PG on behalf of TG v The MEC for Health, Gauteng Province (2014/6003) [2021] ZAGPJHC 351 (19 March 2021)

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[2021] ZAGPJHC 351
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PG on behalf of TG v The MEC for Health, Gauteng Province (2014/6003) [2021] ZAGPJHC 351 (19 March 2021)

REPUBLIC
OF SOUTH AFRICA
IN
THE HIGH COURT OF SOUTH AFRICA
GAUTENG
LOCAL DIVISION, JOHANNESBURG
CASE
NO: 2014/6003
REPORTABLE:
YES
OF
INTEREST TO OTHER JUDGES: YES
REVISED.
NO
DATE:
19 March 2021
In
the matter between:
PG
obo
TG
Plaintiff
and
THE
MEC FOR HEALTH, GAUTENG PROVINCE
Defendant
JUDGMENT
Weiner
J
Introduction
[1]
Claims
for medical negligence against the state rose to a staggering R104.5
billion in 2019, as patients seek redress for harm allegedly
wrought
by SA’s overstretched public health system.
[1]
This case is another which comes before this court on the basis of
the defendant’s alleged medical negligence.
[2]
The plaintiff, as the mother and natural
guardian of her minor child (TG) who was born on 22 November
2004 at the Mofolo Clinic
(the Clinic) sought, in such capacity, to
claim, against the defendant, damages suffered as a result of the
alleged negligence
of the medical and/or nursing staff (the
defendant’s employees) during the plaintiff’s labour and
delivery of TG at
the Clinic. This resulted in TG suffering an
hypoxic ischemic injury (HIE) resulting in neonatal
encephalopathy
(NE)
and cerebral palsy (CP).
[3]
The specific acts of negligence alleged are
that the defendant’s employees:
(a)
failed to properly, sufficiently or
adequately assess the plaintiff’s stage of labour after her
admission to the Clinic;
(b)
failed to monitor the progress of the
plaintiff’s labour and the foetal well-being with sufficient
regularity during the plaintiff’s
labour;
(c)
failed to detect that the foetus was in
foetal distress during the plaintiff’s labour after admission
to the Clinic;
(d)
failed to timeously take appropriate and
effective action to prevent further distress in the foetus or prevent
the foetus from suffering
any harm;
(e)
intervened inappropriately and dangerously
when they realised that TG was in distress by applying fundal
pressure to deliver the
baby.
[4]
It is claimed that TG’s condition is
due to the negligent omissions and actions of the defendant’s
employees in circumstances
in which such conditions were preventable.
[5]
The defendant defended the claim by denying
that any of its employees acted negligently, or that TG sustained an
injury while the
plaintiff was in labour and/or when he was
delivered.
[6]
In
addition, the defendant pleaded that, even if negligence was proved,
there was no causal connection between the negligence alleged
and the
CP suffered by TG. The defendant submitted that the plaintiff was
required to show that the CP was a product of an intrapartum
insult
caused by and/or connected to such negligence.
[2]
The
lack of medical records
[7]
At the trial, the defendant’s counsel
submitted that the plaintiff could not prove her case as the
Maternity
Case record, including that of the antenatal period and intrapartum
period, and the neonatal records, were missing and/or
lost. These
were accordingly not made available by the defendant
.
No further explanation was proffered by the defendant in this regard.
In the defendant’s argument, the submission was made
that as
there were no maternal records, the plaintiff could not show that the
treatment she received was substandard and that it
caused the injury
to TG. This somewhat cynical attitude has been displayed by MECs in
various cases in this, and other divisions,
of our courts.
[8]
In
Khoza
v MEC for Health and Social Development, Gauteng,
[3]
Spilg
J set out possible implications of such missing records:
‘
In
summary, the failure to produce the original medical records which
are under a hospital’s control and where there is no
acceptable
explanation for its disappearance or alleged destruction —
(a)
may result in the inadmissibility of “secondary” evidence
if the interests of justice so dictate, whether
such evidence is of a
witness who claims to have recalled the contents of the lost
document or to have made a note of its
contents on another document;
(b)
cannot of its own be used to support an argument that a plaintiff is
unable to discharge the burden of proof because
no one now knows
whether the original records would exonerate the defendant's staff
from a claim of negligence;
(c)
may result in the application of the doctrine of
res
ipsa loquitur
in an appropriate case;
(d)
may result in an adverse inference being drawn, that the missing
records support the plaintiff's case in matters
where the defendant
produces other contemporaneous documents that have been altered,
contain manufactured data or are otherwise
questionable, irrespective
of whether the evidence of secondary witnesses called in support is
found to be unreliable or untruthful.’
[9]
In
Madida
obo M v MEC for Health for the Province of Kwa-Zulu Natal
,
[4]
Pillay J
discussed this issue as follows:
‘
In
terms of
ss
13
and
3>
17
of
the
National Health
Act 61 of 2003
,
the
defendant’s employees have a statutory duty to preserve and
protect such hospital and medical records. Failure to do so
opens the
defendant’s employees to criminal prosecution
and
liable on conviction to a fine or to imprisonment for a period not
exceeding one year or to both such fine and imprisonment
.
The
Health Professions Council’s Guidelines on the keeping of
patient records dated May 2008 applies to health care practitioners

in both the private and public service. It identifies what
constitutes health records, why documents or materials should be
retained
and what information is compulsory for recording. It
prohibits alteration of records and requires reasons for any
amendments
to be specified on the record. Errors may be corrected but
the date of the change must be entered and the correction signed in
full. The original record must remain intact and fully legible.
Additional entries at a later date must be dated and signed in full.

The guidelines also provide for the retention of health records,
which must be stored in a safe place and if stored electronically

then safeguarded by passwords. In the case of minors,
their
records must be kept until the minor’s twenty-first birthday.
For
mentally incompetent patients the records must be kept for the
duration of the patient’s life. Health records kept in
a
provincial hospital or clinic including the records of minors and
mentally incompetent patients may only be destroyed with the

authority of the Deputy Director General concerned.
I
have detailed the
National
Health Act and
Guidelines
to emphasise their importance and the rationale and seriousness with
which the health professions view the keeping
of patients’
records. So when they are not available when they should be there is
potentially a breach of a rule of law and
codes of good practice.
Non-compliance with statutory requirements and codes of good practice
that impact directly on the health
of members of the public is cause
on its own to refuse the adjournment. To do otherwise would lead to
the mistaken inference that
the court is prepared to condone or
tolerate the illegality. The lack of a bona fide explanation for the
unavailability of the
records fortifies my opinion.’
[10]
These remarks are pertinent in the present
case, where the defendant, despite the absence of such records,
pleaded a bare denial
that its employees were negligent. As stated by
Pillay J in
Madida
—
‘
To
plead “no knowledge” and to put the plaintiff to the
proof of facts that should be easily ascertainable was not a
plea in
good faith. It is hardly the response of a caring health service.
Proof as to whether a medical doctor had attended to
the plaintiff
had to come from the hospital staff on duty at the time and from
their records….’
[5]
[11]
In the
present case, the only records that
were discovered were:
(a)
The birth register which showed:
i.The
name of the plaintiff, date, and time of admission at 07h15 on
22 November 2004.
ii.The
plaintiff tested negative for syphilis, positive for HIV, and she was
not anaemic.
iii.A
male child TG was delivered at 13h00 and both the mother and child
were given a dose of nevirapine to prevent mother to child

transmission of the HIV virus.
iv.Meconium
Stained Liquor was noted when TG was delivered.
v.
Meconium Aspiration.
vi.Apgar
scores of
6/10
at one minute and 8/10 at ten minutes.
vii.TG
had been immunised against polio and given a BCG inoculation at
birth.
(b)
The
Neonatal discharge summary which showed that:
i.
The
Apgar scores were 6/10 at one minute and 8/10 at five minutes.
ii.
Reference
to body proportions/measurements at birth being normal (appropriate)
for the gestation of 38 weeks.
(c)
The Road
to Health record was relied upon as a secondary factual record.
Witnesses
[12]
The following expert witnesses were called
to give evidence in support of the plaintiff’s case:
(a)
Dr K
Frank

Obstetrician Gynaecologist
(b)
Dr George Gericke

Paediatrician and Geneticist
(c)
Professor R.Solomons

Paediatric Neurologist
(d)
Prof J
Smith

Neonatologist/ Paediatrician
(e)
Prof I G
Nolte

Nursing Expert
[13]
A radiologist appointed by the plaintiff,
Dr Ranchod, compiled a radiology report and joint minute together
with the defendant's
radiologist, Dr Weinstein, which was
accepted into evidence without the radiology experts having to give
evidence. It was
accepted that the MRI brain scan dated 30 June 2017
demonstrated features consistent with chronic sequela of a partial
prolonged
HIE.
[14]
The defendant called the following expert
witnesses:
(d)
Professor D Du Plessis

Nursing Expert
(e)
Professor K D Bolton

Paediatrician
(f)
Dr
Koll

Obstetrician Gynaecologist
(g)
Dr V M Mogashoa

Paediatric Neurologist
(h)
Professor A L Christianson
Geneticist
[15]
The plaintiff testified to the facts in the
matter. Sister Elizabeth Nomathansanqa Ndlela (Sister
Ndlela), called by the
defendant, was the midwife who apparently
attended to the plaintiff. She had no independent recollection of the
plaintiff’s
case. Her evidence consisted of a description of
how nurses in her position conduct themselves during a patient’s
labour.
She doubted that the plaintiff’s version of events was
accurate. She however confirmed that the birth register referred to

birth Asphyxia (BA), and Meconium Aspiration Syndrome (MAS) and
Meconium Stained Liquor (MSL) and the Apgar scores as 6/10 after

