1 SAFLII Note: Certain personal/private details of parties or witnesses have been redacted from this document
in compliance with the law and SAFLII Policy
REPUBLIC OF SOUTH AFRICA
IN THE HIGH COURT OF SOUTH AFRICA
(GAUTENG DIVISION, JOHANNESBURG)
CASE NO: 2018/21491
(1) REPORTABLE: YES / NO
(2) OF INTEREST TO OTHER JUDGES: YES/NO
(3) REVISED: YES/NO
In the matter between:
V[...] W[...] : K[…] M[…] obo
V[...] W[...] : C[...] C[...] Plaintiff
and
MEC FOR HEALTH, GAUTENG PROVINCE Defendant
___________________________________________________________________
JUDGMENT
MABASA, AJ
Introduction 1. This is an action for damages in delict on behalf of a minor child afflicted with
cerebral palsy. The core issue for determination is the liability of the defendant (“ the MEC”) for the conduct of its staff at a public hospital during the birth of the child.
Parties
2
2. The plaintiff is KM v[...] W[...] (“Mrs v[...] W[...]” ) who acts in her representative
capacity on behalf of the minor child, C[...] C[…] V[...] W[...] (“C[...]” ) who was born
on 2 March 2008 at the Tshwane District Hospital (“the hospital”).
3. The defendant is the MEC for Health, Gauteng Province.
Background 4. It is common cause that C[...] suffers from cerebral palsy . What is in dispute is
whether the nursing care provided during C[...]’s birth at the hospital fell below the
accepted medical standard, and if so, whether that substandard care caused C[...] to
suffer a brain injury resulting in cerebral palsy.
5. The parties agreed that it would be convenient to separate the issues of
liability from that of the quantum of the plaintiff’s claim. An order to that effect was granted in ter ms of Uniform Rule of Court 33(4) and the matter proceeded to trial
only on the issues of negligence and liability. The quantum of the plaintiff’s claim was
postponed sine die.
6. The trial lasted for 10 days. The plaintiff testified in person. All the experts
testified virtually. The following experts testified on behalf of the plaintiff : Prof GB
Theron ( Obstetrician ); Dr. D Pearce (Paediatric Neurologist); Prof AGW Nolte
(Speciality Nurse ); Prof J Smith (Neonatologist) and Dr. Suzanne O’Hagan
(Neuroradiologist) . The defendant called t hree factual witnesses and the following
experts: Dr. Weinstein (Neuroradiologist); Dr. T M Marishane
(Obstetrician/Gynaecologist); Dr. Mogashoa (Paediatric Neurologist ); Prof K Bolton
(Paediatrician); Prof P A Cooper (Neonatologist).
7. There is a sharp dispute between the Plaintiff’s experts and the Defendant’s
experts on the cause and the timing of the injury. The Plaintiff’s experts say it was the negligence of the nursing staff during labour that led to hypoxia which caused the injury and that the injury had occurred intrapartum. The Defendant’s experts say it
3 was the sepsis that caused apnoea after C[...] was discharged and that it was the
apnoea that caused the injury, which accordingly occurred postnatally.
8. All the expert witnesses had regard to the hospital records and the clinical
notes upon which their opinions were based. The documents are voluminous and
although all testimony was considered, what is reflected here are mostly summaries.
9. Neither the locus standi of any of the parties nor the vicarious obligation of the
defendant is in dispute and the court must determine:
(1) Causal negligence as pleaded in paragraphs 6 to 8.1 1 of the particulars
of the claim.
1
(2) The existence of a duty of care of the staff and the defendant to C[...]
(in utero and as a neonate) and Mrs v[...] W[...], which are disputed in the plea.
Issues
10. The issues for determination are:
i) Whether C[...] suffered a hypoxic -ischaemic brain injury during birth.
(The timing issue).
ii) Whether the defendant or its staff were negligent, and if so, whether
such negligence caused or materially contributed to the hypoxic -ischaemic
brain injury in the sense that the hospital staff , by the exercise of reasonable
professional care and skill , could have and should have prevented the
intrapartum hypoxic -ischaemic brain injury from occurring. (The causative
negligence issue).
The Plaintiff’s version
11. Mrs V[...] W[...] testified that C[...] was her firstborn child. She was 28 years
old at the time of her pregnancy. She attended Skinner Street Clinic and consulted a
private practitioner, Dr. Heyns , on approximately three occasions during the
1 0001- 6 – 0001- 12 Particulars of Claim found on Caselines
4 pregnancy. She stated that her primary reason for consulting Dr. Heyns was to
determine the baby's sex. During these consultations, Dr. Heyns conducted medical
assessments, including measuring her blood pressure, listening to the baby's
heartbeat, and performing a sonographic scan. He informed her that she was expecting a girl and that there were no adverse findings.
12. Mrs v[...] W[...] remained in good health throughout her pregnancy . She also
confirmed that she does not smoke n or consume alcohol.
13. During the early hours of the morning of 2 March 2008, she began
experiencing contractions and proceeded to Tshwane District Hospital for delivery.
14. Mrs V[...] W[...] gave evidence that during the birth process she was
intermittently assessed for dilatation, subjected to a “belt test” and she followed the
bearing down instructions of the midwives in attendance. The birth was difficult, long
and painful.
15. She was attended by three midwives during labour: one positioned at her feet,
another holding her hand, and a third on a stool beside the bed. The third midwife applied pressure to her abdomen above the ribcage in an effort to assist in the delivery. She was instructed to push whilst this third midwife exerted a single force of
fundal pressure resulting in the immediate birth of C[...] by unassisted vaginal
delivery . Upon delivery , C[...] was not crying, and she was accused of having "killed
her child" . The midwife slapped C[...] against Mrs V[...] W[...]’s thigh and took her
behind a curtain. It was only after a few minutes that C[...] started crying. She was
wrapped in a blanket and handed to Mrs V[...] W[...] , and then placed in a crib while
Mrs V[...] W[...] was attended to.
16. After delivery, she and C[...] were transferred to a ward. Later that same
evening she observed that C[...] was not breathing properly and alerted a nurse.
C[...] was taken away and subsequently placed in an incubator.
17. The day following the birth, both Mrs v[...] W[...] and C[...] were discharged
from the hospital. Upon arriving home, she noticed that C[...]’s hands remained
5 clenched in a claw -like position near her head and that she exhibited a bluish- purple
discolou ration around the mouth and face. Concerned, she returned to Dr. Heyns ,
who examined C[...] and provided a referral letter, leading to C[...]’s re -admission to
the hospital.
18. Upon re- admission, blood tests were conducted, and medical professionals
assured Mrs. v[...] W[...] that C[...] would be fine. However, she stated that at no
stage was she informed of any formal diagnosis. She observed that C[...]’s head was abnormally shaped, resembling a “pawpaw”, and that C[...] ’s hands remained
clenched.
19. Mrs. v[...] W[...] further testified that she was unable to breastfeed because
C[...] did not latch and that she did not produce milk. Hospital staff provided her with
formula milk and a syringe for feeding, and she continued to feed C[...] in this
manner after discharge.
20. During cross examination Mrs. v[...] W[...] was questioned regarding whether
the bluish discolou ration around C[...]’s mouth persisted the day after discharge, and
she confirmed that it did. She stated that at approximately midnight, while still in the hospital, C[...] had stopped breathing and was placed in an incubator. Mrs . v[...]
W[...] remained with her until she resumed breathing independently .
21. It was put to Mrs . v[...] W[...] that it is common cause that C[...] suffers from
cerebral palsy, which she confirmed. She testified that upon returning home after discharge, she became increasingly concerned about C[...]’s condition, particularly noting the persistent clenching of the hands and the bluish discolo uration.
22. Mrs V[...] W[...] disputed entries in the hospital records suggesting that she
had been "restless" during labour, maintaining that she was stressed but not restless. She was questioned as to whether the room in which she gave birth was the same as the room where she was initially admitted and she stated that they were
different. She could not recall whether the hospital staff in both rooms were the
same.
6 23. She confirmed that at the time of C[...]’s birth, she was employed as a
qualified daycare teacher. She was shown the hospital records and asked whether
she had ever seen them before, to which she responded that she had not. While she
acknowledged that she was aware of hospital files being opened for both herself and C[...], she stated that she had never seen their contents.
24. Mr Son i (for the defendant) informed her that all state hospitals are legally
required to maintain records, which she acknowledged. She confirmed that various files were opened for C[...]. She also confirmed that she provided information at
different points to different medical personnel.
25. When probed about specific dates and times of the medical events, Mrs . V[...]
W[...] stated that she could not remember exact details. She confirmed that different
nurses and doctors attended to her and C[...] on multiple occasions.
26. She was asked whether she recalled specific medical examinations, including
whether a CTG (Cardiotocography ) was performed or whether a Doppler machine
was used to listen to the baby's heartbeat, and whether she was given pain
medication. She stated that she could not recall these details.
