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[2023] ZAECBHC 8
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A.M obo L.M v Member of the Executive Council for Health, Eastern Cape Province (586/2017) [2023] ZAECBHC 8; 2024 (1) SA 413 (ECB) (25 April 2023)

IN THE HIGH COURT OF
SOUTH AFRICA
EASTERN CAPE DIVISION,
BHISHO
CASE NO: 586/2017
REPORTABLE
In
the matter between
A.M
obo L.M.
Plaintiff
And
THE
MEMBER OF THE EXECUTIVE COUNCIL FOR HEALTH, EASTERN CAPE PROVINCE
Defendant
JUDGMENT
GOOSEN, J.
Introduction
[1]
On 9
June 2011, the plaintiff gave birth to a son, L.M., at Saint Barnabas
Hospital in the Eastern Cape Province. The plaintiff
was 20 years old
at the time. It was her second birth. Her first child was born by
caesarean section. She was admitted to Saint
Barnabas Hospital, in
labour, at 03h25. L M was born by vaginal delivery at 09h00. He was
born in a compromised state, as will
be described below. The
plaintiff and LM were discharged on 10 June 2011.
[2]
On 21
September 2017, the plaintiff instituted action in her personal and
representative capacities against the defendant. She alleged
that the
defendant’s servants, medical personnel employed at Saint
Barnabas Hospital, were negligent in the management and
treatment of
her during labour. She alleged that this negligence caused LM to
suffer a hypoxic ischaemic brain injury (HI injury)
at term
manifesting as cerebral palsy. In consequence, she claimed damages
payable by the defendant.
[3]
The
defendant denied liability. Two special pleas were raised. The first,
concerning the failure to give timeous and proper notice
in terms of
s3(1) of the Limitation of Legal Proceedings against Certain Organs
of State Act, 40 of 2002, was resolved by an order
granting
condonation in terms of s3(4) on 7 May 2019. The second, concerning
the alleged prescription of the claim by the plaintiff
in her
personal capacity, remained alive on the pleadings at trial.
[4]
The
case came to trial on 25 April 2022. It was agreed to separate the
determination of liability from that of the quantification
of damage,
if any. An order to this effect was made at the commencement of the
trial. In relation to liability, two issues had
crystalised. The
pre-trial minute which was signed by the parties identified the
issues for determination as being:
‘
a.
What was the factual cause of the hypoxic ischaemic brain injuries
suffered by the baby resulting
in cerebral palsy and when did the
said injuries occur?
b.
Did negligence (if any) on the part of the Defendant’s staff
cause or materially contribute
to the baby’s hypoxic ischaemic
brain injuries in the sense that the Defendant by the exercise of
reasonable professional
care and skill could have prevented it from
occurring?’
[1]
The proceedings
[5]
The
trial, save for proceedings during which the plaintiff testified, was
conducted on a virtual platform. This occurred by agreement
between
the parties, to accommodate several expert witnesses who were unable
to attend the trial in person. The trial proceeded
over several days.
It was then adjourned to allow for the plaintiff to testify in
person. It was concluded in December 2022.
[6]
The
plaintiff presented the evidence of five expert witnesses. They were
Prof Davies (a neonatologist); Prof Andronikou (a radiologist);
Dr
Kara (a paediatrician); Dr Pearce (a paediatric neurologist); and
Prof Anthony (an obstetrician). The defendant only presented
the
evidence of Prof Rothberg (a neonatologist). The defendant qualified
several other expert witnesses. Joint minutes reflecting
points of
agreement and disagreement between the parties’ respective
experts were prepared and, during the plaintiff’s
case,
reference was made to these joint minutes where relevant.
[7]
As far
as documentary evidence is concerned, the plaintiff produced the
maternity medical kept by the hospital. The plaintiff also
produced
medical records relating to post-natal treatment of LM and the
plaintiff. Extensive reference was made to these medical
records by
the experts, both in their reports and testimony. At the commencement
of the trial Mr McKelvey, who appeared for the
plaintiff, pointed out
that they were not admitted. Accordingly, the normal evidentiary
rules apply. Although it was stated that
the evidential value and
weight to be attached to the records would be addressed at the
conclusion of the trial, Mr McKelvey foreshadowed
plaintiff’s
stance, in his opening address, with reference to the judgment in
HN
v MEC for Health, KwaZulu Natal
,
[2]
where Koen J set out the approach as follows,
‘
Both
parties made extensive reference during the leading of the evidence
to the hospital records which the Defendant had kept, relating
to the
Plaintiff’s confinement at the Greytown Hospital and the birth
of M. At the commencement of the trial, it had been
agreed that the
status to be assigned to these documents inter alia was that they are
what they purport to be without being proof
of the content thereof.
To the extent that there
are records, the Defendant has inter alia relied on a favourable
Apgar score which the nursing staff of
the Defendant had determined
at one minute and five minutes after M’s birth as indicative of
him having been born as a healthy
baby. The Plaintiff, on the other
hand, has relied on references in the official hospital records that
there was ‘foetal
distress’ and ‘cephalo-pelvic
disproportion’ present to support her case. The questions
arising from relate to
the admissibility and the evidentiary value to
be given to these entries appearing in these records.
Statements in the medical
records that are favourable to the Defendant are hearsay where the
author thereof has not been called
to testify, and hence not
admissible. Accordingly, the apparent high Apgar scores relied upon
by Doctor Wildenboer, namely scores
of 7 and 8 out of 10, determined
at 1 and 5 minutes respectively, remain hearsay as the author
determining and recording those
scores was not called to testify
thereto. No application was made for the admission thereof in
evidence in terms of section 3 of
the Evidence Law Amendment Act
1998, but even if there was, it would be unlikely to have succeeded
as there was no evidence that
the author thereof was no longer
available to give that evidence. These scores are in any event, in
the opinion of all four medical
experts who testified, subjective and
to that extent open to debate and unreliable. This was particularly,
as Doctor Kara testified,
that the five-minute score would be
inflated by M’s resuscitation with oxygen. Doctor Wildenboer
agreed. Thus, even if admissible
evidence, no valid conclusion can be
drawn from these scores.
Recordings favourable to
the Plaintiff’s case in establishing negligence and liability
generally, and accordingly damaging
to the Defendant’s case,
made as part of the records kept by the Defendant’s servants,
are however on a different footing.
They constitute admissions by the
servants of the Defendant made in the ordinary course of discharging
their duties, which are
binding against the Defendant. The
Defendant’s staff are obliged to make these statements by
recording the medical position
as it unfolds in the records. They
have an obligation to speak on behalf of the Defendant and dispute
what is recorded, if indeed
incorrect.’
[8]
As in
that case, no application was made for the admission of the hospital
records in terms of s 3 of the Law of Evidence Amendment
Act. I shall
return to the consequences of this, later in the judgment.
[9]
During
the trial, reference was also made to a substantial volume of
published medical and scientific journal articles and textbooks
on
relevant subjects. For reasons which will become apparent, this
material will only be referred to where strictly necessary,
and where
the material to which reference was made was adopted by the expert
concerned.
[3]
It was held, in
Menday
v Protea Assurance Co Ltd
[4]
that:
‘
Where
.. an expert relies on passages in a text book, it must be shown,
firstly, that he can by reason of his own training, affirm
(at least
in principle) the correctness of the statements in that book; and,
secondly that the work to which he refers is reliable
in the sense
that it has been written by a person of established repute or proved
experience in that field. In other words, an
expert with purely
theoretical knowledge cannot in my view support his opinion in a
special field (of which he has no personal
experience or knowledge)
by referring to passages in a work which has itself not been shown to
be authoritative… [T]he dangers
of holding the contrary are
obvious.’
[10]
Finally,
in respect of the unchallenged evidence of expert witnesses, it
remains to point out that it does not necessarily follow
that because
the opinion is unchallenged that it must be accepted. The expressed
opinion must be founded upon facts admitted or
accepted by the
parties or found by the court. And such opinions must be based upon
sound and logical reasoning. It is incumbent
upon the court to
determine whether the expressed opinion, despite being unchallenged,
is to be accepted.
[5]
The facts
[11]
The
plaintiff said that she had attended the antenatal clinic on one
occasion, when she was already six months pregnant. She testified

