improvements can occur to such an extent that there
would be no detection of foetal distress (this is consistent
with
Volpe and other authors);
c)
the
latent phase can last up to 15 hours and is followed by a secondary
energy failure resulting in cell death; and
d)
the
reperfusion of oxygen results in the exit of neurotransmitters which
can result in seizures, cell death and brain swelling;
and
e)
subsequent
progressive signs of encephalopathy result from the underlying
reperfusion injury and the later chemical inflammatory
and metrical
abrasions, which cause possible long-term damage.
[126] In
his opinion, the abovementioned process occurred during the largely
unmonitored hours of the birth, resulting in poor
postnatal sucking,
possible lethargy, eventual swelling, seizures and return of the
child to hospital due to manifestations of
the secondary energy
failure. Around 50% of seizures would occur in the secondary energy
failure stage during the release of electro-transmitters,
associated
with brain swelling.
[127] In
his view it is likely that the neonate was experiencing partial
prolonged ischaemia previously, which now demonstrated
through the
signs of the reperfusion injury i.e. seizures relating to hypoxic
ischaemic encephalopathy. The initial damage occurred,
followed by a
recovery period, followed by a secondary energy failure, followed by
the signs of damaged areas as recovery progresses.
[128]
According to him it must be assumed that the staff must
discharge the plaintiff and the baby based on an apparent normal

labour and delivery, the discussion of feeding options and successful
initiation of breastfeeding.
[129] He
accepted that the MCR reflect neonate was born without the need for
resuscitation and was assessed as normal. He defended
the evidence of
Sr Dilla, stating that she was under the impression that the child
showed the intention to breastfeed, but that
the plaintiff’s
HIV prevented enforced breastfeeding.
[130]
He said that if there was no significant resuscitation of the child
and the significant late intrapartum event occurred, it
would be
highly unlikely that the neonate would be born without respiratory
impairment or would have reacted to physical tactile
stimulation.
[131] In
his view ,Sr Dilla differentiated and knew the difference between a
flat or healthy baby, and her impression was that
the baby was well
enough to be put on the mother’s chest. Placing the child on
the mother’s chest imply that the child
is healthy.
[132]  And
in respect of the joint minute with Prof Davis he stated that:
a)
Sr
Dilla’s evidence of retaining the child on CTG would have
enabled her to listen to the beep sound associated with foetal

heartrate and identify severe foetal heartrate adjustments;
b)
he
disagreed with the statement that the injury could have been
predicted and prevented if the labour were correctly monitored and

managed;
c)
according to him the Apgar
scores had probably not been falsely elevated;
d)
he remained of the opinion
that the child presented with mild encephalopathy at birth. He
disagrees with Prof Davis that the injury
occurred during hospital
admission, stating that the timing of the hypoxic and ischaemic event
could not be timed exactly, and
could have occurred the unmonitored
phase;
e)
he criticised Prof Davis
for diagnosing intrapartum hypoxia and ischaemia, stating that the
features referred to by Prof Davis are
largely absent; and
f)
commenting on the
statement of Prof Davis that 91% of injuries may be predictable and
preventable, he opined that same only applies
to patients who are
been observed during the complete labour.
[133]  He
said that a child with encephalopathy is simply suffering from
symphatic nervous system stimulation, which might
present hyper alert
and only eventually present with respiratory problems, later
presenting in feeding problems and being jittery.
These features
might be difficult for a nurse to detect.
[134]
He agreed with Prof Andronikou and Dr Pearce that the injury
occurred over hours, but maintained that those many hours
likely
occurred during the unmonitored phase of labour.
Submissions on behalf
of the plaintiff
[135]
Mr Wessels submitted that the plaintiff’s case was
strengthened by her evidence in respect of the lack of
monitoring
during birth; the dismal failure of the staff to adhere to applicable
protocols; the absence of evidence to suggest
that she or the foetus
reached the hospital in a comprised condition; or that the foetus was
already suffering from foetal distress
before or upon arrival at the
hospital; and her uncontroverted evidence in respect of neonatal
feeding and sucking difficulties.
And, furthermore, the fact that the
child had seizures, at least from the early morning hours of the 10
th
(2 days after birth) and hypoglycaemia.
[136]
The reassuring foetal condition upon admission leaves the probable
conclusion that the foetus was uninjured on admission,
but went into
distress after admission due to the staff’s failure to monitor
the foetus, which resulted in brain damage of
the mixed type and
encephalopathy.
[137]
He submitted that the court should draw an inference of causal
negligence in the absence of an explanation from the
defendant to
negate the inference.
[138]
The version advanced by the defendant on the aetiology, onset and
process of the hypoxic ischaemic brain injury is premised
solely on
the assumption that the MCR are correct and that the staff acted in
accordance with all protocols. Because of the MCR
entries, the
defendant advanced a defence that the injury could have occurred
during the unmonitored part of the labour.
[139]
He furthermore submitted the factual evidence of the plaintiff is
probable and credible, while the evidence of Sr Dilla
is
reconstructed, the product of guesswork, clearly aimed at exonerating
herself and thus not trustworthy. In addition, the records
are not
nearly contemporaneous, reconstructed, incorrect, contradictory,
inadequate, inaccurate and contain fabricated amendments.The
version
of the plaintiff should accordingly be preferred above the contents
of the MCR and the evidence of Sr Dilla.
[140]
He argued that all other reasonable causes of brain injury have been
excluded. Maternal HIV was not further assessed,
nor was the CD4
count, or the viral load ever recorded or further examined. There is
no evidence of maternal infection or infective
brain injury, and
according to the experts there was no reason to believe that the
pregnancy did not develop normally or that the
foetus was in a
compromised condition upon admission.
[141]
Prof Andronikou gave evidence that the injury occurred over “many
hours”; and an extensive portion and important
parts of the
brain are involved, inclusive of the peri-rolandic area which
contains the motor cortex and sensory cortex (which
allows a child to
function) being severely damaged or destructed. The internal
capsules, which controls movement and the deep nuclei
involvement in
the thalamus is also severely affected and a large portion of the
brain, which includes the peri-sylvian, posterior
watershed and the
occipital areas are damaged.
[142]
The expert evidence showed that there should have been proper
monitoring of the foetus. However, there was no proper
monitoring of
the foetus to detect foetal distress.
[143]
There was probable foetal distress more particularly having
regard to the mechanism of damage described by Prof Davis
and Dr
Chimusoro being that perfusion of oxygenated blood was progressively
impeded as contractions increased towards the end of
labour; (Dr Koll
agreed)
[144]
Proper monitoring would have detected foetal distress and had such
distress been detected and acted upon, as it should
have been, the
outcome would have probably been different for the foetus in that a
healthy neonate was likely to be born.
Submissions on behalf
of the defendant
[145]
Ms Goedhart submitted that it is undisputed that the plaintiff
laboured for approximately 17 hours outside of the hospital
and that
only approximately 4 hours of her labour was supervised.
[146]
The experts agreed that the damage to the baby occurred in the period
of 36 – 38 weeks’ gestation. Given
that no foetal
distress was noted during the plaintiff’s labour, and given
that the plaintiff does not dispute the admission
recordals at 09h20
and 09h30, the greater likelihood is that the injury to the baby
occurred before the plaintiff’s arrival
at the hospital, and
that the baby was in the latent recovery stage during the observed
part of the labour.
[147]
The recordings on the record are all within the normal range and are
not in the least indicative of foetal distress.
None of them come
close to the lowest parameter (110 bmp) or the highest parameter (160
bpm). In addition, the Apgar scores of
9 at one minute and 10 at 5
minutes, are reflective of a normal crying baby.
[148]
The only possible sign of a neonatal encephalopathy was the
difficulty to breastfeed, which it is acknowledged most
new mothers
struggle to do. This would amount to a subtle sign of neonatal
encephalopathy, which was only so identified on a retrospective