resuscitation and 8/10 at five minutes. She conceded that it was
possible that the plaintiff and the foetus may not have been
monitored for a period of two hours. This, she stated, could occur if
the nurses were busy with other patients. She could not recall
if
this occurred in plaintiff’s case. She agreed that the fact
that TG’s condition was poor, and they referred him
to the
Chris Hani Baragwanath Hospital (CHBH) meant that his situation was
serious.
[16]
It was submitted by plaintiff’s
counsel that, in the circumstances, the plaintiff was the only
factual witness and that the
Court would have to make a determination
in respect of the veracity or reliability of the evidence of the
plaintiff, in deciding
the merits of the case.
Common
cause or agreed issues
[17]
The plaintiff was a primigravida (giving
birth for the first time) at the time of the birth of TG on 22
November 2004. The plaintiff
was admitted into the labour ward at the
Clinic at approximately 07h15 on that day, her labour having already
started and having
progressed to the active phase of labour (her
cervix had already dilated more than four centimetres).
[18]
The baby was delivered by vaginal birth at
approximately 13h00. It is recorded in the birth register that the
baby suffered from
birth asphyxia as a complication at birth. TG was
born at full term and his anthropometric measurements and weight were
within
the normal range for a term baby according to the Road to
Health Chart and the mode of delivery.
[19]
TG required resuscitation and oxygen at
birth and was transferred to CHBH on the same day after a delay of
approximately three hours.
The reason for the transfer to CHBH was
recorded as low Apgar scores and birth asphyxia. TG was admitted to
the Neonatal Intensive
Care Unit (NICU) immediately on arrival at
CHBH and remained in the NICU for at least three days, whereafter he
remained in hospital
for a further three weeks.
[20]
TG also presented with a subaponeurotic
haemorrhage (bleeding into the skull) at birth, which resolved during
TG’s stay in
CHBH.
[21]
TG presented with feeding difficulties
during his admission in the NICU and further stay in CHBH, in keeping
with the consequences
of birth asphyxia on the neonatal brain, and
consistent with the sequela of NE.
[22]
TG subsequently developed epilepsy, which
is indicative of an encephalopathy. TG now suffers from mixed spastic
CP and microcephaly
with profound intellectual disability, as well as
a mixed picture of asymmetric spastic quadriplegia and dystonia.
[23]
The MRI brain scan dated 30 June 2017
demonstrates features consistent with chronic sequela of a partial
prolonged HIE. There are
no stigmata of intracranial syndromic
disorder and there are no features to suggest complicated
intracranial sepsis (infection).
The implication of this is that the
child does not suffer from a brain injury which was caused by HIV
infection or AIDS, or inflammatory
infections such as meningitis or
syphilis.
[24]
Although the plaintiff was HIV+, TG is not
HIV infected and the plaintiff had been given a single dose of
nevirapine to prevent
mother to child transmission of the HIV virus,
as was the practice at the time. There is sufficient evidence for
timing of the
partial prolonged HIE to the intrapartum period, birth
asphyxia having been recorded in the discharge summary and notes. The
paediatric
neurologists for both parties are in agreement in this
regard.
[25]
There is no recorded evidence for the
presence of the histological markers of Fetal Inflammatory Response
Syndrome (FIRS) i.e. inflammation
of the umbilical cord, acute
chorioamnionitis, or chorionic villi vasculitis – all
indicators of a pathological placental
condition.
[26]
Clinically, no genetic predisposing
familial or antenatal factors could be identified. There are no
obvious congenital genetic/syndromic
causes for TG’s
neurological deficits.
Defendant’s
conduct of the trial
[27]
Despite
these issues being agreed upon as being common cause,
[6]
the defendant, in effect, ‘threw the book’ at the
plaintiff. The defendant sought to introduce a myriad of evidence
and
literature to show the following: that there was insufficient
evidence to time the HIE as being intrapartum; that the fact
that the
plaintiff was HIV positive was the cause of the CP; that there was a
possibility of chorioamnionitis and/or chorionic
villi vasculitis,
Villitis of Unknown Etiology (VUE) and/or various other infections
which may have caused the HIE.
[28]
It
must be noted that none of these issues were raised by the defendant
on the pleadings. Furthermore, the defendant conducted this
trial in
a most unsatisfactory manner, in effect, a ‘trial by ambush’.
The defendant’s counsel sought to introduce
reams of literature
whilst the plaintiff’s witnesses were testifying. This resulted
in the matter having to stand down on
numerous occasions for the
witnesses to familiarise themselves with the literature. In addition,
the cross-examination of the plaintiff’s
witnesses was at times
insulting and aggressive. On several occasions I had to admonish the
defendant’s counsel in this regard.
It is pertinent to refer in
this regard to
S
v Azov
,
[7]
where
the following was stated in regard to the attitude of the counsel in
cross-examination:
‘
I
think it must be made clear to him, and perhaps to others, that
witnesses who come into court, be they police witnesses or any
other
kind of witnesses, are entitled to the ordinary courtesy one extends
to decent people. Witnesses who give evidence are assisting
the court
in arriving at the truth and in carrying out the administration of
justice. No cross-examiner is entitled to insult a
witness or to
treat him in the manner in which these witnesses were treated,
without there being a very good reason for it. Witnesses
must be
treated with courtesy and respect. They are doing a public duty in
coming to court. That must be borne in mind by both
cross-examiners
and by presiding officers. It was clearly the duty of the magistrate
here to protect these witnesses. I do not
wish to be understood to
say that a witness may never be attacked, but before you can attack a
witness you must at least lay a
foundation to the satisfaction of the
presiding officer that you have grounds for attacking the witness.
Otherwise witnesses must
be treated with respect and with the same
courtesy that you would extend to a man in civilised society. One is
not rude to people
when you speak to them during ordinary social
intercourse, so why should it be any different in a court of law?
Here this cross-examiner
really shocked me in regard to the manner in
which he treated these respectable men. He starts off by attacking
them without any
reason. He seems to assume that they are dishonest
people and that he is entitled to attack and insult them….’
[29]
Unfortunately, the defendant’s
counsel was guilty of the same conduct; more particularly when he
attacked some of the plaintiff’s
experts.
Plaintiff’s
evidence
[30]
The plaintiff testified that she was 38
years old and had a Grade 11 level of education. She was 25 years old
when TG was born.
She has two other children aged six years and three
years, who are both healthy and do not suffer from any of the health
and neurological
deficits which TG has.
[31]
The plaintiff first attended at the Clinic
in about February 2004, when it was found that she was pregnant. She
was tested for HIV
and was found to be HIV positive. The nursing
sisters informed her after the examination that the baby was fine.
She attended at
the Clinic regularly for the next few months.
[32]
On 15 November 2004, the plaintiff
experienced some contraction-like pains in her abdomen and went to
the Clinic where she was kept
overnight. The nursing sister examined
her in the morning and thereafter discharged her to go home.
[33]
On 22 November 2004, she returned to the
Clinic after she discovered a mucous and blood discharge on her
panties just before 06h00.
She also started having contractions and
proceeded to the Clinic. She arrived at the Clinic at approximately
07h00. She was attended
to by a nursing sister who checked her
cervical dilatation manually and then advised the other nurses
present that she was about
to give birth. She was then taken into a
labour room just behind the reception area.
[34]
She was told to lie on a bed and a drip was
put into her arm. The nurse left the room at some stage and only
returned to check if
the drip was working properly, but did not
examine the plaintiff. She testified that the nurse did not examine
her again from the
time when the drip was inserted until she gave
birth. The plaintiff was left in the labour room until she started
screaming because
the pains she was experiencing in her abdomen had
become unbearable. During the intervening period, neither she nor the
foetus
were monitored. She is not sure of the time when she started
screaming, but thinks that it was around 12h00.
[35]
Three nurses came into the labour room when
she started screaming and they then started telling her to push,
which she then did.
When she was told to push, one of the nurses
placed her hand on the plaintiff’s abdomen and pressed onto her
abdomen just
below her breast. The nurse continued to press until TG
was delivered.
[36]
The plaintiff estimated that the time from
when she started screaming until the baby was delivered was
approximately 30 minutes.
When the baby was delivered, he did not
cry, and she heard the nurses saying that one of them should go and
fetch the oxygen.
[37]
A while later, the plaintiff got off the
bed and then saw her baby with an oxygen mask on his face. She was
not allowed to touch
or handle him. She noticed that the baby was
still and was not moving, nor was he making any sounds. One of the
nurses told her
that they were being transferred to CHBH. The nurses
did not inform her why they were taking her and the baby to CHBH,
save to
say that the baby did not cry.
[38]
The ambulance arrived some three hours
later at approximately 16h00 and they then drove to CHBH in the
ambulance, accompanied by
a nurse who held the baby in the ambulance.
On arrival, TG was taken away by the nurses who were still
administering oxygen to
the baby.
[39]
The plaintiff was later informed that TG
was in ICU and that she could only see him the next day. The
plaintiff saw TG in the ICU
the next day in an incubator with pipes
inserted into his nostrils and running into machines and into a
bottle. She was informed
that TG had not yet cried and that he was
unable to feed normally, and was therefore being fed by means of the
pipes which she
was seeing. TG was kept in ICU for about a week, and
was then taken to a ward where he was kept for a further two weeks.
[40]
The plaintiff was discharged from CHBH
after two days while TG was in ICU. She visited the baby every day in
the ICU and in the
ward. TG was kept on an oxygen mask while in the
ward. Whilst in the ward, people from the speech therapy department
assisted her
with training on how to feed TG with a feeding bottle as
TG had difficulty sucking.
[41]
A week after TG was discharged from the
hospital, the plaintiff took him to the antenatal clinic. TG attended
there approximately
once a week for one month. At three months of
age, TG was referred to the CP clinic at CHBH where the plaintiff was
informed that
TG suffered from CP.
[42]
TG is now 13 years old and he cannot walk,
talk, or sit up straight without support. At present, he crawls
around on his knees and
cannot do anything for himself, like feeding
or cleaning himself.
[43]
The plaintiff gave evidence that with the
births of her two other children she experienced the same symptoms
before and during labour
as she did with TG. In those cases, however,
she and her babies were monitored and referred to the hospital for
the children to
be delivered in the hospital.
[44]
The plaintiff stated that she clearly
remembered everything about the birth of TG because the treatment
which she received during
his birth was so different to that which
she received with the birth of the other two children, and her recall
was also clear because
of the trauma surrounding his birth.
[45]
In
cross-examination, other than repeating the plaintiff’s version
and then accusing her of being coached, the defendant did
not put a
version or a defence to the plaintiff. The Court commented that
counsel had traversed each and every one of the plaintiff's

statements without putting forward a version. The position regarding
unchallenged evidence was set out in
President
of the Republic of South Africa & others v South African Rugby
Football Union & others
[8]
to
the following effect:
‘
The
institution of cross-examination not only constitutes a right, it
also imposes certain obligations. As a general rule it is
essential,
when it is intended to suggest that a witness is not speaking the
truth on a particular point, to direct the witness’s
attention
to the fact by questions put in cross-examination showing that the
imputation is intended to be made and to afford the
witness an
opportunity, while still in the witness-box, of giving any
explanation open to the witness and of defending his or her

