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INTRODUCTION
[1] This is a delictual claim wherein the plaintiff is alleging negligence due to sub-
standard care on the side of the Thembisa Hospital staff, resulting in her minor
child sustaining a brain injury . The requirements for a successful claim in delict
are well -established. A plaintiff must prove positive conduct or an omission,
causation, wrongfulness, fault and harm1.
[2] The defendant contends that causation was not proved by the plaintiff because
as a mother with HIV there were various risk factors in existence and highlighted
by the experts that were not excluded in evidence and therefore she didn’t
discharge the onus re sting upon her. They submit absolution from the instance
must be granted due to the two mutually destructive versions before court.
[3] The parties agreed at pre -trial that the matter would proceed on liability only, with
the court to determine specific questi ons2 regarding the defendant's employees'
alleged negligence and the causation of the minor child's brain injury.
BACKGROUND
[4] In 2018 YM3 was 23 years of age. She started with morning sickness and did a
home pregnancy test which turned out to be positive. S he then attended the
Mayibuye clinic for the first time on 13 July 2017 where her first pregnancy was
confirmed. On information she supplied gestation was estimated at 15 weeks.
She had HIV and was on ARV treatment.
[5] She continued her visits to the Clinic a nd on 12 January 2018 she was given a
letter by the clinic sisters to report to the Thembisa Hospital on 19 January 2018
if the baby wasn’t born yet. On her own evidence she did not attend the hospital
as advised, only doing so on 21 January 2018 . This vis it was never recorded

1 Par 51 - NVM obo VKM v Tembisa Hospital and Another (CCT 202/20) [2022] ZACC 11; 2022 (6)
BCLR 707 (CC) (25 March 2022) – Minority judgment: Majiedt J
2 Discussed below in detail
3 Plaintiff on behalf of her minor child
3
anywhere , but YM insisted she gave the nurse her card and the letter from the
Clinic, but after the nurse determined she was not in labour she sent her home.
[6] She then felt lower abdominal pains at 14h00 on Saturday 3 February 2018 and
by 16h00 an ambulance was summoned for her. She was taken to Thembisa
hospital and admitted to casualties where she was monitored spending a
substantial period o f time in the waiting room awaiting a bed.
[7] She was seen by a doctor in the early hours of Su nday 4 February 2018. She
was diagnosed and treated for vaginitis (inflammation or infection of the vagina)
and assessed as post -date (beyond 40 weeks of gestation) . The foetus’s heart
rate was normal according to the CTG (Cardiotocography, electronic foetal
monitoring method recording baby’s heart rate and mother’s uterine contractions
– used during labour to monitor foetal wellbeing and detect potential signs of
distress) and she was then admitted to the labour ward for induction of labour.
[8] The induction was not carried out, a decision which the probabilities in evidence
suggest s was related to her HIV status and the fear of transmission possibilities
between mother and baby .
[9] In the late hours of t he evening when according to plaintiffs evidence she had
excrucia ting pain and had requested a C -section several times a CTG was done
between 22H13 and 22H38 which showed poor variability with a heart rate of
180 bpm (poor variability is when there are minimal or no fluctuations in the foetal
heart rate indicating a potential issue as the brain or central nervous system
control this function , and when the heart stops compensating , dropping below
the base -line it is an indica tion the foetus is running out of oxygen) . There was a
follow up done at 22h4 5 also with poor variability but at 150bpm more in line with
normal which is between 110 -160bpm. It is here , with these CTG’s , especially
the follow up one, where the first foetal distress was observed according to the
experts .
[10] She was returned to the war d and monitored and in the morning she reported to
the nursing staff the baby was no longer kicking. She described herself as tired
and dizzy and when the doctor saw her on Monday 5 February 2018 around
4
10h00 she was informed the baby is not well and she w as re ferred for an
emergency C-section . LM was born at 12h53.
[11] When LM was born, YM never heard her cry and didn’t see her as she was ta ken
to the ICU. She was told her baby was exhausted, distressed and not breathing.
She only saw baby LM the next day in the ICU at around 17h00.
[12] She described in her evidence that LM was on a machine. She looked if she had
convulsions. She was naked and had a hat on her head. There were drips and
she had pipes in her nose. She was told it was necessary as t he machine LM
was on was helping her to breathe and she couldn’t breathe without it. Ulanda
was discharged from hospital after 4 days and LM after 10 days.
[13] She was later told LM is Cerebral Palsy (CP), but no one ever told her what it is.
She describes LM’s problems as having a small head, not walking or talking
normally and her right side is not working properly. The clinic sisters at four
months old told her there was something wrong with LM and she was referred to
hospital where LM was receiving speech, physical and occupational therapy. She
used to take LM monthly , but it seems it isn’t always possible for her to do so as
a single parent who must care for her special needs child.
[14] The res t of the evidence consisted of expert witnesses ’ viva voce evidence and
Exhibits A - C3 which were expert witnesses ’ opinions, agreed upon and
submitted with consent , as they were not called. These were Exhibit:
A - Report by Prof Anna Nolte report (6 Pages)
B - Joint minutes between Dr L Muthelo and Prof Nolte (2 Pages)
C1 - Joint minutes Dr’s T Kamolane and S Dlangamandla (1 Page)
C2 - MRI Brain Dr T Kamolane (3 Pages)
C3 - MRI Brain Dr Dlangamandla (2 Pages)
[15] The plaintiff called in support of her case Dr Meshack Mbokata (Specialist
Obstetrician and Gynaecologist) an d Dr Nosipho Maponya (Specialist
Paediatrician ) and the Defendant called Dr Magdalena Susanna van der Merwe
5
(Specialist Obstetrician and Gynaecologist) and Professor Keith Duncan Bolton
(Specialist Paediatrician )
[16] It is observed that all these specialist were basing their expert opinions on what
they could note from the Hospital records. None of them were actually present
during the period of admission to hospital of YM or at the birth of LM and none
of them actuall y saw or treated them. The experts , whose credentials and
expertise was never questioned , all worked from the premise that if it was not
written in the hospital notes , it was probably not done.
SUMMARY OF THE EXPERT OPINIONS AND THEIR ANALYSIS
[17] I do not in tend doing an in -depth analysis of each witnesses evidence as it was
mostly of expert nature. I will only al lude to relevant portions when deemed
important to do so in this judgment. This because e ssentially, the plaintiff argues
that LM’s condition was pr imarily due to negligent intrapartum ca re4, while the
defendant emphasis es the role of multifactorial causes, particularly neonatal
anaemia, and the limitations and constraints of medical practice in Government
institutions , which they submitted were not s ub-standard in the context of this
case.
[18] What did the respective expert’s evidence amount to? The NURSING experts of
the parties Prof. Nolte (Plainti ff) and Dr Muthelo (Defendant) expressed their
views in Exhibit “B” which was handed in by consent .
[19] Important from the nursing experts is that both agree YM was post -date upon her
admission to hospital and there was no intrauterine resuscitation5 (IUFR)
measures taken at any stage until LM’s birth. Even though there was
disagreement, it would also seem th at the CTG monitoring was too infrequent ,
measured against the prescribed and applicable guidelines .
They also agreed that YM's pregnancy was normal and the foetus grew as
expected, despite her HIV+ status . She was post -date, and didn't follow advice

