Nemes v South Eastern Sydney Local Health District - [2025] NSWSC 418

Supreme Court

New South Wales

Medium Neutral Citation: Nemes v South Eastern Sydney Local Health District [2025] NSWSC 418
Hearing dates: 29 April to 2 May, 9 July, 3 and 4 September, 25 October 2024
Date of orders: 05 May 2025
Decision date: 05 May 2025
Jurisdiction: Common Law
Before: Harrison CJ at CL
Decision:
(1) Judgment for the defendant.
(2) Order the plaintiffs to pay the defendant’s costs.

Catchwords:
NEGLIGENCE – professional negligence – medical negligence – where child has disabilities including infantile seizures and Global Developmental Delay – whether disabilities are a result of a failure to deliver the baby earlier – obstetric evidence – conclave of experts – Civil Liability Act 2002 (NSW) s 5O – where the defendant is a Local Health District – whether the defendant acted in accordance with widely accepted peer professional practice – whether the defendant breached its duty of care – where there are multiple experts with competing opinions – whether any alleged breach of duty of care during labour was causative of the child’s disabilities

Legislation Cited:
Civil Liability Act 2002 (NSW) ss 5B, 5C, 5O

Cases Cited:
Dean v Pope (2022) 110 NSWLR 398; [2022] NSWCA 260
Makaroff v Nepean Blue Mountains Local Health District [2021] NSWCA 107

Category: Principal judgment
Parties: Bendeguz Nemes (Plaintiff - 2019/269249)
Erika Nemes (Plaintiff - 2019/250366)
Zsolt Nemes (Plaintiff - 2019/250377)
South Eastern Sydney Local Health District (Defendant)
Representation:
Counsel:
M Cranitch SC with A Campbell and M Summerhayes (Plaintiffs)
R Cheney SC with B Bradley (Defendant)
Solicitors:
Gerard Malouf & Partners (Plaintiffs)
Makinson d’Apice Lawyers (Defendant)

File Number(s): 2019/269249; 2019/250366; 2019/250377
Publication restriction: Nil

JUDGMENT

HIS HONOUR: Bendeguz Nemes (“Benny”) was born at the Royal Hospital for Women at Randwick at 11.38 on 2 April 2016. These proceedings are concerned with the question of whether the disabilities from which Benny was later found to be suffering, including infantile seizures and Global Developmental Delay, are the result of an alleged negligent failure by the hospital to deliver him earlier or whether they are alternatively unrelated to the timeliness of his delivery, which description must be taken to include the hospital’s management of his antenatal care.
By amended statement of claim filed on 10 July 2020, it is alleged against the hospital, for which the defendant is responsible, that it was negligent by failing to:

(a)   induce labour and contractions at an earlier stage in light of the early rupture of membranes;
(b)   administer prophylactic antibiotics after physical vaginal examinations;
(c)   discontinue Syntocinon when the CTG became abnormal;
(d)   deliver the baby at an earlier time when abnormalities were indicated;
(e)   adequately examine the placenta and to retain it for investigation of the plaintiff’s condition.

An additional issue was identified in a further amended statement of claim filed after the close of evidence. That issue was framed as a failure to:

(f) conduct a foetal scalp test during labour.

These allegations are denied. There is no separate claim made against the midwives.
On 12 April 2024 the Court ordered the separate determination of the following questions:

Did the defendant breach its duty of care by not proceeding to earlier delivery?

Was any purported delay in (1) causative of the plaintiff’s disability?

Did the defendant breach its duty of care by not prescribing prophylactic antibiotics?

Was any purported failure to prescribe antibiotics in (3) causative of the plaintiff’s subsequent disability?

Did the defendant breach its duty of care in the manner in which it augmented the mother’s labour with Syntocinon?

Was the purported manner of administration of Syntocinon in (5) causative of the plaintiff’s subsequent disability?

Having regard to the further amended statement of claim, I will treat the issue of the alleged failure to administer a foetal scalp test during labour as an additional question for determination. Despite the specificity of the separate questions, each falls to be considered under the broadly contested issue of whether or not Benny’s problems were avoidable, in the sense that they were caused by the defendant’s failure to deliver him sooner, or were never preventable in the sense that they were congenital and unavoidable. In either case, the defendant relies upon s 5O of the Civil Liability Act 2002 as a complete answer to the claim.
In my opinion, each of these questions must be answered “No”. My reasons for coming to that conclusion are set out at length in what follows. However, separate questions (3) and (4) can be dealt with quickly. Erika Nemes did not at any stage suffer from an infection of the type to which antibiotics would be expected to respond. On the question of whether it was reasonable not to administer prophylactic antibiotics to Ms Nemes, only Dr Schmidt considered that they should have been administered. None of the other obstetric experts agreed with that opinion. These experts all agreed that, on the balance of probabilities, Ms Nemes did not develop chorioamnionitis or any other infective process. Moreover, these experts also all agreed that the absence of prophylactic antibiotics had no impact on foetal outcome.
Despite the order for the determination of the separate questions, the various joint reports and other expert opinions deal with matters going beyond these separate issues that I am required to determine. For example, the obstetric experts were asked a question concerning disposal of the placenta. Joint Question 6 asked the obstetricians to comment on whether it was reasonable not to retain the placenta following birth. The experts agreed that it would have been preferable for the placenta to be retained. However, there is no evidence before me in the proceedings that suggests any such failure was the cause of any injury or disability from which Benny has been found to suffer. The reasonableness or otherwise of the failure to retain and examine the placenta in this case is unrelated to Benny’s claims.

Background

In the nature of things, the parties have provided me with their respective introductions to this case. For reasons that will become apparent, each party’s take on how to explain their respective cases is understandably replete with emphasis and references that favour their contentions. An understanding and comparison of these differences helps to inform a resolution of the matters in dispute.