that she experienced no complications or illnesses during pregnancy.
The records from the antenatal clinic indicate that on examination

her blood test results were normal and she tested negative for viral
infections. The plaintiff was admitted to Saint Barnabas Hospital,
in
labour, in the early hours of the morning of 9 June 2011.
[12]
During
her testimony, the plaintiff admitted that she had presented a
different history of antenatal clinic attendance to the expert

witnesses with whom she had consulted. When asked to explain why she
had dishonestly inflated the number of antenatal attendances,
she
said that she did not want to appear to be a parent who did not care.
She explained her limited attendances on the basis that
she was
afraid of her employer and did not want to be absent from work.
Although the plaintiff did not create a favourable impression
in this
regard, little turns upon her evidence as to what occurred, in
relation to her pregnancy, prior to her admission. Her account
of her
labour and the birth of LM is, as will become apparent, also not
decisive.
[13]
The
hospital records reflect that the plaintiff was examined on admission
at 03h25 on the morning of 9 June 2011. LM was born at
09h00 by
normal vaginal delivery. At birth LM weighed 2900g and had a head
circumference of 34cm. His length was recorded as 41cm.
The experts,
including those qualified by the defendant but not called, were
agreed that the length was not accurately recorded.
No significance
was attached to this measurement.
[14]
The
maternity records indicate that the baby did not cry at birth and
that active resuscitation, which involved the use of an ‘ambu-bag’