4 Refers to healthcare provid ed to a women and her baby from the onset of labour, through
childbirth and immediately after birth to her and the baby
5 IUFR is a set of procedures aimed at improving oxygen delivery to the placenta and umbilical
blood flow to reverse f oetal hypoxia and acidosis when f oetal distress is suspected .
6
to report at the hospital , as per the letter given to her . The y agreed the midwives
provided substandard care by not initiating intrauterine resuscitation for foetal
distress and by failing to maintain accurate records.
They disagree in that Professor Nolte a rgues that the midwives failed to adhere
to the 2016 Maternity Guidelines by not performing continuous CTG monitoring
for foetal compromise and by not promptly responding to , or reporting a foetal
heart rate of 163 bpm at 05:30. Dr Muthelo disagreed that t here was only one
foetal heart rate recording, stating that there is evidence of monitoring at both
05:30 (163 bpm) and 09:37 (150 bpm). This is however a disagreement on what
happened on the Monday morning of LM’s birth and not Sunday evening, where
all experts agree there was clear foetal distress.
[20] Looking at Exhibit C 1 the joint minute of the two Radiologist experts , Dr.T.K
Kamolane and Dr S .D. Dlangamandla both agree that the MRI brain scan shows
findings consistent with chronic hypoxic ischemic brain injury in a term infant,
specifically a pattern of partial prolonged hypoxic ischemic brain , making genetic
disorders and TORCH infections unlikely causes. They however indicate that a
further review of clinical and obstetrical records is needed to determi ne the cause
and timing of this injury.
[21] Important to note is that TORCH infections6 as well as genetic disorders are
unlikely to have caused LM’s current CP status. Both Radiologists diagnosed
Chronic hypoxic ischemic brain injury (HIE) which is long-term brain damage
resulting from the brain not receiving enough oxygen and blood flow for a period
of time . They diagnosed a pattern of partial prolonged hypoxic ischemic brain ,
which is a specific patt ern of brain injury seen on MRI in individuals who
experie nced a less severe , but sustained lack of oxygen and blood flow to the
brain .

6 A group of diseases ( Toxoplasmosis, Other, Rubella, Cytomegalovirus, Herpes Simplex Virus) that can pass from a pregnant
mother to he r baby, potentially causing serious health issues like birth defects and developmental delays

7
[22] The viva voce evidence of the two Obstetrician -Gynaecologists Dr M. Mboko ta
and Dr M.S. van der Merwe can be summarised as follows:
[23] Dr Mbokota 's view is that YM presented as post -dates with a concerning low
symphysis fundal height, although the initial foetal heart rate was normal. He
stated that a "tip of finger" cervical dilation suggests the start of labour. The
midwife's finding of "tip of finger" cervical di lation, at 18h00 on 3 February 2018
upon admission is an indication that labour had started . He believes the latent
phase should not exceed 8 hours. Postnatally, the baby presented with MAS,
HIE, PPHN, and anaemia, likely linked to hypoxia. An abnormal RI (Resistive
Index)7 on admission indicated potential placental issues , but without testing
results of the placenta, sent for analysis but never received back, this is
unascertainable .
[24] Dr van der Merwe’s view is that Cerebral Palsy is a multifactorial condition. She
highlighted the uncertainty surrounding the gestational age and expressed doubt
that the Plaintiff was in established labour upon admission due to the lack of
progressive cervical changes. She states from the hospital notes the first
definit ive sign of labour was at 09h37 on the 5th of February 2018 , when the
cervix was 2 cm dilated and the membranes had ruptured. She considered a
vaginal infection in a post -term pregnancy unlikely to induce labour and state
induction probably didn’t happen f or fear of HIV transmission between mother
and baby . Relying on newer guidelines, she downplayed the significan ce of a
prolonged latent phase as s he deemed the Cardiotocography (CTG) a poor tool
for assessing foetal well-being . She was of the opinion that the cause and timing
of the minor child's anaemia is unclear. Critically, she stated that the severe
neonatal anaemia in this case would likely have negatively impacted the outcome
regardless of earlier interventions for foetal distress. She acknowledged t he
presence of foetal distress from 22h13 on 04 February 2018, the delayed
decision and execution of the Caesarean section, and the 11 -hour period of
foetal non-monitoring as substandard care.