Plaintiff’s introduction

Ms Nemes is Benny’s mother. She was 37 years of age and in her 5th pregnancy when she presented for antenatal care. Ms Nemes was born in Hungary in 1978. She married George (Zsolt) Nemes in 2006 and moved to Australia in 2009. She became an Australian Citizen in June 2020. George Nemes was born in 1973 in Hungary. He owns a building construction company and carries out residential and commercial building work in Sydney. Benny is their only child.
Ms Nemes had a termination of pregnancy at age 19, followed by three miscarriages, at 7 weeks in 2006, 6 weeks in 2010 and 6 weeks in 2014. She initially consulted Dr Bitsis whom she had seen following her last miscarriage and was allocated to the Midwifery Group Practice model at Royal Hospital for Women for management of her pregnancy with Benny.
Scanning revealed normal foetal growth but also uterine fibroids. She was also treated for thyroid issues. Ms Nemes presented on 29 March 2016 to the midwives’ clinic as she was in pain and had been feeling unwell. Bloods were ordered and CTG monitoring commenced. Dr Bitsis was contacted. Following a reassuring CTG and normal bloods, she was discharged noting that she was to be assessed antenatally on 31 March 2016. According to the antenatal attendance record, Ms Nemes presented to the delivery suite on 31 March 2016 “following possible bradycardia in clinic”. The entry suggests there were notes prepared for this visit, but none has been located within defendant’s Clinical Records. Ms Nemes was discharged.
After a spontaneous rupture of membranes at 01.40 on 1 April 2016 and the commencement of contractions at 04.00, Ms Nemes presented to the hospital. She says she saw a midwife named Tammy who suggested she did not need to be admitted but that she could go home until her contractions became more painful and closer together. Ms Nemes was then seen by three obstetricians (Lee, Kernan and McIntosh) who noted the bradycardia the previous day and also said “CTG this a.m. suspicious – decreased variability”. As a result, Ms Nemes was admitted, nil by mouth at present, and was to have continued foetal CTG monitoring. During the remainder of labour, the defendant assumed care of Ms Nemes, including monitoring the health of both her and the foetus. Benny was ultimately born with the assistance of forceps at 11.38 on 2 April 2016 in a poor state.
The plaintiffs allege that the defendant was negligent in failing to deliver Benny earlier and that if it had done so he would, on the balance of probabilities, have avoided his injuries, including infantile seizures and Global Developmental Delay.

Defendant’s introduction

When Benny was five months old, he was admitted to the Sydney Children’s Hospital on 27 September 2016 under Dr Andrews, a paediatric neurologist, with a six day history of seizures. Following EEGs and MRI imaging, Dr Andrews suspected a left sided brain malformation as the cause of his seizure activity. His seizures evolved into infantile spasms. Benny developed an intractable seizure disorder and Global Developmental Delay. Good seizure control was eventually obtained with Vigabatrin therapy.
Between 2018 and 2020, Benny resided in Queensland and Hungary. He returned to Dr Andrews’ care in April 2020. Dr Andrews documented a history of left posterior cortical malformation on MRI on 18 April 2017 and MRI on 28 September 2017, as well as a recurrence of focal seizures with altered awareness and subtle clinical features to suggest left hemisphere onset from June 2019. Dr Andrews diagnosed ongoing focal seizures. He strongly suspected a left cerebral malformation in the left posterior quadrant of the brain, with concordant semiology of the initial spasms and current partial seizures. Dr Andrews engaged Dr Lawson, a neurologist and Dr Erica Jacobsen, a neurosurgeon, for input. Dr Lawson reported a clear left-sided extensive parieto-occipital cortical dysplasia, a condition where the top layer of the brain does not form properly. The only path to being seizure free was epilepsy surgery in order to remove the abnormal cells.
It is the defendant’s case that Benny was born with a congenital-structural abnormality in the left hemisphere which manifested in a seizure disorder at five months of age with subsequent Global Developmental Delay. The defendants maintain that this dysplasia is an in-utero developmental condition which entirely explains Benny’s condition, and that Benny’s seizure activity is not the result of a perinatal hypoxic brain injury.
As noted earlier, Benny was born at 11.38 hours on 2 April 2016. The Plaintiffs allege that had he been delivered at 9.30 hours, he would have avoided brain injury and his global development disorder.
The defendant’s first response to the allegations is to maintain that it acted at all times in accordance with competent professional practice as contemplated by s 5O of the Civil Liability Act. In short, the defendant contends that in providing the professional services impugned in these proceedings, it acted in a manner that, at the time the services were provided, was widely accepted in Australia by peer professional opinion as competent professional practice. If that is established, the defendant incurs no liability in negligence, and it is unnecessary for the Court to undertake any analysis pursuant to ss 5B and 5C of the Act.
Nevertheless, but in addition, the defendant submits that the plaintiffs’ case fails on both breach of duty and causation.
With respect to breach, Ms Nemes’ labour was managed to a standard consistent with peer professional care in 2016. Augmenting her slow labour with Syntocinon was appropriate: there is no suggestion of uterine hyperstimulation. As Ms Nemes was Group B Streptococcus negative and afebrile, prophylactic antibiotics were not indicated. There is no suggestion that she developed an infective process. The defendant maintains that the CTG trace was adequately monitored and that prior to the second stage of labour there was no clinical indication to expedite Benny’s delivery. When the trace became non-reassuring, Ms Nemes’ care was appropriately escalated with a prompt forceps delivery performed in a competent manner. The decision not to take a foetal blood scalp sample was reasonable. Professor Chapman and Associate Professor Keogh, both obstetricians, are supportive of the care and management provided to Ms Nemes.
With respect to causation, whilst Benny was born in poor condition, it was promptly managed. He improved quickly. There is no evidence of postnatal encephalopathy. Postnatal encephalopathy is not a subtle diagnosis. Professor Nick Evans, a neonatologist and Associate Professor John Keogh, an obstetrician well published in matters of newborn encephalopathy, make plain that, absent newborn encephalopathy, there is no possibility intrapartum hypoxia resulted in Benny’s epilepsy or Global Developmental Delay. Professor Monique Ryan, a paediatric neurologist, also agreed there were no symptoms or signs suggestive of hypoxic brain injury. Consistently with the treater, Dr Andrews, Dr Ryan considered that cortical dysplasia is the cause of Benny’s epilepsy syndrome and cognitive deficits. This cortical malformation occurred during in utero development.
The defendant maintains that any perceived abnormality in Benny’s history is both legally and factually unconnected to the cause of his condition. In short, whereas Professor O’Connor and Dr Schmidt, both obstetricians, attempt to elevate a single feature of the CTG trace from time to time to advance an argument in favour of urgent intervention or delivery, their approach ignores the limited predictive power of CTGs. The weight of the evidence is to the effect that the CTG trace was largely reassuring and that the clinical judgments made by the obstetric team caring for Ms Nemes from time to time were competent, considered and appropriate.
Moreover, whereas Dr Harbord, a paediatric neurologist, would elevate “poor feeding” in the neonatal period to evidence of encephalopathy, this ignores the fact that neonatal encephalopathy is neither a subtle diagnosis nor established solely by the feeding pattern of a newborn. The weight of the evidence is to the effect that Benny was well, had an active suck function, fed from a bottle and gained weight in the neonatal period. Any attachment issues are adequately explained by Ms Nemes’ large breasts and inverted nipples.
Finally, whereas Dr Keenan, a paediatric neuroradiologist, would elevate microbleeds and gliosis seen on Benny’s MRI imaging to evidence of a possible perinatal insult, this ignores the fact that none of Benny’s images contains features compatible with either a mild, moderate, severe or profound hypoxic ischaemic insult. The weight of the evidence is to the effect that microbleeds are often found coincidentally without significance. Likewise, the cause of any gliosis is speculative. It is entirely plausible (if not more likely) that any gliosis seen in later scans is the product of Benny’s well known seizure activity on and from five months of age.
In summary, the defendant contended that it has not been established that Benny suffered any perinatal brain injury which could have materially contributed to his disabilities, namely, irretractable seizures and Global Developmental Delay consequent on known cortical malformation.