to stimulate breathing, and oxygen was used. The plaintiff confirmed
this. She said that the baby was taken away after birth and
she later
saw him in an incubator with tubes in his nostrils. The baby was
assigned Apgar scores of 4/10 at 1 minute and 6/10 at
5 minutes. The
record indicates that he was hypotonic and that his primal reflexes
(Moro, grasp and suck) were absent. He was fed
with a nasogastric
tube. The placenta, on gross examination, was recorded as normal.
[15]
The
plea of prescription of the plaintiff’s claim may be easily
disposed of. The plaintiff explained that she had come to
institute
action against the defendant after meeting a woman at a clinic where
her son received treatment. This was in 2017. She
was referred to an
attorney who advised her. Shortly thereafter this action was
instituted. It was argued that the plaintiff had
been aware that LM
was diagnosed with cerebral palsy from shortly after his birth, and
therefore ought, reasonably, to have known
that she had a claim in
her personal capacity against the defendant. In my view, there is
nothing to gainsay the plaintiff’s
evidence as to when she
acquired knowledge of her rights. Accordingly, the plea of
prescription must fail.
The condition at birth
and cerebral palsy
[16]
Professors
Davies and Johnson and Drs Pearce and Kara concur that LM suffered
from hypoxic ischaemic encephalopathy (HIE) at birth.
They accepted
that although all the diagnostic evidence for encephalopathy, as set
out in the American College of Obstetrics and
Gynaecology (ACOG)
guidelines, was not present, LM presented with sufficient features to
conclude that he suffered from HIE. These
were the low Apgar scores,
the need for resuscitation at birth, the absence of primal reflexes
and the baby’s hypotonic state.
They considered that it was of
moderate severity. Dr Rothberg, who testified for the defendant, also
accepted that LM manifested
HIE at birth. It was therefore common
cause that LM suffered a hypoxic ischaemic insult which caused HIE,
as manifested at birth.
The question was gave rise to the HI injury
and when it occurred.
[17]
It is
apposite to highlight the fact that the experts all drew upon the
maternity records as the factual basis for their opinions.
The
plaintiff’s experts were entitled to do so, notwithstanding the
hearsay nature of the records, for the reasons articulated
in
HN
v MEC for Health, Kwazulu-Natal
.
As in that case, Dr Kara here also expressed the opinion that the
Apgar scores as recorded may well have slightly elevated because
the
baby had been resuscitated. He pointed out that the low Apgar scores
even after resuscitation indicated a condition, at birth,
worse than
suggested by the Apgar scores.
[18]
Dr
Pearce, a paediatric neurologist, consulted with LM and undertook an
assessment of the medical records and expert reports. Her
diagnosis
of LM’s medical condition was that he suffers from a mixed type
of cerebral palsy, i.e., both dyskinetic and spastic,
which is
dystonic. She described this as the most severe form of cerebral
palsy in terms of motor function and speech. She confirmed
that the
clinical picture presented by LM correlates with the brain injury as
depicted in the MRI and as described by Prof Andronikou.
[19]
Dr
Pearce also confirmed that, upon a proper assessment of the maternity
records, LM presented at birth with moderate HIE. Her opinion
was
that the HIE was because of intrapartum hypoxic ischaemia. There was
no evidence in the medical records or history to point
to an
antepartum event or occurrence giving rise to hypoxic ischaemic
insult which would explain the HIE outcome at birth. I shall
return
to this aspect of the matter later in the judgment, since the
possibility of an antepartum causal factor was raised by Dr
Rothberg,
on behalf of the defendant.
[20]
Dr
Pearce dealt with the post-natal care of LM and the fact that he was
discharged within 24 hours of birth. She considered that
the early
discharge was inappropriate given the condition of LM at birth. She
expressed the view that there was a window of opportunity
immediately
post-delivery for treatment which might have mitigated the
progression of the cerebral palsy.
The cause of the brain
injury
[21]
There
is no dispute that LM suffered a profound HI injury to the brain and
that he now presents with severe mixed cerebral palsy.
A key
question, however, was when this injury occurred and what caused it.
[22]
On 7
November 2017, a Magnetic Resonance Imaging (MRI) scan was performed
on LM. Prof Andronikou testified to the interpretation
of the MRI. He
concluded that the MRI displays features of ‘a global insult to
the brain due to hypoxic ischaemic injury
of an acute profound nature
at term.’ There was no dispute about the nature of the injury
pattern. Joint minutes concluded
between Prof Andronikou and both
radiologists qualified by the defendant reflect this concurrence.
[23]
In his
testimony, however, Prof Andronikou provided an explanation for the
description of the nature of the injury and the mechanism
by which
such injury occurs. He said that at the time that he prepared his
report, in 2017, he used terminology which was descriptive
of the
mechanism rather than the injury pattern. This explained his use of
the phrase ‘acute profound’ which might
be contrasted
with the term ‘partial prolonged.’  The MRI images
indicate an injury pattern to a region of the
brain. In this case the
injury is to the basal ganglia thalamus region, i.e., the core or
central grey matter of the brain. Such
injury typically occurs when
there is a global insult which completely shuts off oxygenated blood
to the brain. He stated that
the use of the term ‘acute
profound’ had in fact been misunderstood to refer only to a
sudden and unpredictable event
causing the occlusion of blood supply
to the brain. He explained that the injury pattern was not always
associated with what are
termed sentinel events. In the light of this
he would not now describe the injury as indicating an acute profound
pattern. He would
merely describe the injury pattern as being a basal
ganglia thalamus (BGT) or central core injury.
[24]
He
said the following:
‘
So,
in the past, the words partial prolonged do not describe what you are
seeing in the brain. What you are seeing in the brain
in partial
prolonged, is a watershed. It is an injury between the main vascular
territories. When we used to talk about acute profound,
we are
talking bout whether the injury has affected the [deep] nuclei, the
areas of the brain that have got such a high energy
demand at that
period of your life. And but we were describing or what we knew from
the literature and the time and going, well,
that pattern happens
when the injury is of a short duration and very severe.
I
am glad you called me to court so I can go with the words acute, I
mean many hours. Hours, many hours. With the word prolonged
I mean
like 24 hours, much longer.’
[25]
Prof
Andronikou’s reinterpretation of the word ‘acute’
to suggest an occurrence that is not sudden or takes place
over a
short duration, must be seen against the backdrop of his consistent
assertion that the BGT injury pattern occurs when the
oxygen supply
is completely or near completely shut off. He did not suggest that
the word ‘acute’ is now uniformly
taken by radiologists
to mean something other than a sudden insult of short duration. Prof
Andronikou accepted that the imaging
indicates some measure of damage
in the perirolandic and corticospinal region. This was recorded in a
joint minute concluded with
Dr Swartzberg, a radiologist qualified by
the defendant. Prof Andronikou, however, said the following:
‘…
so,
both of us definitely say that it is acute profound. And then he has
been, he mentions in his report that he thinks there is
a watershed
injury, and I am not completely agreed with this. What I have done is
I cannot disprove considering that there is an
injury involved in the
surface of the brain, the cortex, and that the perirolandic region
which normally fits with the deep nuclei
pattern, is also within the
watershed zone. I have conceded that it is, there is a potential of a
possibility, that there is an
additional watershed injury. But in
fact, without other watershed injuries, that is unlikely. But I
concede that there is, I cannot
exclude the watershed injury as of
course for perirolandic involvement. But basically, we both agreed on
the acute profound components,
and he has suggested a watershed
injury as well, which is a partial prolonged component and I have
excluded that I cannot exclude
that.’
[26]
Dr
Swartzberg did not testify. His analysis of the MRI imaging is not
before the court and not explained. The concession, made on
the basis
that it is not possible to exclude the additional injury features, is
not, as the passage above indicates, a positive
assertion of a
fact-based opinion. On the contrary, Prof Andronikou highlighted the
improbability of such additional injury given
the absence of other,
expected, watershed injuries. I shall return briefly to the effect of
this evidence hereunder.
[27]
Dr
Kara testified about the cause or causes of the HI injury and whether
the injury arose, intrapartum. He examined LM and diagnosed
him as
suffering from dyskinetic cerebral palsy on a gross motor function
scale of 5, which accords with the diagnosis of Dr Pearce.
Regarding
the timing of the HI injury, Dr Kara’s opinion was that it
occurred intrapartum. In support of this conclusion,
he stated that
the only known antepartum factor was the birth of the plaintiff’s
first child by caesarean section because
of preeclampsia. The
measurements of LM taken at birth, particularly his normal weight and
head size, do not point to any growth
restriction in utero.
[28]
Dr
Kara stated that there is nothing to suggest that intrauterine
infection or maternal chorioamnionitis, played any role in the