character. If a point in dispute is left unchallenged in
cross-examination, the party calling the witness is entitled to
assume
that the unchallenged witness’s testimony is accepted as
correct.’
Expert
witnesses
Evidence
of Dr Frank – obstetrician and gynaecologist called by the
plaintiff
[46]
Dr Frank had obtained a history of what had
happened during labour and the delivery of the baby from the
plaintiff by way of an
interview conducted on 19 February 2018.
She opined that it could be deduced that the plaintiff was in active
labour when
she arrived at the Clinic at approximately 07h00 on 22
November 2004. She was at least four centimetres dilated on
admission. As
a primigravida, the plaintiff would have dilated at one
centimetre per hour. She should therefore have taken between six to
eight
hours to dilate fully.
[47]
She referred to what was contained in the
birth register. It was noted that there was meconium aspiration,
meaning that TG had aspirated
meconium at some stage during the
delivery. Such aspiration can present as pneumonia-like symptoms. As
a child only starts breathing
after delivery, TG could not have
aspirated the meconium prior to his delivery and must have aspirated
the meconium during or after
delivery when he took his first few
breaths. The maternity register further indicated that Meconium
Stained Liquor was noted when
the child was delivered, indicating
that the child was probably in distress during the labour and/or
delivery period.
[48]
Meconium aspiration is preventable by
either meconium infusion, or the more practical method of suctioning
the meconium out of the
baby’s trachea once the baby is
delivered, thereby preventing the meconium from entering the
respiratory system. In general,
the nursing sisters delivering the
baby would suction the baby immediately on noticing the presence of
meconium at birth.
[49]
TG suffered birth asphyxia, which is a
condition where the baby is depressed, has low Apgar scores; the baby
would be flat, not
crying, have low tone, and be blue instead of
pink, and would need assistance with breathing or resuscitation –
which occurred
in this case with TG.
[50]
There are several causes of birth asphyxia.
In the present case, there is no record or evidence of intrauterine
infection, cord
around the neck, an abnormal presentation or shoulder
dystocia, which are some of the causes. In Dr Frank’s opinion,
the
birth asphyxia could have been caused by the meconium aspiration.
The thick meconium could have occurred because the baby was
compromised
during the course of labour, and it could have occurred
at the time of delivery as well. It would have been possible to
detect
that the baby was being compromised before delivery if correct
monitoring occurred.
[51]
The protocol for the care of a pregnant
woman admitted into the labour ward before giving birth is as
follows:
(a)
Her vital signs i.e. blood pressure, pulse,
urine, and temperature would be recorded every two hours.
(b)
She will have a vaginal examination hourly
from six centimetres dilated.
(c)
The foetal heart rate will be listened to a
half hour before, during, and after contractions.
(d)
When the cervix is fully dilated (ten centimetres), then the
foetal heart rate must be monitored at intervals of five minutes.
[52]
The purpose of this protocol is to detect
any abnormalities in the condition of the mother and the foetus. From
such closer monitoring
the doctor or midwife would get an indication
of the condition of the baby. It will give the practitioner an idea
if the baby is
coping with the labour, or is in distress during the
contractions.
[53]
If the baby is in distress in this period
before its birth and is imminently deliverable, i.e. the mother is
ten centimetres dilated,
then the nurses will encourage her to bear
down or push the baby out. If she is not imminently deliverable, i.e.
she is about seven
centimetres dilated, if the foetal heart rate is
not reassuring, then she must be transferred to a hospital where a
caesarean section
can be performed.
[54]
Foetal monitoring and foetal heart rate
monitoring is critically important as it would indicate the condition
of the baby, and if
not reassuring, would prompt an intervention to
deliver the baby.
[55]
Based on an assumption that the plaintiff
was admitted to the Clinic at approximately 07h00, she would have had
to be examined at
least three more times before she was fully
dilated. The foetus should then have been monitored every 30 minutes,
at least seven
times before 12h00, and at least ten more times in the
period from 12h00 to when TG was delivered at 13h00. That is 17
examinations
in the period from 08h30 to 13h00. If the plaintiff was
allowed to labour by herself for six hours without being attended to,
and
without the foetus being monitored, then her treatment was
substandard.
[56]
Dr Frank did not believe that the use of
fundal pressure was safe. Fundal pressure means that the uppermost
part of the uterus is
being squeezed manually in order to get the
baby out. The use of fundal pressure often resulted in damage to the
mother and child,
such as a ruptured liver, fractured ribs, ruptured
uterus and foetal injuries and conditions, such as the subaponeurotic
haemorrhage,
which TG presented with at birth. Fundal pressure could
cause a cord compression if the cord was in a position where it could
be
pushed against the maternal pelvis. The cord compression could
have caused the birth asphyxia if the foetus was compressed against

the bony pelvis and the cord is trapped between the foetus and the
pelvis. This did not appear to be the situation in the present
case.
[57]
One of the reasons why fundal pressure
would be employed, is if the doctors or midwives were worried about
the well-being of a baby
and could not get the baby out fast enough,
or could not get the mother to a theatre for a caesarean section or
deliver the baby
by vacuum or forceps. In other words, it would be
used if there was an emergency situation.
[58]
In this case, Dr Frank believes that when
the nurses saw the meconium stained liquor, they realised that this
baby was in trouble
and needed a rapid delivery, and that is why
fundal pressure was applied.
[59]
As the injury was a partial prolonged HIE
brain injury, adequate monitoring of the mother and foetus would have
shown that TG was
in distress, was having decelerations or prolonged
bradycardia (low heart rate). If the nurses had been monitoring the
baby appropriately,
they would have picked this up timeously; they
would have been able to arrange to transfer the mother and baby to a
tertiary centre
such as CHBH, where the mother and baby could have
received a better standard of care during the labour and delivery.
[60]
Neither Dr Frank, nor Dr Kohl (the
obstetrician and gynaecologist called by the defendant) dealt with
the effect of the plaintiff’s
HIV status and/or the presence of
infection on TG’s condition in their reports or the joint
minutes. Despite this, the defendant’s
counsel cross-examined
Dr Frank extensively in this regard. Dr Frank noted that the
plaintiff was HIV positive but was only
placed on ARV’s seven
years after the birth of TG, and deduced from this fact that the
mother was healthy, and had a high
CD4 count with a low viral load.
Both mother and child were also given nevirapine during the labour
and after delivery, to prevent
mother to child transmission of the
HIV virus.
[61]
In commenting on the mother’s health
status at the time of the birth of TG, Dr Frank noted that the
mother’s haemoglobin
level was 10.7. She further noted that, in
general, women who are infected with HIV, who are immune compromised
generally have
a haemoglobin lower than 10.7, the deduction from this
being that the plaintiff was not yet immune compromised, although
infected
at the time.
[62]
If one took into consideration the
objective facts recorded, such as the fact that the baby was not
crying at birth, that the baby
required resuscitation and needed
oxygen immediately at birth, that the baby was transferred to CHBH
and was admitted to the NICU
and remained in the hospital for three
weeks, the Apgar scores of 6/10 at one minute, 8/10 at five minutes
and 10/10 at ten minutes
(from the discharge summary), are not
credible.
[63]
Dr Frank believes the Apgar scores may have
been inflated and a baby with birth asphyxia and meconium aspiration
would certainly
not be able to score 10/10 on an Apgar within ten
minutes. Further, that common logic dictates that a healthy baby
would not be
taken to the ICU.
[64]
Under cross-examination, which was in the
main aimed at Dr Frank’s lack of expertise,
the
defendant’s counsel questioned the expertise of Dr Frank by
suggesting that she had ventured an opinion in the area of
HIV in
which she did not have a full qualification. He further accused her
of not having credibility amongst her peers, in that
she had not
published relevant research in peer reviewed journals. Dr Frank
responded that her expertise and training was
in the field of
obstetrics and gynaecology, but that it was necessary for her to have
knowledge of HIV treatment protocols as treating
and delivering HIV
positive women was part of her training and her daily tasks as an
obstetrician and gynaecologist.
[65]
Dr Frank practiced as an obstetrics and
gynaecology specialist in the labour ward at CHBH from 2006 to 2012,
having qualified as
a medical doctor in 1999, and having been an
intern from 2000 to 2006 when she became a specialist. In addition,
she taught obstetric
students at the hospital, performed surgery and
supervised Master’s in Medicine students in their research for
their theses,
and was also an examiner at the University of
KwaZulu-Natal.
[66]
Dr Frank was published in the American
Journal of Obstetrics and Gynaecology, which Mr Pauw himself had
acknowledged as one of the
highest ranking peer review bodies. In
addition, she was published in the South African Journal of
Obstetrics and Gynaecology and
the British and Italian Journals of
Obstetrics and Gynaecology.
[67]
Dr Frank conceded that her knowledge and
experience of CP was limited as it was not her area of
specialisation, but she was also
not totally uninformed as to the
causes of CP or how it related to antenatal and intrapartum causative
factors.
[68]
Counsel for the defendant further suggested
that the finding by Dr Frank that at birth there was thick meconium
present was false
as it is not mentioned in the available records.
Dr Frank replied that the fact that the child suffered meconium
aspiration
at birth, according to the records, indicates that there
was thick meconium. In addition, Dr Frank pointed out that the
child
was diagnosed with respiratory distress syndrome which could
very easily have been caused by Meconium Aspiration Syndrome.
[69]
To the suggestion that the child had
congenital pneumonia at birth, Dr Frank responded that the note
was merely a query and
not a diagnosis of pneumonia. Further, that
the results of tests done on the baby were put into the hospital file
at least three
weeks after the tests were done. If the child had
congenital pneumonia, it would have been investigated and confirmed.
There was
no such note in the file.
[70]
It
was put it to Dr Frank that HIV exposure (i.e. when the mother is HIV
positive while the child is in utero) is associated with
an adverse
outcome or morbidity in new born babies. This he based on a study
done in Botswana (the Botswana study).
[9]
[71]
Dr Frank responded that the sample size in
the study for the article was too small to be of much significance,
and the results were
confounded by a high number of premature births
which were included in the sample cohort, and that prematurity was
found to be
a significant risk factor for CP in Botswana.
[72]
The article, in fact, concluded as follows:
‘
Cerebral
Palsy is an important and common contributor to childhood disability
in low-resource settings. The relative contributions
of major risk
factors for cerebral palsy in Botswana differ significantly from
those described in high resource settings, with
infection, birth
complications and maternal HIV being major contributors. Of note,
these are all potentially preventable risk factors,
suggesting that
interventions in birth practices and neonatal care could make a
significant impact in decreasing rates of cerebral
palsy in Botswana
.
Further studies are necessary to
confirm maternal HIV as a risk factor for cerebral palsy and to
characterize the mechanism by which
HIV increases the risk of
cerebral palsy.
’
[Emphasis added]
[73]
Dr Frank conceded, in regard to fundal
pressure, that the literature was inconclusive in relation to the
possible injury to the
foetus. However, she stated that, in 2004,
fundal pressure was an acceptable practice in hospitals, but not in
clinics.
[74]
Dr
Frank was recalled at a later date and confronted with articles with
which the defendant attempted to show that maternal recall
of labour
and birth was poor.
[10]
Dr Frank commented that the articles merely showed that some
women remember some aspects of birth and labour better than others,