27. She was questioned regarding an entry indicating that she was asked to push
at 19h 00, to which she stated she did not recall. It was put to her that she was noted
as being "very restless and uncooperative" during delivery, which she denied. She confirmed that C[...] was born at 20h 05.
28. When asked whether an episiotomy was performed, she stated that she did
not know what it was. Mr Soni explained the procedure as a “cut in the uterus ,” but
she maintained that she could not remember.
29. Mrs. v[...] W[...] was asked whether C[...] was kept with her after birth, to which
she replied in the negative. It was put to her that C[...] ’s colour was recorded as pink
after the birth , but she stated that she could not recall. She was also questioned
about the baby's reflexes and meconium passage, to which she responded that she could not recall.
7
30. She disputed claims in the medical records that she "was not pushing well."
stating that she followed the nurses’ instructions to push.
31. She was questioned about the timing of her legal action. She stated that she
first contacted a lawyer in 2015 after discussing the matter with her brother, a law student at the time. Mr Soni suggested that her claim was a recent fabrication, which
led to a debate regarding the relevance of her brother's involvement.
32. She was shown the particulars of claim and amendments but stated that she
had never seen them before. It was put to her that the term "you killed your baby" did not appear in the particulars of claim.
33. It was put to her that the hospital records showed an entry that she had a UTI
(urinary tract infection) and took antibiotics on 2 February 2008. Her response was that she could not remember.
34. Mrs. v[...] W[...] testified that the events occurred 16 years ago and that she
was unable to recall all details. Mr Soni highlighted the discrepancies between her
testimony and hospital records and stated that the court would be asked to accept the records as correct. 35. It was put to her that fundal pressure was not recorded in the medical records,
which she disputed, maintaining that it had been used during delivery. She also insisted that a staff member had stated, "You killed your baby."
36. During re- examination, Mr Uys (counsel for Mrs v[...] W[...] ) questioned her
regarding the particulars of claim and amendments. She reiterated that she had never seen these documents before that day.
Plaintiff’s expert witnesses
37. Dr. O’ Hagan, stated that her evidence is based on current peer -reviewed
literature and clinical guidelines, including authoritative texts such as those authored
8 by Prof. Joseph Volpe and reports by the American College of Obstetricians and
Gynaecologists (ACOG).2
38. She testified that h ypoxic -ischemic brain injury arises when insufficient oxygen
reaches the brain cells. This pathological condition may occur in various clinical
settings and manifests in distinct patterns depending on the developmental stage of
the brain. Neonatal hypoxic -ischemic injury is particularly sensitive to the age and
maturation of the patient, which significantly influences radiographic appearance on MRI.
39. MRI patterns of injury vary depending on the patient's age, and these patterns
evolve over time from hyperacute to chronic phases. She emphasised the
importance of identifying the brain structures involved, as this helps determine the injury mechanisms. Established literature supports the significance of central patterns (e.g., basal ganglia and thalami involvement) and peripheral patterns. These are the predominant classifications recogni sed in both clinical and academic
contexts. She notes that historically, the term "acute profound hypoxic -ischemic
injury" was used to describe a sudden and severe interruption of oxygen supply.
40. However, recent advancements in literature since approximately 2018 have
shifted the preferred terminology to more precise anatomical descriptions, such as “basal ganglia- thalamus (BGT) injury,” often with perirolandic cortical involvement.
This evolution in nomenclature is reflected in current standards of radiological and
neuropathological practice. In this case, the injury pattern observed in C[...] involved
the basal ganglia and thalami. According to her testimony this pattern does not
necessarily result from a single acute event, as there are now recognized mechanisms that can cause this injury from prolonged or partial hypoxia, which may involve intermittent asphyxia,
41. In C[...]’s case , the MRI reveals chronic -phase findings characterized by T2 -
weighted hyperintensities in the bilateral thalami and putamina, more pronounced on
the right. These findings are consistent with chronic cytotoxic oedema and neuronal
2 Caselines 0005- 296.
9 loss. Notably, the brainstem and cerebellum are spared, and there is no radiological
evidence of watershed injury.
42. According to Dr. O’Hagan, MRI is capable of depicting gross anatomical injury
but cannot resolve individual neuronal injury. For visuali sation of injury patterns, a
sufficient volume of tissue must be involved. Images are typically acquired in sagittal, axial, and coronal planes, with axial views offering particular utility in identifying hypoxic -ischemic changes .
43. The MRI in C[...]’s case demonstrates a severe Grade 3 parasagittal
perirolandic injury, with abnormal T2 signal extending into the paracentral lobule and supplementary motor area. At the level of the basal ganglia, bilateral symmetric hyperintensity is noted in the thalami and putamina. These findings are consistent with a BGT pattern of injury, and the absence of watershed injury supports a non-diffuse pathophysiology.
44. She clarified that i n term neonates , that is babies defined radiologically as
those born at or beyond 36 weeks of gestation, BGT structures are metabolically
active and heavily myelinated, rendering them selectively vulnerable to hypoxic injury.
45. C[...]'s MRI findings align with the deep nuclear injury pattern involving
bilateral thalami, putamina, perirolandic cortex, and possibly the hippocampi. This pattern is symmetric and central, characteristic of what literature terms “cerebrocortical deep nuclear injury.” There is significant atrophy, ventricular
dilatation, and microcephaly, but no evidence of congenital anomalies or infections.
46. Although historically associated with single acute profound sentinel events,
emerging consensus —including Volpe’s 2018 and 2023 editions, the 2019 ACOG
guidance, and Wis nowski (2021)
3acknowledges that this pattern may result from
3 Volpe, Joseph J., and Terrie E. Inder, editors. Neurology of the Newborn. 7th ed., Elsevier, Jan. 8,
2024. American College of Obstetricians and Gynecologists. “Neonatal Encephalopathy and
Neurologic Outcome.” Obstetrics & Gynecology , vol. 123, no. 4, 2014, pp. 896– 901. Reaffirmed
2019. Newborn Brain Society –endorsed Wisnowski et al. article (2021)
10 either a single acute sentinel event, or prolonged partial hypoxia with intermittent
near-total asphyxial episodes .
47. Dr. O’ Hagan provided the fol lowing helpful illustrative analogy ; if a child is
repeatedly submerged in water (like being thrown into a swimming pool) with each
recovery being incomplete, eventually, the child’s capacity for recovery is exceeded,
resulting in injury. This scenario is analogous to repeated uterine contractions that progressively reduce oxygenation during birth. In a similar example intermittent
pressure, like stepping on a garden hose gradually reduces water flow until it ceases
entirely . This represents how repeated partial hypoxic events may culminate in
permanent brain injury.
48. In summary she testified that the MRI findings in C[...]’s case are indicative of
chronic BGT- type injury consistent with current neuropathological and radiological
classifications. These findings are in line with accepted contemporary literature and reflect a sophisticated understanding of neonatal brain injury mechanisms.
49. She noted that i t is not within the scope of the radiologist’s expertise to confirm
the occurrence of a sentinel event. Rather, her role is to accurately identify and
categorize anatomical injury patterns. In this case, the imaging findings are consistent with a BGT injury pattern, which, according to current medical consensus, may be attributable to either acute or serial hypoxic events.
50. For this specific case, MRI showed characteristic signs of injury in the basal
ganglia and thalami, along with severe perirolandic cortex involvement. She emphasi sed that while MRI cannot confirm the precise cause of the injury, it clearly
shows a pattern of injury consistent with the BGT (basal ganglia -thalamus) pattern,
which can result from either a single severe event or multiple less severe events over time.
Newborn Brain Society Guidelines and Publications Committee, et al. “Neuroimaging in the Term
Newborn with Neonatal Encephalopathy.” Seminars in Fetal and Neonatal Medicine, vol. 26, no. 5,
Oct. 2021, Article 101304, doi:10.1016/j.siny.2021.101304.
11 51. Dr. O’Hagan highlighted that this injury pattern is well -documented in the
literature, including work from prominent sources like Volpe's neonatology texts and
the Newborn Brain Society.4 She further clarified that MRI, rather than CT scan , is
crucial for detecting these types of injuries, and suggested that the injury could have been caused by serial partial insults rather than a single acute episode.
52. Under cross examination Mr Son i put it to her that this pattern could only result
from a single acute profound event , but Dr. O’ Hagan disagreed, stating that the
absence of a clear sentinel event does not exclude prolonged hypoxia as the cause.
She maintained that C[...]’s MRI shows a basal ganglia- thalamus (BGT) and
perirolandic injury pattern, which aligns with evolving literature recogni sing
that prolonged partial asphyxia can cause BGT injury.
53. Dr. O Hagan rejected the term "acute profound" hypoxic -ischemic injury , citing
that medical literature since 2018, including works by Wisnowski and Miser, has
moved away from this terminology in favour of anatomical descriptions like BGT
injury .