development of the cerebral palsy. The presentation of HIE at birth
suggests an HI injury having occurred intrapartum. He said
that the
MRI scan establishes that the injury occurred at term. This excludes
an early antenatal injury, i.e., prior to 35 weeks
gestation. The
fact that the baby required resuscitation at birth; was hypotonic,
unable to feed and the absence of reflexes all
point, on the
probabilities to an intrapartum insult. Dr Kara referred to a study
by
Rennie
et
al
[6]
which
suggested that 80% of cases resulting in dyskinetic cerebral palsy
are because of intrapartum hypoxic ischaemia. This probability
is
supported by the 2014 Revision of the ACOG criteria.
[29]
Dr
Kara’s opinion was supported by Prof Davies and Prof Anthony.
Dr Rothberg expressed the view that a pathway to cerebral
palsy that
involved antepartum factors could not be excluded. It was accepted by
all the expert witnesses that there was, in this
case, no evidence to
suggest the occurrence of a sentinel event, such as maternal
haemorrhaging, placental abruption, prolapse
or occlusion of the
umbilical cord or some other unexpected and catastrophic event during
labour or birth. A joint minute between
Prof Davies and Dr Rothberg
was presented in evidence. The minute records the following points of
agreement:
(a)
That
LM suffers from permanent brain damage in the form of a mixed
cerebral palsy with severe impairment because of a hypoxic ischaemic

brain injury.
(b)
That
the MRI is in keeping with a hypoxic ischaemic brain injury.
(c)
That
the neonatal encephalopathy presented at birth was most probably due
to hypoxic ischaemia.
(d)
That
the recorded growth parameters are appropriate for gestational age.
(e)
That
chronic hypertension, intrauterine congenital factors or genetic or
other syndromes can be excluded as possible causes of the
pathology;
and
(f)
That
the monitoring of the plaintiff during labour was not according to
the published VBAC (vaginal birth after caesarean section)