Civil Liability Act 2002 (NSW): s 5O

Defendant’s submissions

The question posed by s 5O is whether the professional acted in a “manner” that at the time the service was provided was widely accepted in Australia by peer professional opinion as competent professional practice. This requires identifying the manner in which the professional acted and asking whether those actions were at the time widely accepted as competent professional practice. The “manner” refers to what the professional did and the issue is whether what the professional did is what a wide body of that professional's peers would have done in that circumstance: Dean v Pope (2022) 110 NSWLR 398; [2022] NSWCA 260 at [236] per Ward P; at [314] per Brereton JA; at [266] per White JA.
The evidence of Professor Chapman and Dr Keogh, corroborated further by Dr Stamatopoulos and Dr McCormack, bears out that in its management of Benny’s delivery, the hospital staff acted at all times in a manner that was widely accepted in Australia by peer professional opinion in 2016 (and today) as competent professional practice. Closely read, neither Dr Schmidt nor Professor O'Connor advances a proposition to the effect that the management of the delivery here fell short of what was widely accepted by obstetric peers in 2016 as competent professional practice. In short:

The interpretation of the features on the trace during the first stage of labour was reasonable. The trace was not pathological during that stage and a wide body of peers would not have considered assessment of foetal welfare by foetal blood scalp sampling or expedited delivery absent a pathological trace.

When the trace became concerning during the second stage of labour, this was promptly escalated in accordance with the Guidelines. Dr McCormack made the clinical judgment to proceed to expedited delivery and to not delay delivery so as to perform foetal blood scalp sampling. The decision to expedite delivery at that time was valid and in accordance with what a wide body of professional peers would have done in that circumstance.

There is a genuine division in obstetric opinion as to whether Syntocinon should have been ceased or continued ahead of an attempt at instrumental delivery in a patient with a non-reassuring trace. Whilst not universal, the defendant submitted that I would be satisfied that the clinical decision to continue Syntocinon in the circumstances of Ms Nemes’ labour was in accordance with what a wide body of professional peers would have done in that circumstance.

Ms Nemes was GBS negative and afebrile at all material times. A wide body of professional peers would not have commenced her on prophylactic antibiotics during her labour.

Although born in poor condition, Benny recovered quickly and was well shortly thereafter. There was no clinical indication for him to be transferred to the NICU for care. The decision to dispose of the placenta absent significant persisting pathology in the newborn was consistent with what a wide body of professional peers would have done in that circumstance.

The “defence” based on s 5O is made out. The defendant submitted that I should find that it does not incur a liability in negligence.

Plaintiffs’ submissions

In Makaroff v Nepean Blue Mountains Local Health District [2021] NSWCA 107 Simpson AJA made the following observations as to the applicability of s 5O to a Local Health District (at 237):

"There is a further basis on which the applicability of s 5O may be doubted. Section 5O provides a defence to ‘a person practising a profession’. While doctors Rannard and Lee and were undoubtedly persons practising a profession, neither was named as a defendant. The named defendant was the Local Health District, a body corporate constituted under the Health Services Act 1997 (NSW). While recognising the corporate personality of the first respondent, it is difficult to see that a local health authority is ‘a person practising a profession’, although it may be (and in this case admittedly it was) vicariously liable for any negligence established against any of its employees."

The plaintiffs submitted that, as a matter of statutory construction, s 5O does not apply in these proceedings as the defendant was not practising a profession.
In any event, the negligence alleged against the hospital is framed in a general sense as a failure to deliver Benny at an earlier time. These allegations encompass the totality of the obstetric care, including antenatal management, management during labour and the decisions of the accoucheur. Undoubtedly the care provided to the mother and her baby during this period came from doctors and midwives who may have been practising a profession. However, they do not incur a liability in negligence in their professional capacity as they are covered by their employer pursuant to the principles of vicarious liability.
The defendant's submissions highlight the problems that the hospital has in raising a s 5O “defence”. The only evidence that was led which identified the manner in which the professional acted was obstetric evidence. This, it is suggested "bears out that in its management of Bendeguz' delivery, the hospital staff acted in a manner that was widely accepted in Australia by peer professional opinion in 2016 (and today) as competent professional practice". [emphasis added]
In short, the plaintiffs submitted that obstetric evidence cannot bear upon the efforts of the midwifery team who oversaw Ms Nemes’ observations and would bring in the doctors when they thought it was necessary. It was conceded by Dr Innes that the midwives were the experts in interpreting a CTG, yet the defendant called none of the midwives in charge of the care of the mother and baby.
In these circumstances, the plaintiffs submitted that the defendant is unable to establish a defence under s 5O and the matter should be determined according to the principles of negligence.

Consideration

Paragraph 29 of the defence dated 25 March 2020 is in the following terms:

“29. In further answer to the whole of the Statement of Claim, the defendant says:
(a) At all material times, the defendant was engaged in the practice of a profession.
Particulars

(i) The defendant by its agents or servants provided professional medical and nursing services to the plaintiff and his mother at the admission to the Royal Hospital for Women (the Hospital) in April 2016.