54. Mr Soni suggested that the old terminology was still used in some practices as
late as 2020, but Dr. O’Hagan emphasi sed that this terminology implies causation
rather than just anatomical damage, which is why it is now discouraged. She
explained that the current understanding of hypoxic -ischemic injury recogni ses
that multiple mechanisms , including prolonged partial asphyxia or serial hypoxic
events, can lead to BGT injury, not just a single catastrophic event.
55. Mr Soni asked whether BGT injury could result from multiple hypoxic episodes
postnatally, and then she confirmed that such a pattern could indeed emerge
from prolonged or severe hypoxia after birth .
56. Mr Soni raised concerns about the relevance of primate studies in supporting
human medical conclusions. Dr. O’Hagan acknowledged the limitations but affirmed
that findings from primate models suggest patterns similar to those observed in
4 Dr. Joseph Volpe, ‘Cerebral Visual Impairment (CVI): Important Challenge for Neonatology
https://newbornbrainsociety.org/commentaries -volpes -view/
12 human infants . She maintained that while conclusions in medical literature may not
be definitive, the strong body of evidence supports the view that cumulative hypoxic
events can result in BGT injury, reflecting the evolving understanding in the field.
57. Prof. Anna Nolte, an expert midwife, provided detailed evidence about the
purpose of guidelines for healthcare workers providing obstetric and anaesthetic services in public hospitals. These guidelines addr ess the lack of standardised
protocols in primary and secondary healthcare, which has led to high pregnancy -
related deaths. They focus on identifying and managing complications, including timely referrals to higher levels of care.
58. She also explained maternal care protocols, stating that a partogram is a
chart /graph that tracks maternal and foetal condition, labour progress, including
cervical dilation, uterine contractions, and foetal descent. Alert and action lines monitor labour progress, with action required if dilation exceeds set thresholds.
59. She explained the stages of labour and the importance of the four P’s of
labour: the Passenger (foetus, position, head moulding, condition), the Passage
(maternal pelvis and birth canal), the Powers (strength and frequency of uterine
contractions), and the Patient (maternal condition and readiness for delivery). The stages of labour are first stage (cervical dilation up to 10 cm, with specific monitoring frequencies during latent and active phases), second stage (begins at full dilation and ends with delivery), and third stage (delivery of the placenta). 60. Foetal monitoring is crucial to detect signs of distress. Normal foetal heart rate
(FHR) is 120– 160 bpm. Variability below 5 bpm or decelerations indicate potential
distress and require intervention. Monitoring intervals vary by labour stage, with additional monitoring during the second stage and after contractions.
61. Signs of foetal distress include abnormal FHR, lack of variability, or
meconium -stained liquor. In such cases, the staff should immediately position the
mother laterally , administer oxygen and IV fluids, and perform a vaginal exam to
exclude cord prolapse. If delivery is imminent, proceed with vacuum delivery; otherwise, prepare for caesarean section.
13
62. Newborns are assessed using the APGAR score at 1 and 5 minutes to
evaluate breathing, muscle tone, colour, and responsiveness. Routine care is provided if the baby is born at term with clear amniotic fluid, breathing/crying, good muscle tone, and pink skin.
63. She mentioned that labour management tools include a Doppler (handheld
device) for monitoring foetal heart rate and a cardiotocography (CTG) for continuous monitoring of heart rate and contractions, with stored tracings in patient files.
64. Prof. Nolte reviewed C[...]’s obstetric clinical records. The records show that
Mrs V[...] W[...] walked in at 6 :50 am, was a primigravida (first pregnancy) at 40
weeks’ gestation, and had complained of lower abdominal pain since 3h 30 am that
morning.
65. A CTG was done, and it was described as reactive, suggesting normal foetal
heart rate variability and reactivity. However, the contractions probe was not working,
meaning one of the two CTG probes (the one that measures uterine contractions)
did not register. Prof. Nolte explained that this probe is typically placed on the top
part of the maternal abdomen to monitor contractions. It is crucial to monitor both the
foetal heart rate and contractions simultaneously for meaningful interpretation.
66. Despite the probe malfunction, the midwife palpated contractions manually.
The record shows 2 contractions in 10 minutes, a standard way to quantify frequency. The midwife interpreted the CTG as reactive and performed a vaginal examination, assessing cervical dilatation, station, effacement, and application, bulging membranes, and completed a full maternal assessment.
67. Mrs V[...] W[...] was admitted to the waiting room for further management.
During the latent phase, the foetal heart rate was 145 bpm, strong contractions occurred at 10h00, blood pressure, pulse, and temperature were recorded, and no problems were found.
14 68. Mrs V[...] W[...]’s labour partogram (“the partogram”) was compared with the
guideline partogram (“the guideline partogram”). Prof. Nolte explained that the
guideline partogram is more detailed and standardised for assessing foetal distress,
especially when interpreting foetal heart rate in relation to contractions. The provincial record partogram (used for Mrs V[...] W[...]) only provides a line for writing
foetal heart rate, without guidance on variability or decelerations. The guideline recommends recording foetal heart rate before, during, and after a contraction.
69. Prof. Nolte pointed out that the provincial record partogram lacks the
necessary detail to differentiate heart rate readings before and after contractions. Symbols like circles or crosses should be used for this purpose, but they are absent. The provincial record partogram and notes also do not indicate whether the foetal
heart rate was recorded relative to contractions.
70. At 12h00, the Active Phase Record of Labour (a contemporaneous note of
progress) shows a foetal heart rate of 140 bpm, moderate to strong contractions, and
an unclear note indicating 3 contractions in 10 minutes. This matches the
partogram’s stable heart rate of 130 bpm at 11h30.
71. Prof. Nolte observed that from 12h00 to 14h00, contractions were consistently
described as strong and occurred at a steady frequency (3 in 10 minutes). However, from 14h00 onwards, the partogram shifted to simply describe contractions as ‘strong’, as indicated by changes in the graph’s shading or colouring.
72. At 17h30, the patient was 9 cm dilated, but the partogram does not record the
strength or frequency of contractions. Only a single foetal heart rate entry is visible.
She compared this with the active phase record of labour which shows the following:
• 13h30 – Moderate contractions, likely “3 in 10”
• 15h30 – Strong contractions, 3 in 10, and 8 cm dilation
• 17h30 – Strong contractions and 9 cm dilation
73. 19h00 – Patient found with strong contractions, but not reassessed at 18h 30.
The birth occurs at 20 h05.
15 74. During the second stage of labour, the cervix is fully dilated (10 cm) but Mrs
V[...] W[...] is noted as restless and uncooperative. Clinical guidelines allow up to 2
hours before pushing once the cervix is fully dilated, especially if the head of the
foetus still high. 75. Another concerning factor is that the level of the foetal head is not recorded.
On the partogram the descent is marked as “1” consistently at 11 h30, 13h 30, 15h 30,
and 17h 30. From 17h 30 onward, no station data is recorded, indicating no tracking
of descent at a crucial stage of labour.
76. Moulding and caput remain unmarked (indicated by a dash). Effacement is
poorly recorded and possibly misrepresented as values like ‘4’, ‘3’, and ‘2’, which Prof. Nolte explains is invalid. Effacement should be noted in centimetres or
percentages. Application (how well the foetal head is applied to the cervix) is consistently marked as ‘fair’.
77. Prof. Nolte noted that the patient’s labour progress as recorded in the
partogram was as follows: at 11h30, she was in the active phase at 5 cm dilation,
progressing to 6 cm at 13h30. However, this was slower than expected, as she had
crossed the alert line.
78. From 13h 30 to 15h 30 and 15h 30 to 17h 30, progress resumes at the expected
1 cm per hour. However, expected dilation of 10 cm at 17h 30, is only recorded as
reached at 19:00. This delay means she had crossed both the alert and action lines
on the partogram, the latter typically signalling the need for hospital -level intervention
if in a community clinic.
79. Prof. Nolte explained that each block on the partogram represents an hour. By
19h00, the dilation curve would be four hours beyond the alert line, placing it on the action line, which supports concerns about delayed or inadequate clinical response.
80. The second stage of labour began at 19h00, as per the earlier entry. She
explained the clinical management algorithm: if the head is still high after full dilation, there is a 2 -hour window for descent before pushing starts. If the head is on the
16 perineum, the pushing phase allows for 45 minutes. If the patient starts pushing, the
45-minute rule applies before the second stage is considered prolonged. This was
not followed.
81. The third stage ended at 8h 15 pm. There is no record of a doctor assisting
during labour .
82. Prof. Nolte further testified that C[...]’s b irth metrics were all within normal
parameters for a full -term female baby; weight 3.314 kg, length 52 cm, and head
circumference 33 cm .
