THE SUPREME COURT OF APPEAL OF SOUTH AFRICA
JUDGMENT
Not Reportable
Case No: 272/2022
In the matter between:
MEMBER OF THE EXECUTIVE
COUNCIL OF HEALTH AND SOCIAL
DEVELOPMENT, GAUTENG
PROVINCIAL GOVERNMENT APPELLANT
and
F B M
(obo L P M) RESPONDENT
Neutral Citation: MEC of Health and Social Development of the Gauteng
Provincial Government v M (272/2022) [2024] ZASCA 21
(05 March 2024)
Coram: DAMBUZA AP and SALDULKER, NICHOLLS, MABINDLA-
BOQWANA and GOOSEN JJA
Heard: 07 March 2023
Delivered: 05 March 2024
2
Summary: Delict – claim for medical negligence damages – minor born with
brain injury sustained during birth – whether hospital staff were negligent – if so,
whether such negligence caused the brain injury – evidence did not establish that
the hospital staff were negligent.
3
_______________________________________________________________
ORDER
________________________________________________________________
On appeal from: Gauteng Division of the High Court, Johannesburg (Wilson
AJ, with Weiner and Mudau JJ concurring) sitting as a court of appeal:
1. The appeal is upheld with costs, including the costs of two counsel where
so employed.
2. The order of the full court is set aside and substituted with the following:
‘The appeal is dismissed with costs, including the costs of two counsel
where so employed.’
________________________________________________________________
JUDGMENT
________________________________________________________________
Dambuza AP and Nicholls JA (Saldulker, Mabindla-Boqwana, and Goosen
JJA concurring):
[1] This appeal is against an order of the full court of the Gauteng Division of
the High Court , Johannesburg (Wilson AJ, with Weiner and Mudau JJ
concurring). That court overturned a judgment of the trial court of the same
division (Molahlehi J) which held that the appellant, the Member of Executive
Council for Health and Social Welfare for the Gauteng P rovincial Government
(MEC)1, was liable for damages suffered by the respondent, Ms M’s child, L, as
a result of a brain injury which it found to have been sustained during L’s birth.
1 In April 2012 this Department was split into - a separate provincial department of health and a department of
social development. However, in this judgment we continue t o refer to the parties as they we re in the pleadings,
the trial court, and the full court.
4
[2] The primary questions in this appeal are whether the medical staff at
Tshwane District Hospital were negligent in the care and treatment of Ms M, the
mother of L , and whether such negligence caused the consequent medical
condition from which L presently suffers . This appeal is with the leave of this
Court.
[3] L was born at Tshwane District Hospital on 18 May 2010. His mother, Ms
M arrived at the hospital in the early hours of the morning of that day as an
‘unbooked’ patient, with no ante-natal records. She was admitted at 01h45 in the
latent stage of labour , with ruptured membranes. L was born at 15h10, on the
same day, by natural delivery, with Apgar score s of 1 at one minute, 7 at five
minutes (assisted through resuscitation ), and 8 at ten minutes (assisted through
resuscitation). At birth he was flaccid , acidotic and had to be placed on a
ventilator.
[4] On 15 January 2014 Ms M instituted an action in the Gauteng Division of
the High Court , claiming damages against the M EC for medical negligence on
the part of the hospital ’s staff. In the summons she alleged that L suffered a
hypoxic-ischaemic encephalopathy (HIE or brain injury)2 during birth as a result
of negligence by the hospital staff . This resulted in L suffering cerebral palsy
which continues to afflict him, she alleged.
[5] She pleaded various acts of negligence on the part of the hospital staff . In
the main, her case was that her labour was unduly prolonged and that the hospital
medical staff failed to take a decision at 13h10 to deliver the baby by caesarean
section. The contention was that L suffered the brain injury due to perinatal
2 A type of brain dysfunction (brain injury) that occurs when the brain experiences a decrease in oxygen or blood
flow. It can occur before, during labour and delivery or after birth. https://www.massgeneral.org as of 4 February
2024.
5
asphyxia3 which caused him to sustain severe brain damage, resulting in cerebral
palsy (CP), mental retardation and epilepsy.