(b) At all material times, the defendant provided professional services to the plaintiff and his mother in the manner that was widely accepted in Australia by peer professional opinion as competent professional practice.
Particulars

(i) On 1 April 2016, Erica Nemes (the mother) had spontaneous rupture of membranes at home. She was admitted to the Hospital at 0830 hours with mild contractions every 4 to 6 minutes lasting approximately 60 to 90 seconds.
(ii) At 1140 hours on 1 April 2016, a digital vaginal examination was undertaken and in April 2016 this was standard practice of a significant body of peer professionals prior to starting Syntocinon.
(iii) Routine prophylactic antibiotics after vaginal examination with ruptured membranes was not practised by the majority of peer professionals in April 2016 except in circumstances of an antenatal swab showing Group B Streptococcus or a maternal fever, neither of which the mother had.
(iv) At 0312 hours on 2 April 2016, Syntocinon was commenced to augment labour.
(v) Commencing augmentation of labour 24 hours after spontaneous rupture of membranes was appropriate and in accordance with peer professional practice in April 2016.
(vi) From about 0935 hours on 2 April 2016, the CTG showed a series of deep decelerations with contractions and reduced variability at times and this pattern continued until 1030 hours.
(vii) When the CTG changes persisted, appropriate steps were taken to expedite delivery and in April 2016 it was not consistent with standard practice of a significant body of peer professionals to have intervened sooner.
(viii) By 10 minutes of age, the plaintiff appeared to be totally recovered from the initial respiratory depression and there was no indication to examine the placenta further.
(ix) In April 2016 and now, the peer practice is to dispose of the placenta once a basic examination by the accoucheur has occurred except where significant persisting pathology was present in the baby.

(c) In the circumstances and as particularised above, in its management of the plaintiff and the mother in April 2016, the defendant acted in a manner that (at the time that medical and nursing services were provided) was widely accepted in Australia by peer professional opinion as competent professional practice.
(d) Further and in the alternative, if, which is denied, section 5O requires that the defendant acted pursuant to a practice that was in existence at the relevant time then the defendant says that the manner in which it acted including in doing the things referred to in paragraph (b) (i)-(ix) above, accorded with or was pursuant to a practice that was in existence at the time for the management of patients in labour and delivery.
(e) The defendant states that on the basis of the matters pleaded and particularised at paragraph (b) (i)-(ix) above, it does not in the circumstances incur a liability in negligence to the plaintiff pursuant to section 5O of the CLA.”

By reason of the view I have formed concerning the separate questions, and the way that my answers dispose of the proceedings, the issue of whether or not the hospital is a professional and as such entitled to raise the s 5O response, and whether if it is, it has established that it operated in accordance with widely accepted practice, achieve less significance than might otherwise have been the case. Moreover, there was no evidence from either party specifically tailored to the question of whether what the hospital did at the time of Benny’s birth accorded with such a widely accepted practice. Rather, the experts directed attention to the different issue of whether what was done in specific ways concerning foetal scalp monitoring, the administration of Syntocinon, retention of the placenta and the administration of prophylactic antibiotics was appropriate. Opinions about these and other specific activities performed in the course of the antenatal care and ultimate delivery were always not unanimous.
However, if the issue is limited to the more general question of whether the hospital acted in accordance with widely accepted peer professional practice in delivering Benny in the manner and at the time that it did, I consider that the hospital acted in accordance with such a practice. It must go without saying that the course of the birth of every infant is potentially different from any other. The decisions about whether to deliver vaginally or to intervene surgically before that occurs are inevitably informed by changing circumstances in a dynamic situation. There is not always or necessarily only one course that must be followed. The exercise of professional judgment by equally qualified professionals may legitimately lead to different approaches.
Section 5O does not require the establishment of a universally accepted practice. Nor does the expression of a different opinion negate the defendant’s ability to rely upon the provision. Section 5O understandably emphasises the importance of a widely accepted practice, acknowledging the possibility that more than one solution to the same problem may qualify. In the present case, I am satisfied on the evidence that the defendant’s approach to Benny’s delivery accorded with what was widely accepted in Australia by peer professional opinion as competent professional practice at the time.

separate Question 1: did the defendant breach its duty of care by not proceeding to earlier delivery?

This is an obstetric issue.
The obstetric experts produced a report following a joint session on 18 January 2023. The several matters to which their expert attention was directed included whether Benny’s delivery was negligently delayed. The experts present were Dr John Schmidt, Professor Mike O’Connor, Professor John Keogh and Professor Michael Chapman. The Joint Report deals with a series of sub-issues, some of which are referable to one or more of the other questions, such as prophylactic antibiotics and placenta disposal. However, with respect to the present issue, the experts’ opinions may be gleaned from their answers to Joint Question 1, dealing with interpretation of the CTG trace. The obvious significance and relevance of this trace emerges from the uncontroversial fact that all experts express opinions upon the basis of records assembled from or at the time of Ms Nemes’ labour and not from any observations that they were able to make themselves at the time.
Joint Question 1(a) is as follows:

1. Please provide your interpretation of the CTG trace performed on 1 and 2 April 2016, including:
(a) By reference to its features, whether the trace was reassuring, suspicious or pathological and if so, during what periods?

Professor Chapman considered that the trace “was never pathological” although it was “occasionally non-reassuring”. He thought it was “consistent with the majority of CTGs we see during labour”. Dr Schmidt, in contrast, was of the view that the tracing at 01:50 on 2 April 2016 “showed features with significant foetal compromise which required immediate attention”. It was his view that “urgent action” was required at 01:40 hours.
Professor Keogh provided a more expansive answer, parts of which it is helpful to record at length:

“I think this trace, prior to the onset of the second stage, is within the normal range. There are periods of decreased variability and periods of normal variability with accelerations in the foetal heart rate. This represents a normal sleep/wake cycling within the trace, which is a reassuring feature.
In the second stage of labour, there are atypical variable decelerations, and that represents that this baby may be becoming acidotic, or has the potential to become acidotic. Consequently, and appropriately, the staff responded to this by stopping her pushing and making the decision to move to theatre and deliver by the most appropriate means when they got there. After they stopped the pushing, the trace shows a stable baseline. Though variability in this period after cessation of pushing is borderline, there are no decelerations and there would have been no acute concern.
When they get to theatre there is an acute complication following the topping up of the epidural, probably associated with a fall in maternal blood pressure causing acute decompensation. It is important to realise that they had to top up the epidural to deliver the baby with forceps, so it was good they did this in theatre where urgent delivery was possible even if turned out that forceps delivery was not appropriate.
The isolated decelerations which occur from time to time in this trace are reasons to keep on monitoring the baby, but they are not reasons to deliver, because they are self-resolving or respond to a change in maternal posture (which facilitates placenta blood flow) or to stopping the Syntocinon. They are interspersed with periods of normal and reassuring trace.
Although in the second stage the baby had a non-reassuring trace suggesting that he may be developing some acidosis, he is not in any way acutely threatened. It is not until they are in theatre and the epidural is topped up that the baby is acutely threatened, as is demonstrated by the trace, just prior to delivery. At no stage prior to the baby being in theatre following the epidural top-up did I have any concern that the baby was in acute trouble.
I point out that urgent action was taken in theatre. By moving to a rapid and skilful forceps delivery at this stage, a baby was born who, despite having evidence of acute decompensation in the cord gases, required minimal resuscitation and had a completely normal post-natal course till 5 months of age.
My summary would be that
(i) this trace is within normal limits all through until the second stage of labour; and
(ii) that any periods of concern are interspersed with periods of reassuring trace. I would see this as sleep/wake cycling, which is reassuring. In the second stage, there are certainly concerns raised, but I am reassured by the fact that when the mother stopped pushing, the trace reverted to within normal limits until she received the epidural top-up in theatre, following which the appropriate response of urgent delivery was made.”