83. Her Apgar Scores:1 Minute: Score of 4/10, with 1 each for heart rate,
respiratory effort, muscle tone, colour, and 0 for reflexes . 5 Minutes : Improved to
6/10. Reflexes and respiratory effort showed slight improvement; cyanosis persisted. 10 Minutes : Reached 9/10, with all parameters scoring 2 except reflexes
(1).
84. Prof. Nolte explained C[...]’s lack of reflexes (0 at 1 minute) as a sign of
hypoxia, which affected her neurological response at birth. Normally, newborns respond to stimuli, but C[...] was initially unresponsive.
85. A score of 4/10 at one minute was concerning. Resuscitative efforts, including
oxygen administration, improved C[...]’s condition. Ideal scores are 9– 10, with scores
below 7 indicating clinical concern. C[...] passed meconium, cried, and was
resuscitated with 2L oxygen and suction. These observations were likely made after 10 minutes of birth.
86. Prof. Nolte noted late decelerations in the first tracing on the CTG, suggesting
foetal distress. The second tracing showed a prolonged deceleration after contractions, while the third tracing indicated tachycardia, possibly also indicating foetal distress.
87. It is recorded that the CTG was s topped because the patient was too restless.
Despite restlessness, continuous monitoring using a Doppler device should have
17 been continued after these late decelerations, which should have prompted
immediate medical intervention, including intrauterine resuscitation.
88. In summary , Prof Nolte’s evidence was to the effect that Mrs v[...] W[...]’s
labour progressed slowly, with cervical dilation crossing the alert line by 13:30. Despite some progress, her active labour phase remained suboptimal, with delayed cervical dilation and increasing foetal heart rates. Pethidine and Atarax were administered, and Mrs V[...] W[...] became very restless and uncooperative during
labour. Continuous foetal monitoring was compromised due to poor CTG contact, and foetal heart rate recordings were incomplete —especially during the second
stage of labour between 18h 30 and 20h 05. An alive female infant was delivered at
20h05 with low Apgar scores of 4, 6, and 9, requiring oxygen and suction
resuscitation. Though initially stable, the baby exhibited poor sucking reflexes and was later discharged despite feeding difficulties and early signs of distress.
89. Therefore, it is her opinion that the care rendered was sub- standard: maternal
and foetal observations were not performed according to national maternity
guidelines, the slow labour progress was not escalated, foetal distress was not timely
recogni sed, and a vulnerable newborn was prematurely roomed- in and discharged
without appropriate medical referral.
90. Under cross -examination, Prof. Nolte maintained her belief that decelerations
were likely pathological . She disagreed with the version put to her that Dr.
Marishane’s view is that variability was preserved and decelerations were artefacts
caused by poor transducer contact. She stressed that decelerations, regardless of
variability, warrant caution and further monitoring.
91. Prof. Theron also provided detailed evidence on the partogram entries, which
will not be repeated as it largely corresponds with Prof. Nolte’s observations .
Notably, he also observed that cervical dilatation was slower than expected. Labour
progression was documented as follows: at 11h 30 – 5 cm , at 15h30 – 8 cm , at
17h30 – 9 cm, at 19h 00 – fully dilated (10 cm) .
18 92. Under normal circumstances, the cervix should dilate by 1 centimeter per
hour. However, Mrs V[...] W[...] ’s progress was slower than anticipated, as one would
normally expect full dilation (10 centimeters ) by 17h30. The slow progress should
have prompted the midwives to notify the attending doctor at the hospital.
93. He also confirmed that t he partogram used during Mrs V[...] W[...]’s 2008
delivery was outdated. Maternity care guidelines introduced a new version in 2006 or 2007. The revised partogram has a new action line, two hours to the left of the original, indicating prompt intervention when labour progresses to this line. However, in this case measures to expedite delivery were not implemented.
94. The CTG tracings showed baseline variability , but also periods of lost
contact and decelerations . Poor quality in some areas, partly due to maternal
restlessness .
95. He testified that nursing staff must report any deviations from expected clinical
patterns, especially concerning foetal conditions during labour. Continuous foetal
monitoring is crucial, and decelerations in the foetal heart rate should be interpreted
in the context of uterine contractions. Early decelerations may coincide with
contractions, while variable decelerations may occur independently. Late decelerations, which begin after a contraction’s peak and return to baseline, indicate foetal distress.
96. During labour, especially the second stage, continuous cardiotocography
(CTG) is crucial. Mrs v[...] W[...] was restless, which is normal during the second
stage, especially for first -time mothers. The records indicate that the CTG was
stopped. However, foetal heart rate should be assessed with each contraction,
before, during, and after, using either CTG or a Doppler every 30 minutes. Maternal
observations are usually done every two hours.
97. At full cervical dilation (10 cm), the decision was made to instruct the patient to
push. However, the records show that Mrs V[...] W[...] was restless, not pushing
effectively, and uncooperative, each rated at 3+. While midwives are expected to provide guidance during this stage, standard practice dictates that pushing should
19 only begin when the foetal head is less than two- fifths above the pelvic brim ( here it
is noted as 1/5 on the partogram). A first -time mother is generally given 45 minutes
for effective pushing; if delivery has not occurred by then, the midwife must alert the
attending physician for potential intervention.
98. Progress during labour must be closely monitored. Slow cervical dilation,
particularly between 8 and 9 cm, should raise concerns about a potential prolonged second stage. Reassessment should occur within an hour of noted stagnation, and if progress remains inadequate, the physician must be informed promptly to evaluate for surgical or assisted delivery.
99. According to Prof. Theron the foetal heart rate monitoring was inadequate.
The CTG documentation lacks sufficient correlation between decelerations and uterine contractions, making it unreliable for assessment of the foetal condition.
100. Mrs V[...] W[...]’s labour lasted 16 hours, with the second stage lasting 1 hour
and 5 minutes. Cervical dilation from 5 cm at 11h30 should have reached full dilation
by 16:30. However, it progressed slowly between 15h30 and 19h00, suggesting an
abnormal labour pattern. A timely reassessment at 17h30, when dilation had only
advanced from 8 to 9 cm, could have allowed for corrective action. The delay in response likely contributed to the adverse outcome.
101. He stated that s igns of foetal compromise were evident as early as 14h 20,
according to the CTG tracings. Allowing labour to continue into a prolonged and
difficult second stage under such conditions was inadvisable. The "golden rule" in such cases is to suppress labour and proceed with a caesarean delivery when foetal
well-being is at risk.
102. Notably, fundal pressure was applied at delivery. T his manoeuvre is
controversial and not endorsed in clinical training due to associated risks. In this case, its contribution to the adverse outcome is considered minimal, though its use remains a point of concern.
20 103. Prof. Theron noted that insofar as the condition of the foetus at birth is
concerned, the neonatologist is the most appropriate person to evaluate neonatal
outcomes. Howeve r, the presence of poor muscle tone and lack of responsiveness
are alarming signs, warranting serious concern from an obstetric perspective.
104. During cross -examination, it was put to him that Dr. Marishane is of the view
that there was no delay in delivery, citing the World Health Organization’s position. Dr. Marishane further argues that there was no evidence to suggest instrumental
delivery was indicated, and that if used, it is often blamed for cerebral palsy, and there was no need to expedite delivery.
105. Prof. Theron disagreed. He believed that if the attending physician had been
promptly notified when slow progress was observed (at 13h 30, 15h 30, and 17h 30),
the doctor would have been more alert to the potential for a difficult delivery. Early notification could have prevented the prolonged second stage of labour.
106. Regarding the CTG it was put to him that Dr. Marishane argues that the
tracing from 14h 17 onward shows poor contact of the transducer, and that the
observed decelerations, though accompanied by good variability, are not pathological.
107. Prof. Theron disagreed with this proposition. The FIGO classification system
clearly distinguishes between normal, suspicious, and pathological CTG tracings. Even if light decelerations occur with good variability over 30 minutes, the pattern should be considered pathological. The FIGO classification says a pathological CTG has a sustained baseline foetal heart rate below 100 beats per minute. However, prolonged decelerations —especially if they last 20 to 30 minutes —are abnormal,
even with good variability.
108. Prof. Theron says the CTG data, particularly from 14h17 to 14h47, clearly
shows a 30- minute period of decelerations that meet the criteria for a pathological
CTG. This should have prompted concern about the foetal condition and immediate intervention, rather than allowing labour to continue.
21 109. Prof. Smith , explained that neonatal encephalopathy is a condition
characterised by altered consciousness, changes in primitive reflexes, difficulty
latching, sucking, and swallowing, and altered muscle tone, which can make a baby hypertonic, hypotonic, or fluctuate between these states. Seizures may also occur. Encephalopathy is a general term for these features, but they can be caused by factors other than intrapartum hypoxic -ischemic injury. Therefore, when evaluating
cases of cerebral palsy, it is important to excl ude other potential causes that might
mimic encephalopathy.