7 RI is a calculated value used in Doppler ultrasound to assess blood flow resistance in a vessel
8
[25] The Obstetrician -Gynaecologist experts agree on the presence of foetal
distress from 22h13 on 04 February 2018, the substandard delays in proceeding
with the Caesarean section and the lack of adequate foetal monitoring. They also
agreed on the postnatal presence of anaemia and the abnormal RI value.
[26] Their main disagre ement lies in their interpretati on of when labour commenced.
Dr Mbokota relied on the initial "tip of finger" cervical dilation, while Dr van der
Merwe emphasis ed the absence of progressive cervical changes and raised the
possibility of infection influencing the initial finding. They also differed on the
significance of the latent phase and, most importa ntly, on the issue of causation.
Dr van der Merwe attributing a significant role to the severe neonatal anaemia in
the eventual outcome, a factor D r Mbokota touched on , but did not emphasis e
as a potentially overriding cause.
[27] The two expert paediatricians who testified was Dr Maponya (Plaintiff) and Prof .
Bolton (Defendant).
[28] Dr Nosipho Maponya , presented expert testimony centred on the assertion that
LM's, neurological injuries stemmed primarily from intrapartum hypoxia. Her
analysis focus on the substandard care rendered according to her at birth ,
specifically the documented absence of essenti al resuscitation equipment and
adequately trained personnel who could assist Dr Naidoo , who as one person
did a two person job . Dr Maponya holds the view that this deficiency directly and
significantly worsened any pre -existing or developing hypoxic insult .
[29] Her core argument is a clear causal pathway : a failure in basic, life -saving care
at birth led to or worsened the lack of oxygen (hypoxia), which in turn manifested
as Hypoxic Ischemic Encephalopathy (HIE), Persistent Pulmonary Hypertension
of the New -born (PPHN), and ultimately the observed developmental delays. She
opines that the child's anaemia was a consequence of this hypoxic event ,
evidenced by the low initial haemoglobin levels, rather than a primary etiological
factor. While acknowledging Foetal -Maternal Haemorrhage (FMH) as a potential
cause of anaemia in other contexts, she found no evidence of its occurrence in
LM’s case. S he downplayed the role of the mother's HIV status , focusing instead
on the immediate impact of the birth asphyxia.
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[30] She made several significant statements to bolster the Plaintiff's allegations of
negligence. They are that there w as a fundamental breach of the duty of care
owed to a vulnerable new -born. That the prolonged 11 -hour gap in foetal CTG
monitoring and the 2.5 -hour delay in perfor ming the Caesarean section fell below
the acceptable standard of care.
[31] Although she agreed with Professor Bolton's concept of Neonatal
Encephalopathy (NE)8 as a "gateway" her emphasis fell on the link between the
hypoxic -ischemic insult and the resulting encep halopathy, and that probably the
MAS and PPHN cause d the long -term neurological damage to LM. She remained
resolute that her conclusion of hypoxic injury based on the clinical picture was
correct even though it was not in line with the so called ACOG9 (American
College of Obstetricians and Gynaecologists ) criteria Dr Bolton was relying on.
[32] Her testimony was a powerful and direct argument for causation rooted in
demonstrable negligence focusing on the failure to provide basic medical
necessities in the immediate postnatal period, a time of critical vulnerability for
LM, who was already compromised. The absence of working suction, a bag -
mask, oxygen, and an incubator at the moment of birt h, according to her ,
represents a significant departure from the expected standard of care. This
failure, in her expert opinion, directly impeded effective resuscitation and
worsened any preceding hypoxic insult.
[33] Her assertion is that the anaemia was a con sequence of hypo xia and directly
contradicts Dr Bolton’s argument that the anaemia was due to FHM .
[34] The strength of Dr. Maponya's evidence provides a compelling argument for a
direct and significant causal link between the substandard postnatal care and th e
child's hypoxic brain injury. Her testimony is consistent and directly addresses
the core elements of a delictual claim: duty of care, breach of that duty, causation,
and harm. T he factual evidence placed before court supports her account of staff

8 It's a broad term indicating a problem with the new-born baby's brain and nervous system (neurological
function ) in the first few days of life .
9 In the context of new-born’s hypoxic -ischemic encephalopathy (HIE) and its potential link to cerebral
palsy, refer to a set of clinical and laboratory findings that i ncrease the likelihood that a new -born's
neurological impairment was caused by an acute intrapartum hypoxic event.
10
and equipment shortages in an emergency hospital theatre and probable
mismanagement of LM’s condition as a result thereof at an extremely critical time
directly after her birth.
[35] Profess or Keith Duncan Bolton, presents a viewpoint emphasis ing the multi -
factori al causes of Cerebral Palsy (CP). He suggests that CP in this case is likely
the result of a complex interplay of proximal (at birth) and distal (before or after
birth) risk factors, rather than a singular negligent event. He identifies Neonatal
Encephalop athy (NE) as a key intermediary stage in the development of CP,
noting its presence in LM. A central point of his view is the significant role of
severe anaemia, likely caused by foetal -maternal haemorrhage (FMH)10
occurring shortly before birth, as a major proximal risk factor. He also highlights
maternal HIV and post -datism as distal risk factors predisposing LM to NE and
CP.
[36] In evidence he downplayed the direct causal link between the delayed
Caesarean section and CP , attributing the delay partly to systemic staffing and
overcrowding issues experienced in State Hospitals . His view is that the value of
CTG in preventing CP is limited. Whilst acknowledging initial equipment issues,
he believes resuscitation was ultimate ly adequate. His main conclusion is that
multiple risk factors, both pre -existing and peri -partum11, contributed to LM’s CP.
[37] The contradictions in his evidence arise from his agreement on a "sentinel event"
near birth potentially contributing to acute brain injury and anaemia , which can
be seen as downplaying the multifactorial aspect he insist ed was present .
Additionally, while deeming resuscitation adequate, he acknowledges (evident
from his notes) the frustration caused to Dr Naidoo by the lack of equipment
during this emergency , suggesting a potential negative impact.
[38] The key concessions he made include acknowledging that a component of brain
injury occurred intrapartum, agreeing on the likely timing of the acute profound