[6] The MEC denied liability , pleading that there was no negligence on the
part of the hospital staff. He pleaded that any duty of care owed to Ms M and the
baby she was carrying was circumscribed by, and subject to the reasonable
financial, human, and other resources available to the Department of Health to
equip staff and maintain the hospital. It was asserted that the hospital rendered
the best service it could to Ms M. However, in the event of the court finding that
the monitoring of the foetus was insufficient, such deficiency was not causally
connected to the cerebral palsy suffered by L.
[7] It was common ground that on her admission in the ear ly hours of the
morning, Ms M was connected to a cardiotocography (CTG) machine.4 At first,
the CTG tracings (partogram) were ‘non-reassuring’. This was resolved by
application of Ringers Lactate.5 The CTG machine was allowed to run for another
30 minutes and was described as ‘re -assuring with good variability’. Ms M was
then monitored with a Doppler at 4h00, 6h00, 8h00 and 10h00. Over this period
the foetal heart rate was recorded as being between 142 and 147 beats per minute,
3 ‘Perinatal asphyxia or birth asphyxia, results from an inadequate intake of oxygen by the baby during the birth
process – before, during or just after birth. Decreased oxygen intake can result in chemical changes in the baby’s
body that include hypoxemia, or low levels of oxy gen in the blood, and acidosis, in which too much acid builds
up in the blood.’ https://www.hopkinsmedicine.org as of 4 February 2024.
4 The CTG is a machine used to monitor the heartbeat of a foetus and the mother’s contractions during labour. It
generates a printout on which traces depicting the baby’s heartbeat over time are recorded. The three indicators to
look out for when reading CTG tracings are: first, the rate of the foetal heartbeat, second, the baseline variability,
and third decelerations in the heartbeat. A foetal heartbeat of between 110 -160 beats per minute (bpm) is
considered normal. Baseline variability refers to the extent of variation between one heartbeat and the next. When
the heart rate deviates from the normal baseline variability this can be a sign that the foetus has initiated defence
mechanisms as a result of decreased levels of oxygen. The presence of variability suggests that the nervous system
of the foetus is still undamaged. Dece leration occurs when the heart rate is reduced to less than 15 beats per
minute. This may signal that the foetus is becoming hypoxic, or it may indicate something less sinister.
5 This is a ‘type of isotonic, crystalloid fluid further classified as balance d or buffered solution used for fluid
replacement. The content of Ringer’s Lactate include s sodium, chloride, potassium, calcium and lactate in the
form of sodium mixed into a solution with an osmonality of 273 mOsm/L and pH of about 6.5. See
https://ncbi.nlm.nih.gov, (the National Library of Medicine of the United States of America ) as of 28 February
2024.
6
thus falling within the normal range of 110 -160 beats per minute. The next CTG
assessment was performed at 06h24. The partogram was again described as ‘re-
assuring’. A handwritten note by the senior midwife Sister Motshwene recorded
that the CTG assessment should be repeated after one hour. This was not done.
[8] Ms M went into the first stage of active labour at 7h30. Sometime thereafter
she was seen by a doctor 6 who referred to a ‘reassuring’ partogram . At 11 h30,
after a further foetal heart rate assessment, she was transferred to the labour ward.
The foetal heart rate was again assessed with a Doppler a t 12h00, 12h30 and
13h00. The next CTG assessment commenced at 12 h40 and the machine ran
continuously until approximately 15h00. A note at 13h30 recorded that the foetal
heart rate was 1607 beats per minute with slight decelerations. A further written
note was made to ‘report CTG to Sr Motshwene’. Foetal distress was diagnosed
at 14h30 and Ms M was prepared for a caesarean section. However, she became
fully dilated at 14 h45, after being wheeled into theatre, and she delivered L
naturally at 15h10.
[9] Ms M’s case was, in the main, constructed around two aspects of her baby’s
birth. First, she contended that the CTG partogram showed that a decision should
have been taken at 13h10 on the day of L’s birth, to have her deliver the baby by
caesarean section. Aligned to this , was the contention that L’s foetal heart rate
should have been monitored by a CTG machine for the whole period that she was
at the hospital, or that Ms M should have been put back on the CTG machine at
some stage before 12h40. Had that be en done , irregularities in L’s heartbeat
would have been observed sooner, and the decision to perform a caesarean section
would have been taken prior to brain injury occurring.