110. He stated that neonatal encephalopathy, appearing within the first few hours
to two or three days after birth, in conjunction with cerebral palsy, and alternative causes ruled out, suggests intrapartum hypoxic -ischemic injury. Labour and delivery
events are critically evaluated, starting with the antenatal period to check for maternal hypoxic illness or predisposing conditions, then moving to the intrapartum period.
111. He agreed with Prof. Theron’s explanation that CTG tracings during labour
showed serious warning signs that the foetus was at risk for a long time, but no
effective intervention was taken.
112. He stated that C[...] was born in a state of secondary apnea, not breathing,
with bradycardia, and requiring resuscitative measures, as confirmed by Prof.
Cooper. Secondary apnea is severe and can be fatal if left uncorrected. It suggests a preceding period of primary apnea, indicating a hypoxic insult during the second stage of labour, when maternal pushing intensifies the forces. Despite clear CTG warnings during this critical period, appropriate intervention was not initiated, leaving the baby in a compromised condition.
113. He explained that during labo ur, the foetus experienced progressive hypoxia,
a lack of oxygen, that gradually depleted its energy reserves. This culminated in a
critical event, described metaphorically as going over a "waterfall edge," where the foetus transitioned from primary to secondary apnoea. This stage involves
significant acid-base imbalance, due to a shift to anaerobic metabolism , leading
to acidosis and multi -organ effects .
22
114. At birth, C[...] was compromised and required resuscitation, although no blood
gas test was performed to confirm the metabolic state, a key missed opportunity.
She was later diagnosed with early -onset neonatal encephalopathy , initially mild but
worsening after an inappropriately early discharge. C[...] was readmitted to hospital
within 5.5 hours of discharge with more severe symptom s, including cyanosis at
home.
115. The brain injury pattern, affecting the basal ganglia, thalamus, and perirolandic
cortex, suggests acute profound hypoxic -ischemic injury, requiring 10– 20 minutes of
severe circulatory failure. However, no evidence supports such a prolonged collapse. The previous expert witnesses (like Dr. O Hagan) believe progressive hypoxia during
labour, especially in a vulnerable foetus, led to decompensation, as evidenced by foetal heart rate abnormalities.
116. Prof. Smith is of the view that t here is no indication of antenatal brain injury ,
and the injury was not caused postnatally. Both Pro f Nolte and Ther on pointed out
how the midwives missed warning signs , and inadequate ly managed foetal
distress during labour . After birth, further substandard care, particularly the failure to
admit C[...] to high or intensive care, as per 2006 Department of Health guidelines ,
potentially worsened her condition.
117. Neonates face a critical recovery period in the first six hours after birth, during
which they are vulnerable to secondary energy failure due to factors like hypoglycaemia, seizures, infection, hyperthermia, and oxygen mismanagement. C[...] exhibited feeding difficulties, desaturation episodes, and seizures, which were
poorly monitored. Oxygenation management was inadequate, with non- standard
practices like ‘double oxygen’ delivery. Despite these challenges, she was eventually
was stabilised and transferred to Pretoria Academic Hospital
118. The results of C[...] ’s blood tests and l aboratory findings showed evidence
of metaboli c acidosis , kidney injury , elevated inflammatory markers , and possible
dehy dration . Although a urinary tract infection (UTI) was suspected, urine cultures
did not confirm this .
23
119. More i mportantly, Prof. Smith stated there is no credible evidence linking the
UTI to the specific brain injury , which is not typically associated with infection- related
patterns. Literature supports that neonatal infections more commonly cause white
matter injury , not the deep grey matter injury seen in this case.
120. C[...] had various episodes of s eizure activity consistent with moderate
encephalopathy . This further supports a significant perinatal hypoxic event.
The cranial ultrasound performed three days post -birth showed no signs of pre-
existing injury or infection, reinforcing that the insult occurred during labour .
121. Finally, Prof Smith is of the view that while studies show inflammation may
worsen hypoxic -ischemic injury, there is no conclusive evidence that it played a
significant role in this case. Systematic reviews found no clear link between perinatal
infection and worsened outcomes in neonatal encephalopathy, and further research is needed.
122. Dr. Debbie Pearce testified that C[...] display s profound disability with mixed -
type cerebral palsy, predominantly dystonic in nature, which is considered one of the
most severe presentations . She is totally dependent her caregivers for daily
activities .
123. According to Dr. Pearce her injuries align with a PBGT injury pattern typical
of chronic hypoxic -ischemic injury, likely resulting from intrapartum hypoxia. There is
no evidence of genetic, inflammatory, or infective pathology on imaging.
124. In a j oint minute with Dr. Mogas hoa the experts agreed on:
• The mixed nature of cerebral palsy ;
• Presence of multiple comorbidities ;
• A diagnosis of Grade 2 neonatal encephalopathy ;
• MRI findings indicative of chronic PBGT pattern injury ;
125. Dr. Mogashoa deferred interpretation of MRI to radiologists and acknowledged
infection as a possible contributing cause of hypoxia. Both experts deferred final
24 conclusions on infection and postnatal care to neonatology experts. Possible causes
of neonatal encephalopathy considered included:
• Hypoxic -ischemic encephalopathy (HIE) (primary diagnosis)
• Infection
• Congenital anomalies
• Metabolic disorders
• Placental insufficiency
• Intrauterine growth restriction
• Inborn errors of metabolism
126. Despite some evidence of infection (e.g., raised WCC, CRP, and a UTI
diagnosis), the dominant cause of C[...]’s condition was deemed to be intrapartum
hypoxia.
127. In their application of the of ACOG criteria the following were noted:
• Neonatal encephalopathy (Grade 2) was present
• Apgar scores (6 at 5 minutes, 9 at 10 minutes) did not meet the <5
threshold
• No cord blood gases available
• MRI findings consistent with HIE
• No confirmed sentinel event
• Multisystem involvement (neurological, renal) present
128. Dr. Pearce noted that according to the mother’s presentation of the clinical
history, C[...] did not cry immediately at birth, and stopped breathing later that night .
Convulsions occurred within 24 hours . She was readmitted on the same day with
oxygen needs and feeding difficulties . Following re-admission, she was d iagnosed
with a UTI and had a non- contributory lumbar puncture.
129. She agree d with the previous experts who testified on behalf of the plaintiff
that the deterioration of C[...]’s condition post-discharge was part of a continuum of
the initial hypoxic insult, not a new event.
25 130. Dr. Pierce stated that insofar as the infection was concerned no microbial
growth was confirmed. While infection may have been a risk factor, it was not
the primary cause. The clinical and radiological evidence supports hypoxic -ischemic
encephalopathy as the central aetiology.
131. With regard to the timing of the injury no significant antenatal risk factors were
identified. The pattern and chronic nature of injury suggest that it occurred shortly
before delivery, not antenatally or postnatally.
132. During c ross-examination she stated that ACOG criteria are not a checklist but
rather guide. The Apgar scores and absent cord gas data were acknowledged as
limitations. Neurological dysfunction is a prerequisite of neonatal encephalopathy
and therefore not listed as an additional system involvement. Apnoea was
interpreted as neurological in origin, with respiratory distress potentially reflecting acidosis.
Defendant ’s expert witnesses
133. Dr. Marishane testified that the progression of labour was within normal limits.
A delay occurred between 5 cm and 6 cm cervical dilation, lasting approximately two
hours, but this did not cross the action line on the partogram. Historically, a cervical
dilation rate of 1 cm/hour during the active phase was used as a standard, but this
assumption , especially for first -time mothers , has been scientifically discredited. The
WHO no longer recommends this outdated threshold, recognizing that labour
progresses at different rates for different women. Reliance on this standard has led
to unnecessary interventions, including caesarean sections and artificial labour
augmentation.
134. He stated that he idea that caesarean section prevents cerebral palsy is not
supported by credible evidence. Caesarean sections , whether elective or
emergency , have not been shown to reduce the incidence of cerebral palsy . Only
a small fraction of cerebral palsy cases are caused by acute intrapartum hypoxia.
Notably, emergency caesarean sections are associated with a higher incidence of
26 cerebral palsy, likely because these procedures are usually performed after foetal
injury has already occurred.
135. He cited the 2018 WHO review and provided the following insights:
• There is no universally accepted definition for prolonged first stage of
labour.
• Traditional thresholds used to define prolonged labour were based more
on clinical custom than scientific evidence.
• The WHO meta- analysis found no sound justification for using strict time
limits to diagnose prolonged first -stage labour.
• Therefore, the term “prolonged first stage” is now viewed as vague and
unsuitable for guiding interventions.
136. Regarding the second stage of labour he said that t his stage begins at full
cervical dilation and ends with delivery. FIGO recommends a maximum of two
hours for this stage. WHO permits up to three hours in women receiving epidural
anaesthesia. In Mrs V[...] W[...]’s case, the second stage did not exceed the two- hour
limit.