10 Refers to the leakage or transfer of foetal blood cells into the mother's bloodstream during
pregnancy, labo ur, or delivery .
11 The period preceding or following child birth usually events that occurred during the last month of
gestation or the first few months after delivery, with reference to the mother.
11
injury and severe anaemia in the last 30 minutes of labour, and conceding that
the damage caused the NE.
[39] He defers to obstetricians on whether detectable damage constituted
substandard care. He agrees NE is a common pathway to CP and the importance
of preventing NE. He confirms that post -datism causes complications, HIV in
mother’s increases meconium aspiration risk, and that the brain dama ge likely
occurred around birth. Also that PPHN is a postnatal risk, and the lack of
resuscitation equipment and delays in cooling possibly wors ened the existing
condition , which was actually a medical catch twenty two situation . He
acknowledges the difference between association12 and causation13 from the
expert reports he relied on , regarding HIV and NE , but maintains that CP is not
a simplistic single -event outcome . This as the Plaintiff’s counsel put it to him that
his expert reports only shows associations and not actual causation .
[40] In essence, Professor Bolton's evidence aims to establish that while
acknowledging some s ubstandard care and intrapartum events, the child's CP is
best understood within a framework of multiple contributing factors, with a strong
emphasis on pre -existing and likely unavoidable factors like severe anaemia due
to probable FMH, alongside distal r isks. He argues against attributing CP solely
or directly to specific acts of negligence during labour.
ARGUMENTS BY PLAINTIFF AND DEFENDANT
PLAINTIFFS ARGUMENTS
[41] The Plaintiff argues that the clear sequence of events – the documented foetal
distress, the p rolonged failure to act, the condition of the baby at birth, and the
subsequent diagnosis of hypoxic ischemic brain injury – strongly suggests that
the hospital staff’s negligence directly caused the child's cerebral palsy. They
submit the Defendant's alte rnative explanations as speculative and unsupported
by the presented evidence.