6 The evidence was that the clinic did not employ specialist doctors but only general practitioners.
7 The actual note referred to 60 beats per minute but it is accepted that this was an error and it should have been
160 beats per minute.
7
[10] This contention was based on the evidence given by Ms M’s obstetrician,
Dr Murray, that if the CTG had been repeated prior to 12h40, an abnormal pattern
would have been diagnosed earlier, and a plan made for a caesareansection to be
performed before the foetus became acidotic. According to her, from 12h40 the
traces depicted a pathological foetus, even though there was normal variability.
From that time two atypical decelerations, and a baseline foetal heart rate of 160
bpm were pre sent on the partogram . When these features persisted for the 30
minutes ending at 13h10, the foetus became pathological. The decision to perform
an emergency c aesarean-section should have been taken at that time , and the
failure by the hospital staff to do so was sub-standard medical care, she opined.
[11] The second aspect on which Ms M relied was the contents of joint minutes
prepared by medical experts, including radiologists Dr A Weinstein and Prof.
Savvas Andronikou. The Magnetic Resonance Imaging (MRI) scan on which the
radiologists based their opinion was done when L was 4 years and 5 months old.
The radiologists agreed that the MRI demonstrated features in keeping with acute
profound hypoxic ischemic injury . They also agreed that because the findings
were isolated, they required clinical correlation. In their minute they recorded that
they had observed a bilateral ‘T2/flair’ 8 hyperintensity of the child’s putamina,9
these being features of an acute profound hypoxic ischaemic injury. They agreed
that the MRI scan demonstrated an ‘acute profound HII [Hypoxic Ischaemic
Injury] that occurred in a term brain at 37 weeks or [older] probably in the
perinatal time period . . . ’. They also agreed that the involvement of the basal
ganglia in a HII, in general, indicates an acute profound event. In addition, they
8 This stands for ‘T2-weighted Fluid-Attenuated Inversion Recovery’, an area of high intensity on types of MRI
scans of the brain of a human reflecting lesions produced largely by damaging of the myelin sheath surrounding
neurons and axonal loss.
9 A paired structure that is part of the nuclei that form the basal ganglia – which is responsible for motor control
and other functions of the brain.
8
agreed that the injury to L’s brain was limited to the putamina and that the other
deep grey structures as well as the hippocampi,10 the Peri-Rolandic11 regions and
cerebellar vermis had been spared. They stated that the neurological outcome
should be assessed clinically , by obstetricians, for determination of a more
accurate time and cause of injury.
[12] Dr Andronikou, the radiologist who testified for Ms M, was of the opinion
that if the baby’s heart had been monitored 24 hours a day by CTG, it might have
been possible to pinpoint when the sentinel event occurred by observing the
deteriorating foetal heart rate on the CTG. He persisted in the view that the assault
on L’s brain was acute profound, and likely to have been caused by hypoxia. The
MRI imaging, he said , indicated that something severe had happened to the
foetus, although it did not show the period when the injury occurred.
[13] Paediatric neurologists Drs D Pearce (for Ms M) and J Rademeyer (for the
MEC) also prepared a joint minute intended ‘to assist the court in respect of
causation/origin of the timing of [L’s] diagnosis and neurological disability’.
They did a neurological examination on L on 13 April 2017 and 8 A ugust 2017
respectively, and also considered the joint minute prepared by the r adiologists.
They agreed that L suffered from ‘mixed cerebral palsy (predominantly
dystonic12) with a superimposed right hemiplegia and gross motor functional
classification scale 1V [which were ] indicative [of the fact ] that L’s physical
impairments severely restricted his movements’.
[14] The neurologists agreed that a diagnosis of early onset of HIE II (neonatal
encephalopathy) could be made based on the history and the limited clinical
10 Complex brain structure embedded deep into the temporal lobe. https://www.ncbi.nim.nih.gov > pmc
11 Central lobe of the brain. . https://www.ncbi.nim.nih.gov > pmc
12 Involuntary muscle twitch.
9
records available. Whilst they agreed that foetal distress was evident in L more
than 12 hours prior to delivery, they also resolved to defer to the obstetricians the
question of appropriate management of that observation. They could not agree on
whether there could be other causes for the cerebral palsy other than the HIE. Dr
Pearce opined that because the MRI findings were not consistent with infection,
congenital brain abnormalities, genetic and metabolic disorders, or cranial
haemorrhage, the most probable cause of the injury to L’s brain was intrapartum
or peripartum hypoxia.