Professor O’Connor did not respond directly to this question in terms. However, his appended table at page 367 of the Court Book suggests that from 1:40-4:40 on 2 April 2016, the decelerations were either pathological or non-reassuring. His table also noted periods of non-reassuring variability from 21:00-21:50 on 1 April 2016, and from 01:50-2:30 and 09:40-10:10 on 2 April 2016. His table also indicated pathological variability on 2 April 2016 from 04:00-05:20. Professors Chapman and Keogh expressly disagreed with Professor O’Connor’s table, consistently with the views earlier recorded. Moreover, Professor Chapman said he “would totally concur with Dr Keogh’s comments re Prof O’Connor’s interpretation of the trace”.
Joint Question 1(b) is as follows:

(b) Whether the features of the trace indicated a need for earlier augmentation of labour, and if so, when?

All experts agreed that the answer to this question was “No”. However, the following answer by Dr Schmidt should also be noted. He said this:

“We are looking in terms of length of time since rupture of membranes as well. After 12 hours, I would like to think the baby should start to be delivered by augmentation, that is around 12 hours after the ruptured membrane, with an endeavour to deliver the baby within about 24 hours.”

Professor Chapman immediately responded, saying “Dr Schmidt’s views are not consistent with the majority of peers or most hospital protocols”. Dr Keogh also observed that “we have all four agreed that there were no features of the trace that required earlier augmentation.”
Joint Question 1(c) is as follows:

(c) Whether the features of the trace indicated a need for earlier delivery of the baby by Caesarean section, and if so, when?

It is convenient to record what each doctor said in response to this question as follows:

“PROF O’CONNOR: There were two episodes, and I think it goes back to what Dr Schmidt was saying about the prolonged deceleration at 01:40 hours, on 2 April. So, that would certainly be an indication to get the baby out, I would have thought, unless there was reassuring [inaudible] of the foetus.
…
DR KEOGH: When I review the trace at 01:40, it is not at all clear that the foetal heart rate was down to 80 beats per minute. The fall from 130bpm at 01:41 is very sudden and goes straight down to the maternal rate. This is not how foetal heart rate decelerations develop. From here it varies in parallel with the maternal heart rate trace and is in fact I believe a recording of the maternal heart rate.
This is something that happens frequently in practice and requires readjustment of the recorder, together with action taken to correct underlying risk factors in case the recorded rate is foetal. It would be completely in keeping with repositioning the mother at that time. It looks to me that quite a bit of the trace down the bottom completely overlies the maternal trace. We can’t in fact say that the baby’s heart rate was down for 8 minutes.
As far as the deceleration at 01:10 is concerned, it lasts for just over 2 minutes (not four minutes) and is both self-resolving and followed by accelerations. It therefore just required ongoing observation. I would say there is NO point in this trace where a Caesarean section is indicated, unless when they got her to theatre following the epidural top-up the baby was not quickly deliverable vaginally.
The decision to take her to theatre was reasonable. The decision to assess her there and see whether or not she needed to be delivered by Caesarean or by forceps was reasonable. When they got there, in fact, she was deliverable by forceps and the baby was quickly and expertly delivered by forceps.
My reading of this trace is that there was never a point where a Caesarean section was indicated, unless when they got her to theatre the baby had not been suitable for vaginal delivery.
DR SCHMIDT: I concur that foetal scalp blood sampling should have been performed at that stage. She was fully dilated at about 8 o’clock. Head at the spines. No attempt was made then to deliver her, but she went for another 3.5 hours with Syntocinon stimulation increasing incrementally with quite significant atypical decelerations.
Foetal tachycardia associated with prolonged deceleration at 01:40 indicated requirement for urgent action, the abnormal CTG was not recognised by medical carers, so that although a valuable opportunity for foetal assessment was missed, I don’t know why there wasn’t attempted delivery at 08:10 when she was fully dilated with head level with the ischial spines (engaged) in an occipito-anterior position.
DR KEOGH: In 2016, when this happened, and even now it was common place to wait for an hour at full dilatation, if the epidural is working, to allow for descent of the head. The trace at that stage was normal and remained normal for the next hour. Actual pushing lasted, as can be seen on the CTG, for just under an hour. There was no reason to jump in and deliver since assisted delivery carries risk to both mother and baby.
PROF CHAPMAN: I agree with Professor Keogh.”

Joint Question 1(d) is as follows:

(d) Did the CTG trace indicate the need for foetal scalp blood sampling?

Professor O’Connor said it did. Dr Schmidt agreed, indicating his opinion that foetal sampling was necessary shortly after deceleration at 01:40. He said this:

“The second stage was complicated by indecision, in my opinion. The baby probably could have been delivered easily, analgesia being an effective epidural block. The foetus was in a favourable position for delivery and there were no other issues contraindicating delivery. The foetal head was level with the spines whereby the baby probably could have been delivered in theatre at 8 o’clock. The baby wasn’t delivered then.