12 Possible link, but not conclusive
13 Actual relationship between cause and effect
12
[42] The Plaintiff submits that the hospital staff were negligent in their management
of the Plaintiff's labour and the foetal distress experienced by her baby. They
contend that for eseeable harm was not acted upon when foetal distress was
detected at 22h13 on 4 February 2018, a clear sign of danger. Despite this, no
immediate or adequate intervention was taken for approximately 14 hours until
the emergency C -section at 12h53 on 5 Feb ruary 2018. This constitutes sub -
standard care and a breach of guidelines, specifically in the failure to
continuously monitor the foetus with a CTG, initiate intrauterine resuscitation,
and perform an emergency C -section within the guideline of one hour a fter the
diagnosis of foetal distress.
[43] Consequently, the Plaintiff argues that the prolonged period of foetal distress and
the subsequent hypoxia and ischemia are the most probable cause of the child's
neonatal encephalopathy and resulting cerebral palsy. They firmly reject the
Defendant's alternative causation theories, such as the child's HIV exposure or
an unspecified infection causing the brain injury, as speculative, unsupported by
the evidence, and contradicted by their own expert's concessions regard ing the
timing and cause of the anaemia.
[44] The Plaintiff supports their arguments with the following common cause facts and
concessions made. The plaintiff's admission to hospital, without being in active
labour, and having been in good health (both she and the foetus) since her
Mayibuye clinic day s up until 22h13 on 4 February 2018, forms the factual basis.
All experts agreed that the first signs of foetal distress appeared at the
aforementioned time and date. This occurred after YM was admitted for an
induction of labour, which never happened. Whe n foetal distress was diagnosed
(22h13 on 4 February 2018), the maternity guidelines required continuous CTG
monitoring, which did not occur. There was spontaneous rupture of membranes
with meconium -stained liquor, further indicating foetal distress before the
emergency C -section was ordered. The guidelines stipulate emergency C -
sections must happen within an hour; however, the order was given around
10h00 and the baby was born at 12h53 – almost three hours later – without a
proper explanation for the delay .
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[45] Further, there was a concession by Dr van der Merwe that the acute profound
injury likely occurred in the last 30 minutes and probably caused the anaemia.
The Plaintiff argues that the lack of oxygen and suctioning equipment in the
theatre was negligent and caused a crisis, evident in LM's condition at birth:
being floppy, not crying, cyanosed, meconium aspirated, and in respiratory
distress. This also delayed her transfer to the NICU. The Plaintiff submits that
these events led to the diagnosis of a mix ed pattern hypoxic ischemic brain injury
and neonatal encephalopathy, ultimately resulting in cerebral palsy .
[46] The plaintiff’s critique on Prof. Bolton’s evidence was that his theories regarding
HIV exposure and anaemia as primary causes are not supported b y the cited
studies , the facts of this case and are contradicted by his own concession about
the timing of the anaemia. They emphasize the distinction between association
and causation in scientific studies which they said he tried to elevate to
probabilit ies in this matter , whilst only being possibilities if further research is
conducted.
[47] The Plaintiff quoted various pieces of case law to establish the legal principles of
negligence and causati on, to argue that the hospital staff’s conduct fell belo w the
required standard of care and to support the inference of n egligence based on
the evidence. They also provided case law to counter the Defendant's potential
alternative explanations, and to emphasize the importance of basing expe rt
opinions on proven facts and not studies with association which are possibilities,
but not probabilities in this matter
DEFENDANT S ARGUMENTS
[48] The Defendant argues that the child's cerebral palsy is likely the result of a
complex interplay of various risk factors, some potentially pre-existing . Their
evidence was aimed to demonstrate that the outcome in LM’s circumstances
cannot be solely and directly attributed to negligent actions or omissions by the
hospital staff during the final stages of labour. They highlight the uncertaintie s in
the Plaintiff's history and the presence of other plausible contributing factors to
counter the Plaintiff's claim of direct causation due to negligence.
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[49] The Defendant's main arguments are that Cerebral Palsy (CP) is a complex
condition with multiple p otential antenatal, intrapartum, and postpartum
contributing factors, making it difficult to pinpoint a single cause. They contend
that, despite some shortcomings, the clinical notes provide a generally good
picture of the management of the Plaintiff's pre gnancy and labour. They submit
it cannot be definitively stated that baby LM's condition is purely due to a failure
of staff at Tembisa Hospital to provide adequate care during labour and delivery.
They also argue that the significant delay between the dia gnosis of foetal distress
and delivery on 5 February 2018 might have been unavoidable in an
overcrowded health system with limited resources and the need to prioritise
patients.
[50] Furthermore, the Defendant highlights several factors that complicate the
causation argument: the Plaintiff's uncertainty about her last menstrual period,
making accurate gestational age determination difficult; the Plaintiff's
greenish/yellowish vaginal discharge indicating an infection, which could have
implications for the cervi x and potentially contribute to complications for LM; and
the initial resistance index (RI) of 0.8 at term being high, suggesting potential pre -
existing issues with blood flow to the baby (intrauterine growth restriction). They
submit that labour only defi nitively started at 09h37 on 5 February 2018 with
cervical changes (2cm dilation) and spontaneous rupture of membranes, arguing
that earlier signs were not conclusive of active labour. Therefore, it cannot be
said that labour was delayed, as the spontaneou s rupture of membranes on the
morning of 5 February 2018 was the clear sign of labour onset.
[51] Regarding causation, the Defendant submits that the anaemia LM was born with
was not caused by the foetal distress experienced during labour, but by factors
such a s the mother's HIV status, potential post -datism, and the abnormal
resistance index, which could have predisposed the baby to hypoxia. They
maintain that LM's condition can be attributed to a combination of pre -existing
factors and events that are not sole ly attributable to negligence during the final
stages of labour.
[52] The Defendant largely supports their view with the evidence of their experts, who
testified that CP is complex and multifactorial. They contend that the hospital
15
notes show reasonable managem ent was provided within a difficult,
overcrowded hospital setting. They highlight the plaintiff’s uncertainty regarding
the gestational age due to her unclear menstrual history, and that the greenish
discharge was a sign of potential infection. The elevate d resistance index at term,
they argue, was potentially indicative of a pre -existing issue. Furthermore, they
submit that YM's labour observations, which require cervical changes and regular
contractions, were not consistently documented to definitively st ate when active
labour started, except when the membranes ruptured, which is a clear sign of
labour onset. Dr van der Merwe specifically indicated that the foetal distress did
not cause the anaemia, attributing it to a pre -existing risk factor like HIV.
[53] The Defendan t further submits that Drs Mboko ta and Maponya, the Plaintiff's
own experts, conceded several crucial points: that HIV was a risk factor for
hypoxia and that an HIV infection could contribute to brain damage; and that a
vaginal infection could p redis pose LM to hypoxia. Dr Mboko ta also agreed that a
prolonged gestational period carries risks for the baby, including placental
insufficiency and meconium -stained liquor, and Dr Maponya concurred that post -
datism poses a risk. They highlight that the i nitial RI of 0.8 was agreed to be
abnormal, suggesting potential intrauterine growth restriction. Crucially, the
Defendant points out that Dr Mboko ta agreed the baby's anaemia was not
caused by foetal distress, and Dr Maponya also stated that hypoxic ische mia
does not cause anaemia. Furthermore, Dr Maponya agreed that several factors,
including severe congenital anaemia, maternal HIV, meconium -stained liquor,
meconium aspiration, PPHN, post -datism, and neonatal infection, could have
contributed to the brain damage.
ANALYSIS
[54] I find to properly understand the views of the Plaintiff and Defendant it must be
broken down in very understandable language. This especially for my benefit as
the Judge who must rule on the presented very intricate medical facts with mostly
experts expressing their medical opinions that are nuanced, sometimes
conceded and sometimes based on inference (association) not necessarily
suppo rted by the facts of this matter.
16
[55] My understanding therefore of the Plaintiff’s case is that LM has c erebral palsy
because the hospital staff were negligent before and during YM’s labour, and
throughout the delivery process until after birth .
[56] The Plaintiff contends that the hospital staff ignored clear signs of danger,
specifically foetal distress, for a n unacceptably long period (14 hours and 40
minutes), and failed to deliver LM timeously. Furthermore, no interventions were
undertaken to initiate intrauterine resuscitation when distress was noted or in the
period preceding surgery, thereby causing her t o be born hypoxic (lacking blood
flow and oxygen to the brain).
[57] The Plaintiff further asserts that the hospital staff did not have the necessary
equipment ready when LM was born in distress, having aspirated meconium14
and required immediate assistance. Th is alleged lack of proper care, it is argued,
directly caused LM to suffer birth asphyxia15 resulting in a hypoxic ischemic
incident and severe brain damage.
[58] The Plaintiff's emphasis is therefore on the asphyxia (lack of oxygen in the blood)
causing a hypo xic-ischemic incident, damaging LM's brain due to insufficient
oxygen and blood flow. This situation was worsened by the fact that she was
birthed in distress and that insufficient emergency resuscitation equipment was
available to prevent or mitigate furt her damage. The Plaintiff believes the
chronological timeline of events and the established facts of this case strongly
support their claim, rendering any excuses or alternative causes for LM's
condition untenable given the evidence.
[59] The defendant says CP is a complicated condition wit h many possible causes,
and it is not fair to blame everything that happened in hospital and in the delivery
room on a single event . Whilst there might have been some things the hospital
staff could have done better and faster, the staff were doing their best in trying
circumstances .