reconstruction of the events.
[149]
She argued that the evidence does not support an HIE just before
delivery or in the time where the plaintiff was under
the care of the
defendant’s personnel. A baby who suffered an HIE at that late
stage would not present with good Apgar scores,
especially one who
allegedly did not cry for either 30 minutes or one hour. A neonate
who did not cry at birth and who did not
receive resuscitation is
unlikely to have survived, given the level of fall-out reported.
[150]
The seizures on day two are indicative of a reperfusion injury, where
the main injury occurred at a time distal to the
birth, and where the
signs of neonatal encephalopathy, if any, at birth were subtle.
[151]
She submitted that the experts agreed that the ACOG criteria for an
intrapartum injury have not been met, in that an
Apgar score of 5 or
less must be present, there was no umbilical gas showing academia,
there was no neonatal imaging available
to confirm, nor was there
multi-organ system failure, as only one organ, that is neurological
dysfunction, was present.
[152]
She argued that there was no evidence that foetal distress was
present. It has not been demonstrated to have been present,
nor that
it was discernible. Nor has it been demonstrated that the hospital
staff ought to have, or even could have, expedited
delivery to avoid
the injury. The plaintiff has not proven an absence of monitoring.
[153]
That half hourly monitoring instead of hourly monitoring on the part
of the hospital staff would have identified foetal
distress, of which
there is no evidence, is complete speculation. Inferences can only be
drawn from established facts. Instead,
the plaintiff relies on a
reconstruction of events and a reverse-engineering to make out a case
for negligence.
[154]
The Apgar scores were evidently contemporaneously recorded, because
the plaintiff left the clinic with the Road to Health
Chart (RTHC)
that mirrors what was in the MCR, and could not have been fabricated
after the fact.
[155]
The plaintiff could not only speculate as to when there may have been
an indication of foetal distress. Whilst Sr Dilla’s
credibility
may be questioned in relation to her subsequent insertions, there was
no discernible motive for Sr Dilla to have fabricated
the records
from after 09h20 until the birth of the Lingomso, including the Apgar
scores. There are a number of cross-references
across the records
(observations, Partogram and nursing notes) relating to the
plaintiff’s labour which are consistent. It
would have required
a lot of foresight to fabricate all of the entries from 09h20
onwards. She argued that such a level of fabrication
is improbable.
It is equally improbable that Sr Dilla would have simply vaccinated
an infant who, on the plaintiff’s version,
must have been
manifestly ill at the time of discharge.
[156]
She submitted that speculation as to when the insult may have
occurred, also means that it becomes speculative as to
whether any
intervention may have changed the outcome.
[157]
She accordingly submitted that the plaintiff has failed to discharge
the onus upon her of proving causative negligence
on the part of the
defendant’s personnel.
[158]
Regarding the allegation that the defendant’s
personnel failed to monitor and treat the plaintiff
from 07h30 until
13h00, save for vaginal examination at 10h00 in consequence of which
the child suffered foetal distress, Ms. Goedhart
submitted that the
case presented at trial is different to what has been pleaded
initially by the plaintiff and in a statement
to attorneys on 23
January 2018.
[159] Plaintiff’s
claim of not having been assessed, save for the assessment at 10h00,
is not born out by the record.
Not only is it uncontested that
the plaintiff was assessed by Sr Dila at 09h20 and Dr.
Ntshokota at 09h30, but the plaintiff
also accepts that at those
times, there was nothing detectably wrong with the foetus.  The
case presented at trial is different
to what had been pleaded
initially by the plaintiff and in her statement, in the original
particulars of claim, in her reports
to the expert and in the
application for condonation..
[160] The
absence of monitoring, which is denied, does not cause foetal
distress as alleged by the plaintiff.  Monitoring
can only serve
to detect foetal distress which is detectable (and it is not always)
and may, if detected, alert the medical personnel
to a suspicion of
foetal distress.  The question is then whether, if it were
detectable and confirmed, whether at that point
in time, there is
anything that could be done to avoid the cerebral palsy.
[161] Regarding
the contention that the defendant’s personal failed to
determine foetal distress, failed to apply intrauterine
resuscitation
measures and failed to immediately deliver the child promptly upon
determining foetal distress, Ms. Goedhardt argued
that there is no
evidence of foetal distress on the record, nor has any been elicited
in evidence. Since there is no factual evidence
of foetal distress,
intrauterine resuscitation was not warranted.
[162] And
regarding the contention that the defendant’s personnel failed
to provide any or adequate treatment of the
plaintiff or her foetus
so as to prevent the development of foetal distress or hypoxic
ischemic encephalopathy or meconium aspiration
syndrome or superadded
hypoglycaemia, Ms. Goedhardt argued that the only evidence that the
baby suffered HIE is on the MRI, performed
on 25 May 2018 when he was
two years and three months old, which is evidence of HIE, partial or
prolonged and acute profound pattern
injury.  There was no
evidence of discernable foetal distress, there was no evidence of
meconium aspiration syndrome and the
superadded hypoglycaemia evident
on the MRI is not causative of HIE in and of itself, but superadded.
[163]
Regarding the assertion that the defendant’s personnel failed
to monitor and manage the plaintiff’s labour
and the condition
of her unborn baby during labour as required by the maternity care
guidelines, Ms. Goedhardt argued that Sr Dilla
was challenged
repeatedly under cross-examination with regard to the use of the
CTG.  She was not undermined in this regard
and was consistent
in her evidence that she had used the CTG.
[164]
Her evidence in this regard is supported by the fact that at
12h20 and 11h20 she recorded two readings of the foetal
heartrate.
This is explained by the fact that, at the time she wrote her notes,
the reading on the CTG had changed.
[165] Regarding
the allegation that the defendant’s personnel failed to
appreciate that the plaintiff’s baby was
born with hypoxic
ischaemic encephalopathy, she argued that the assertion by the
plaintiff regarding the presence of encephalopathy
at birth is based
on her evidence that the baby did not cry or suck at birth.
However, there is evidence on the MCR and the
RTHC that the baby was
sucking.
[166]
Under cross-examination, the plaintiff twice testified that the baby
was breastfed while she was in hospital.
The plaintiff’s
experts conceded that a first time mother might have difficulty in
establishing breastfeeding at the outset.
The inability to suck
would not in and of itself have been a self-evident sign of
encephalopathy to the nursing personnel, particularly
under
circumstances where the plaintiff was not a high-risk patient. The
labour progressed normally and the Apgar scores were normal.
[167]
She argued that while there is evidence on the MRI that the baby
suffered super-added hypoglycaemia, the plaintiff’s
own experts
attribute that to the baby’s poor sucking and that this was as
a consequence of the alleged encephalopathy at
birth.  Professor
Davis, in cross-examination, conceded that mild encephalopathy can be
missed in the early stages after birth
and that this would be more
prevalent in a rural hospital where the care of the baby falls to
nursing personnel.
[168]
Regarding the assertion that defendant’s personnel failed
properly to assess the plaintiff’s baby immediately
after birth
and to diagnose the baby as suffering from HIE, she argued that it
was established that the only evidence that may
have presented itself
to the defendant’s personnel was the poor sucking, which could
also be attributable to the plaintiff
being unable to breastfeed as a
first time mother.
[169]
The plaintiff’s evidence regarding when the baby started crying
was inconsistent.  In court she said it was
30 minutes. She
advised Dr. Kara that it was 30 minutes.  She advised Dr.
Chimusoro and Prof Davis that it was after an hour.
This
evidence would mean that the baby was born flat.  In such an
event, Sr Dilla would not have recorded Apgar scores of
9 and 10.
The baby would also not have been admitted to the post-natal ward,
but rather to the neonatal ward.  Such
a baby would also not
have been vaccinated on 9 February 2016.
[170]
Regarding the allegation that the defendant’s personnel
failed to introduce measures, treat and manage the encephalopathy