but all women remembered some aspects of the labour better,
especially if it was associated with a traumatic or negative outcome.
[75]
Despite the relentless challenge to her
expertise, Dr Frank’s evidence remained consistent that, based
on the narrative given
by the plaintiff, as well as the information
obtained from the available medical records, the care given to the
plaintiff and the
baby was substandard.
Evidence
of Dr Kohl – obstetrician and gynaecologist called by the
defendant
[76]
Dr Kohl’s initial evidence was that
he was unable to give an opinion due to the lack of obstetric
records. His further comments
were based purely on hypothetical
scenarios put to him by counsel for the defendant.
[77]
Dr Kohl stated that it was highly unlikely
that plaintiff was left unattended for six hours. In addition, he had
no reason to doubt
the Apgar scores, despite the evidence that TG was
asphyxiated at birth and taken to CHBH as he was considered very ill.
He did,
however, made the following concessions:
(a)
That continuous foetal monitoring was
critical to detect foetal distress.
(b)
There should have been foetal monitoring at
least every five minutes in the second stage of labour.
(c)
That even though low Apgar scores were not
conclusive of the poor condition of the baby, they are a strong
indicator and useful
tool to assess the condition of the child at
birth.
(d)
That if the evidence of the plaintiff is
accepted by the Court, the care given to the plaintiff and the foetus
was substandard.
[78]
Dr Kohl furthermore testified that, with
proper monitoring, if there was foetal distress, it could and should
have been detected
at an early stage, and that intervention would
have led to a positive result for the newborn. The process of labour
should be monitored
through any of the known mechanisms of assessment
to monitor foetal heart rate patterns and the increase and decrease
thereof before,
during, and after contractions. He did not dispute
the evidence of Dr Frank that if foetal distress was suspected, plans
could
have been made to transfer the plaintiff to CHBH.
Evidence
of Professor Nolte – nursing specialist called by the plaintiff
[79]
The evidence of Professor Nolte was clear,
that based on the history given by the plaintiff, the nursing sisters
were grossly negligent
in the following respects:
(a)
They did not monitor the plaintiff.
(b)
They did not monitor the foetus and
therefore missed important indicators of foetal distress.
(c)
They did not identify the significant risk
factors in the maternal HIV when the plaintiff was admitted.
(d)
The failed to follow the correct protocols
in delivering the baby by using fundal pressure when it is
specifically prohibited in
the training of nurses and midwives.
(e)
They allowed the plaintiff to give birth
without any medical assistance, when clearly there was a difficulty
in the birth which
necessitated a resort to the dangerous procedure
of fundal pressure.
Evidence
of Professor du Plessis – nursing specialist called by the
defendant
[80]
Professor du Plessis did not dispute the
proper protocol for the management of labour and maternal and foetal
monitoring. She commented
that HIV holds the potential of
opportunistic infection, but could take the matter no further.
Evidence
of Professor Johan Smith and Professor Bolton – paediatric and
neonatal specialists
[81]
Professor Johan Smith, the paediatrics and
neonatology expert called by the plaintiff, is the head of Neonatal
Services at the Tygerberg
Hospital and the head of the neonatal
intensive care unit at the University of Stellenbosch University
Hospital since 1987.
[82]
In the pretrial minute, Professor Smith and
Professor Bolton (called by the defendant) could not find common
ground in relation
to the cause of TG’s CP:
(a)
Professor Smith stated that the Apgar score
of 6/10 at one minute was probably an ‘assisted’ score
after resuscitation.
Professor Bolton disagreed, stating that that
scenario is only one such possibility. It was equally probable to
speculate that
the child’s clinical condition at birth
reflected the presence of severe respiratory distress.
(b)
Professor
Smith opined that moderate and severe encephalopathy is attributable
to asphyxia in 60% of cases, most of which evolve
during labour.
[11]
Professor Bolton partially agreed, but stated that these authors
defined NE as being caused by asphyxia according to blood gas
and CTG
anomalies, which are not available in this case. The authors noted
that their patients with asphyxia and NE had low five-minute
Apgar
scores (<7/10 in 77% and <4/10 in 44% of cases). In this case
the five-minute Apgar score was 8/10. Professor Smith
doubted the
Apgar score at five minutes, having regard to the condition of TG and
the fact that he was immediately referred to
CHBH.
(c)
Professor Bolton stated the following in
the joint minute:
‘
Children
born to HIV mothers in low-resource settings in Southern Africa [the
Botswana study] have been shown to be at increased
risk for
developing CP and this risk is not affected through the transmission
of the HIV to the foetus, but likely to be due to
the effect that the
HIV infection has on the placenta.
The
mother’s HIV status probably had a deleterious effect on
placental function and this then played an important role in
the
development of brain damage and that infection with HIV is associated
with chorioamnionitis which in turn is associated with
cerebral
palsy….’
Professor
Bolton referred to a study regarding the effect of HIV on placenta
from Bangkok, Thailand (the Bangkok study)
[12]
which
showed that:
‘
Although
HIV-infected women were more likely than HIV-uninfected women to have
placental inflammatory lesions,
but that
placental inflammatory lesions were not associated with increased
perinatal HIV transmission.’
(d)
Professor Smith noted that in the Bangkok
study, placentas from the HIV-positive group were characterised by
decreased weight and
an increased number of marginal infarcts
relative to the HIV-negative group.
(e)
Professor Bolton stated that (1) recent
evidence from Southern Africa (the Botswana study) has shown that
postnatal infection including
early-onset pneumonia was strongly
associated with later development of CP; and (2) that in this case
the baby was thought to have
evidence of congenital pneumonia; and
(3) this early infection may have been associated with
chorioamnionitis and probably played
an important role in the
aetiology of CP.
(f)
Professor Smith was of the view that the
Botswana study included the whole spectrum of gestations, including
premature births of
gestations below 32 weeks, which are known to
influence incidences of CP. Of the subjects with CP studied (56),
only eight had
gestational age <32 weeks. The authors acknowledged
that they did not have sufficient data in this study to allow them to
differentiate
between potential mechanisms causing CP related to HIV.
(g)
Professor Bolton stated that the major risk
factors for CP in Botswana included birth complications (50%),
neonatal infection (23%)
and maternal HIV. Serious neonatal infection
was defined as culture-proven sepsis, severe pneumonia, or
meningitis, but the actual
percentages were not reported.
(h)
Professor Bolton observed that in this
case, the severity of the respiratory distress was not commented on
in the neonatal discharge
summary. Professor Smith noted that the
discharge summary indicated a possibility, rather than a probability,
that there was congenital
pneumonia, which is different to an
infection acquired after birth, and there certainly was no meningitis
or culture-proven septicaemia.
(i)
Professor
Smith noted that if there was possible chorioamnionitis as referred
to by Professor Bolton, chorioamnionitis among neonates
with
encephalopathy has been associated with a lower risk of brain injury
and adverse outcomes, whereas signs of neonatal sepsis
carried an
elevated risk.
[13]
He noted
that neonatal infection was not defined as pneumonia, but according
to the presence of a positive blood culture or combined

haematological derangements associated with neonatal fever. A
positive blood culture was not reported in the present matter,
otherwise
the neonatal summary would have recorded it, and the
reference to ‘congenital pneumonia?’ indicates that this
diagnosis
was uncertain, or not proven.
(j)
Professor Bolton disagreed. He stated that
the neonatal caregivers noted respiratory distress and ascribed this
to pneumonia. He
quoted a study which stated that:
‘
Pneumonia
in newborn infants is often difficult to diagnose and often difficult
to distinguish from other causes of respiratory
distress... Although
many investigations including white cell counts, blood cultures,
C-reactive protein, etc are performed, they
lack the necessary
sensitivity and specificity to accurately diagnose pneumonia’.
[14]
(k)
Professor Smith stated that it is alleged
that external abdominal pressure was applied. If this allegation is
borne out in Court,
the following should be noted:-
i.Fundal
pressure is understudied and remains controversial in the management
of the second stage of labour;
ii.Application
of fundal pressure on a delivering woman was ineffective in
shortening the second stage of labour;
iii.Fundal
pressure is associated with shoulder dystocia and foetal acidosis;
iv.There
was evidence for a traumatic delivery if one considers the recording
of a subaponeurotic haemorrhage (SAH) and one has
to consider a
contributory role for external abdominal pressure;
v.The
mechanism through which external abdominal pressure probably
contributed towards the development of HIE was recently described
as
‘cranial compression ischemic encephalopathy’.
[15]
They opined
that
intrapartum events, including asphyxia in term foetuses, account for
significant amounts of subsequent neurological handicap,
including
CP. In their review, they trace the development of the understanding
of
the forces of labour as a mechanism of foetal head trauma and
subsequent foetal neurological injury.
(l)
Professor Bolton stated that the lack of
contemporaneous records of the labour makes it speculative regarding
the allegation that
abdominal pressure was applied. According to him,
this seems unlikely if, as recorded by Dr Mogashoa (the Paediatric
Neurologist
called by the defendant), ‘the delivery was not
difficult’. Thus, Professor Bolton concluded, the mother’s
various
versions should be tested in Court.
(m)
Professor Smith summarised the position as
follows:
‘…
considering
the available limited factual records, the allegation that there was
application of external fundal / abdominal pressure,
his own
experience with alleged birth asphyxia cases and the scientific
literature, he concludes that the foetal brain was probably
subjected
to partial prolonged hypoxic ischaemia during the period between
07:00 and 13:00. It is likely (probable) that the combined
effects of
uterine contractions (placental blood flow) during the active phase
of labour and external fundal pressure during the
second stage of
labour, significantly contributed towards the development of cerebral
(brain) ischaemia, cranial compression ischaemic
encephalopathy and
birth trauma (SAH), which ultimately lead to the development of
cerebral palsy.’
(n)
Professor Bolton disagreed in this regard.
He was of the view that—
‘
In
the absence of appropriate, contemporaneous clinical records of the
labour and delivery, it is speculative as to whether there
was
sub-optimal care offered by the defendants during labour. The
obstetric experts, rather than a paediatrician and neonatologist,

should be relied upon to comment on care of the mother.’
(o)
Professor Smith further noted:
‘
When
an acute sentinel event such as uterine rupture, placenta praevia,
abruption placenta or cord prolapse is reasonably excluded,
the most
common causal factor underlying intrapartum hypoxic ischaemic brain
injury (neonatal encephalopathy) is suboptimal obstetric
care. In the
present case none of the aforementioned sentinel factors were
recorded in the available medical notes…’
(p)
Professor Smith concluded that, based on a
balance of probabilities, foetal distress and a non-reassuring foetal
condition probably
occurred before birth because the probability that
early neonatal encephalopathy occurs with foetal distress is higher
than the
probability that encephalopathy occurs without foetal
distress. Professor Bolton disagreed with this statement, regarding
it as
speculation.
(q)
Professor Smith was of the opinion that:
‘Suboptimal obstetric care was probably the avoidable causal
factor and therefore
had birth been appropriately expedited, the
outcome was probably completely avoidable.’ Professor Bolton
disagreed with this
conclusion.
Evidence
of Professor Smith (additional to that contained in the joint
minutes)
[83]
TG suffered from birth asphyxia and HIE
Grade 2. This, in layman’s terms, is an injury to the child’s
brain caused by
deprivation of blood and oxygen to the brain.
[84]
‘
Grade 2’ refers to the
severity of the injury being a moderate injury on a sliding scale
from one to three, with one being
mild and three being the worst kind
of injury. When the clinicians write this diagnosis, it means that
they were under the impression
that this HIE is the mechanism of the
brain injury and the encephalopathy.
[85]
When the congenital pneumonia occurs during
the pregnancy near to the time of delivery, one would link it to a
maternal infection;
the probability is that there is chorioamnionitis
in a mother who would present with fever, tender uterus, pus draining
from the
vagina, foul smell, or a combination of such things. If
there was chorioamnionitis there would be a footprint or record of
the
infection with regard to treatment and antibiotics for the
infection. None of these was present with the plaintiff.
[86]
In the absence of infection, just pure
asphyxia
per se
will
result in respiratory distress. It is more likely on the
probabilities, and supported by his experience and the literature,