137. During c ross examination Dr. Marishane initially resisted applying a strict 1
cm/hour dilatation standard, citing WHO's evolving stance, but eventually conceded
that the action line had been crossed by 19h 00. He also acknowledged that
an examination at 18h 30 was omitted but maintained that intervention was not
mandatory at that point because the patient was already in hospital.
138. With regard to foetal monitoring and CTG analysis Dr. Marishane disputed
Prof. Theron’s interpretation, attributing CTG unreliability to maternal restlessness ,
and claimed that standard tools like Doppler or stethoscope could suffice. He
insisted that t he nursing records showed no abnormalities , and no escalation was
warranted unless documented concerns existed.
139. Mr Uys challenged Dr. Marishane's reliance on nursing records that lacked
detail on heart rate timing relative to contractions , as well as the a bsence of
documented abnormalities as a basis to conclude there were none.
27
140. Dr. Marishane defended his stance, asserting that he interpreted the
records in good faith. Clinical trust in the nursing staff is standard unless there's
evidence of error. His analysis did not reflect bias but followed accepted practice.
141. Dr. Weinstein stated that his report describes abnormalities observed in a 10-
year-old C[...]’ s MRI, particularly affecting the bilateral thalamus, putamen, corona
radiata, and periventricular subcortical white matter. He characterized the injury as an “acute profound” pattern, meaning it resulted from a short, severe hypoxic event,
with no signs of a “partial prolonged” injury, indicating the absence of an extended
hypoxic episode.
142. Dr. Weinstein explained that the MRI, taken when C[...] was over 10 years old,
showed no recent injury , supported by the lack of diffusion restriction on the
diffusion- weighted imaging sequence. However, he acknowledged the limitations of
MRI in determining the precise timing or cause of an injury, stating that such
conclusions require correlation with clinical, laboratory, and serial imaging data.
143. He noted that t he cranial ultrasound done on day 4 of C[...]’s life was normal.
There were no signs of mass effect, echogenic abnormalities, or early oedema
changes typical of perinatal hypoxic events. This, according to Dr. Weinstein, makes
it unlikely that the injury occurred shortly before or during labour.
144. While both Dr. Weinstein and Dr. O’Hagan agreed on which brain
regions were affected, they differed on the terminology. Dr. O’Hagan preferred
anatomically descriptive terms and cited the Wisnowski article , which cautions
against traditional pathophysiological labels. In contrast, Dr. Weinstein defended the
use of “acute profound”, citing long- standing international neuroradiology literature,
including work by Prof. Barkovich and Dr. Masser , asserting that these terms remain
valid when paired with clinical context.
5
5 Caselines 0006 -32
28 145. Dr. Weinstein addr essed interpretations from the Wisnowski article , stating
that while some animal studies suggest intermittent hypoxia could lead to basal
ganglia- thalamus (BGT) injury, there is no clinical evidence in humans supporting
this assumption. He emphasized that such a pattern usually reflects a single, severe
hypoxic event , even if it was clinically silent at the time.
146. Dr. Weinstein categorised C[...]’ s injury as fitting the acute profound profile ---
severe, short -duration hypoxia affecting metabolically sensitive regions. There
were no features of a watershed pattern, which would suggest a more prolonged or
intermittent event.
147. Under cross examination Dr. Weinstein accepted that here were periods of
slow progress , especially between 15h30 and 17h 30, and again until 19h00.
According to protocol, this met the definition of slow progress and could cross the
action line on the partogram , prompting medical review or intervention. Although
clinical judgment also plays a role, the observed delays warranted closer monitoring and possibly escalation of care.
148. He also accepted that delays in the first stage can increase the risk of second-
stage delays . Therefore, proactive management was warranted once full dilation was
reached at 19h00, given the earlier background of delay . He agreed it would have
been reasonable to involve senior clinicians at that point .
149. With regard to the CTG tracings Dr. Weinstein acknowledged that The CTG
was not ideal for stand- alone decision- making. Decelerations and reduced
variability were observed. He also agreed that i n such cases, clinicians should
use alternative monitoring methods (e.g., handheld Doppler or stethoscope). The
CTG could have warranted heightened vigilance and possibly intervention.
150. Dr. Weinstein acknowledged several shortcomings in clinical management ,
including delays in reassessment , failure to escalate, and insufficient documentation.
He supported the view that these issues fell short of expected standards but maintained that the available evidence was insufficient to conclusively establish
causation.
29
151. Prof. Bolton was of the view that even though C[...] had low APGAR scores
at birth , she was breathing but not crying, which is not unusual . She
received supplemental oxygen and suctioning, but no records showed positive
pressure ventilation (PPV) , bagging, or intubation. He stated such interventions
would typically be documented if performed.
152. C[...]’s vital signs were monitored and a raised temperature ( 36.1 –37.4°C)
was recorded. This was not seen as abnormal. Blood pressure and oxygen
saturation were not measured, which P rof. Bolton deemed standard unless she was
in intensive care.
153. The nursing notes and a control chart documented feeding difficulties such as
a poor latch and unsatisfactory sucking reflex . C[...] was fed with formula ( NAN) .
154. She was placed on oxygen and later appeared pink, indicating improvement.
Prof Bolton acknowledged poor sucking reflex is more concerning than poor latch
and requires closer observation. He agreed that babies showing such signs should
be carefully monitored before discharge.
155. Mr Uys put it to him that C[...] displayed early signs of HIE (hypoxic -ischemic
encephalopathy) . Prof Bol ton initially denied clear evidence of encephalopathy , but
conceded that if the mother’s account is accurate and C[...] was placed in an
incubator she should not have been discharged . Prof. Bolton stated that he did not
have records on the incubator use and did not comment on it .
156. Prof. Smuts is employed at Steve Biko Academic Hospital . She is of the view
that C[...] ’s treatment followed hospital protocol s;
antibiotics and anticonvulsants were administered for seizures, apnoea, and
breathing issues . She supported neonatal sepsis , potentially caused by maternal UTI
and antibiotic use during pregnancy as the cause of the injury.
157. This is in contrast with the neonatologists who attributed the injury
to intrapartum hypoxia .
30
158. She maintains that C[...] ’s clinical presentation and treatment were reasonable
and appropriate. The brain injury was likely due to poor circulation, possibly linked
to infection- related hypoxia/sepsis .
159. She was testifying as a factual witness , not offering expert conclusions
on obstetrics or causation.
160. Mr Uys questioned her neutrality , citing her employment at the defendant
hospital . Mr Soni clarified that her evidence was limited to factual testimony , not
expert opinion. As a result, portions of her evidence that exceeded her factual
witness role was disallowed especially any speculative medical conclusions .
161. Prof. Cooper stated that C[...] presented with secondary apnoea at birth ,
suggesting a significant hypoxic event occurred before or during delivery . He agreed
that f eeding issues can signal mild neonatal encephalopathy , although other signs
(e.g., jitteriness, hyper alertness ) were not observed initially . Thus , while feeding
concerns were noted, clinical evidence of encephalopathy was limited in the early
period.
162. Prof. Cooper explained that elevated respiratory rates and heart rates just
under 100 bpm can be considered normal in term infants , especially when other vital
signs are stable. These signs alone did not justify intensive investigation unless
accompanied by additional symptoms.
163. He noted that i deally, newborns should be monitored hourly for 6– 12 hours
post-resuscitation for signs of encephalopathy. In C[...]’s case observations
were intermittent, not hourly. A doctor assessed her after 13 hours , finding no signs
of encephalopathy . Prof. Cooper stated that the lack of neurological
deterioration supported a reasonable discharge decision.
164. He stated that the timing of the injury , whether pre-labour, intrapartum, or
postnatal —could not be definitively established from available evidence.
31 165. With regard to the l aboratory findings he pointed out that e levated CRP and
the presence of band cells in the FBC indicated inflammation . He agreed with Prof.
Smith that such markers cannot differentiate between inflammation cause
by infection or hypoxic injury .
166. Although Prof. Cooper initially dismissed postnatal injury as a cause, he
conceded that that a note regarding "bradycardia" had been misread (not "severe
bradycardia"), and he conceded that the records did not support postnatal hypoxia.
167. He raised the possibility of a pre-labour injury , possibly triggered
by undisclosed traditional medicines causing uterine contractions or foetal stress. He
also acknowledged intrapartum injury due to repetitive hypoxic episodes as a
possibility, but not a probability based on the evidence. Prof. Cooper did not agree
with UTI as a primary cause of septicaemia but agreed it could have been
a contributing factor .
168. Prof. Cooper said at discharge, the baby did not display signs of moderate
encephalopathy , which would be easily recognizable, even by non- specialists.
169. Upon readmission, C[...] had clear signs of moderate encephalopathy (e.g.,
decreased consciousness, seizures).