after birth to prevent further brain injury, she argued that there
was no obvious encephalopathy present when the baby was born,
given
the Apgar’s of 9/10 and 10/10.  Fitting only occurred
after discharge.  All Saints Hospital is a district
hospital and
does not have the capabilities to perform head cooling treatment.
[171]
And regarding the allegations that the defendant’s personnel
failed to retain the baby in hospital to undergo
treatment for the
encephalopathy, she argued that no encephalopathy was noted at birth
or at discharge.  The plaintiff testified
that she breastfed the
baby at hospital, which is why no warning signs were raised about the
premature discharge.  The only
record of poor sucking and
lethargy in the new-born baby is by the plaintiff herself.  Her
evidence in this regard is inconsistent
and has varied between the
different experts she had seen.
[172]
Ms Goedhart also argued that the evidence of Sr Dilla is to be
preferred to that of the plaintiff.  She criticised
the
plaintiff as an inconsistent witness and in this regard pointed to
discrepancies which in her submission related to: whether
she took
her anti-retroviral treatments; the time of the onset of her labour;
whether she was attended to in the labour; by whom
she was seen; the
times when she was assessed and the number she was assessed; the
condition of the baby at birth and when the
baby first cried; the
issue of whether the baby could suck or not and whether she breastfed
or sip fed the child in hospital; and
when the baby suffered
seizures, the number of seizures and the management of the seizures.
.
[173]
She submitted that despite her evidence regarding the seizures, the
plaintiff nonetheless failed to return to the clinic
for check-ups.
The RTHC has entries which do not pertain to the child and begs into
question veracity of those entries.
The plaintiff was
discharged with the RTHC. Sr Dilla confirmed that she wrote into the
RTHC the Apgar scores and she administered
the vaccinations.
[174]
The RTHC also reflects exclusive breastfeeding on discharge and mix
feeding (breast and cup).  It has also been
demonstrated that
both plaintiff and her attorney of record deposed to a false
affidavit in order to obtain condonation.
This included making
reference to an incorrect hospital.
[175]
Consequently the plaintiff has been demonstrated to be mendacious in
her affidavit to obtain condonation and inconsistent
about facts
falling peculiarly within her knowledge, and which she would have
been expected to be consistent about.
[176]
Under the circumstances where both the plaintiff and Sr Dilla had
demonstrated to be untruthful, the objective
recordals of the MCR of
the time of the birth must be carry greater weight, bearing in mind
that, at that time, neither party had
contemplated any claim.
[177]
The plaintiff’s claim is based on speculation that in three
hours and fifty minutes that the plaintiff was in
labour at the ASH
and prior to the baby’s delivery, something went wrong and was
missed.  Sr Dilla’s evidence
on the other hand is that the
labour was indeed monitored, albeit hourly, that during the time the
FRH was monitored and recorded
six times, all of which fell within
normal parameters, that the baby was assessed and found to be well at
birth.
[178]
While the guidelines require a hand held Doppler for every thirty
minutes, a CTG machine was used and it did not reflect
any abnormal
FHR.  Dr Ntshokota had confirmed that the hospital did have a
CTG machine at the time, and the nursing staff
used them.  He
also explained what the procedure was for managing the child that
needed resuscitation and confirmed that he
was not called in this
instance to resuscitate a minor child.  The subsequently
inserted entries are all irrelevant to the
issue as to whether there
had been an omission to note foetal distress at the time.
[179]
She that if the two conflicting versions are considered in the
light of the guidelines for resolving conflicting factual
versions as
set out in
Stellenbosch Farmer’s Winery Group Ltd and Others
vs Matel and Others
2003 (1) SA 1
SCA, the version of Sr Dilla is
more probable.
[180]
She accordingly submitted that the plaintiff has also failed
to establish that the negligence of the defendant’s
personnel,
if any, caused the child’s injury
Discussion
[181]
The test for negligence is whether a reasonable person in the
position of the defendant would foresee the reasonable
possibility of
his or her conduct injuring the person of another or his or her
property and causing him or her patrimonial loss;
would take
reasonable steps to guard against such occurrence; and that the
defendant has failed to take such steps. (
Kruger v Coetzee
1966(2)
SA 428 (A) at 430E-F)
[182]
Thus the plaintiff is required to prove, on a balance of
probabilities, that the defendant’s employees failed to
exercise
reasonable skill and care, in other words, that their
conduct fell below the standard of a reasonably competent
practitioner in
their field and that the aforesaid negligence caused
the child’s injury. A medical practitioner is bound to employ
reasonable
skill and care, and is liable for the consequences if he
or she does not. (
Goliath v Members of the Executive Council for
Health, Eastern Cape
2015 (2) SA 97
(SCA))
[183] The
plaintiff is not required to prove that the inference she contends
for is the only reasonable inference. It is sufficient
for her to
convince the court that the inference advanced “is the most
readily apparent and acceptable inference from a number
of possible
inferences”. (
Goliath
(supra), at para. 19)
[184]
The court should select a conclusion that it deems to be the more
natural appraisable conclusion from amongst several conceivable
ones,
even though that conclusion may not be the only reasonable one. The
inferences drawn from the facts must be based on proved
facts and not
matters of speculation. (
AA Onderlinge Assuransie Beperk v De Beer
1982 (2) SA 603
(A))
[185]
This process is achieved on qualitative assessment of truth and
inherent probabilities of evidence of witnesses and on ascertainment