that when encephalopathy is diagnosed during the early neonatal
period, that there must have been foetal distress during labour
and
birth.
[87]
Having regard to the history that the
plaintiff gave regarding the condition of the child at birth i.e.
that the child did not cry,
the child was lying very still and not
moving, he was resuscitated, placed in an incubator and transferred
to CHBH, where he was
placed in ICU with tubes in his nose for
feeding and breathing, and after his discharge was referred to the CP
clinic – the
probable time at which the hypoxia and
encephalopathy occurred is in the intrapartum phase. That is, during
labour and birth at
which the child sustained the asphyxia and the
development of the CP.
[88]
The Apgar scores recorded in the available
hospital records do not make sense if one has regard to the known
objective factors,
such as the condition of the child at birth and
the need to admit the child to the NICU at CHBH immediately after
birth.
[89]
It does not make sense that they would
resuscitate the baby and then immediately decide to send the baby to
CHBH with an Apgar score
of 8/10. There was no clear reason to refer
TG to CHBH, as 8/10 is a normal score. If the baby arrived at CHBH
and scored 10/10
then that would indicate that TG was perfectly
healthy. In his experience he has found that clinics and midwife
clinics sometimes
overestimate or inflate the Apgar scores.
[90]
From the perspective of a neonatologist,
the HIV-positive status of the mother did not highlight a higher risk
for abnormal neurodevelopmental
outcome for the child, the mother
having taken nevirapine before the birth. He stated that there are no
studies that show conclusively
that HIV is noted as an independent
cause for CP. HIV did not give you a higher risk profile, so there is
no conclusion that can
be drawn from studies from Botswana and other
places, as obstetric care in South Africa is better than that in
Botswana.
[91]
Growth restriction is the long standing
effect of inadequate placental function. Infection like HIV kills a
baby if it is severe
enough and is contracted in close proximity to
labour and delivery; whereas placental pathology caused by some
infection is contracted
weeks before delivery in the majority of
cases, and would be evident from the mother’s symptoms. There
is no evidence that
this occurred.
[92]
Various
articles
[16]
were put to
Professor Smith by the defendant’s counsel for comment. When
presented with the article titled
‘
The
Villitis of unknown etiology: noninfectious chronic villitis in the
placenta’ (the third Redline article)
[17]
Professor Smith stated that if Villitis of Unknown Etiology (VUE) was
implicated in having caused a placental pathology which resulted
in
the hypoxia and CP, the VUE would cause preterm labour, still birth
and intrauterine growth restriction – none of which
are present
in this matter. In addition, if the CP was caused by VUE, it would be
of a different kind from the spastic quadriplegic
and/or dyskinetic
CP. Linking VUE and CP causally by way of a hypoxic mechanism
involving the placenta would be a quantum leap
as there is no clear
cut definite brain pathology for such a link. The proposition is all
speculation. There is not a specific
categorisation of the type of CP
that may be caused by VUE. The article does not include any HIV
cases.
[93]
Professor Smith discounted the Botswana
study as neonatal infections were defined as culture proven sepsis,
severe pneumonia or
meningitis. But the actual percentages were not
reported, and complications occurred in half of those cases.
Association between
maternal HIV and CP has not been previously
described and required further investigation.
[94]
In regard to the Bangkok study, Professor
Smith commented that the article states that with an HIV positive
population, there was
more chorioamnionitis. There was no
chorioamnionitis present in the plaintiff’s case.
[95]
If there was a placental abnormality
causing hypoxia, the foetus would show that by an abnormal foetal
heart rate and heart rate
pattern which is then equated to foetal
distress and would then be detectable, if proper monitoring occurred.
In any event, if
the brain injury was sustained in the weeks before
delivery there would, on the probabilities, be a non-reassuring
foetal heart
rate pattern and the probability that the brain would
have already started shrinking in the weeks prior to the labour. In
other
words, the baby would have had a much smaller head
circumference out of proportion to what TG had.
[96]
There is evidence of meconium aspiration,
which negates the diagnosis of congenital pneumonia. The query of
congenital pneumonia
is just a query and not a diagnosis. It was not
confirmed in the discharge summary.
[97]
Having considered the multi-pronged,
multi-faceted, multi-disciplinary involvement and what respective
experts for the plaintiff
described, including genetics, neurological
outcome, and the radiology picture (of which there is agreement
between the plaintiff
and defendant) one has to conclude that
intrapartum asphyxia is the most likely cause of the child’s
injury. As this was
a partial prolonged HIE brain injury, the failure
to monitor the foetus’ heart rate amounted to substandard care,
as proper
monitoring would have picked up the foetal distress in a
timely way, allowing the defendant’s employees to refer the
plaintiff
to CHBH timeously.
Evidence
of Professor Bolton (additional to that contained in the joint
minutes)
[98]
Professor Bolton conceded that he is not a
neonatologist and that he is careful not to claim to be what he is
not. However, within
the field of his expertise as a paediatrician,
he confirmed that the HIE occurred in the intrapartum phase.
[99]
He opined that, in view of the plaintiff’s
HIV positive status, the condition of the child may have been caused
by exposure
of the child to HIV – although this did not mean
that the child was HIV infected. However, he conceded that given the
status
of the available research material in respect of the
association between HIV exposure and possible adverse birth outcomes,
he was
unable to say that the Court should consider the HIV as a
probable cause of the outcome.
[100]
Professor
Bolton explained that chorioamnionitis had an effect on the amniotic
sac, placenta, and umbilical cord and was the most
common cause of
prematurity, especially in developing countries. He stated further
that it is the response to an infection that
causes the damage, and
that there is no way of detecting this damage during pregnancy.
However, the latest consensus statement
from the American College of
Obstetricians and Gynaecologists in 2014,
[18]
says that unless you have examined the placenta histologically, one
cannot determine the cause of CP.
[101]
The examination would include histological
chorioamnionitis, microscopic histological chorioamnionitis,
microscopic histology, culture
histology and clinical histology.
Professor Bolton states that on the medical evidence available, the
baby most likely had pneumonia.
An X-Ray can confirm pneumonia, or it
can look like meconium aspiration. But at this point, it is all
speculation.
[102]
On
the Mowbray study,
[19]
Professor Bolton stated the article ‘supports the fact that HIV
positive mothers have got more hypoxic ischemia in their
entrance
than HIV negative mothers…. In the worst case scenario that
hypoxic ischemia kills the baby and it is born stillbirth.’

With reference to the Botswana study, Professor Bolton stated that a
lot more evidence needs to be published but that that they
‘found
a significant increased incidence of CP rather than neonatal
encephalopathy, the end result.’ In response to
Professor
Smith’s criticism of the Botswana study, Professor Bolton
responded, ‘So we have got two articles neither
of which were
the greatest articles, but showing evidence that, at least in an
African context in the developing world, certain
causative factors
are associated with CP.’
Evidence
of Dr Solomons – the paediatric neurologist called by the
plaintiff
[103]
Dr
Solomons testified that based on his examination of the child as well
as his consideration of the respective expert reports,
by a process
of deduction and elimination of causal factors, he had reached the
conclusion that TG had suffered HIE in the intrapartum
period. He
further explained that based on the finding that there was bifrontal
narrowing, the probability that the HIE occurred
in the intrapartum
phase was stronger. In addition, he indicated that the finding of
multi-cystic encephalomalacia
[20]
was also a further indicator that the HIE occurred in the intrapartum
phase when looked at in conjunction with the history of the
labour as
given by the plaintiff. This is also confirmed by the radiologists in
their reports.
[104]
The cross examination of Professor Solomons
did not focus on his findings, but rather sought to establish the
possibility of an
infectious cause for the HIE. He considered other
possible causes, such as infection, by indicating that the fact that
the baby
was of normal weight is in contradiction to an antepartum
event or to a placental problem as that would have resulted in
intrauterine
growth restriction.
[105]
With regard to the causal implication of
chorioamnionitis, his evidence was that there would have been
specific symptoms for chorioamnionitis
in the mother, which include a
foul smelling discharge and maternal fever, none of which were
reported. If sub-clinical chorioamnionitis
(no symptoms evident) was
suggested, it could only be determined by a histology. He concluded
that there was no evidence of chorioamnionitis,
and the suggestion in
the circumstances is merely speculative and not probable. All the
literature referencing chorioamnionitis
or foetal inflammatory
response syndrome indicates that the outcome would be a preterm
infant.
[106]
In relation to pneumonia being a possible
cause, his evidence was that you would need a very severe pneumonia,
and a child that
is shocked enough to require cardio compressions to
be administered, in order to lead to postnatal HIE.
[107]
With regard to the suggestion of
intercranial sepsis, Professor Solomons pointed out that the MRI
excludes sepsis as a cause. If
the injury had occurred after the
child had been delivered, it would have been a significant event and
would have been something
clearly mentioned in the discharge summary.
[108]
Professor
Solomons differed from Dr Mogashoa, the paediatric neurologist
called
by the defendant. He opined that a baby born HIV negative, but
suffering from CP, could only be connected to the mother’s
HIV
positive status, with premature birth, low weight with a specific
brain injury and MRI picture-periventricular leukomalacia.
[21]
This did not occur in TG’s case.
[109]
Professor Solomons testified that the
mother’s narrative of labour is consistent with the MRI ‘holes
in the frontal
area of the brain’. It was consistent with
partial prolonged HIE and occurred for 15-30 minutes. Professor
Solomons stated
that that, in the absence of supporting evidence, he
had to rely completely on the mother’s history.
[110]
Professor Solomons maintained that, in the
literature, there is no support for a link between HIV and
a term infant. On HIV, the following
articles were put to Professor Solomons and he maintained that HIV is
not associated with this
case:
(a)
The Botswana study associating HIV exposure
with encephalopathy: he indicated that the article is unreliable as
the sample size
was too small to draw a valid conclusion; the type of
CP involved is not indicated; and the study clearly refers to an
association
and not causation. He refuted the attempt to implicate
HIV infection or HIV exposure as a probable cause of the
encephalopathy.
He stated that if HIV was somehow implicated, it
would have manifested in premature labour. Further that the MRI would
have shown
a specific pattern which does not appear in this case.
Professor Solomons maintained that, in the literature, there is no
support
for a link between HIV and
a
term infant.
(b)
The Bangkok study: he pointed out that the
high water mark of the study is an association, not causation, and
that it is based on
placental histology which is not available in
this case. The reference is therefore speculative. Professor Solomons
discounted
this article as it is not applicable, as TG does not have
specified spastic CP, which was the issue considered in the Bangkok
study.
(c)
A study
titled ‘Placental pathology in full-term infants with
hypoxic-ischemic neonatal encephalopathy and association with

magnetic resonance imaging pattern of brain injury’:
[22]
Professor Solomons stated it does not speak to HIV itself but rather
analysis of placentas in relation to CP, and at term CP’s.
[111]
The Redline articles: Professor Solomons
discounted as being
studies
on placentas and chorioamnionitis but not specific to CP.
Evidence
of Dr Mogashoa – paediatric neurologist called by the defendant
[112]
Dr Mogashoa conceded that the baby suffered
a HIE in the intrapartum phase, although she stated that it is
difficult to accurately
time such an injury. Dr Mogashoa further
conceded that the evidence which she gave with regard to the
implication of HIV and
chorioamnionitis, based on the literature,
cannot be used to prove causation, as it only rises to the level of
an association.
Dr Mogashoa referred to the ACOG criteria that a
depressed baby does not mean it is HIE, there are many causes.
Children with
low Apgar scores turn out normal; children with high
Apgar scores can develop CP.
[113]
She stated that maternal HIV infection
could still be an associated factor, as just because the baby is HIV
negative, does not mean
that there are no problems during labour. She
referred to the ACOG statement, which provides that there should be a
multi-dimensional
assessment. The take home message of the Botswana
article is that maternal infection plays a role in placental
pathology and the
outcome of the child and subsequent CP. The Bangkok
article stated that with HIV positive mothers, there was more
chorioamnionitis.
In many cases, sub-clinical chorioamnionitis
occurred; no symptoms were present which would alert the nurses to
foetal distress.
[114]
Dr Mogashoa indicated that, in the absence
of records, one cannot come to a definite conclusion. Without knowing
the effect of HIV,
it is difficult, with certainty, to say what
caused the HIE.
[115]
Dr Mogashoa stated that there are
various forms of placental abnormalities. The fact
that the baby was HIV negative does not mean that there was no
problem with the
pregnancy. One may not understand the pathology and
the mechanisms behind it, but the study suggests that the HIV, even
though
it is not transmitted to the baby, is associated with a lot of
problems in the placenta. They found abnormality in the placenta
in
the form of chorioamnionitis. Chorioamnionitis and villitis of
unknown origin (VUE) are examples of these. Chorioamnionitis
is more
common. In the Bangkok Study it is said that VUE is actually a remote
issue and it can therefore be excluded in a scenario
where HIV may
have affected the placenta.
[116]
There are three possible, most likely
causes of the respiratory distress. Firstly, MAS; secondly, HIE,
because the babies are born
with metabolic acidosis and they have
difficulty in breathing; and, thirdly, pneumonia.
[117]
HIV causes lots of problems with infection
‘but what we do not know at this point in time is how it
affects brain injury,
we are still in the dark about the mechanisms
that it affects and therefore we cannot draw conclusions from it and
the studies
as they stand at present.
The
association between maternal HIV and CP requires further
investigation.
Because there is a higher
chance of a HIV infected mother having chorioamnionitis,
chorioamnionitis as a cause for the HIE, must
be one of the
considerations in this case.’
[118]
The plaintiff’s counsel suggested to
Dr Mogashoa that the Bangkok study suggests that the chorioamnionitis
has the opposite
effect; it says it has a protective effect. At the
end of the study, it says chorioamnionitis was associated with lower
risk of
moderate to severe brain injury. The study also stated that
with ‘neonatal encephalopathy, chorioamnionitis was associated