Professor Keogh disagreed. He reasoned as follows:

“I would say [it] would have been reasonable to do a foetal blood sample in the second stage. I don’t think there was ever a situation before that where we were actually significantly worried about the baby, and so no needed to do a scalp sample. The scalp samples are not common practice, certainly not in the private sector.
In the second stage, around 10:20, it would have been reasonable to do a scalp sample, it would have been one option, but what they have done instead is take her to theatre for delivery. I think they have taken an alternative and very reasonable step there. Any urgency they felt would have been relieved when they saw the trace become acceptable once the pushing stopped.
So yes, I think in the second stage it was reasonable to do a scalp sample at around 10:20, but it was also reasonable to take an alternative path of action, which is just as good.
…
I disagree with Dr Schmidt about how easy forceps delivery was likely to be at 08:00. When the head is above the spines there is no place for forceps delivery in modern obstetrics. When the head is just below the spines, it is a borderline decision to deliver with forceps at this stage. Some would be happy to apply forceps, but many would be reluctant. The higher the foetal head at the application of forceps, the higher the likelihood of complications for mother and baby. I think it is a sensible choice when the head is just at the spines to wait for further descent, unless you are acutely concerned about the welfare of the baby.
When they were waiting in that first hour they were not concerned about the well-being of the baby. As the mother started to push, they became concerned. Then they stopped pushing, got the doctor to come and then they made a decision to go to theatre. When they stopped pushing the trace became reasonable again and the pressure was off, so they had a chance to take time to get to theatre and top up the epidural and make this as comfortable and safe as possible.

Everything changed when the foetal heart rate crashed after the epidural was topped up. You can see that on the CTG. Then they acted with urgency and expertise and delivered the baby. The fact that they were in theatre and consequently had paediatric, anaesthetic and obstetric expertise, created a buffer of safety that would not have been there in labour ward, with the midwife and the doctor being the only people typically present.”

Professor Chapman was of the following view:

“The primary goal of labour is a normal vaginal delivery. Unless there are reasons to intervene, that is the goal. The reason they were probably turning up the Syntocinon was that probably the contractions had drifted off to be less frequent and so to get the head to come down so she can have a normal delivery, they increased the Syntocinon. At no point was there hyperstimulation, in my view, during that time. The decelerations that we see are almost certainly due to her pushing and the compression of the baby’s head, which is a physiological response.
Going back to both questions, one in relation to augmentation, why are they doing it, it is pretty straightforward. Why didn’t they deliver the baby, because they were hoping for a vaginal delivery. The midwives were hoping for a vaginal delivery. Given there were, in their view, and John Keogh’s and in my view, no abnormalities during labour to hasten delivery.”

Joint Question 1(e) is as follows:

(e) Did the CTG trace demonstrate hyperstimulation of the uterus, and if so, when?

The unstated but accepted context in which this issue achieves relevance is that when labour contractions come too close together or last too long in the earlier stages of labour, the supply of blood and oxygen to the foetus will or may diminish, and foetal distress can occur when the unborn baby becomes oxygen-deprived. This can cause harm to the foetus, including hypoxia, ischaemia and acidosis.
Professor O’Connor answered yes to this question. None of the other experts shared his view.
Professor Chapman said no. He thought that the CTG trace never met any definition of hyperstimulation. Professor Keogh was of the same view. He said that “There is absolutely no evidence of hyperstimulation in this trace, at all. At all”. Dr Schmidt indicated that he also could not see hyperstimulation.
Joint Question 4(a) asked of the obstetricians was also concerned with the timeliness of Benny’s delivery and is as follows:

4. Please comment on the reasonableness of the decision to attempt forceps delivery in theatre, including:
(a) Whether there was any indication for more urgent intervention?

With the exception of Dr Schmidt, who did not in terms offer an answer to the question, all experts agreed that there was no indication for more urgent intervention. Professor Keogh’s answer was the most detailed, as follows:

“No. Had the trace remained abnormal in that period when they were trying to get her to theatre, that might have been different, but because the trace became acceptable in that period, there was no urgency until there was a sudden onset of bradycardia in theatre. As soon as that happened the baby was very quickly delivered. The rapid deterioration followed by quick and expert delivery is why the baby responded so quickly to minimal resuscitation and so quickly normalised his gases after birth.”

Joint Question 4(b) is as follows:

(b) Whether mechanical delivery with forceps was appropriate in the circumstances?

The experts were unanimous in answering this question yes.

Consideration: Separate Question 1

The defendant did not breach its duty by failing to deliver Benny at an earlier stage.
In my opinion, the overwhelming tone of the expert obstetric opinion is that Ms Nemes’ labour with Benny proceeded normally. Normally does not mean without incident or in the complete absence of fluctuations in readings or other indications of foetal wellbeing and progress over time. The experts all agree that there were occasions where Benny’s status was effectively suboptimal. However, these occasions were passing or transitory and resolved. None was of a kind that mandated immediate or earlier delivery.
It is important in this context that I indicate that the question of what the objective and observable data suggest or say about Benny’s condition in the period between his mother’s presentation to the hospital and his delivery are definitively matters for expert opinion. Even though the evidence in this case included, for example, the tender of CTG traces, and even though the parties made submissions about what the traces revealed and when, it is trite to observe that I must be guided by, in this instance, obstetric or similar expert opinion in order to be able to form a view and make a finding on the balance of probabilities about it. When there are competing opinions, that task necessarily includes an evaluation of the witnesses whose expertise is marshalled to assist me.
In this case, although I have referred almost exclusively so far to the written responses provided by the experts in their joint report, I also had the opportunity to see and hear each practitioner give evidence in joint session at the hearing. I consider that the evidence given by Dr Keogh was particularly impressive. He gave me the distinct impression that he was giving evidence that was based upon an impassioned but wholly disinterested view of the facts. Even though he was advocating for a particular point of view, he was not at any stage in my opinion attempting to endorse a particular outcome in order to support the party that retained him or doing so in the face of evidence to the contrary. I found his reasoning process to be balanced and logical and ultimately entirely persuasive.
Dr Keogh’s view was that there were no indications, in the form of abnormalities or suspicious traces or otherwise, that mandated or even warranted a hastened delivery. Professor Chapman shared that view.
Professor O’Connor and Dr Schmidt were of a different opinion. I respect their views. However, without meaning or appearing to be unduly critical of either expert, I did not gain the impression that Professor O’Connor or Dr Schmidt was able to say more than it would have been preferable if Benny had been delivered earlier, rather than that he should have been.
For example, Professor O’Connor referred to the fact that there were two episodes of prolonged deceleration which he thought “would certainly be an indication to get the baby out…unless there was reassuring [inaudible] of the foetus”. For better or worse, I am unable to translate that opinion into one that suggests it was critical that Benny should have been delivered sooner. Put another way, an earlier delivery may have been possible without causing harm to either Benny or his mother. That is a different matter entirely from saying that it was negligent obstetric practice at the time not to do so.
This question should be answered “No”.

separate Question 2: Was any purported delay in (1) causative of the plaintiff’s disability?