14 Baby’s first stool and a clear sign of distress
15 Lack of oxygen or an excess of carbon dioxide in the body causing breathing difficulties
17
[60] The Defendant emphasises that, based on the hospital notes, LM presented with
other significant indicators of factors contributing to CP, visible before, during,
and after birth. These incl uded YM’s post -datism, her HIV status, and vaginal
infection, along with the medications used for their treatment and their possible
effect on LM. The severe anaemia (indicated by a low RI at admission) is also
highlighted. Due to the presence of these var ious other factors, the Defendant
submits that the Plaintiff has not discharged the onus of proving that the staff’s
actions directly caused the CP.
FINDINGS ON THE FACTS
[61] I conclude from the expert evidence presented that YM was post term when she
was eve ntually admitted to hospital. Her pregnancy was normal apart from her
being HIV positive.
[62] LM has confirmed permanent brain damage (Chronic hypoxic ischemic brain
injury) that was caused by insufficient blood flow and or oxygen reaching her
brain.
[63] I accep t that clear labour was only diagnosed at 09h37 on 5 February 2018, but
that at that time there was already clear signs of foetal distress noticed at 22h13
on 4 February 2018 which was not acted upon or properly monitored by CTG.
This noted distress was agreed upon by all the experts and lasted for 14 hours
and 40 minutes for LM.
[64] An emergency C -section was ordered at 10h00 on 5 February 2018, and despite
admitted medical guidelines that it should have been performed within an hour ,
LM was only born at 12 h53, two hours and fifty three minutes later.
[65] At birth, LM was in severe distress. Dr Naidoo, who, even according to Dr Bolton,
performed a sterling 'one -person job meant for two,' did not have the basic
resuscitation equipment available. This situation l ikely exacerbated LM’s already
poor hypoxic condition.
18
[66] I accept, even though there was only r eluctant agreement , that a sentinel event
occurred 30 minutes before LM’s birth and that she was probably delivered just
in time to prevent a stillbirth .
APPLICATION OF LAW TO FACTS: NEGLIGENCE
[67] In answering the five questions formulated for answer I find as follows: On
question 1 - Whether or not the defendant’s employees who cared for the
plaintiff during her admission and treatment in hospital delivered s ub-
standard care as alleged by the plaintiff?
[68] The answer is an unequivocal, YES. My acceptance of a prolonged latent phase,
foetal compromise not acted upon, multiple missed opportunities for intervention,
and the baby's compromised condition at birth , are all deviations from accepted
medical practice, and establish es that the defendant's employees delivered sub -
standard care as alleged .
[69] On the prolonged latent phase issue, my finding is based on the fact that YM was
admitted for induction, which never took place. Although a plausible explanation
was given for this omission, it is clear from her individual situation — considering
her post -datism, HIV status, possible labour, vaginal infection, and her
complaints (that went unheeded) from Sunday evening ( 4 February) to Monday
morning (5 February), when an emergency C -section was eventually ordered —
that she required, and indeed almost demanded, much more attention and care
from the medical staff than was provided.
[70] On question 2 - Whether or not the defend ant’s employees negligently
prolonged the plaintiff’s labour? The answer is YES. YM was in clear foetal
distress from 22h13 on 4 February 2018, as agreed to by all the experts. This
distress was not acted upon definitively. This inaction led to a subsequen t delay
in calling for the emergency C -section, which procedure was also executed
beyond the acceptable guidelines. This indicates that the defendant's employees
negligently prolonged the plaintiff's labour, thereby allowing a significant and
unacceptable period of foetal compromise to occur.
19
[71] On question 3 - Whether or not the defendant’s employees were negligent
by failing to timeously recommend an emergency Caesarean Section (C -
Section) and perform one without undue delay? The answer is YES. The
experts agreed upon, clear signs of foetal distress at 22h13 on 4 February 2018
warranted a timely recommendation and execution of an emergency C -section.
The significant delay until the baby's birth at 12h53 on 5 February 2018, almost
three hours after the decisi on for the C -section taken at 10 h00, and nearly fifteen
hours after the initial signs of distress, directly contravenes medical guidelines
and constitutes clear negligence.
[72] On question 4 - Whether or not the failure to provide intrauterine
resuscitation (I UFR) after having diagnosed foetal distress and while
awaiting a Caesarean Section was negligent? The answer is YES. Following
the diagnosis of foetal distress at 22h13 on 4 February 2018, the failure to
implement intrauterine resuscitation measures during the prolonged waiting
period until the emergency C -section, which was only performed much later,
constitutes a deviation from the accepted standard of procedure and care and is
therefore negligent .
[73] On question 5 - Whether or not the failure to heed warning signs indicated
foetal compromise and take appropriate measures to avoid harm to the
baby was negligent? The answer is YES. The clear signs of foetal distress
noted at 22h13 on 4 February 2018 were critical warning signs of foetal
compromise. The f ailure to act upon these signs for an extended period, including
the delay in performing the emergency C -section and the omission of intrauterine
resuscitation, demonstrates a negligent failure to heed these warnings and take
appropriate measures to avoid harm to the baby.
[74] Negligence is therefore apparent in respect to all the questions posed. There was
a clear duty of care on Thembisa Hospital and its medical staff. Various
deviations from accepted medical practice were either apparent or admitted.
Therefo re, answering all the questions supra with a 'YES' is unavoidable.
APPLICATION OF LAW TO FACTS: CAUSATION
20
[75] A delictual claim requires more than j ust negligence. Causation must also be
proved. Causation , in medical terms, is established where there is a dire ct link
between the healthcare provider's negligent actions or omissions and the
patient's resulting harm. It's not simply about showing a mistake was made; it's
about proving that the mistake made caused the harm .
[76] In this matter, therefore, the plaintiff needs to show, on a balance of probabilities,
that the hospital employees' negligent actions — such as failing to properly
attend to YM’s specific circumstances and complaints, not properly monitoring,
reporting, an d taking definitive action on the foetal distress noted, and delaying
the emergency C -section — actually caused the baby's brain injury. The plaintiff
argues that but for the negligence, the baby would not have suffered the hypoxic
event leading to cerebra l palsy, and that this outcome was a foreseeable
consequence of the negligent medical care.
[77] This is where the argument of the defendant lies. They agree that some aspects
of care could have been better, and even seek to exculpate their staff in parts.
Professor Bolton agrees there were some issues with the care provided, but he
argues that despite these, LM still had several pre -existing vulnerabilities [post -
datism, potential impact of maternal HIV, and significantly, severe anaemia likely
from Foetal -Maternal Haemorrhage (FMH)] that made her susceptible to
Neonatal Encephalopathy (NE) and Cerebral Palsy (CP). He maintains that
these factors are the more significant contributors to LM’s outcome. He remains
adamant that CP is a complex condition with multip le potential pathways, and
attributing it solely to the alleged (and now found by the court) negligence is an
oversimplification.
[78] There has been a lot of confusion lately in court arguments and judgments where
factual causation is at issue , regarding whet her the so called “but for” or Lee test
would be applicable. It must be realised that it is actually only one test wherein
flexibility under Lee16 is recognised against the rigidness of “but for17”. The
underlying principle of factual causation remains, but the way the question is