with no risk of brain injury’. Therefore, plaintiff’s
counsel contended that one cannot draw any firm conclusions from
the
study that the Court can rely on. One study says chorioamnionitis
causes brain injury, the other says there is lesser risk
for brain
injury where there is chorioamnionitis. In addition, the study
indicated that they are unsure whether the condition resulted
from
HIV itself, or as a result of the anti-retroviral treatment that HIV
positive mothers were given.
[119]
Dr Mogashoa responded that she ‘was
quite satisfied to conclude that HIV is associated with increased
intrapartum morbidity,
increased mortality, increased problems in the
infants who are HIV exposed even though they are uninfected because
‘we have
to use what we have in front of us, some of it may be
conflicting but we know from the countries with increased prevalence
of HIV,
that we have got problems.’
Evidence
of Dr Gericke and Professor Christianson
[120]
The two geneticists excluded infections or
genetics as probable causes for the HIE.
Literature
[121]
Professor
Solomons, Professor Bolton
and
Dr
Mogashoa
referred to
the
article ‘Neonatal Encephalopathy and Neurological Outcome,
Second Edition:  Report of the American College of Obstetricians

and Gynaecologists’ Taskforce on Neonatal Encephalopathy’
from the American Academy of Pediatrics (the ACOG statement),
which
states:
[23]
‘
To
determine the likelihood that an acute hypoxic–ischemia event
that occurred within close temporal proximity to labor and
delivery
contributed to neonatal encephalopathy, it is recommended that a
comprehensive multidimensional assessment be performed
of neonatal
status and all potential contributing factors, including maternal
medical history, obstetric antecedents, intrapartum
factors
(including fetal heart rate monitoring results and issues relating to
the delivery itself), and placental pathology….’
[122]
Of importance are the following points made
in the article:
‘
There
are several well-defined patterns of brain injury and their evolution
on MRI that are typical of hypoxic–ischemic cerebral
injury in
the newborn, including deep nuclear gray matter or watershed cortical
injury. If a different pattern of brain injury
or evolution of injury
exists on MRI, then alternative diagnoses should be actively pursued
(eg, metabolic and genetic investigations).’
[123]
It appears from the ACOG statement that the
definition of neonatal encephalopathy is—
‘…
a
clinically defined syndrome of disturbed neurologic function in the
earliest days of life in an infant born at or beyond 35 weeks
of
gestation, manifested by a subnormal level of consciousness or
seizures, and often accompanied by difficulty with initiating
and
maintaining respiration and depression of tone and reflexes.’
[24]
[124]
One has to look at the clinical status of
the baby during labour, during and at birth in the neonatal period,
and the subsequent
outcome to determine if the baby fits the criteria
for intrapartum hypoxia. There are certain requirements before one
can diagnose
neonatal encephalopathy and the cause thereof. ACOG
looks at, inter alia:
(a)
the condition of the baby at birth and
refers to the Apgar scores;
(b)
the condition of the baby in the neonatal
period that speaks to neonatal encephalopathy and the staging;
(c)
whether there was a sentinel event.
[125]
Dr Mogashoa stated that in the 2014 ACOG
guidelines, the ACOG task force on neonatal encephalopathy and CP
reflects that multiple
causes can lead to brain injury in term
infants, not just oxygen deprivation around the time of birth. The
task force states that
a comprehensive, multidimensional assessment
should be performed, as described above. The task force considers
that multiple factors
act together with resultant encephalopathy and
resultant injury to the brain.
[126]
ACOG requires that the medical
practitioners look for risk factors during the labour, called
proximal risk factors, and then look
at how the labour was managed.
This helps one to conclude when the insult occurred. According to the
ACOG statement, an Apgar score
less than five at five and at ten
minutes is supportive of intrapartum hypoxia. The Apgar score remain
helpful to determine what
the condition of the child was at birth,
the need for resuscitation and the response to resuscitation and as
one goes on with the
resuscitation, the lower the Apgar remains, the
more likely the chance of morbidity.
Fundal
pressure
[127]
The plaintiff contended that the literature
in respect of the risks associated with the application of fundal
pressure support the
version or proposition of the plaintiff that the
most probable cause of the injury is a mechanical event such as cord
compression
or meconium aspiration. I am unable to decide, on the
probabilities, whether the fundal pressure contributed to or caused
the injury.
There was insufficient evidence in this regard. I
therefore will not take this issue into account in analysing the
evidence and
coming to a conclusion.
The
effects of the plaintiff’s HIV positive status on TG’s
condition
[128]
The defendant referred to several articles,
some of which have been dealt with above, in support of its
proposition that there was
an association between HIV exposure,
intrapartum asphyxia and the development of CP in children born to
HIV infected mothers.
[129]
The plaintiff argued that the articles
referred to by the defendant all clearly indicate that at this point
in time much more research
has to be done before any conclusions can
be drawn with regard to a causative connection between HIV exposure
in neonates, and
the development of neonatal encephalopathy resulting
in CP.
[130]
The other articles referred to by the
defendant:
(a)
‘
The
effect of maternal HIV infection on maternal conditions and perinatal
deaths in southwest Tshwane’:
[25]
The plaintiff submitted that what the article demonstrated is the
occurrence of a higher rate of spontaneous preterm births, infection

and intrapartum asphyxia in the HIV mothers coupled with a higher
rate of antepartum deaths, spontaneous abortion or stillbirths.

Further, it referred to an increase of intrapartum asphyxia in HIV
infected babies and not to HIV exposed but uninfected babies
such as
in the present case. The article concluded that:
‘
The
significant increase of intrapartum asphyxia in HIV infected babies
was unexpected and unexplained…. A possible explanation
is
that these fetuses had severe congenital infections that were
mistaken for intrapartum asphyxia. Alternatively, previous
intra-amniotic
infections might make the fetus more susceptible to
hypoxia during labour due to the fetal immune response syndrome. The
numbers
of fetuses involved are small and this observation will need
to be confirmed by other studies.’
(b)
The Mowbray study: the defendant sought to
show, by way of this study, that there was an association between HIV
exposure and morbidities
such as neonatal encephalopathy. Whilst the
study purported to confirm such an association, the results of the
study reports: ‘In
2008, there were 54 babies diagnosed with
neonatal encephalopathy (predominantly hypoxic ischaemic
encephalopathy), 16 in HIV positive.
31 in HIV negative and 7 in
untested women.’ It is argued by the plaintiff that the quoted
statistic runs counter to the
case which the defendant wishes to make
for the proposition that HIV exposed children are more likely to
suffer a neonatal encephalopathy.
(c)
‘
Meconium
aspiration syndrome in infants of HIV-positive women: a case-control
study’:
[26]
The purpose
of referring to this study was to show that HIV positive women had
significantly
more
meconium-stained amniotic fluid than HIV negative women and that
infants born to HIV positive women showed higher rates of
Meconium
Aspiration Syndrome.
While
the study found that there was more meconium-stained amniotic fluid
and higher MAS in HIV positive as opposed to HIV negative
mothers and
infants, the authors stated that—
‘
We
were not able to determine whether it was the HIV infection itself or
the fetal exposure to ART that led to meconium passage,
possibly
through fetal distress.
What
is however significant is the repetition of the fact that fetal
distress can cause increased production of meconium by the
fetus.
Therefore, it is important to prevent fetal distress.’
(d)
‘
Placental
pathology in HIV infection at term: a comparison with HIV-uninfected
women’:
[27]
the
plaintiff contended that this article debunks the suggestion by the
defendant that a positive HIV status will result in more
placental
lesions than for HIV negative women. The study is significant as it
was conducted at hospitals in Cape Town and makes
the following
conclusions:
‘
Our
findings are notable for the limited differences observed at the
placental level between the HIV- infected and uninfected women

without adverse birth outcomes.’
[28]
The
legal framework
[131]
As stated above, the plaintiff is the only
factual witness who gave evidence.  Sister Ndlela, had no
recollection of the plaintiff’s
case and could only confirm
what appeared on the birth register.
[132]
In a trial action—
‘…
it
is fundamental that the opinion of an expert must be based on facts
that are established by the evidence and the court assesses
the
opinions of experts on the basis of “whether and to what extent
their opinions advanced are founded on logical reasoning”.
It
is for the court and not the witness to determine whether the
judicial standard of proof has been met.’
[29]
[133]
Adapting the approach taken by the Supreme
Court of Appeal (SCA) in
MV Pasquale
:
‘
[T]he
court must first consider whether the underlying facts relied on by
the witness have been established on a prima facie basis.
If not then
the expert's opinion is worthless because it is purely hypothetical,
based on facts that cannot be demonstrated even
on a prima facie
basis. It can be disregarded. If the relevant facts are established
on a prima facie basis then the court
must consider whether the
expert’s view is one that can reasonably be held on the basis
of those facts. In other words, it
examines the reasoning of the
expert and determines whether it is logical in the light of those
facts and any others that are undisputed
or cannot be disputed. If it
concludes that the opinion is one that can reasonably be held on the
basis of the facts and the chain
of reasoning of the expert the
threshold will be satisfied. This is so even though that is not the
only opinion that can reasonably
be expressed on the basis of those
facts. However, if the opinion is far-fetched and based on unproven
hypotheses then the onus
is not discharged.’
[30]
[134]
In
PriceWaterhouse
Coopers Inc v National Potato Cooperative Limited
,
[31]
the
court said:
‘
The
basic principle is that, while a party may in general call its
witnesses in any order it likes, it is the usual practice for
expert
witnesses to be called after witnesses of fact, where they are to be
called upon to express opinions on the facts dealt
with by such
witnesses.’
[135]
Similarly,
Wessels JA, in dealing with the nature of an expert’s opinion,
in
Coopers
(South Africa) (Pty) Ltd v Deutsche Gesellschaft für
Schädlingsbekämpfung MBH
,
[32]
stated—
‘…
an
expert’s opinion represents his reasoned conclusion based on
certain facts on data, which are either common cause, or established

by his own evidence or that of some other competent witness. Except
possibly where it is not controverted, an expert’s bald