of which of the two versions is more probable. The court’s
estimate of the credibility of the witnesses is inextricably linked

to the consideration of probabilities, and the court is required to
consider these factors simultaneously.
[186]
Where a plaintiff is not in a position to produce evidence on a
particular aspect, less evidence will suffice to establish
a prima
facie case where the matter is peculiarly within the knowledge of the
defendant. In such a situation there is an evidentiary
burden upon
the defendant to show what steps were taken to comply with the
standards required.
[187]  The
factual disputes arising from the irreconcilable versions proffered
by the plaintiff and Sr Dilla, respectively,
must be resolved on the
basis of the following principles enunciated by the Supreme Court of
Appeal in
Stellenbosch Farmers Winery Group Ltd v Martell Et Cie
2003 (1) SA 11
(SCA), at 14I-15D:
“To come to a conclusion on the disputed issues a court must
make findings on (a) the credibility of the various factual

witnesses; (b) their reliability; and (c) the probabilities. As to
(a), the court’s findings on the credibility of a particular

witness will depend on its impression about the veracity of the
witness. That in turn will depend on a variety of subsidiary factors,

not necessarily in order of importance, such as (i) the witness’
candour and demeanour in the witness-box, (ii) his bias,
latent and
blatant, (iii) internal contradictions in his evidence, (iv) external
contradictions with what was pleaded or put on
his behalf, or with
established fact or with his own extracurial statements or actions,
(v) the probability or improbability of
particular aspects of his
version, (vi) the calibre and cogency of his performance compared to
that of other witnesses testifying
about the same incident or event.
As to (b), a witness’ reliability will depend, apart from the
factors mentioned under (a)(ii),(iv)
and (v) above, on (i) the
opportunities he had to experience or observe the event in question
and (ii) the quality, integrity and
independence of his recall
thereof. As to (c), this necessitates analysis and evaluation of the
probability or improbability of
each party’s version on each of
the disputed issues. In the light of its assessment of (a), (b) and
(c) the court will then,
as a final step, determine whether the party
burdened with the onus of proof has succeeded in discharging it. The
hard case, which
will doubtless be the rare one, occurs when a
court’s credibility findings compel it in one direction and its
evaluation
of the general probabilities in another. The more
convincing the former, the less convincing will be the latter. But
when all factors
are equipoised probabilities prevail.”
[188]
It is common cause that Sr Dilla had tampered with the MCR entries
after copies thereof were provided to the plaintiff’s