[15] Dr Rademeyer’s opinion was that the mild involvement of basal ganglia
observed was not consistent with a severe hypoxic event. She maintained that
there was no evidence that other causes of HIE had been investigated and insisted
that the MRI findings were not in keeping with peripartum13 hypoxia. However,
she agreed in the joint minute that a diagnosis of HIE could be made from records
showing partially compensated metabolic acidosis in L’s blood that was taken
more than an hour after delivery. She was also satisfied that there were no other
identifiable causes of the injury to Baby L’s brain injury. She still referred back
to the MRI findings which, she said, were not in keeping with peripartum
hypoxia.
[16] Dr Pearce saw L when he was 6 years 11 months. He accepted that the MRI
scan showed that the damage to the brain was limited to the putamina only, which
meant that the lesion was not extensive. He also admitted that the brain injury
could have occurred after birth, but stated that because this was not what Ms M
told her, and from all the available records, there was no evidence to suggest this.
He agreed that the complete cause of L’s cerebral palsy was uncertain.
13 ‘Peripartum’ means ‘the period shortly before, during, and immediately after giving birth’.
https://profiles.umassmed.edu as of 14 February 2024.
10
[17] The obstetricians, Drs Murray (for Ms M) and Archer (for the MEC) agreed
in their joint minute that the cerebral palsy from which L was suffering, was likely
caused by intrapartum hypoxia which occurred at an undefined time. They also
agreed that although at some stage prior to 14 h00 the CTG showed a pattern of
recurrent decelerations, variability remained normal. Only from about 14h00 did
the foetal heart rate rise and variability fall.
[18] In addition, the obstetricians agreed that although there were decelerations
or signs of distress on the ear liest partogram generated by the CTG, the foetus
was ‘likely, overall in a good condition at that stage’ as indicated by its positive
response to the administration of the Ringer’s Lactate.
[19] The trial court dismissed Ms M’s claim , having found that it could not
conclude that the injury to L’s brain was sustained intrapartum, or that the hospital
staff was negligent. With the leave of this Court the matter was appealed to the
full court, which overturned the decision of the trial court and held that the MEC
was 100% liable for any proven or agreed damages arising from L’s brain injury.
The full court held that the trial court should have found that:
‘Ms M’s foetal condition on admission was good, but that the first CTG gave cause for concern;
that continuous CTG – or at least two hourly – monitoring ought to have been implemented,
but it was not; that the foetal condition deteriorated further at 13:30, to the extent that the senior
midwife on duty would have taken immediate action had she been told about it; that the
situation deteriorated rapidly after 14h30; that L was born hypoxic; and that L’s cerebral palsy
probably resulted from a brain injury that occurred during labour.’
[20] There are a number reasons why the conclusion reached by the full court
that the standard of care afforded to Ms M was sub-standard cannot be sustained.
First, it is evident that the conclusion of the full court was based on the
First, it is evident that the conclusion of the full court was based on the
understanding that Dr Murray was of the opinion that the foetal condition became
pathological at 06h24. Based on this understanding t he full court reasoned that
11
there was ‘deterioration’ in the foetal condition between 07h00 and 12h40 in the
early hours of the morning, which ‘rendered L’s brain injury foreseeable ’.
Therefore, CTG monitoring should have been continuous, and when the
partogram was not reassuring at 13 h10, there should have been prompt
intervention to deliver the baby, the court found. It concluded that the failure to
monitor with CTG constituted below par medical care.
[21] However, it was not Dr Murray’s evidence that the foetus became
pathological at 06 h40 and that its condition deteriorated thereafter . In fact, Dr
Murray accepted that although the partogram had been non-reassuring when Ms
M was first put on the CTG, it became reassuring for hours after the Ringer’s
Lactate was administered . The conclusion by the full court that at 06h24 the
decelerations demonstrated such degree of abnormality as to be regarded as
requiring closer than standard care ignores the positive response to the
administration of the Ringer’s Lactate.