statement of his opinion is not of any real assistance. Proper
evaluation of the opinion can only be undertaken if the process
of
reasoning which led to the conclusion, including the premises from
which the reasoning proceeds, are disclosed by the expert….’
[136]
An
opinion of an expert must therefore be based on facts which have been
proven before the court. An opinion based on facts not
in evidence
has no value for the court.
[33]
A court has to ascertain whether the opinions expressed by the
experts are based upon facts proved to it by way of admissible
evidence. It is with this principle in mind that the facts of the
matter, as well as an analysis of the experts’ evidence,
must
be considered.
[137]
As set out above, other than Sister Ndlela,
the defendant called no other factual evidence to dispute the
plaintiff’s version.
Such version was, in effect, not
challenged in cross-examination.
[138]
In
Ratcliffe
v Plymouth and Torbay Health Authority
,
[34]
Lord
Justice Brooke made the point that:
‘
It
is likely to be a very rare medical negligence case in which the
defendants take the risk of calling no factual evidence, when
such
evidence is available to them, of the circumstances surrounding a
procedure which led to an unexpected outcome for a patient.
If such a
case should arise, the judge should not be diverted away from the
inference of negligence dictated by the plaintiff’s
evidence by
mere theoretical possibilities of how that outcome might have
occurred without negligence: the defendants’ hypothesis
must
have the ring of plausibility about it….’
[139]
It
suffices for the plaintiff to convince the court that the inference
that they advocate is the most readily apparent and acceptable

inference from a number of possible inferences.
[35]
In
Caswell
& Powell Duffryn Associated Collieries
,
[36]
Lord Wright remarked—
‘
Inference
must be carefully distinguished from conjecture or speculation. There
can be no inference unless there are objective facts
from which to
infer the other facts from which it is sought to establish. In some
cases, the other facts can be inferred with as
much practical
certainty as if they had been actually observed. In other cases, the
inference does not go beyond reasonable probability.
But if there are
no positive proved facts from which the inference can be made, the
method of inference fails and what is left
is mere speculation or
conjecture.’
[140]
When
a plaintiff is not in position to produce evidence on a particular
issue, less evidence will suffice to establish a prima facie
case
where the matter is peculiarly within the knowledge of the defendant.
A shifting burden will be placed on the defendant to
show that steps
were taken to comply with the standards to be expected. The overall
onus
nevertheless
remains with the plaintiff.
[37]
In
McIntosh
v Premier, Kwazulu-Natal and Another
,
[38]
the
SCA held that:
‘
The
second inquiry is whether there was fault, in this case negligence.
As is apparent from the much-quoted dictum of Holmes JA
in
Kruger
v Coetzee
1966 (2) SA 428
(A) at 430E -
F, the issue of negligence itself involves a twofold inquiry. The
first is: was the harm reasonably foreseeable?
The second is: would
the
diligens paterfamilias
take reasonable steps to guard against such
occurrence and did the defendant fail to take those steps? The answer
to the second
inquiry is frequently expressed in terms of a duty. The
foreseeability requirement is more often than not assumed and the
inquiry
is said to be simply whether the defendant had a duty to take
one or other step, such as drive in a particular way or perform some

or other positive act, and, if so, whether the failure on the part of
the defendant to do so amounted to a breach of that duty.
But the
word “duty”, and sometimes even the
expression
“legal duty”, in this context, must not be confused with
the concept of “legal duty” in
the context of
wrongfulness which, as has been indicated, is distinct from the issue
of negligence….
…
The
crucial question, therefore, is the reasonableness or otherwise of
the respondents’ conduct. This is the second leg of
the
negligence inquiry. Generally speaking, the answer to the inquiry
depends on a consideration of all the relevant circumstances
and
involves a value judgment which is to be made by balancing various
competing considerations, including such factors as the
degree or
extent of the risk created by the actor's conduct, the gravity of the
possible consequences and the burden of eliminating
the risk of
harm….’
[141]
In
Goliath
v MEC for Health Eastern Cape
,
[39]
Ponnan JA stated:
‘
When
an inference of negligence would be justified and to what extent
expert evidence would be necessary would no doubt depend on
the facts
of the particular case. Questions of absolution from the instance at
the close of the plaintiff’s case aside, a
court is not called
upon to decide the issue of negligence until all of the evidence is
concluded (
Arthur v Bezuidenhout and
Mieny
at 573H). Thus any such
explanation as may be advanced by a defendant forms part of the
evidential material to be considered in
deciding whether a plaintiff
has proved the allegation that the damage was caused by the
negligence of the defendant or its servants
(
Osborne
Panama SA v Shell & BP
at 897G –
H). Here, although the procedure performed on Ms Goliath was under
the control of the MEC's employees, and what
they did or did not do
was exclusively within their direct knowledge, none of those
employees were called to testify.’
[142]
Ponnan
JA referred to and adopted Lord Justice Brooke’s comments in
Ratcliffe
v
Plymouth and Torbay Health Authority.
[40]
[143]
In
Meyers
v MEC, Department of Health, EC,
[41]
Ponnan
JA, in dealing with the onus of proof found that, once the plaintiff
had given an acceptable explanation for her claim, it—
‘
was
sufficient as to place an evidentiary burden upon [the doctor] to
shed some light upon the circumstances attending [the plaintiff’s]

injury. Failure to do so meant that, on the evidence as it then
stood, he ran the risk of a finding of negligence against him.
For,
whilst … the plaintiff, bore the overall onus in the case,
[the doctor] nonetheless had a duty to adduce evidence to
combat the
prima facie case made by [the plaintiff]. It remained for him to
advance an explanatory (though not necessarily exculpatory)
account
that the injury must have been due to some unpreventable cause, even
if the exact cause be unknown.’
[144]
The
defendant conceded that the plaintiff’s evidence was
uncontroverted. It was however submitted that, in spite of this,
her
evidence should not be accepted. Reference was made to
Siffman
v Kriel
.
[42]
The defendant contended that the version put up by the plaintiff was
so improbable that it should be rejected. It reiterated the

submission that the plaintiff was a rehearsed witness, without
offering any reason therefor.
[145]
The
submission was that one cannot infer that once something has gone
wrong or not in accordance with what was expected, there must
have
been negligence on the part of the defendant.
Buthelezi
v Ndaba
[43]
was
referred to in this regard. It was submitted that the appropriate
approach to the evidence would be to ask, with reference to
all the
evidence that was admitted, whether a reasonable person in the
position of the defendant would have foreseen injury to
the plaintiff
and have taken steps to guard against it. Reference was made to the
locus
classicus
in this regard
Kruger
v Coetzee
,
[44]
as refined in
Mukheiber
v Raath & Others
.
[45]
If this test is applied to the evidence at hand and, in particular,
to the fact that there is no complete record of what had transpired

during birth and the neonatal period, the answer is that one cannot
know what happened. In the absence of such primary knowledge,
the
defendant contended that it is difficult (if not impossible) to draw
any inference of negligence on the part of the defendant.
[146]
This approach would depend upon the Court
rejecting the plaintiff’s evidence as highly improbable.
Unfortunately, our court
records are filled with cases in which the
negligence of the defendant’s employees in failing to monitor
patients properly,
recording issues inaccurately (if at all) and
generally displaying conduct that does not befit medical
practitioners, is proven.
On Sister Ndlela’s own version,
expectant mothers can be left unattended and unmonitored for two
hours on occasion, if the
nurses are busy with other patients. There
appears to be no reason to reject the plaintiff’s version of
events, which is
not improbable.
Analysis
of possible results of the plaintiff’s HIV positive status
[147]
The plaintiff contended that the
defendant’s case for implicating HIV as a distal factor in
causing the encephalopathy suffered
by the child, is that the HIV
positive status of the mother may have resulted in the placenta
having been affected to the extent
that it may have resulted in
reduced blood flow to the foetus, and therefore less oxygenation and
perfusion. This reduced perfusion
then led to the brain of the foetus
being affected and resulting in an encephalopathy.
[148]
The plaintiff submitted that the literature
referred to by both parties indicated that the theory of causation of
injury suggested
by the defendant is unlikely, and that the more
probable cause is a mechanical injury or event which resulted in a
deprivation
of blood to the foetal brain intrapartum which in turn
led to hypoxia, foetal distress, and a resulting encephalopathy.
[149]
The plaintiff contended that the injury
shown on the MRI, and on which the radiologists agree, is a partial
prolonged HIE. This
is an important criterion for establishing the
timing of the injury to the intrapartum or peripartum phase of labour
and the nature
of the injury as a partial prolonged HIE, and not one
caused by a metabolic or infectious agent (as suggested by the
defendant).
[150]
The literature referred to by the defendant
eliminates the likelihood of VUE having been present in the
plaintiff; alternatively,
there is insufficient evidence to be drawn
from the literature for either VUE or chorioamnionitis to be the
cause of the HIE.
[151]
In relation to the Bangkok study, the
plaintiff pointed to the finding that:
‘
Our
findings that villitis occurred less often in HIV infected women may
be related to HIV associated immunosuppression and suggests
a
diminished capacity to develop an inflammatory response.’
[46]
[152]
In relation to the Botswana study, the
plaintiff submitted that the defendant sought to show, by way of this
article, that there
was an association between HIV exposure in
neonates from HIV positive mothers and the development of neonatal
encephalopathy and
the sequela of CP. The plaintiff submitted that
the study is misplaced in the present case, as the purpose of the
study is aimed
at low resource settings and obtaining a better
understanding of the unique risk factors affecting children with CP
in such low
resource settings, and how to optimise resource
allocation and preventative strategies.
[153]
That objective is stated very clearly in
the abstract on the first page of the article. The conclusion of the
study is stated as
follows:
‘
Modifiable
risk factors such as maternal HIV infection should be targeted as a
potential strategy to reduce the incidence of cerebral
palsy in
Botswana. Further studies are necessary to determine the optimal
preventative and treatment strategies in this population.’
[47]
[154]
The conclusion of the Botswana study
states—
‘
Cerebral
Palsy is an important and common contributor to childhood disability
in low-resource settings. The relative contributions
of major risk
factors for cerebral palsy in Botswana differ significantly from
those described in high-resource settings, with
infection, birth
complications, and maternal HIV being major contributors. Of note,
these are all potentially preventable risk
factors, suggesting that
interventions in birth practices and neonatal care could make a
significant impact in decreasing rates
of cerebral palsy in
Botswana.’
[48]
[155]
The plaintiff contended that the study
cannot be applied to a South African setting, as there are major
differences between the
resources available in South Africa as
opposed to Botswana. It was further argued that the conclusion sought
by the defendant that
HIV exposure is associated with neonatal
encephalopathy is not one of the conclusions reached in the study.
The study also makes
the point that further studies are necessary to
confirm maternal HIV as a risk factor for CP and to characterise the
mechanism
by which HIV increases the risk of CP.
[156]
It was argued by the plaintiff that the
defendant raised the issue of HIV as a possible distal factor merely
to muddy the waters
as it has not placed any cogent evidence before
the Court to show that HIV exposure may have caused the neonatal
encephalopathy
and CP the child suffered.
[157]
The defendant’s witnesses, Professor
Bolton and Dr Mogashoa, both conceded that HIV exposure as a
contributing factor required
more research.
Conclusion
[158]
It was submitted that by the
plaintiff that it is more probable that the negligence of the
midwives is the proximal cause of the
injury which the child suffered
in that they:
(a)
Failed to monitor the plaintiff properly
during her labour;
(b)
Failed to monitor the unborn child
regularly and appropriately to detect any foetal distress and
therefore did not note that the
child was in distress timeously;
(c)
Failed to take appropriate action or
interventions to stop the child from suffering distress;
(d)
Applied a risky and dangerous procedure to
deliver the child when they discovered the distress thereby injuring
the child further.
[159]
Despite vigorous and extended
cross-examination, the defendant did not succeed in establishing that
the plaintiff was dishonest
or coached in presenting her testimony.
The plaintiff claimed that neither she nor TG were examined or
monitored as required by
the maternity guidelines.
[160]
The radiological evidence is not disputed.
The injury was a partial prolonged ischaemic event. Properly
monitored, the foetal distress
during this period should have been
picked up and the necessary interventions should have occurred.
[161]
As stated earlier in this judgment, it is
of significance that very fundamental issues were agreed to by the
parties before the
commencement of the trial. These included:
(a)
It is recorded in the birth register that
the baby suffered from birth asphyxia as a complication at birth.
(b)
TG required resuscitation and oxygen at
birth and was transferred to CHBH on the same day after a delay of
approximately three hours.
(c)
The reason for the transfer to CHBH was
recorded as low Apgar scores and birth asphyxia.
(d)
The MRI brain scan, dated 30 June 2017,
demonstrates features consistent with chronic sequela of a partial
prolonged HIE. There
are no stigmata of intracranial syndromic
disorder and there are no features to suggest complicated
intracranial sepsis (infection).
The implication of this is that the
child does not suffer from a brain injury which was caused by HIV
infection or AIDS, or inflammatory
infections such as meningitis or
syphilis.
(e)
There is sufficient evidence for timing of
the partial prolonged HIE to the intrapartum period.
(f)
There is no recorded evidence for the
presence of the histological markers of Foetal Inflammatory Response
Syndrome (FIRS) i.e.
inflammation of the umbilical cord, acute
chorioamnionitis or chorionic villi vasculitis – all indicators
of a pathological
placental condition.
[162]
Despite these agreed issues, the defendant
sought to introduce evidence in contradiction to the agreement
reached in relation to
the timing of the partial prolonged HIE to the
intrapartum period; the presence of acute chorioamnionitis or
chorionic villi vasculitis;
the fact that the child does not suffer
from a brain injury which was caused by HIV infection or AIDS, or
inflammatory infections.
[163]
The evidence introduced by the defendant is
inconclusive on all those issues and in most cases, speculative.
There is simply no
conclusive evidence that the plaintiff’s
positive HIV status had the consequences suggested by the defendant.
In the absence
of contradictory evidence, the plaintiff’s
version (supported by the expert evidence on the consequences of
substandard care)
that she was not monitored and that such
substandard care resulted in TG suffering birth asphyxia and the
resultant neonatal encephalopathy
and CP must be accepted.
Therefore,
the following order is made:
1.
It is declared that the defendant is liable
for 100% of the plaintiff’s damages, as proved or agreed,
arising from the birth
of TG born on 22 November 2004.
2.
The defendant shall pay the plaintiff’s
costs.
S
E WEINER
JUDGE
OF THE HIGH COURT
GAUTENG
LOCAL DIVISION, JOHANNESBURG
This
judgment was handed down electronically by circulation to the
parties’ and/or parties’ representatives by email
and by
being uploaded to CaseLines. The date and time for hand-down is
deemed to be 10h00 on
19 March 2021.
Dates
of hearing:

24 – 26 April 2018
13 – 17 August 2018
20 – 24 August 2018
28 January – 1
February 2019
2 December 2020
Defendant’s
supplementary heads of argument:
22 December 2020
Plaintiff’s
supplementary heads of argument:
16 January
2021
Date
of judgment:

19 March 2021
Appearances:
Counsel
for the Plaintiff:

Adv. D Brown
Instructing
Attorneys:

Du Plessis Attorneys
Counsel for the
Defendant:

Adv. Pauw SC; Adv. R Mansingh
Instructing
Attorneys:

State Attorney
[1]
Article in
Business
Live, dated 27 January 2020, titled ‘Medical negligence claims
against the state soar to R104bn’ accessed
at
https://www.businesslive.co.za/bd/national/health/2020-01-27-medical-negligence-claims-against-the-state-soar-to-r104bn/
.
[2]
In
relation to causation, Gorven AJA, writing for the majority, in
AN
obo EN v Member of the Executive Council for Health, Eastern Cape
[2019]
4 All SA 1
(SCA) stated at paras 3-4:
‘…
The
wrongful conduct must cause the wronged person to suffer loss. The
first step in proving this is to prove that the wrongful
conduct of
the staff caused the baby to suffer brain damage. The appellant
accordingly bore an onus to prove this. Wrongfulness
should not be
conflated with factual causation.
The
test for factual causation is whether the act or omission of the
defendant has been proved to have caused or materially contributed

to the harm suffered. Where the defendant has negligently breached a
legal duty and the plaintiff has suffered harm, it must
still be
proved that the breach is what caused the harm suffered….’
[3]
Khoza
v MEC for Health and Social Development, Gauteng
2015
(3) SA 266
(GJ) para 47.
[4]
Madida
obo M v MEC for Health for the Province of Kwa-Zulu Natal
[2016]
ZAKZPHC 27 paras 10-12.
[5]
Ibid
para 20.
[6]
And
further confirmed in the defendant’s heads of argument where
it is stated: ‘6. The matters dealt with under the
heading
“The issues which are common cause or agreed in the joint
minutes” are not in dispute.’
[7]
S
v Azov
1974 (1) SA 808
(T) at 810F – 811A.
[8]
President
of the Republic of South Africa & others v South African Rugby
Football Union & others
2000 (1) SA 1
(CC) para 61.
[9]
Baphaleng Mononkwane
et
al
‘Risk Factors for Cerebral Palsy in Children in Botswana’
(2017) 77
Paediatric
Neurology Journal
73.
[10]
BP Yawn
et
al
‘Maternal Recall of Distant Pregnancy Events’ (1998) 51
Journal
of Clinical Epidemiology
399.
[11]
Jonsson
M
et
al
‘
Neonatal
encephalopathy and the association to asphyxia in labor’
(2014) 211
American
Journal of Obstetrics and Gynecology
667.e1-667.e8.
[12]
DA
Schwartz
et
al
‘
Placental
abnormalities associated with human immunodeficiency virus type 1
infection and perinatal transmission in Bangkok, Thailand’

(2000) 182(6)
The
Journal of Infectious Disease
1652-1657.
[13]
Jenster,
M
et
al
‘
Maternal
or neonatal infection: association with neonatal encephalopathy
outcomes’ (2014) 76
Pediatric
Research
at
93.
[14]
Edwards
MO
et
al
‘
Respiratory
Distress of the Term Newborn Infant’ (2013) 14
Paediatric
Respiratory Reviews
29-37.
[15]
BS
Schifrin
et
al
‘
Cranial
compression ischemic encephalopathy: Fetal neurological injury
related to the mechanical forces of labor and delivery’
in L
Zhang and LD Longo (eds)
Stress
and Developmental Programming of Health and Disease: Beyond
Phenomenology
(2014)
at 651-688.
[16]
RW
Redline & MA O'Riordan ‘Placental lesions associated with
cerebral palsy and neurologic impairment following term
birth’
(2000) 124
Archives
of Pathology & Laboratory Medicine
1785-1791;
RW
Redline ‘Severe fetal placental vascular lesions in term
infants with neurological impairment’ (2005) 192
American
Journal of Obstetrics and Gynaecology
452-457;
and RW Redline ‘Villitis of unknown etiology: noninfectious
chronic villitis in the placenta’ (2007) 38
Human
Pathology
1439-1446. (The Redline
articles).
[17]
‘
The
Villitis of unknown etiology: noninfectious chronic villitis in the
placenta’ (note 16 above).
[18]
‘
Neonatal
Encephalopathy and Neurologic Outcome, Second Edition’ (2014)
133 Pediatrics e1482-e1488 (the ACOG statement).
[19]
D
Kennedy
et
al
‘
The
effect of maternal HIV status on perinatal outcome at Mowbray
Maternity Hospital and referring midwife obstetric units, Cape
Town’
(2012) 18
South
African Journal of Obstetrics and Gynaecology
6-10.
[20]
The
softening or loss of brain tissue after cerebral infarction,
cerebral ischemia, infection, craniocerebral trauma, or other

injury.
[21]
A
type of brain injury that affects premature infants. The condition
involves the death of small areas of brain tissue around

fluid-filled areas called ventricles. The damage creates ‘holes’
in the brain.
[22]
JC
Harteman
et
al
‘
Placental
pathology in full-term infants with hypoxic-ischemic neonatal
encephalopathy and association with magnetic resonance
imaging
pattern of brain injury’ (2013) 163
The
Journal of Pediatrics
968-995.
[23]
The
ACOG statement (note 18 above).
[24]
Ibid
at e1484.
[25]
RC
Pattinson
et
al
‘
The
effect of maternal HIV infection on maternal conditions and
perinatal deaths in southwest Tshwane’ (2010) 2
Facts,
Views & Visions in ObGyn
227-231.
[26]
SK
Gupta
et
al
‘
Meconium
aspiration syndrome in infants of HIV-positive women: a case-control
study’ (2016) 44
Journal
of Perinatal Medicine
469-475.
[27]
E
Kalk
et
al
‘
Placental
pathology in HIV infection at term: a comparison with HIV-uninfected
women’ (2017) 22
Tropical
Medicine & International Health
604-613.
[28]
Ibid
611.
[29]
MV
Pasquale della Gatta; MV Filippo Lembo; Imperial Marine Co v
Deiulemar Compagnia di Navigazione Spa ZASCA
2012
(1) SA 58
(SCA) para 25. See also
Michael
& another v Linksfield Park Clinic (Pty) Ltd & another
2001 (3) SA 1188
(SCA) paras 34-40.
[30]
Ibid
para
26.
[31]
PriceWaterhouse
Coopers Inc & others v National Potato Cooperative Ltd &
another
[2015]
ZASCA 2
;
[2015] 2 All SA 403
(SCA) para 80.
[32]
Coopers
(South Africa) (Pty) Ltd v Deutsche Gesellschaft für
Schädlingsbekämpfung MBH
1976
(3) SA 352
(A)
at 371F-G.
[33]
PriceWaterhouse
(note 31 above) para 99.
[34]
Ratcliffe
v Plymouth & Torbay Health Authority & Anor
[1998]
EWCA Civ 2000
(11 February 1998)
[35]
AA
Onderlinge Assuransie-Assosiasie Bpk v De Beer
1982
(2) SA 603
(A); see also
Cooper
&
Another
NNO v Merchant Trade Finance Ltd
2000
(3) SA 1009 (SCA).
[36]
Caswell
v Powell Duffryn Associated Collieries Ltd
[1940]
AC 152
at
169–170.
[37]
Monteoli
v Woolworths (Pty) Ltd
2000
(4) SA 735
(W) para 27.
[38]
McIntosh
v Premier, Kwazulu-Natal and Another
2008
(6) SA 1
(SCA) paras 12 & 14.
[39]
Goliath
v Member of the Executive Council for Health, Eastern Cape
[2014] ZASCA 182; 2015 (2) SA 97 (SCA) para 17.
[40]
Ratcliffe
(note
34 above).
[41]
Meyers
v MEC, Department of Health, EC
[2020]
ZASCA 3
;
2020 (3) SA 337
(SCA)
para
71.
[42]
Siffman
v Kriel
1909 TS 538.
[43]
Buthelezi
v Ndaba
[2013] ZASCA 72
;
2013 (5) SA 437
(SCA), where it was held that
negligence was not to be inferred from a concession by the surgeon
that something must have gone
wrong during the operation. It was
dependent on evaluation of the reasoning underlying conflicting
expert opinions.
[44]
Kruger
v Coetzee
1966
(2) SA 428
(A) at 430E-F.
[45]
Mukheiber
v Raath and Others
[1999]
ZASCA 39; [1999] 3 All SA 490 (A).
[46]
The
Bangkok study (note 12 above) at 1655.
[47]
The
Botswana study (note 9 above) at 73.
[48]
Ibid
at 76.