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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.  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 terms 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 three 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 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 8.11 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 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 nor 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 clenched in a claw-like position near her head and that she exhibited a bluish-purple discolouration 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 discolouration 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 discolouration.

 

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.

 

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 Soni (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 19h00, 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 20h05.

 

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.

 

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 by Prof. Joseph Volpe and reports by the American College of Obstetricians and Gynaecologists (ACOG).[2]

 

38.  She testified that hypoxic-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 recognised 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 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 visualisation 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 in 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 Wisnowski (2021)[3]acknowledges that this pattern may result from either a single acute sentinel event, or prolonged partial hypoxia with intermittent near-total asphyxial episodes.

 

47.  Dr. O’ Hagan provided the following 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 it 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 emphasised 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.

 

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 Soni 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 recognising 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 emphasised 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 recognises 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 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 address 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.

 

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 3h30 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.

 

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 18h30. The birth occurs at 20h05.

 

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 11h30, 13h30, 15h30, and 17h30. From 17h30 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 13h30 to 15h30 and 15h30 to 17h30, progress resumes at the expected 1 cm per hour. However, expected dilation of 10 cm at 17h30, 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 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 8h15 pm. There is no record of a doctor assisting during labour.

 

82.  Prof. Nolte further testified that C[...]’s birth 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 stopped because the patient was too restless. Despite restlessness, continuous monitoring using a Doppler device should have 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 18h30 and 20h05. 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 recognised, 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 11h30 – 5 cm, at 15h30 – 8 cm, at 17h30 – 9 cm, at 19h00 – fully dilated (10 cm).

 

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 the 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 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 signs of foetal compromise were evident as early as 14h20, 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. This 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.

 

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. However, 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 13h30, 15h30, and 17h30), 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 14h17 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.

 

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 exclude 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 labour, 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.

 

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 symptoms, 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 there is no indication of antenatal brain injury, and the injury was not caused postnatally. Both Prof Nolte and Theron pointed out how the midwives missed warning signs, and inadequately 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 laboratory findings showed evidence of metabolic acidosis, kidney injury, elevated inflammatory markers, and possible dehydration. Although a urinary tract infection (UTI) was suspected, urine cultures did not confirm this.

 

119.  More importantly, 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 seizure 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[...] displays 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 joint minute with Dr. Mogashoa 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 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 diagnosed with a UTI and had a non-contributory lumbar puncture.

 

129.  She agreed 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.

 

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 cross-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 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 this 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 cross 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 19h00. He also acknowledged that an examination at 18h30 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 the 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 absence of documented abnormalities as a basis to conclude there were none.

 

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 the 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]

 

145.  Dr. Weinstein addressed 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 17h30, 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 in 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.

 

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 Prof. 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 Bolton 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 protocols; 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 .

 

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 feeding 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 ideally, 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.

 

165.  With regard to the laboratory findings he pointed out that elevated 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.

 

173.  They evaluated the case using the ACOG’s essential criteria 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:

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 she did not issue any instruction to discontinue oxygen support. She assumed the baby remained on oxygen when transferred to the ward, in line with her 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

 

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. She 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 Harriet 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 Harriet 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.

 

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 characterised 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 appeared 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 courts have warned “that the evidence of a single witness to a fact, there being nothing to throw 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.

 

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?

 

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—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 there 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 backdrop 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

 

211.  In determining factual 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.

 

218.  The evidence canvassed in the aforegoing 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: -

(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 Africa

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