guidelines.
[30]
It was
Prof Davies’ evidence that the HI injury occurred intrapartum.
He stated that the intrapartum period poses the greatest
risk to the
foetus. The BGT injury pattern is not only associated with what is
described as an acute or sudden and profound hypoxic
ischaemic event.
It can also be observed where the hypoxic ischaemia is partial and
occurs over a period. He referred, in this
regard, to the results of
a study conducted by
Smith
et
al
[7]
in support of his opinion.
I shall touch upon this study hereunder.
[31]
Both
Prof Davies and Anthony described the mechanisms of hypoxic ischaemic
injury as follows: a decrease in the level of oxygen
in blood
supplied to tissue gives rise to a neurological response in the
foetal brain. Oxygenated blood is shunted away from less
vital or
critical, peripheral areas of the brain to the deeper tissues and
core centres of the brain. This is an autonomic response
which serves
to protect those core structures from damage. Brain tissue in the
peripheral and surface areas may suffer damage because
of the absence
of an oxygenated blood supply. The compensatory shunting of blood to
protect core tissue can result in damage observed
in the ‘watershed’
areas, i.e., at the furthest extremities of blood vessels. It is in
this context that reference
was made to ‘partial prolonged’
insults where the blood supply is constrained in successive events
over a period. In
such instances the damage is seen on an MRI in the
peripheral areas. In the case of a sudden ‘profound’
event, where
little or no oxygenated blood is available the damage
occurs in the basal ganglia-thalamic region since it is, in the
foetus, the
most metabolically active region of the brain.
[32]
This
description accords with that provided by Prof Andronikou. The
Smith
study,
to which both Prof Andronikou and Anthony were contributing authors,
involved a retrospective analysis of 10 medico-legal
cases of
neonatal encephalopathy-cerebral palsy survivors who sustained
intrapartum hypoxic ischaemic basal ganglia-thalamic pattern
injury
in the absence of a sentinel event. The results of the study suggest
that a BGT pattern injury may occur in the absence
of a sentinel
event where there is evidence of foetal distress or a non-reassuring
foetal heart rate in the form of abnormal cardiotocography
(CTG)
readings during labour.
[33]
The
assertion made by
Smith
et al
,
is that the term ‘acute profound’ has come to be
associated with obstetric events which occur in the period
immediately
prior to birth and which result in a BGT injury pattern.
Such description of the pattern as ‘acute profound’
should
be avoided in radiological descriptions, the article suggests,
since a BGT pattern may arise from sub-acute insults over a prolonged

period.
[34]
The
association of the term ‘acute profound’ with sudden
short duration events, no doubt arises from the plain meaning
of the
words themselves and the descriptions of events as presented in
evidence before the courts. This can be gleaned from several

judgments dealing with cases such as the present. In
AN
obo EN v MEC for Health, Eastern Cape
[8]
,
Gorven AJA (as he then was) said:
‘
An
acute profound hypoxic ischaemic event, such as in the present case,
must be distinguished from a partial prolonged hypoxic ischaemic

event. An acute profound event means a sudden, not progressive,
event. A partial prolonged event causes damage to the white matter,

or peripheral structures, of the brain.’
[35]
This
was based upon acceptance of the evidence of Prof Van Toorn (another
contributing author to the
Smith
paper),
as stated by the learned judge;
[9]
‘
The
mechanisms giving rise to these two types of brain damage are
uncontroversial. Professor Van Toorn, Head of Paediatric Neurology
at
Tygerberg Childrens’ Hospital and Stellenbosch University, was
called by the appellant. He gave clear and uncontroverted
evidence on
this issue. During labour, the blood to the brain is supplied from
the placenta along the umbilical cord (the cord).
If there is an
inadequate supply of oxygen, the brain shunts the limited blood from
the peripheries to the deep grey matter. This
is designed to protect
the deep grey matter which is the most vulnerable matter due to its
higher metabolic rate. When shunting
takes place, damage occurs to
the white matter of the brain. This means that if there is some blood
supply, but it is inadequate,
damage occurs to the white matter. If
there is no blood supply at all, none is available to shunt to the
deep grey matter. In that
instance, only the grey matter will be
damaged. The MRI scan shows only damage to the grey matter in the
present case. No damage
to white matter was evident.’
[36]
The
evidence in that matter established that there had been compression
of the cord and that it had constituted a sentinel event
which was
not predictable nor possible to detect timeously by way of foetal
monitoring. The apparent concern of the
Smith
article
with the radiological description employed does not alter the fact
that a particular injury pattern arises from each of
the mechanisms
by which such injury occurs. In each case the injury pattern as
established on MRI will provide insight into the
mechanism by which
it occurred. Prof Davies and Prof Anthony confirmed this.
[37]
Prof
Andronikou’s suggestion that ‘acute’ may also
relate to events that take many hours, does not accord with
the
description of the pathogenesis of injury given by Prof Davies and
Anthony. The pattern of brain injury noted by Prof Andronikou
did not
include features of injury caused by partial and prolonged hypoxic
insult, or as suggested by Prof Anthony with reference
to the
Smith
study,
a series of sub-acute hypoxic insults over a period.
[38]
Prof
Anthony said that even in the absence of a sentinel event, a BGT
injury pattern could occur because of repeated and prolonged