attorneys, including the
ex post facto
completion of the
partogram. When she cross-examined the plaintiff, Ms Goedhart put to
her that Sr Dilla admitted to having made
the changes, but asserted
that she was merely inserting what she had done contemporaneously.
[189]
However, when Sr Dilla testified, she simply denied having made
the changes. She was obviously lying and made a very
poor impression
on the court. The question then is whether those changes to the MCR
are indeed immaterial and inconsequential,
as Ms Goedhart has
submitted.
[190] Ms
Goedhart has sought to explain her submission by arguing that Sr
Dilla’s dishonesty must be understood in the
context of her
realising that she has committed a criminal offence and fearing
prosecution. She argued that the untampered portions
of the record
nevertheless corroborates Sr Dilla’s testimony and it should
therefore be preferred to that of the plaintiff,
for the reasons that
I have mentioned earlier.
[191] I
do not agree with this submission. Sr Dilla’s dishonest,
ex
post facto
tampering with the records is only part of the
problem. During cross-examination by Mr Wessels, it became apparent
that she did
not take the completion of the records seriously, nor
did she fully understand the import of what she was doing.
[192]  She
clearly had no understanding of how to measure and note Apgar scores,
to my mind, has lied about having used
a CTG, purported to assess
aspects of the child’s condition that she clearly had no clue
what they mean, and appeared to
have confused the child with another
baby.
[193] She
had known that she must record her findings and had appreciated the
importance thereof. Yet, she did not record that
she was using a CTG
without paper. All the experts were under the impression that she was
auscultating and the plaintiff had also
asserted that she had been
auscultating.
[194]  She
also did not record the findings of the CTG nor did she record the
foetal heartrate before and after the contractions,
as she knew she
was supposed to record. She conceded that she had no independent
recollection of the events, yet insisted that
she had used a CTG when
there was no record thereof.
[195]  She
also admitted that the mild contractions were all recorded on the
partogram at the same time. This spans a
period of two hours. Dr
Chimusoro had testified that it was clear that the strong
contractions were all done simultaneously. She
had recorded mild
contractions on the partogram, but wrote in the clinical notes that
they were moderate.
[196] The
heartrates recorded on the partogram differ from those in the
clinical notes. In addition, on the partogram, clinical
features of
the foetus at 10h20 had not been filled in.
[197]
At 20h20 she writes on the partogram “liquor is clear at
20h20”. This could, however, only be established
if the
membranes have ruptured. On the summary of labour, she writes rupture
of the membranes happened at 12h50.
[198] Her
recording of the Apgar scores are also clearly misleading. She
admitted that the Apgars were not taken at one and
five minutes
respectively, as depicted on the record, but that she had made a
general assessment of the child as she handled the
baby in the third
phase. All these entries were written up 30 minutes after birth and
from her memory.
[199] She
clearly does not know how to do Apgar scores, if one has regard to
her evidence as compared to what the modalities
of scoring indicated
on the Apgar score. Her first examination of the neonate is also
problematic. Everything is recorded as normal
even there were male
and female genitalia. She does not know how to test the moro reflex
and muscle tone, but purported to record
findings in respect thereof.
She also admitted that the features of another child may have been
substituted.
[200]
Her recordals regarding feeding are also misleading. She never
saw the child breastfeeding, although that is the impression
that is
created in the records. She also did not have any further contact
with the neonate within an hour after birth and did not
assess
breastfeeding, sucking reflex or blood sugar levels.
[201] Dr
Koll had testified that if there were an intrapartum hypoxic event
(which is common cause) and hypoxic encephalopathy
after birth (which
is also common cause) there must have been foetal distress. He also
described how the hypoxia increases in an
ascending fashion as
contractions increased towards birth. The records are therefore
obviously incorrect.
[202] I
accordingly agree with Mr Wessels’s submission that the
recordings of Sr Dilla after 09h20 are false or unreliable.
[203]
Sections 13
and
17
of the
National Health Act, No. 61 of 2003
,
place a duty on the hospital to keep and maintain medical records. It
is a criminal offence to alter or tamper with medical records.
In
Khoza v MEC for Health and Social Development, Gauteng 2
015 (3) SA
266
in (GJ), at para. 42, it was recognised that medical staff
responsible for maintaining the patient’s medical records have

the most to gain by ensuring the safekeeping as the records “as
they are surest way of demonstrating that they had monitored
and
carried out proper procedures. The same staff members also have the
most to gain by the disappearance of the contents of the
patient’s
file if they failed to carry out their duties”.
[204]
Mr Wessel correctly submitted that it was common cause that the staff
did not monitor the labour as required in terms
of the Maternity Care
Guidelines (the guidelines). The plaintiff testified that the
foetus’s heartrate was only tested by
Sr Dilla at approximately
09h20, and by the doctor afterwards. There was therefore, on her
version, non-compliance with the guidelines.
[205]
Furthermore, the records as they stand, also indicate that
there was non-compliance with the guidelines, in that the
foetal
heartrate was supposed to be checked every half an hour in the active
phase, but it was only done every hour. The instruction
in the
guidelines state that monitoring must be done before and after a
contraction to detect deceleration. On the defendant’s
own
version that did not happen.
[206]
I am accordingly satisfied that the evidence has clearly
established negligence on the part of the defendant’s
staff.
[207] Insofar
as causality is concerned, Mr Wessels urged me to assess it by taking
into account; the common cause aspects;
what factual version should
be accepted in this instance; whether the plaintiff’s version
is correct or that of Sr Dilla;
the nature and probable mechanism of
the damage and; the features exhibited by the baby after birth.
[208]
The criterion for determining factual causation, namely the
well-known “but-for test” was formulated as follows