[22] Secondly, the suggestion that CTG monitoring of L’s heart rate would have
facilitated the detection and avoidance of a sentinel event is unsubstantiated. The
radiologists, having observed the injury to the basal ganglia (albeit confined to
the putamina), agreed that L sustained acute profound HII . They were unable to
pinpoint when this occurred. Although Dr Rademeyer sought to suggest that that
might not be so, she offered no clear or logical basis for such opinion . The
evidence to the effect that L suffered an acute profound brain injury intrapartum
was overwhelming. T he other experts were consistent in their opinion in that
regard.
[23] The approach adopted by this Court in determining whether there has been
a breach of the legal duty to administer reasonable health care and skill in
12
circumstances such as these is to distinguish between an acute profound and a
partial prolonged HII. In NSS obo AS v MEC for Health, Eastern Cape Province14
this court set out the distinction as follows:
‘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.’
[24] In Member of the Executive Council for Health, Eastern Cape v Z M15 this
court said the following:
‘The significance of this conclusion is an important matter. It was explained, in the course of
the trial, by the expert obstetrician and gynaecologist, Dr Buchmann, who testified on behalf
of the appellant. He testified that there is a distinction between an intrapartum acute profound
brain injury (‘an acute profound injury’) and an intrapartum prolonged partial brain injury (‘a
prolonged partial injury’). An acute profound injury is severe, with total or near-total asphyxia
(deficient supply of oxygen); it is of short duration, and sudden onset, and generally occurs 30
minutes before delivery. A prolonged partial injury is less severe, with partial asphyxia; it
develops slowly over several hours; it is often preceded by a deteriorating foetal heart rate that
gives a warning of developing hypoxia, that is, lack of oxygen. . . .’
[25] With reference to academic writings, this Court has held that authoritative
peer-reviewed literature does not support the view that monitoring of the foetal
heart by CTG provides prior warning of a sentinel event. In AN v MEC for Health,
Eastern Cape16 this court held that:
‘. . . In a number of studies, monitoring of the foetal heart did not support the case that there
would probably have been prior warnings of a sentinel event. Okumura et al conducted a study
would probably have been prior warnings of a sentinel event. Okumura et al conducted a study
where, in some cases, the origin of the fetal bradycardia could not be determined. Monitoring
actually indicated the well-being of these foetuses until sudden fall of the foetal heart rate. No
14 NSS obo AS v MEC for Health, Eastern Cape Province [2023] ZASCA 41 para 6. See further the authorities
cited in that judgment.
15 Member of the Executive Council for Health, Eastern Cape v Z M ZASCA (576/2019) [2020] ZA4SCA 169
(14 December 202) para4.
16 AN v MEC for Health, Eastern Cape [2019] ZASCA 102; [2019] 4 All SA 1 SCA paras 24 and 25.
13
warning was given. In another study, Murray et al17 studied three groups of infants where CTGs
were available. The third group, with nor mal CTGs on admission, suffered acute sentinel
events without warning. Pasternak & Gorey 18 concluded in their study that in 9 of their 11
patients, ‘fetal monitoring was thought to be reassuring until the onset of the terminal
bradycardia, supporting the pr emise that the hypoxic -ischaemic insult occurred at the end of
labor and was acute and severe.’ Finally, a standard text, Williams Obstetrics,19 warns:
“‘There are several fallacious assumptions behind expectations of improved perinatal outcome
with electro nic monitoring. One assumption is that fetal distress is a slowly developing
phenomenon and that electronic monitoring permits early detection of the compromised
fetus.’” .20
The appellant’s witnesses were unable to point to any contrary literature. They appealed to the
court a quo to accept what they said had been their experience. But this cannot be said to prevail
in the face of compelling peer-reviewed literature’.
[26] In this case there was no evidence of a sentinel event. The contention that
a sentinel event would have been detected and avoided if reasonable care had
been taken is based on the reverse reasoning that because L suffers from CP there
must have been a detectable and avoidable sentinel event during his birth. The
courts have cautioned a gainst commencing with an unfavourable outcome and
working backwards in search of a cause. Hornbuckle J warned that with the
benefit of the knowledge that there has been a neurologically unfavourable birth
outcome, a plaintiff’s attorney ‘can take any foet al monitor strip and make a
malpractice case out of it’.21
17 D Murray, M N O'Riordan, R Horgan, G Boylan, J R Higgins, C A Ryan ‘Fetal Heart Rate Patterns in Neonatal
Hypoxic-Ischemic Encephalopathy: Relationship with Early Cerebral Activity and Neurodevelopmental
Outcome’ (2009) American Journal of Perinatology 26:8 605 at 608.