sub-acute ischaemic events which overwhelm the foetus’ capacity
to compensate for the hypoxia. He described the process as
the straw
that breaks the camel’s back. There was, however, no
radiological evidence to suggest partial restriction of blood
flow to
the foetal brain on multiple occasions during the plaintiff’s
labour. There was no evidence to suggest multiple occlusions
of blood
flow to the foetal brain during labour. What remains in the evidence,
is that the brain injury arose because of a global
insult which shut
off the supply of oxygenated blood to the foetal brain completely or
almost completely, for a sufficient duration
to give rise to the BGT
pattern injury.
[39]
Dr
Rothberg, as indicated, postulated the possibility of an antepartum
component to the HIE presented at birth. He accepted that
LM suffers
from a mixed cerebral palsy following neonatal encephalopathy. This,
he suggested is associated with late antepartum
or intrapartum
hypoxic-ischaemic insult. He referenced an article published by
Bhorat
et al
[10]
which
contends that causation of cerebral palsy should not simply be based
upon an intrapartum perspective with radiological confirmation.
Dr
Rothberg’s opinion regarding a possible antepartum hypoxic
ischaemic event was, however, not based upon any facts. There
is no
evidence to support a finding that it is probable that the birth
outcome arose because of some antepartum event. Dr Rothberg
also
suggested that there is a growing awareness that placental
malfunction or pathology plays a role in the development of HIE
and
resultant cerebral palsy. In this case, the gross examination of the
placenta indicated that there was no abnormality. The
placenta was
not sent for histology. The fact that there may be a body of
scientific opinion which favours histological investigation
of
placental function to determine its role in HIE-cerebral palsy
outcomes, does not assist the defendant. There is no evidence
to
suggest that placental function was relevant. It is, in my view, not
for the plaintiff to prove that the birth outcome was not
the result
of placental malfunction where there is no indication that the
placenta was not normal.
[40]
I am
satisfied that the evidence established that LM suffered a profound
global hypoxic ischaemic insult, intrapartum, which shut
off
oxygenated blood flow to the foetal brain completely or almost
completely, causing the BGT pattern injury. It is not possible
on the
evidence to determine when the insult causing injury occurred. Nor,
in the absence of a defined or recognised sentinel event,
why the
insult occurred.
The management of
plaintiff’s labour
[41]
I turn
now to the second issue, namely whether the medical staff at the
hospital were negligent in the management of the plaintiff’s

labour and whether such negligence caused, or materially contributed
to the injury suffered by the baby.
[42]
Prof
Anthony expressed the view that the maternity records reflected a
clear failure to monitor the plaintiff’s progress of
labour in
accordance with the published guidelines for vaginal birth after
caesarean section (VBAC). In this case the plaintiff’s
prior
history presented as a risk factor which necessitated careful
monitoring of the foetus’ condition during labour. The

monitoring, he said, was substandard. Prof Anthony’s view was
supported by all the expert witnesses, including Dr Rothberg.
[43]
I
accept that the failure to employ a CTG or to auscultate the foetal
heart rate and record the results in accordance with the VBAC

guidelines, constitutes a breach of the duty of care owed by the
medical staff to the plaintiff and her unborn foetus. It was known

that the plaintiff’s prior caesarean section and preeclampsia
presented elevated risk during labour. The failure to ensure
proper
and effective monitoring of the foetal condition during labour
created a risk that the medical personnel would not be able
to act
with reasonable expedition as required to prevent injury to the
plaintiff or foetus.
[44]
The
defendant presented no evidence to gainsay the inference of
inadequate monitoring to be drawn from the maternity records. Prof

Anthony suggested that the failure to monitor the foetal heart rate
appropriately caused the baby to suffer the HIE with ensuing
cerebral
palsy outcome. He described the foetal response to successive partial
hypoxic events. At each event variations in the
heart rate would
occur. These would be detectable as accelerations and decelerations
measurable in relation to the contractions
of the uterus during
labour. Where the foetal heart is compromised in its ability to
normalise after a contraction or a hypoxic
ischaemic event,
bradycardia, a deceleration of the heart rate when compared to the
base heart rate, would be evident. This would
indicate hypoxic foetal
distress. Since the process of labour necessarily places the foetus
in some hypoxic distress, effective
and careful monitoring of the
foetal heart rate during labour is required. The monitoring, by CTG
or by auscultation, would enable
foetal distress to be detected so
that appropriate interventions may be made to protect the mother and
foetus.
[45]
In
this instance, he said that the effect of the inadequate monitoring
of the foetal heart rate was that foetal distress was not
detected
and the medical staff were not able to act to mitigate foetal
distress or expedite the delivery of the baby. It was this
failure
which, in the opinion of Prof Anthony, caused LM to suffer the HI
injury which manifested as HIE at birth and resultant
mixed cerebral
palsy.
[46]
Dr
Rothberg, while accepting that the monitoring was sub-standard, did
not support the conclusion that the failure to monitor properly,