This issue was examined by the obstetricians, the paediatric neurologists and the neuroradiologists in their respective joint reports.
The obstetric experts’ answer is to be found in their recorded responses to their Joint Question 5 which is as follows:

5. Please comment on whether the CTG trace and foetal/neonatal condition was consistent with an hypoxic ischaemic encephalopathy or neonatal injury sustained during birth?

This area of inquiry is a very significant aspect of the present proceedings. For that reason, although experts in other areas of specialty deal with it, it is important and instructive that the opinions of the obstetricians who felt able to proffer opinions on the topic are recorded in detail.
Professor Chapman conceded that it was not his area of expertise beyond what he experiences in the labour ward. However, he was of the opinion that what happened with this baby was not consistent with HIE: Benny was depressed at birth but recovered very quickly and subsequently went to his mother, which is not consistent with HIE.
Professor Keogh answered as follows:

“DR KEOGH: No. No-one has suggested that this baby has Hypoxic Ischaemic Encephalopathy other than Professor Michael Harbord, and he says it is because the baby found it difficult to breast-feed. It is very clear that the baby had no difficulty feeding from a bottle. He only had difficulty feeding from his mother’s breasts. The midwives state at several points that this was because the mother’s nipples were short and flat, so they were hard to attach to.
If this was evidence of encephalopathy then nearly half of all babies on the post-natal ward would be said to be encephalopathic, so common is this scenario of difficulty breast feeding. In every other way this baby behaved completely normally in the newborn period. He was only taken back to the nursery because someone looked at the cord blood gases and thought ‘that’s lower than what we thought. We didn’t expect that in such a well-looking baby’.
After 3 hours observation he was put back on the ward because it was clear that everything was fine in terms of consequences of birth complications. There is absolutely no evidence at all this baby had newborn encephalopathy, and consequently we can say definitively this baby did not have a birth-related brain injury. There is an absolute requirement that a baby, who has received a birth related injury severe enough to cause permanent brain damage, go through a phase of newborn encephalopathy. There is no mechanism whereby a baby has a birth related brain injury, severe enough to cause permanent brain injury, and then has a normal postnatal course in the days that follow.
This is made clear in the International Consensus Statement ‘A template for defining a causal relation between acute intrapartum events and cerebral palsy’ published in the BMJ in 1999 on which I am an author. I also claim expertise in this area because I was an author on the ‘Western Australian Neonatal Encephalopathy study’ which remains the largest study of this condition in the world and was published in back-to-back papers also in the BMJ in 1998. These principles are also clear from the work of Nelson and Ellenberg and the work of Blair and Fiona Stanley (Australian of the Year).
Professor O’Connor has said that low Apgars are associated with neurodevelopmental problems, and of course that is true. However, this is not a causal association. Low Apgars do not cause brain injury. They reflect some other problem which may in a small number of cases be associated with brain injury.
This baby was acidotic and that may have caused the low Apgars here. Acidosis did not however cause the brain malformation which this baby has, and which is so well described in later MRIs, becoming increasingly clear as the baby aged. This cortical dysplasia in the baby’s left occipital, parietal and posterior frontal lobes was due to the baby’s brain not being properly formed during intrauterine development, and not from brief exposure to adverse conditions in labour.
I want it to be very clear to the court that no matter how Professor O’Connor seeks to present the data, there is absolutely no possibility at all that this baby’s neurological outcome was in any way associated with his birth. It remains rare to be able to be so clear in most cases, but the absence of encephalopathy in this case excludes an intrapartum cause for brain damage.”

Dr Schmidt declined to comment as it was not his field of expertise. Professor O’Connor did not think Benny had HIE.
It is also in my view very instructive to note the evidence of Professor Keogh given in the joint obstetric evidence session before me on 4 September 2024:

“WITNESS KEOGH: Yeah. So I, I think it’s really important that we state here that there is a absolute invariable pathway from intrapartum injury to long-term neurological damage. If you have an intrapartum injury severe enough to cause long-term neurological injury, there is no pathway between those two that does not pass through a baby having newborn encephalopathy. In other words, if you do not have newborn encephalopathy in the newborn period, you absolutely did not have a neurological injury as a consequence of your birth. If you have something that is so severe that you irreversibly damage your brain, you do not waltz through the newborn period as a newborn, as a normal newborn.
You end up in intensive care. You need assistance with ventilation. You need support of your blood pressure. You, you have evidence of renal damage. There is no pathway that brings you to long-term neurological damage without there being newborn encephalopathy. This baby did not have newborn encephalopathy and the idea that one or two hours of observation in the ICU would have made any difference is unreasonable at the very least. A diagnosis of newborn encephalopathy is not a subtle diagnosis. These babies are unwell. They do not go to the ward and just sit with their mothers. They are not something that you do not notice.
These babies are hyper-reflexic, they’re irritable, they’re crying all the time, they, they are agitated, they’re hypertonic. They are not normal babies. This baby never ever, ever, ever showed any sign of newborn encephalopathy. I can say with absolute 100 per cent confidence that the long-term neurological injury that this baby demonstrates is unrelated to the birth because it never became encephalopathic. I’m not saying this baby doesn’t have that long term injury; it definitely does, but it’s due to a developmental congenital anomaly in the baby’s brain and it was there before the labour and if I had delivered this baby by Caesarean section electively at 39 weeks we would still be seeing this same baby today with the same neurological injury and there’s no doubt about that.”