170. He acknowledged that if these signs were present but missed, then discharge
would have been inappropriate.
171. Dr. Mogashoa participated in two joint expert minutes with the plaintiff’s
paediatric neurologist, Dr. Pearce. Her evidence largely followed the criteria outlined
by ACOG (American College of Obstetricians and Gynaecologists ) for
assessing intrapartum hypoxia as a potential cause of neonatal encephalopathy and
cerebral palsy .
172. Both experts agreed that C[...] exhibited Grade 2 neonatal encephalopathy ,
indicative of moderate hypoxic -ischemic injury . C[...] met several ACOG criteria for
considering intrapartum hypoxia as part of the causal pathway to cerebral palsy.
32
173. They evaluated the case using the ACOG’s essential criteri a for intrapartum
hypoxia:
1. Apgar Scores:
o Documented Apgar scores were 4 at 1 min, 6 at 5 min, and 9 at 10
min.
o Dr. Mogashoa emphasized that Apgar scores are subjective and must
be interpreted cautiously.
2. Umbilical Cord pH :
o No umbilical cord blood gas was available.
o Dr. Mogashoa acknowledged that such data would help confirm
intrapartum hypoxia but recognized its unavailability at district hospitals.
3. Neuroimaging (MRI and Cranial Ultrasound) :
o MRI showed a PBGT pattern (perirolandic, basal ganglia, and thalami)
associated with acute profound injury.
o Cranial ultrasound performed early in life was normal.
o Dr. Mogashoa deferred to the radiologist, Prof. Lotz, and noted
that MRI findings do not rule out infection because inflammation is not
typically visible 10 years later.
4. Multisystem Involvement :
o C[...] had documented renal dysfunction, haematological abnormalities ,
and neurological signs .
o These findings were consistent with systemic hypoxia .
5. Timing and Type of Brain Injury:
o No definitive indication of whether injury occurred antenatally,
intrapartum, or postnatally.
o Dr. Mogashoa reiterated ACOG’s view that injury can occur at multiple
stages —before, during, or after birth.
6. Exclusion of Other Causes:
o Dr. Pearce excluded other causes based on available data.
o Dr. M disagreed, asserting that infection (particularly UTI) was not
excluded and may have contributed to hypoxia.
7. Outcome: Cerebral Palsy Type:
33 o CP was diagnosed with mixed -type cerebral palsy ,
predominantly dyskinetic—a pattern consistent with intrapartum injury per
ACOG.
174. In a second joint minute Dr. . Mogashua consistently highlighted the possible
role of infection (UTI or systemic) in priming the foetus , leading to increased
susceptibility to hypoxic injury. She acknowledged that there were no definitive
culture results were available. The CSF findings (via lumbar puncture)
were inconclusive due to a bloody tap.
175. Under Cross examination she conceded that for a postnatal cause of PBGT
injury to be plausible, severe circulatory collapse with resuscitation lasting over 10
minutes would be required.
176. Dr.. Mogashua agreed that intrapartum hypoxia occurred, but contended that
infection contributed to or caused it , aligning her interpretation with the broader multi -
factorial approach recommended by ACOG .
177. While agreeing that many ACOG criteria were met, she stopped short of
concluding that intrapartum hypoxia was the sole cause of the injury .
The defendant’s factual witnesses
178. Dr. Sibeko testified that she was the attending doctor at the time of C[...] ’s
birth. She was called to assess the newborn because the baby was not breathing
adequately and required suctioning and supplemental oxygen. Upon attending, Dr.
Sibeko recorded that the neonate was "still under resuscitation with oxygen."
179. She confirmed that s he did not issue any instruction to discontinue oxygen
support. She assumed the baby remained on oxygen when transferred to the ward,
in line with h er contemporaneous note.
180. During her evidence, Dr. Sibeko reviewed the clinical notes, Apgar scores,
and nursing documentation. She had no independent recollection of the event
34
181. Under cross -examination Dr. Sibeko agreed that normal reflexes would
typically correlate with an Apgar score of 9 or 10; that entries noting "colour pink" and "suctioned" appeared to be recorded after 10 minutes of life.
182. Her own clinical note indicated that the neonate was still receiving oxygen
when she assessed her. Sh e confirmed that stopping oxygen support must be based
on a doctor’s instruction and he had given no such order. The neonate was
transferred to the ward while still on oxygen.
183. Sister H arriet is qualified nurse and midwife who was employed at the
hospital in March 2008. She is currently working in Saudi Arabia. She has no
independent recollection of the child’s birth or related events.
184. Her name appears in hospital records as assisting with the delivery, while
another sister is recorded as the delivering midwife. She confirmed her involvement
based solely on documentation, not personal memory. She denied authoring several
entries in the clinical file that are attributed to her or mention her name.
185. A form titled “Examination of the Neonate” lists Sister H arriet as the examiner.
She denied completing or writing this form and confirmed that the handwriting was not hers. She explained that nursing protocol requires the individual who conducts
an examination to personally document all findings, positive and negative.
186. She acknowledged that if she did not complete the form, it must have been
completed after the fact, raising concerns about the form’s reliability and accuracy.
187. Sister Harriet stated that the use of fundal pressure during delivery is not
accepted midwifery practice and should not have been performed. She emphasized
that all care actions must be properly documented at the time they occur. Only one
midwife should perform and record each neonatal assessment; duplicate or retrospective entries are not standard practice. Therefore, if the neonatal
examination form was not completed by her contemporaneously, it casts doubt on the accuracy of the recorded findings.
35
Assessment of the factual witnesses: the plaintiff
188. Mrs V[...] W[...] provided a coherent account of a traumatic experience that
occurred 16 years ago. She consistently narrated key facts, such as the timeline of her pregnancy, the hospital admission, and the subsequent readmission of her C[...] ,
which supports her overall credibility. Her detailed recollection of C[...] ’s physical
condition (clenched fists and ‘ pawpaw ’ shaped head) , and her own emotional
responses , lends a degree of authenticity to her account.
189. Notwithstanding the above, her testimony is marked by several instances of
uncertainty. Under cross -examination, she frequently admitted to an inability to recall
specific details (such as exact times, procedural specifics, and certain entries in the hospital records), which she attributed to the passage of time and the stressful
nature of the events.
190. These inconsistencies and discrepancies were highlighted by Mr Soni to
challenge the reliability of her evidence. However, her emotional responses,
including moments when she became visibly upset and required time to compose herself, indicate that the events had a lasting impact. In fairness to her , Mr Soni’s
description of a medical procedure called an episiotomy was incorrectly described as suturing a “ tear in the uterus ” instead of the perineum. This may have been
confusing.
191. Mrs v[...] W[...]’s demeanor during her testimony was characteri sed by a lack
of sophistication and an apparent simplicity. She presented herself in a straightforward and unadorned manner, which may reflect her limited familiarity with legal and technical terminology. Her responses were candid but occasionally marked by a hesitancy that suggested a less polished articulation of her experiences , and it
appear ed to be delivered in a manner consistent with a layperson recounting a
traumatic personal event.
192. I am mindful of the fact that she was a single witness, and that the court s have
warned “that the evidence of a single witness to a fact, there being nothing to throw
36 discredit thereon, cannot be disregarded. Moreover, no matter how serious the
allegations might be, the onus of proving facts in a civil case is discharge on the preponderance of probabilities and not on any higher standard.”
6
193. It was also stated by the Supreme Court of Appeal in Petersen and Another v
Minister of Safety & Security ,
7 that not every error made by a witness or
inconsistency will affect his credibility. Various considerations are highlighted in that case, such as whether a contradiction is an honest mistake, material, and advances
or prejudices a party’s case, or whether it results from erroneous observation in a
confused situation, or can be attributed to defective recollection. Ultimately, ‘in each
case, the trier of fact must make an evaluation; taking into account such matters as the nature of the contradictions, their number and importance, and their bearing on other parts of the witness’s evidence.’
8
194. Mrs V[...] W[...]’s straightforward narrative and emotive responses suggest she
is earnest in her testimony, even though inconsistencies were noted. However, these
inconsistencies are not material and could be attributed in part to the fact that the
birth happened 16 years ago.
195. On the probabilities , many key aspects of Mrs v[...] W[...]’s testimony appear
highly plausible and are corroborated by independent evidence and hospital records.
I therefore accept her evidence as truthful .
Assessment of the defendant’s factual witnesses
196. The hospital staff, understandably, do not remember the event. The lack of
independent recollection by factual witnesses reduces the probative value of their evidence.
6 HAL obo MML v MEC for Health, Free State (1021/20190 [2021] ZASCA 149 (22 October) 2021 at
para 95 referring to Da Mata v Otto NO 1972 (3) SA 858 (A) at 869C, approving Wigmore Wigmore
on Evidence 3 ed, vol 7 at 260. Ley v Ley's Executors and Others 1951 (3) SA 186 (A) at 192 – 193.