caused the baby to suffer a brain injury which it otherwise would not
have suffered. He placed considerable reliance upon entries
on the
partogram contained in the maternity records. The entries involve 12
foetal heart rates recorded between admission and the
delivery of the
baby. These entries were all ‘normal’ or fell within a
‘normal range’ for the foetus.
[47]
Dr
Rothberg relied upon these recorded heart rates to support two
propositions. The first was that the recordings indicated normal

heart rates throughout the labour. There was, therefore, no
indication of any abnormality or foetal distress. The record
therefore
does not support the proposition that there was a
non-reassuring foetal condition during labour evidencing hypoxic
ischaemia which
might explain the outcome. The second, concerned the
proposition that proper foetal heart rate monitoring would have
placed the
staff in a position to prevent the injury suffered by the
foetus. He said that the fact that the recorded heart rates were
single
rates, rather than rates recorded both before and after
contractions, was inconsequential. He stated that it was highly
improbable
that the heart rates that were recorded, were recorded at
a time when there was no sign of distress or bradycardia, which on
Prof
Anthony’s testimony would have been present. This suggests
that the monitoring would not have had any impact upon the result.
[48]
The
difficulty with this evidence is that it relied upon entries in the
maternity record which were not proved. The person who made
the
entries and who took the heart rates did not testify. The record of
heart rates, upon which the defendant relied was hearsay
evidence.
The consequence is that there is no admissible evidence to support
the propositions advanced by Dr Rothberg. Dr Kara’s
view was
that the rates were of little value in determining the condition of
the foetus during labour since they are only single
rates taken at
the indicated times.
[49]
Dr
Rothberg’s further evidence was that CTG monitoring is, in any
event, an imperfect tool for determining the condition of
a foetus
during labour and there is no evidence to suggest that foetal heart
rate monitoring necessarily reduces the probability
of HIE and
cerebral palsy. It is, in my view, unnecessary to engage in the
debate about the efficacy or otherwise of CTG and foetal
heart rate
monitoring. The determination of causation in relation to a negligent
act or omission is a matter which falls to the
court, having regard
to the facts established before it.
[50]
Prof
Anthony explained his reasoning with reference to an analogy of a
child standing alongside a busy road. No one is watching
the child,
who runs into the road and is struck by a car. If the child is found
lying in the middle of the road with traumatic
injuries, it is
reasonable to infer that he was struck by a car. It is also
reasonable to infer that the outcome occurred because
no-one was
watching. If someone was watching the outcome could have been
prevented by appropriate intervention.
[51]
The
analogy, in my view, was flawed. It does not contain sufficient
fact-based premises to allow the final inference to be drawn.
To find
that the failure to properly monitor the foetal heart rate and
condition during labour caused, in the sense that it materially

contributed to, the brain injury, would require additional facts to
be inferred since there is no evidence to establish the existence
of
those necessary facts. It would need to be inferred that the
monitoring would have indicated that the foetal heart rate was

abnormal, and that the foetus was in distress. It would need to be
inferred that the indication of foetal distress would occurred
at a
time when successful intervention could have taken place.
[52]
Regarding
the first requirement, namely that the monitoring would have
indicated foetal distress, the only evidence to support this
was that
which described the mechanism of a partial prolonged hypoxic
ischaemic insult. In such instances, abnormal foetal heart
rates are
likely to occur. But the evidence does not point to such mechanism of
injury. Even if it was accepted that there would
at some stage have
been an indication of foetal distress, there is no basis to determine
when that might have occurred, given the
acute profound mechanism of
injury, nor whether the intervention would have averted the injury.
[53]
In
AN
obo EN v MEC for Health, Kwazulu-Natal
Molemela
JA
[11]
usefully set out the
approach to establishing causal negligence, as follows:
‘
In
Minister
of Safety and Security v Van Duivenboden
,
this court stressed that a plaintiff is not required to establish the
causal link with certainty, but only to establish that the
wrongful
conduct was probably a cause of the loss, which calls for a sensible
retrospective analysis of what would probably have
occurred, based
upon the evidence and what can be expected to occur in the ordinary
course of human experience. In
Minister
of Finance & others v Gore NO
this
court aptly held that the application of the ‘but-for’
test is not based on mathematics, pure science, or philosophy.