18 J F Pasternak & M T Gorey ‘The Syndrome of Acute N ear-Total Intrauterine Asphyxia in the Term Infant’
Pediatric Neurology 18(5) 391 at 396.
19 F G Cunningham, K J Lenovo, S L Bloom, C Y Spong, J S Dashe, B L Hoffman, B M Casey & J S Sheffield
Williams Obstetrics 24 ed (2014)496.
20 Article in BJM Electronic Foetal Monitoring and our epidemic of Caesarean births (SEE CB 218 -235)
21 Hornbuckle J, Vial A, etc see f/n 21 page 229.
14
[27] Similarly in Goliath v MEC Health, Eastern Cape 22 this court cautioned
that a doctor should not be held negligent simply because something went wrong.
It cited with approval the remarks made by Lord Denning in Hucks v Cole [1968]
118 New LJ 469 (1993) that to hold a doctor negligent simply because something
went wrong, would be to impermissibly reason backwards from effect to cause.
If we accept, as we must, that the evidence overwhelmingly pointed to L having
sustained an acute profound hypoxic ischaemic event which occurred
intrapartum, then based on th e evidence of Ms M’S own expert s the injury
sustained by L was not one that might have been reasonably foreseeable.
[28] During cross-examination Dr Murray was constrained to acknowledge that
the CTG is not a perfect tool with which to monitor the foetal heart during labour
because of its ‘low specificity’. The substantial body of evidence that was
tendered at the trial on academic writings regarding the value of CTG in averting
or reducing HIE, is not conclusive on the issue. At best the evidence showed that
on an interpretation of the partogram in terms of both the American College of
Obstetricians and Gynaecologists (ACOG) and National Institute for Health and
Care (NICE) clinical guidelines, 23 acidosis may be deduced in category III
(ACOG) or pathological (NICE) partogram.
22 Goliath v MEC Health Eastern Cape 2015 (2) SA 102 (SCA) para 9.
23 Dr Murray preferred the NICE guidelines which are evidence based health and care clinical guidelines
recommended in the United Kingdom, while Dr Archer preferred the ACOG guidelines. Each one of them
explained how a program is interpreted and managed under their preferred system, with Categories I, II, and III
partogram on the ACOG grading comparable to normal, suspicious and pathological under the NICE guidelines.
Category 1 traces are characterised by a baseline heartbeat of 110 -160 per minute; moderate variability; no
variable accelerations or decelerations. These are all strongly predicative of a normal fetal acid base. Category 11
traces are those that don’t meet the criteria of Category 1. According to Dr Archer because they are not
characterised by a lack of variability, they are not associated with foetal acidosis, and should not be associated
with brain damage. They are non -reassuring and require some intervention such as moving the patient onto her
side and administering fluids, but not necessarily delivery. Category III traces are characterised by recurrent late
decelerations or recurrent variable decelerations with no variability. They are strongly predicative of acidosis. Dr
Archer stated that it is accepted internationally that fetal brain damag e will not occur until there is an abnormal
acid base of a ph of less than 7b and a base excess of more than 12.
Under NICE guidelines Normal is where the fetal heart beat is between110 -160; variability is 5-25bpm; no
decelerations; and accelerations are p resent. A trace is characterised as suspicious when there is one non -
reassuring feature. It is pathological when there are two or more non -reassuring features present. (CB298 -301)
15
[29] Dr Archer insisted that the 06h40 traces were only suspicious and not
pathological, because variability was good, and that from 14h00 the traces were
merely non-reassuring (category II on the ACOG grading system), because there
was no total loss of variability. He explained that under ACOG, brain injury is
likely to occur in category III CTG traces, which would be indicated in recurrent
late decelerations with no variability. However, he readily accepted that if the
baby had been born at 14h20 it was not likely to have been acidotic as variability
was normal on the partogram until 14h30. But he was unwilling to speculate as
to what happened thereafter. Her evidence suggests that the insult occurred within
an hour of the delivery. However, the fact that the injury occ urred during that
period does not mean that it was necessarily attributable to negligence by the
hospital staff.