7Petersen and Another v Minister of Safety & Security [2010] 1 All SA 19 (SCA) (Petersen) paras 6-7.
8 S v Oosthuizen 1982 (3) SA 571(T ) at 576G - H cited with approval in Petersen supra n7.
37 The law
197. It is trite that the criterion adopted by our law to establish whether a person
acted negligently is the objective standard of the reasonable person, the bonus paterfamilias. The test for determining negligence was laid down in the seminal
judgment of Holmes JA in Kruger v Coetzee
9 and stated as follows;
i) Whether a reasonable person (in this case, a reasonable midwife or
doctor) in the position of the defendant would foresee the reasonable possibility of harm occurring;
ii) And, if so, whether they would take reasonable steps to guard against
such occurrence;
iii) And whether the defendant failed to take those steps.
198. In the case of an expert, the requisite standard is articulated by
Molemela JP in the minority judgment in HAL obo ML v MEC
10 as follows; “the
yardstick by which the conduct of healthcare professionals is gauged, … is a notional standard set by a reasonable healthcare professional with their experience and qualification in their circumstances. Thus, the question is whether healthcare professionals in the position of the hospital staff would
have foreseen the reasonable possibility of their conduct causing harm and, if so, whether they would have taken steps to guard against that harm”.
199. In the context of healthcare, and especially obstetrics, this standard must be
applied with the nuance recognised in Michael v Linksfield Clinic (Pty) Ltd
11. Having
regard to the evidence of expert witnesses, the court must assess not whether the
conduct aligned with best practice or guidelines, but whether it deviated so materially from accepted professional norms that no reasonable practitioner would have acted
similarly.
Was the harm to C[...] reasonably foreseeable?
9 1966 (2) SA 428 (A) at 430 E -G.
10 H A L obo M L v MEC for Health, supra n 6.
11 2001 (3) SA 1188 (SCA).
38 200. The clinical timeline shows prolonged labour with documented signs of foetal
distress, including non- reassuring CTG patterns with late decelerations from 14h30
onwards. These were not followed by escalation or continuous monitoring.
201. Expert evidence from Professors Nolte and Theron establishes that the 2007
Maternity Guidelines were not followed in material respects. While deviation from a guideline is not per se negligence, in this case, such deviation coincided with recognised clinical indicators warranting urgent review or escalation.
202. The failure to act on key indicators (e.g., crossing the partogram's alert line at
13h30 and the action line at 19h00, and foetal distress at 14h30) constitutes a breach of the duty of care. No steps were taken to summon a doctor or reassess the foetus timeously.
203. The midwives had access to clear clinical tools (CTG, partogram) to foresee
the potential for hypoxic injury. The foreseeability threshold is not of certainty, but of reasonable possibility.
204. Accordingly, a reasonable midwife in the position of the defendant’s
healthcare professionals would have conducted proper monitoring, at the very least
by further CTGs on a continuous basis, and would have detected the signs of foetal
distress, and therefore would have reasonably foreseen the possibility of harm to the
foetus.
Would a reasonable midwife have taken steps to guard against such harm?
205. Once foetal distress is identified, standard practice is urgent reassessment
and, if necessary, surgical delivery. This action was not taken.
Did the defendant fail to take such steps ?
206. The midwives did not alert the doctor at several critical stages. These lapses
prevented timely reassessment and intervention . A reasonable healthcare
professional in the defendants’ position would have taken definitive steps —
39 escalation, continuous monitoring, and timely intervention —to avert foetal
compromise. The midwives failed to take those steps.
207. I am satisfied that , on the probabilities , the healthcare professionals were
negligent. What remains is to determine the nexus between the negligent conduct of the midwives and C[...]’s brain injury.
Did the negligence of the healthcare professionals cause C[...]’s injury?
208. It is well- established that causation has two elements, namely: (i) the factual
issue, the answer to which can be determined by applying the ‘but for’ test; and (ii) legal causation, which answers the question whether the wrongful act is linked sufficiently closely to the harm suffered; if the harm is too remote, then the re is no
liability.
12
209. In various judgments , the SCA has cautioned against a rigid application of the
‘but-for’ test
13 stating that it does not require “the precision of mathematics, pure
science or philosophy; instead, it requires the invocation of common sense, where
things are viewed against the back drop of everyday life experiences .”14
210. Similarly , in Minister of Safety and Security v Van Duivenboden 15 it observed
that a determination of a causal link was not an exercise in metaphysics; rather, it
ought to be based on the evidence adduced and what can happen in the ordinary
course of human affairs. Therefore, the appellant did not need to prove the causal
link with certainty but only needed to establish that the wrongful conduct of the
hospital staff was the probable cause of the loss.
The factual issue
12 56 International Shipping Company (Pty) Ltd v Bentley 1990 (1) SA 680 (A) at 700E -I.
13 Hal supra citing Mashongwa v Passenger Rail Agency of South Africa [2015] ZACC 36; 2016 (3) SA 528 (CC);
2016 (2)BCLR 204 (CC) and the judgments quoted therein.
14 Minister of Finance and Others v Gore N O 2007 (1) SA 111 (SCA) ; [2007] 1 All SA 309 (SCA) para 33.
15 2002 (6) SA 431 (SCA); [2002] 3 All SA 741 (SCA).
40 211. In determining f actual causation in this case the test is: “ but-for” the failure to
escalate care, would the injury likely have been avoided?
212. Expert testimony from Dr. O'Hagan and Prof. Smith supports the conclusion
that the brain injury is consistent with a partial prolonged hypoxic event, which is preventable through timely intervention. Although imaging alone cannot pinpoint timing, clinical signs strongly correlate with intrapartum injury.
213. The injury's timing is narrowed to the intrapartum period through consistent
findings from multiple experts (Nolte, Theron, O'Hagan, Smith, Pierce) .
214. Prof. Cooper’s evidence suggesting uncertainty does not establish a
competing probable cause. At best, it raises a speculative possibility, which is insufficient to disturb the balance of probabilities standard.
215. Dr. Weinstein and Prof. Smuts proposed alternate theories (e.g., infection and
postnatal factors), but these were not supported by reliable contemporaneous data
or pathology reports. Notably, Prof. Smuts conceded the absence of documentation,
weakening the infection hypothesis.
216. Thus, on a holistic view of the evidence, the negligent monitoring and failure to
act on foetal distress was more likely than not a factual cause of C[...]’s brain injury.
Legal causation
217. In Lee v Minister for Correctional Services
16 the Constitutional Court held that
in the case of systemic omission, it is sufficient for a claimant to prove that the
negligent omission materially increased the risk of harm occurring. Even if I were to
accept that the precise but-for nexus is uncertain due to overlapping factors, the
cumulative failure to monitor, record, and escalate during labour increased the risk of
an otherwise preventable intrapartum brain injury.
16 2013 (2) SA 144 (CC) ,
41 218. The evidence canvassed in the a foregoing paragraphs permits a finding that
the inadequate monitoring during Mrs v[...] W[...]’ prolonged labour , and the repeated
partial hypoxic events led to C[...] suffering a partial prolonged type of brain injury,
culminating in cerebral palsy. This is the more probable version.
219. In the result, causative negligence has been proven on a balance of
probabilities, thus rendering the respondent vicariously liable for damages.
Conclusion and relief
220. The conspectus of evidence, taken together, demonstrates multiple breaches
of established obstetric and neonatal protocols .
221. These failures collectively amount to substandard care, which plausibly
contributed to C[...] ’s adverse neurological outcome.
222. Accordingly, all the evidence canvassed suffices to prove all the elements of
delictual liability on a balance of probabilities. I am satisfied that the plaintiff
succeeded in discharging the onus of proof .
223. In these circumstances, I intend issuing an order declaring that the MEC is
liable for 100% of C[...] ’s proven or agreed damages arising from her brain injury.
224. As regards costs, the general rule is that the successful party should be given
his costs, and this rule should not be departed from except where there are good grounds for doing so, such as misconduct on the part of the successful party or other exceptional circumstances. I can think of no reason why I should deviate from this
general rule and costs should therefore be awarded against the defendant in favour of the plaintiff.
ORDER
Accordingly, I make the following order: -
42 (1) It is declared that the defendant is liable for 100% of the damages that are
proven or agreed to be due to the plaintiff in her capacity as parent and
natural guardian of her minor child arising from her brain injury.
(2) The defendant shall pay the plaintiff’s costs of the determination of this
issue relating to his liability, including the costs of Counsel .
D MABASA
ACTING JUDGE OF THE HIGH COURT
JOHANNESBURG
For the Plaintiff : Adv P Uys instructed by Edeling Van Niekerk Attorneys .
For the Defendant : Adv V Soni SC and Adv T Mlambo instructed by State Attorney
South Afric a