16 Focuses on the contribution of the negligence to the harm by way of increased risk or lost opportunity .
17 But for the Defendant's negligent conduct, would the harm to the Plaintiff have occurred?
21
framed and the factors considered in answering it can differ depending on the
complexity of the causal chain and whether the situation falls under the standard
"but-for" test (still preferred) or the Lee exception.
[79] In Lee t he Consti tutional Court differed from the lower courts (CPD and SCA) by
moving away from a strict "but -for" test and adopting a more flexible approach to
factual causation. This approach took into account the systemic nature of the
defendant's failures, the state's constitutional duties, and the need to prevent
injustice in cases involving vulnerable individuals. The Constitutional Court was
willing to find causation present, where the lower courts were not, because they
adopted a wider and more constitutionally ali gned view of what causation means.
[80] Lee would be applicable in cases where the harm that ensued was closely
connected to an omission by a party who carries a duty of care to prevent the
harm. It focuses on whether the defendant's conduct (the series of omissions)
played a substantial role in bringing about the harm. In cases involving multiple
contributing factors and a series of omissi ons, the court wou ld ask: “Did the
conduct of the party wit h the duty of care significant ly help cause the harm
even if it's difficult to say the harm wouldn't have occurred ?” This question
embodies the core of the Lee test. It acknowledges situations with multiple
contributing factors where pinpointing a single " but-for" cause is problematic.
[81] The “but for” test enquires whether the harm was inevitable to the plaintiff
regardless of the defendant's actions. If the answer is "yes," it suggests the
defendant's breach was not a factual cause under this traditional te st. The
question to be asked is: “Would the harm likely have happened anyway, even
if the defendant had done what they were supposed to do?"
[82] In Mashongwa v PRASA18 paragraph 65, Mogoeng CJ, states th at following i n
the Constitutional Court's judgment of Lee v Minister for Correctional Services19.
[65] “ It seems to me that the approach adopted in Lee is
particularly apt where the harm that has ensued is closely