[30] Dr Murray had initially asserted that under the NICE guidelines, at 13h10
the partogram traces s ignalled a pathological foetus. However, t his stance
changed once she saw the original partogram. She then sent a text message (SMS)
to Dr Archer on 3 September 2017 advising that:
‘. . . based on the fact that we have seen the original ctgs, I need to amend some of my points
where I comment on there being no rate. Also I am happy and raise no comment about the fact
that they are category 2 traces until the last hour. The management thereof we need to discuss.’
[31] Having found that CTG monitoring would not have made a difference, it
is not necessary to consider the contention by Ms M that the hospital staff were
negligent in failing to adhere to the guidelines stipulated by the Department of
Health when attending to her. In any event it was accepted that the decision to
perform a caesarean section (14h30), and L’s delivery happened within one hour
of each other as stipulated by the guidelines. Ms M’s case on negligence can
This is when the fetal heart is more than 180 beats per minute or less than 100; the variability is less than 5 or
more than 25 for less than 90 minutes and that there are variable decelerations present for more than 50% of the
contractions for less than 30 minutes or a single prolonged deceleration lasting more than 3 minutes .
16
therefore only be limited to the alleged fai lure to monitor the foetal heart beat
continuously by CTG or to taking the decision to perform a caesarean section
later than 13h10, which has been discussed already. Ultimately Ms M failed to
demonstrate that the hospital staff acted negligently in attending to her during L’s
birth. This also means that she failed to prove that some wrongful conduct on the
part of the hospital staff caused the injury to L’s brain.
[32] Much was made of the admission into the record, of the evidence of Prof
Izelle Smuts, a lso a paediatric neurologist, on the first day of the trial at the
MEC’s instance. The full court found that Prof Smuts’ evidence should not have
been admitted because ‘it sought impermissibly to undo agreements previously
reached by the parties’ experts’. In addition, the court found that, ‘it was never
made clear which of the expert agreements the evidence sought to undo, and
because there [was] no indication on the record that there was good cause for the
introduction of the evidence in these circumstances’.
[33] The circumstances which led to the admission of the expert evidence of a
further paediatric neurologist are not apparent from the record. And, as the full
court remarked, there is no indication in the judgment of the trial court whether
there was consideration, by that court, of the effect of the departure from the
previous agreements; particularly on the fact that L suffers from CP as a result of
the brain injury. In addition , this Court has discouraged departure from
agreements previously reached by experts.24
[34] Prof Smuts’ evidence led to revised joint minutes of the other experts. Her
evidence indeed impacted on issues which had been agreed on between the
experts, the most significant of which was the condition in which L presented,
when he was born. She cast doubt on the previously uncontested evidence that L
24 Bee v Road Accident Fund [2018] ZASCA 52; 2018 (4) SA 366 (SCA) para 65.
17
was born flaccid, that his low Apgar score at birth was indicative of HIE, and that
L suffered from CP. She highlighted his large brain size (megalocephaly), a large
head (macrocephaly), both of which, according to her, are inconsistent with CP,
which generally presents with microcephaly (a small head). She emphasised the
unexpected divergence between the MRI imaging and the clinical findings and
remarked on the absence of multi-organ failure in L’s case.
[35] We agree that the trial court should not have allowed Prof Smuts’ evidence
without a substantive application setting out factors on which it could properly
exercise its discretion. However, we are satisfied that, even without reference to
Prof Smuts’ evidence and the events pursuant thereto, Ms M did not establish
negligence on the part of the hospital staff and the MEC.
[36] In the result the following order is made:
1. The appeal is upheld with costs, including the costs of two counsel where
so employed.
2. The order of the full court is set aside and substituted with the following:
‘The appeal is dismissed with costs , including the costs of two counsel
where so employed’.
______________________
N DAMBUZA
ACTING PRESIDENT
_______________________
C HEATON NICHOLLS
JUDGE OF APPEAL
18
Appearances
For the appellant: P Pauw with him U R D Mansingh
Instructed by: State Attorney, Johannesburg
State Attorney, Bloemfontein
For the respondents: D T V R du Plessis SC with him P Uys
Instructed by: Wim Krynauw Attorneys Inc, Johannesburg
Martins Attorneys, Bloemfontein