by Corbett CJ in
International Shipping Co (Pty) Ltd v
Bentley
1990(1) SA 680 (A)
([1989]
ZASCA 138) at 700E – H.
“
What it essentially lays
down is the enquiry — in the case of an omission — as to
whether, but for the defendant's wrongful
and negligent failure to
take reasonable steps, the plaintiff's loss would not have ensued. In
this regard this court has said
on more than one occasion that the
application of the 'but-for test'  is not based on mathematics,
pure science or philosophy.
It is a matter of common sense, based on
the practical way in which the minds of ordinary people work, against
the background of
everyday-life experiences. In applying this
common-sense, practical test, a plaintiff therefore has to establish
that it is more
likely than not that, but for the defendant's
wrongful and negligent conduct, his or her harm would not have
ensued.  The
plaintiff is not required to establish this causal
link with certainty.”
[209] Thus
a plaintiff is not required to establish a causal link with
certainty, but only that the wrongful conduct was probably
a cause of
the loss. This calls for sensible retrospective analysis of what
would have probably occurred, based upon the evidence
and what can be
expected to occur in the ordinary course of human affairs, rather
than an exercise in metaphysics. The correct
approach is not to
search for scientific certainty, but to assess where the balance of
probabilities lie on a conspectus of all
the evidence adduced in the
case (
Minister of Safety and Security v Van Duivenboden
2002
(6) SA 341
SCA at 25);
Minister of Finance and others v Gore N.O.
2007 (1) SA 111
(SCA); (
Michael and another v Linksfield Park
Clinic (Pty) Ltd and another
2001 (3) SA 1188
(SCA), at 1201).
[210]  In
Lee v Minister for Correctional Services
2013 (2) SA 144
(CC),
it was held that:
“
In the case of an
omission, the but-for test requires that a hypothetical positive act
be inserted in the particular set of facts,
the so-called mental
removal of the defendant’s omission. This means that reasonable
conduct of the defendant would be inserted
into the set of facts.
However, as will be shown in detail later, the rule regarding the
application of the test in positive acts
and omission cases is not
inflexible. There are cases in which a strict application of the rule
would result in injustice, hence
a requirement of flexibility.”
[211] And
in
Mashongwa v Praza
2016 (3) SA 523
(CC), the Constitutional
Court cautioned that:
“
Lee never sought to
replace pre-existing approach to factual causation. It adopted an
approach to causation premised on a flexibility
that has always been
recognised by the traditional approach. It is particularly where the
harm  that has ensued is closely
connected to an omission of a
defendant that carries the duty to prevent the harm. Regard been had
to all the facts, the question
is whether the harm would nevertheless
have ensued, even if the omission had not occurred. However, where
the traditional but-for
test is adequate to establish a causal link
it may not be necessary, as in the present case, to resort to the Lee
test.”
[212]  In
Oppeldt v Department of Health
2016 (1) SA 325
CC, at paras.
34 to 50, the Constitutional Court held that the but-for test
requires flexibility and a common sense approach when
the issue of
causation has to be decided on the ground of an alleged negligent
omission, as opposed to a negligent commission,
and explained that:
“
While it may be more
difficult to prove a causal link in the context of a negligent
omission then of a commission, Lee explains
that the but-for test is
not always the be all and end all of the causation enquiry when
dealing with negligent omission. The starting
point, in terms of the
but-for test, is to introduce into the facts a hypothetical
non-negligent conduct of the defendant and then
ask the question
whether the harm would have nonetheless ensued. If, but for the
negligent omission, the harm would not have ensued,
the requisite
causal link would have been established. The rule is not inflexible.
Alternately, it is a matter of common sense
whether the facts
establish a sufficiently close link between the harm and the
reasonable omission.”
[213]
To my mind it is significant that the plaintiff and the foetus
appeared to have been in good health prior to labour,
with no
indication of damage or vulnerability before the commencement of
labour. The plaintiff started to feel labour pains by
approximately
16h00 on 8 February 2016. Labour did not commence at that time, but
probably sometime later, as according to Dr Koll
it is difficult to
establish when labour commences.
[214] The
plaintiff was examined in hospital at 09h20 by Sr Dilla, who found
her to be in good clinical condition, with foetal
movements felt and
the foetus being in a reassuring condition. The doctor who examined
the plaintiff and foetus 10 minutes later,
also found the same. The
child was born at 13h50.
[215] The
child had encephalopathy of at least Grade 1, which was classified as
Grade 2 after developing seizures. He suffered
a hypoxic ischaemic
injury of the partial prolonged type, combined with acute profound
injury features compatible with hypoglycaemia.
The injury would have
occurred over many hours and was extensive, in that large portions of
the brain of the child had been damaged,
especially in relation to
those areas governing motor ability.
[216] The
Apgar scores of 9/10 and 10/10 were not done in the standard way, but
it was a general impression noted by Sr Dilla
after handling the
baby. The child had cerebral palsy and the records had been tampered
with years after the event in some important
respects.
[217]
If Sr Dilla’s recordings were to be accepted, there is no
indication of any abnormality during labour or until
discharge the
following day. One would thus have expected a normal child. Yet, it
is common cause that the child suffered serious
and extensive brain
injury. Her version does therefore simply not accord with the
undisputed expert testimony.
[218] Ms
Goedhart’s submission that the unaltered portions of the MCR
corroborate Sr Dilla’s testimony, can only
be upheld if the
integrity of those entries are unassailable. As I have explained
above, this is clearly not the case.
[219] As
I have said earlier, my impression was that Sr Dilla was a dishonest
and unreliable witness who had knowingly tampered
with official
hospital records and had lied about it. Her recordings simply does
not accord with the preponderance of the expert
testimony, which
concluded that there was something seriously wrong with the neonate.
I am therefore of the view that no
reliance can be placed on her
testimony and recordals on the MCR.
[220]
According to the plaintiff, the baby did not cry after birth and when
brought to her, could not feed from the breast
and had to be fed with
a cup. The implication of not crying after birth is that there was
respiratory distress and depleted responses
to stimulation. This
version accords with the expert evidence, as well as with the
probable outcome that would be expected with
the birth of an hypoxic
neonate with encephalopathic  reaction after birth.
[221] Ms
Goedhart has urged me to exclude only those entries which had been
compromised by the
ex post facto
changes, and to accept those
entries which, according to her, were clearly made contemporaneously
and in respect of which there
is no evidence to suggest that they are
unreliable. In this regard she referred me to
AM obo KM v MEC for
Health, Eastern Cape
(699/17)
[2018] ZASCA 141
(1 October 2018),
where the Supreme Court of Appeal found that the correct approach is
to accept the undisputed parts of the record
and to exclude the
disputed parts. The court in that matter any event found that the
alteration of the records was a neutral factor.
[222] The
situation here is of course entirely different. The defendant’s
experts, in particular Prof Rothberg, has constructed
a defence based
on the assumption that the records are correct. Prof Rothberg has
obstinately refused to contemplate the possibility
that Sr Dilla, who
has been shown to be an unreliable and dishonest witness, has also
lied about crucial entries, for instance
the manner in which the
Apgar scores were taken and whether she had used a CTG.
[223] As
I have mentioned earlier, when she was cross-examined by Mr Wessels,
it was clear that she had based her scoring on
general observations
of the child’s appearance and made the entries half an hour
later. She was also unable to explain why
she did not record that she
had used a CTG when she was, by her own admission, aware of the
importance of keeping accurate records.
More concerning was the fact
that she was quite prepared to make entries regarding aspects of the
child’s condition when
she clearly lacked proper understanding
of what they mean and how to test for them. These entries were also
simply incompatible
with the condition of a baby that had by all
accounts suffered severe brain damage.
[224]
While Prof Rothberg has persisted with his speculative
hypothesis that the child had suffered the insult before the