Rather, it is a matter of common sense, based on the practical way in
which the ordinary person’s mind works against the
background
of everyday life experiences. The flexible approach reflected in the
above judgments was adopted by the Constitutional
Court in
Lee
.
The issue of causation
recently received attention in the case of
Mashongwa v PRASA
.
In
Mashongwa,
the Constitutional Court pointed out that
Lee
never sought to replace the pre-existing approach to factual
causation, rather, it adopted an approach to causation premised on
the flexibility that has always been recognised in the traditional
approach as reflected in the authorities referred to above. In

re-stating the ‘but-for’ test in
Mashongwa,
the
Constitutional Court settled the law on this aspect. It pointed out
that the imputation of liability to the wrongdoer depends
on whether
the harmful conduct is either too remotely or sufficiently closely
connected to the harm caused. It emphasised that
where the
traditional but-for test is adequate to establish a causal link, it
may not be necessary to resort to the
Lee
test.’
(Footnotes omitted)
[54]
In my
view, the application of the traditional ‘but-for’ test
is adequate in this case. The extended inferential reasoning
set out
above is not supported by the evidence. It comes close to reasoning
from the result to the cause. I am accordingly unable
to find that
‘but-for’ the failure to monitor the foetal heart rate,
the injury would not have occurred.
[55]
It
follows therefore that I am unable to find that the plaintiff has
established that the defendant is liable for the loss suffered.

Regarding costs, I am not prepared to impose the usual costs order. I
come to this conclusion on the basis that the circumstances
of the
matter are tragic. LM suffered a catastrophic injury during birth,
the consequences of which are stark. This case is yet
another matter
in which evidence of systemic failure and neglect has emerged about
the care and treatment provided in a public
health facility under the
control of the defendant. Our courts have lamented this situation on
several occasions. In
AN
obo EN v MEC for Health, Kwazulu-Natal
[12]
,
Gorven JA said,
‘
Far
too often this court is confronted with serious and serial negligence
in hospitals falling under the respondent. Whether or
not the
negligence can be said to have caused harm in the delictual sense, it
is clear that studied neglect of standards has become
pervasive in
many such hospitals. Those reliant upon their services are receiving
substandard care.’
[56]
In
this case, as in that matter, the medical staff were found to be
negligent, although it could not be found that the negligence
caused
the harm suffered. The ongoing and persistent failure to ensure that
persons who are dependent upon public health facilities
in the
province, receive proper care and treatment deserves censure. For
this reason, I would deprive the defendant of the costs
which would
ordinarily follow the result.
[57]
In the
result, the plaintiff’s claims are dismissed.
G. GOOSEN
JUDGE OF THE HIGH
COURT
Dates
heard: 25, 26, 28 & 29 April 2022
5,
6, 7 & 14 December 2022
Date
delivered: 25 April 2023
Appearances:
For
the Plaintiff
C
McKelvey
Instructed
by
Enzo
Meyers Attorneys
121
Devereux Avenue
Vincent
East
London
For
the Defendant
B Dyke
SC / N James
Instructed
by
Norton
Rose Fulbright South Africa
Sutton
Square
c/o
Smith Tabata Attorneys
Queens
Road
King
Williams Town
[1]
In a
pre-trial checklist submitted in accordance with case management
requirements and to facilitate determination of set-down
for trial,
the issues for determination are framed as follows:
‘
Whether
the defendant’s employees were negligent in the management of
the plaintiff’s labour and whether there was
any causal
relationship between such [negligent] management and the minor
child’s condition.’
[2]
HN
v MEC for Health, KwaZulu Natal
[2018]
ZAKZPHC 8 (4 April 2018) at para 6 – 7.
[3]
See
S
v Collop
1981
(1) SA 150
(A);
S
v Harris
1965
(2) SA 340
(A) at 344C-D.
[4]
Menday
v Protea Assurance Co Ltd
1976
(1) SA 656
(E) at 569H.
[5]
Michael
& another v Linksfield Park Clinic (Pty) Ltd & another
2001
(3) SA 1188
(SCA);
[2002] 1 All SA 384
;
[2001] ZASCA 12
para 36 –
37.
Buthelezi
v Ndaba
2013
(5) SA 437
(SCA);
[2013] ZASCA 72
para 1.
[6]
Rennie
JM, Hagmann CF, Robertson NJ.
Outcome
after Intrapartum Hypoxic Ischaemia at Term
,
Semin Fetal Neonatal Medicine, 2007 Oct; 12(5):397-407 Epub 2007 Sep
7.
[7]
Smith
J, Solomons R, Vollmer L, Langenegger EJ, Lotz JW, Andronikou S,
Anthony J.
Intrapartum
Basal Ganglia-Thalamic Pattern Injury and Radiologically Termed
‘Acute Profound Hypoxic Ischemic Brain Injury’
Are Not
Synonymous
American
Journal of Perinatology (Am J Perinatol), 4 Nov 2020.
[8]
AN
obo EN v MEC for Health, Eastern Cape
(585/2018)
[2019] ZASCA 102
(15 August 2019) par 13. See
M
v MEC for Health, Eastern Cape
(699/17)
[2018] ZASCA 141
(1 October 2018) at par 58 -60;
The
Member of the Executive Council for Health, Eastern Cape v DL obo AL
(Case
no 117/2020)
[2021] ZASCA 68
(03 June 2021) par 21.
[9]
Ibid
par 14.
[10]
Bhorat
et al, S Afr Med J 2021; 111 (Suppl 1): 280-288.
[11]
Fn 8
above para 48 – 49.
[12]
Fn 8
above par 28.