18 2016 (3) SA 528 (CC)
19 2013 (2) SA 144 (CC)
22
connected to an omission of a defendant that carries the duty
to prevent the harm . In those circumstances, the question one
asks in the context of factual causation is whether the harm
would probably have ensued even if the defendant had
complied with its duty . However, where the traditional but-for
test is adequate to establish a causa l link, it may not be necessary
to resort to the Lee test."
[83] The question(s) posed in paragraph 3 supra relating to causation is :
1. Whether the negligence as alleged by the plaintiff
above resulted in the Plaintiff’s minor child suffering
a (HIE) hypoxic -ischemic incident (Brain injury due to
lack of oxygen) due to birth asphyxia (Lack of oxygen
in the blood) causing her to sustain severe brain
damage?
OR
2. Whether the cause of the minor’s brain injury is the
following according to Prof. Bolton:
2.1 Severe Congenital Anemia – CDA - (blood disorder
where significant lower than normal levels of red
blood cells, lead to severe deficiency in oxygen
transport through the body)
2.2 Maternal HIV infection
2.3 Meconium stained liquor (MSL – Amniotic fluid with
greenish / brown colour, due to the presence of
meconium, which is the baby’s first stool) and
meconium aspiration syndrome (MAS – When a new -
born breathes into their lungs during or shortly after
birth meconium)
23
2.4 Persistent Pulmonary Hypertension (PPHN –
Condition where a new -born’s circulation system
doesn’t adapt to life outside the womb, causing the
blood vessels in the lungs to remain constricted, with
resultant reduced blood flow to the lungs and low
oxygen levels in baby’s blood)
2.5 Post Datism (A pr egnancy that has extended more
than 14 days past the 40 weeks of gestation –
expected delivery date)
2.6 Neonatal infection (disease or virus contracted by a
new-born from before birth – in utero - to within the
first 28 days of life)
[84] The causation question presented for answer is a one , OR, the other option. I
however intend to deal with both (even if just cursory) before indicating my
conclusion.
[85] On question 1, and on the probabilities, the answer is YES. Dr Maponya and the
other evidence adduced by the plaintiff rely directly on the timeline of events to
link the substandard care to the outcome. Her testimony indicates there were
clear signs of prolonged foetal distress that were not adequately acted upon.
There was a significant delay in performing the emergency C -section. Crucially,
in this latent phase from distress being noted to the C -section, there was no
indication that intrauterine resuscitation was performed.
[86] The baby's severely compromised condition at bir th—indicative of asphyxia
(floppy, not crying, cyanosed, meconium aspirated, respiratory distress) —along
with the lack of essential resuscitation equipment and personnel immediately
after birth, all further exacerbated LM’s hypoxic state. The resultant dia gnosis of
hypoxic -ischemic brain injury (HIE) is, therefore, the direct consequence of
insufficient oxygen and blood flow to the brain, which, I find, was caused solely
by the attending staff’s negligence. I agree with this assessment.
24
[87] The questions in 2. 1 – 2.6 relate to Professor Bolton’s assertion that LM’s HIE
was multifactorial. He argues that several pre -existing and peri -partum factors
likely contributed to the Neonatal Encephalopathy (NE) and Cerebral Palsy (CP),
suggesting that the CP was likely t he result of a complex interplay of these factors
rather than solely due to the alleged negligence during the final stages of labour.
[88] The factors he listed, which correlate with the questions, are: Severe Congenital
Anaemia , which he argued could have imp aired oxygen transport; Maternal HIV
infection , identified as a distal risk factor; Meconium Stained Liquor and
Aspiration , which he acknowledged as a sign of foetal distress and a respiratory
complication if aspirated at birth, affecting the lungs; Persis tent Pulmonary
Hypertension (PPHN) , which he noted as a postnatal condition affecting
oxygenation where a baby fails to adjust to its new surroundings after birth; Post -
Datism , which he cited as a risk associated with prolonged gestation; and
Neonatal infe ction .
[89] Regarding the latter, Professor Bolton indicated it must be assumed, due to the
medication used in treating LM in ICU, that she had some kind of infection, as
these infections can be caused by various pathogens, including bacteria, viruses,
fungi, and parasites, to which new -borns are particularly vulnerable due to their
immature immune systems.
[90] The problem with Professor Bolton, and for that matter the other experts who
testified viva voce for the defendant, is that they all tried to offer alternat ive
possible risk factors that could have independently or cumulatively contributed
to LM’s brain injury. Crucially, Professor Bolton’s evidence, on which the above
questions require answers, was not always based on the available facts of this
matter.
[91] Professor Bolton conceded two very important aspects: first, that there is a
difference between association and causation – as discussed in paragraph 39
supra – given that the expert material he relied upon showed more association
than causation in relation to LM’s specific facts. Second, he conceded that a
component of LM’s brain injury occurred intrapartum, agreeing on the likely
timing of the acute profound injury and severe anaemia in the last 30 minutes of
25
labour, and further conceding that this damage caused the Neonatal
Encephalopathy (NE)
[92] This concession is significant because it acknowledges that a critical harmful
event occurred during the delivery pr ocess itself, aligning with the plaintiff's
argument that negligence during this time contributed to the brain injury. While
Professor Bolton still maintained his multi -factorial argument, acknowle dging a
direct injury occurring so close to birth weakens h is stance that the CP was solely
or primarily due to pre -existing or unavoidable factors. This is indicative that the
negligent management during those crucial final minutes contributed to and
exacerbated LM’s acute injury.
[93] Professor Bolton’s view that Foetal -Maternal Haemorrhage (FMH) likely occurred
shortly before birth, causing the severe anaemia, is unsupported by evidence as
no blood was drawn from YM to confirm this contention. Furthermore, while the
placenta (due to th e low RI) was sent for analysis, the results were never
received to confirm placental issues. Crucially, on the evidence presented, there
was no real indication of excessive blood visible during the birthing process that
would explain the severe anaemia LM had at birth.
[94] Professor Bolton was particularly defensive regarding the equipment available,
or rather unavailable, in the emergency operating theatre. He sought to argue
that despite the absence of certain equipment, proper help was still afforded by
the Paediatrician who assisted LM. However, the absence of this essential
equipment in an emergency situation such as this is, under the circumstances,
untenable.
[95] In conclusion on the aspect of causation, I find that Dr Maponya’s evidence
provides a direct causal link between the alleged negligence (especially the delay
in intervention and lack of resuscitation) and the hypoxic -ischemic injury. This
finding stands against Professor Bolton’s mostly unsupported offering of a
broader multiple risk hypothesis th at could have caused the brain injury.
LEGAL POSITION
26
[96] The legal principles governing negligence, causation ('but for' test), inferential
reasoning, and the duty of care owed by medical professionals are well -
established in our law.
[97] I consider ed the standard of care as in Kruger v Coetzee20, foreseeability
Mukheiber v Raath21, the drawing of inferences where factual evidence is ab sent
or disputed Minister of Safety and Security v Van Duivenboden22, and the
rejection of implau sible alternative explan ations Ratcliffe v Plymouth and Torbay
Health Authority23 in coming to my findings.
[98] In Standard Chartered Bank of Canada v Nedperm Bank Limited24, it was
clarified that for liability to result, the precise nature or extent of the loss or the
exact manner of harm need not be foreseeable. It is sufficient if the general
nature of the harm and the general manner of its occurrence were reasonably
foreseeable. This principle is relevant in LM’s case , suggesting that even if the
exact severity of her CP was not pre dictable, the harm resulting from untreated
foetal distress was indeed reasonably foreseeable.
[99] In Minister of Safety and Security v Van Duivenboden , the court addressed
causation, affirming that a plaintiff does not need to establish the causal link with
certainty, but only that the wrongful conduct was probably a caus e of the loss.
This principle was pivotal in the courts assessment whether the hospital staffs
negligence was the probable cause of the child's brain injury.
[100] The Constitutional Court in Minist er of Finance and Others v Gore NO25 further
elaborated on factual causation, emphasizing a common -sense, practical
approach rather than a purely scientific or philosophical one. A common -sense
assessment of th is cases timeline of events and th e lack of tim ely intervention
points strongly to the hospital staffs omissions as the cause of the injury to LM.

20 1966 (2) SA 428 (A)
21 1999 (3) SA 1065 (SCA)
22 2002 (6) SA 431 (SCA)
23 1998 PLNR 146
24 1994 (4) SA 747 (A)
25 2007 (1) SA 111 (SCA)
28

For the Applicant:






For the Respondent:







Dates heard: 3 -7; 10 -14 March 2025

Judgment finalised: 20 May 2025

Judgment delivered after redaction and

revision : 22 May 2025
Advocate D Brown assisted by Ms

N. Radebe (Attorney) instructed by

Jerry Nkeli & Associates Inc.


Advocate(s) MM Gwala SC & HL

Kelaotswe instructed by The State

Attorney