plaintiff was admitted to hospital, had sufficiently recovered to
present with reassuring heartrate upon admission, and only after

birth presented with features of HIE, Dr Koll conceded that if the
plaintiff’s version is accepted, and the court accepts
that the
injury occurred intrapartum, then foetal distress would most probably
have incurred intrapartum,
[225] Mr
Wessels has launched a sustained and comprehensive assault on Prof
Rothberg’s testimony. He submitted that on
the probabilities
and logic, the testimonies of the plaintiff’s experts must be
accepted and that of Prof Rothberg rejected
as being illogical, bias
and speculative. In order to put his criticisms of Prof Rothberg’s
testimony into proper perspective,
it is perhaps necessary to explain
the legal principles relating to assessment of expert testimony. They
are as follows:
(a)
an
expert’s opinion represents his or her view based on facts
which are either common cause or established. The opinion can

accordingly only be accorded weight if the facts upon which that
opinion is based are found to exist. (
Coopers
(S.A.) (Pty) Ltd v Deutsche Schädlingbekämpfung MBH
1976
(3) SA 352
(A);
(b)
although
experts are, by virtue of their specialized knowledge and skill,
better qualified than the presiding judge to draw inferences,
the
probative value of an expert’s testimony must be considered in
the same manner as that of any other witness. The court
is
accordingly not bound by an expert’s opinion;
(c)
an
experts’ testimony can only be of value to the court if he or
she is found to be neutral and impartial;
(d)
an
expert must not advocate his or her client’s case or
selectively examine only the evidence that support his or her
client’s
case and ignore other relevant evidence.
(
PriceWaterhouseCoopers
Inc v National Potato Co-op Ltd
[2015]
2 All SA 403
(SCA), at paragraphs 98-99); and
(e)
an
expert’s bald statement of his or her opinion is of no
assistance to the court unless it is uncontroverted. The expert
must
accordingly fully disclose the premise on which his or her reasoning
is based and the process of the reasoning which led to
the
conclusion.
[226] Does
Prof Rothberg’s testimony pass muster when assessed in the
light of the abovementioned principles? I think
not. While I think
that Mr Wessels’s depiction of Professor Rothberg as a “hired
gun” who tried to advocate his
client’s case at all costs
is a trifle harsh, I do agree with his submission that the former’s
testimony contravened
the principles applicable to expert witnesses
in various respects.
[227] Prof
Davis testified that the process of multiple partial prolonged
hypoxic ischaemic episodes resulted in a cumulative
mixed acute
profound and partial prolonged injury, that the partial prolonged
insults would have manifested through changes in
foetal heartrate and
a foetal condition and that appropriate intervention could have been
instituted successfully.
[228] Dr
Kara confirmed that there is little to support an antenatal insult,
the undoubted encephalopathy and particularly
seizures in the first
36 hours of life is likely the result of brain injury during birth,
as supported by the MIR and the type
of cerebral palsy suffered by
the child.
[229]
Dr Koll conceded that foetal distress probably occurred during
the late intrapartum period, resulting in hypoxia and
ischaemia and
associated hypoxic ischaemic encephalopathy.
[230] Dr
Chimusoro testified that perfusion of oxygenated blood was
progressively impeded as contractions increased towards
the end of
labour, a hypoxic event prior to admission would probably have
presented through foetal heartrate abnormalities upon
admission and
hypoxic event with recovery without any intrauterine resuscitation
was  highly unlikely obstetrically.
[231] Only
Prof Rothberg has proffered a different opinion. Mr Wessels submitted
that he is a neonatologist who stopped clinical
practice in 1994,
which is 27 years ago and since then appeared to have been involved
in academic pursuits and training of therapists.
It is common cause
that obstetrics is not within his field of expertise and he conceded
that the possibility of prolonged foetal
distress prior to admission,
with subsequent recovery, needs further comment by the obstetrician.
I agree with this submission.
[232]
It appears that Prof Rothberg has constructed a defence that the
damage occurred after commencement of labour until admission
in
hospital. This falls squarely in the field of obstetricians, of which
he acknowledged not to be an expert. He accordingly had
no basis to
dispute the evidence of Dr Chimusoro, who stated that if the foetus
were suffering from hypoxia it would not have recovered
without of
the mother being resuscitated.
[233] Prof
Rothberg also disputed Dr Chimusoro’s evidence that according
to the principles stated in ACOG, if a patient
would present with a
category 1 foetal heartrate pattern (the normal heartrate) that
convert to a category 3, it is suggestive
of an hypoxic ischaemic
event. It is axiomatic that the heartrate obviously would have had to
change to have the outcome that what
was seen in the child. This
supports Dr Chimusoro when he said that on probabilities the child’s
damage was done after admission
to hospital, because the foetus had a
normal heartrate on admission.
[234]
Mr Wessels has correctly argued that Prof Rothberg conceded that he
had no facts to support his opinion, but relied on literature
which
stated that it can happen that you can have hypoxic damage before
labour that can recover significantly to exhibit an uncomplicated

labour. The articles which he referred to, are mainly irrelevant and
others do not support his opinion. His opinion was that the
damage
occurred after labour commenced. Mr Wessels submitted that the
features exhibited by the control group of children mentioned
in the
article are not the same as the child in this case and the article is
thus not supportive of Prof Rothberg’s theory.
Notwithstanding
extensive research by him he could not find any support in the
literature otherwise he would surely have submitted
it.
[235]
Prof Rothberg’s reasoning was to my mind strained and
illogical in certain respects. He said that he does not
know what the
cause for the hypoxic event was. He conceded that if the baby is not
born approximately 40 minutes after acute profound
damage sets in,
the baby is usually dead. On that basis the baby should on logical
reasoning have been dead by the time the plaintiff
was admitted to
the hospital. His opinion, however, is that the damage to the brain
and heart, for unexplained reasons, stops before
admission to the
hospital. The foetus then must have recovered sufficiently to be in a
reassuring condition on admission. However,
it is common cause that
the baby did not recover and has suffered extensive damage according
to Prof. Andronikou.
[236]
I am consequently of the view that Prof Rothberg’s
hypothesis was speculative and without any factual basis.
[237] The
plaintiff testified that she was only examined once by the nurse and
once by the doctor each time with a fetuscope.
She was not examined
again thereafter until birth. There was then a period of
approximately three and a half hours of unmonitored
labour during
which time the stress on the baby increased with the increasing
strength of contractions and the risk of hypoxia
increasing up to
birth. In my view it is more probable that the damage occurred in the
time. The expert testimony has confirmed
that the damage could have
been prevented if there was proper monitoring, which would have
detected an abnormal heartrate during
the buffer stage before damage
is done to the brain. This would have allowed an intervention by way
of maternal resuscitation and
caesarean section before the damage
occurred. The damage is therefore closely connected to the failure to
monitor as required by
the guidelines.
[238] I
am accordingly of the view that the reassuring condition of the
foetus upon admission, compels the conclusion that
the foetus went
into distress thereafter and the hospital staff’s negligent
failure to monitor the foetus resulted in it
suffering brain damage
of the mixed type and encephalopathy.
Order
[239]
In the result the following order issues:
1.
The
defendant is helped liable for the plaintiff’s agreed or proven
damages arising from the cerebral palsy suffered by the
minor child,
Lingomso.
2.
The
determination of the quantification of the plaintiff’s claim is
postponed sine die.
3.
The
defendant shall pay the plaintiff’s costs relating to the
merits, together with all preserved costs, such costs must be
paid on
the party and party scale, and shall include:
(a)
the costs of the
preparation of the expert reports and qualifying fees, if any, of the
following expert witnesses:
(i)
Prof Andronikou –
Radiologist;
(ii)
Prof Davis –
Neonatologist;
(iii)
Dr Kara –
Paediatrician
(iv)
Dr Pearce –
Paediatric neurologist; and
(v)
Dr Chimusoro –
Obstetrician and Gynacologist.
(b)
Costs of two counsel.
4.
The defendant shall pay
interest on the aforesaid costs at the current prescribed legal rate
of interest, calculated from 30 days
of
allocatur
or agreement, to date of payment thereof.
_________________________
J.E. SMITH
JUDGE OF THE HIGH COURT
Appearing
on behalf of the Plaintiff:

Adv. Wessels SC with Mr Uys
Instructed
by:

NONXUBA INC.
Plaintiff’s Attorneys
345 Rivonia Boulevard
Ground Floor, Block B 2
Edenburg, Rivonia
2191
JOHANNESBURG
REF. NO: ZMMN/FM/MAT725
Service Address:
14 Stewart Drive
Berea
East London
Appearing
on behalf of the Defendant:
Adv. Goedhart SC with Ms Cassim
Instructed
by:

ZILWA ATTORNEYS
Defendant’s Attorneys
100 High Street
P O Box 2141
GRAHAMSTOWN 6140
Our ref.: AF Basson/lab/M434