The paediatric neurologists, Dr Michael Harbord and Professor Monique Ryan, produced a joint report dated 20 December 2022. They were asked a series of questions directed to the elucidation of their respective opinions on Separate Question 2. These are considered in turn.
Question 1 asked the experts to comment upon whether, on the balance of probabilities, Benny suffered from intrapartum hypoxia and ischaemia. The experts disagreed on this issue.
Dr Harbord was of the opinion that Benny suffered from intrapartum hypoxia and ischaemia. That was because there were foetal heartrate abnormalities during the labour and he required active resuscitation after delivery. In particular, regular spontaneous respirations did not occur until after 5 minutes of age. Moreover, Dr Harbord noted that there was severe acidosis on the arterial cord gas with a pH of only 6.99, which is accepted as being severe for the purposes of establishing the presence of birth asphyxia. Dr Harbord also considered that there were signs of HIE with poor feeding.
Professor Ryan accepted that there was intrapartum hypoxia, as demonstrated by the changes in Benny’s heart rate and low pH present at birth on the cord blood, plus the need for resuscitation. However, Professor Ryan considered that the hypoxia was transient and did not lead to hypoxic ischaemic brain injury: Benny’s pH normalised quickly, the resuscitation time was relatively minimal, and his presentation returned to normal thereafter. Professor Ryan was of the opinion that blood tests and other investigations were probably not performed because Benny was felt to present normally: such investigations would usually be undertaken only if there were concerns about the baby’s status.
Moreover, Professor Ryan did not consider that the imaging changes seen on the MRI scan were suggestive of or consistent with hypoxic ischaemic brain injury. She considered that the changes subsequently seen in the white matter of Benny’s brain related to toxicity from anti-convulsant Vigabatrin and that Benny’s seizures resulted from a cortical dysplasia in the left temporal parietal and occipital lobes, as reported by the consultant neuroradiologist Dr Coleman. Professor Ryan considered that these abnormalities were very different from those expected after an hypoxic ischaemic brain injury at birth.
Furthermore, the feeding difficulties seen in the first few days after birth were transient and were contemporaneously attributed to the maternal factors of large breasts and inverted nipples. These difficulties were neither persistent nor severe.
Question 2 asked whether there were any clinical signs which to the experts’ observation in the neonatal period were consistent with HIE. The experts disagreed on this issue.
Dr Harbord considered that there were signs of HIE because on 3 April 2016, Benny was uninterested in feeding. On both 3 and 4 April he required feeds by spoon or syringe, which indicated an inability to feed by sucking.
Dr Ryan accepted that Benny had feeding difficulties but noted that these resolved within 5 days when he was discharged. Benny did not have any other signs or symptoms that would be expected to be present if he had neonatal encephalopathy. For example, there were no abnormalities of tone or responsiveness and no seizures or other neurological abnormalities identified by the paediatric resident when Benny was checked.
Professor Ryan emphasised that a baby with significant neonatal encephalopathy would never have feeding difficulties as an isolated or single manifestation of that condition: there would always be other signs and symptoms to support such a conclusion.
Dr Harbord disagreed with Professor Ryan’s assumption that if Benny had exhibited any neurological symptoms in the neonatal period they would have been identified and recorded in the clinical notes by the treating nurses and doctors.
Question 6 asked Dr Harbord and Professor Ryan what was the most likely cause or what were the most likely causes of Benny’s alleged brain injury, seizures and cognitive deficit.
Dr Harbord considered that these things were caused by birth asphyxia: there was no evidence that there was any other cause for Benny’s neurological abnormalities. In particular, Dr Harbord did not consider that there is any cerebral dysplasia. Dr Harbord was not, in his capacity as a paediatric neurologist, convinced that there was any dysplasia in Benny’s left hemisphere shown in the imaging. However, he deferred to the radiologists when it came to the interpretation of the MRIs.
Professor Ryan, by way of contrast, remained of the opinion that Benny’s neurological deficits resulted from focal cortical dysplasia in the left cerebral hemisphere, causing the development of severe epilepsy in infancy, or what is called West syndrome: this resulted in Benny’s persisting neurological deficits.
The final group of experts who offered opinions on this question were the neuroradiologists, Dr Ross Keenan and Associate Professor Lee Coleman. Their joint report following a conclave is dated 14 December 2022. This joint report is particularly detailed and correspondingly difficult to summarise fairly. However, two general matters do emerge from this report. First, Dr Keenan and Professor Coleman disagree about what the radiological images say about the cause of Benny’s disabilities. Secondly, neither expert is able to assert that his opinion is definitively supported by what the radiological images show and each expert agreed that there was a significant amount of speculation involved in their respective interpretations. In that context, the following matters should be noted.
Benny underwent an MRI of his brain on 28 September 2016. Each expert agreed that the images showed the presence of microhaemorrhages, observed in the form of three black dots in Benny’s right cerebellar hemisphere. There was also asymmetry in myelination being the formation of a myelin sheath around a nerve to allow for improved conduction. Professor Coleman considered that the asymmetry was evident albeit subtle. Doctor Keenan agreed. He noted that myelination is a dynamic process and takes time to evolve. He was not able to say whether this was delayed myelination, hypomyelination, being an inability to produce myelin at normal levels, or something else. The answer was conjectural.

Professor Coleman and Dr Keenan agreed that the microhaemorrhages were present but that there was no associated hemisphere atrophy or malformation. Dr Keenan thought that the microbleeds were pathologic. He emphasised that they should not be present in a brain and should not be present in the cerebellum. He considered that the microbleeds in Benny’s brain had potential clinical significance. The experts were unable to agree upon what that significance might be. In summary, Professor Coleman and Dr Keenan disagreed on the significance of microbleeds but were otherwise in full agreement on this topic.
A second MRI of Benny’s brain was performed on 18 April 2017, when he was 12 months old. Benny was by then on Vigabatrin. The experts agreed that there were indications of Vigabatrin related neurotoxicity, or cytotoxic oedema.
Professor Coleman described what he observed as a case of dysplastic development or, in lay terms, a badly made brain. The experts offered these interpretations of the radiological features:

“PROFESSOR COLEMAN: We agree on the Vigabatrin effect and agree on the abnormal left parietal lobe, where we agree there is asymmetry in myelination, the cause of which is yet to declare itself, if it ever does declare itself. It could be developmental and there could have been an associated antenatal or postnatal seizures, which has impaired what was poorly made in the first instance.
DR KEENAN: We’re not sure on the causation at this stage, we agree on the findings but we don’t know the causation.”

A third MRI of Benny’s brain was performed on 28 September 2017. The Vigabatrin toxicity had resolved. The scan was otherwise relevantly uninformative for present purposes.
A fourth MRI of Benny’s brain was performed on 13 January 2020. After referring to the features observed on this scan, the experts said this:

“DR KEENAN: From my point of view, the question is are these actually another sign of acquired brain injury? We have the black dots and we have white dots. The black dots just happen to be in the cerebellum. The white dots just happen to be in the hemispheres.
Having thought about this very carefully, it seems too big a burden for these to be physiologic. Now they are non-specific, they don’t tell us exactly what’s caused them, but I think this may well be a signature of additional acquired brain injury in the hemispheric white matter. If you like, we’ve now gone from black dots to adding on maybe some white dots in the white matter.
My supposition that they both represent acquired brain injury and on the background of this we have this asymmetry, which [Professor Coleman] and I have talked about, which has been there on all the scans and it’s an asymmetry of, a more diffuse asymmetry of the white matter, if you like, and is probably more likely than not an acquired brain injury. It’s probably a different process.
One of the confusing things here is I think we have a couple of processes potentially going on. In the background we have this sort of, if you ignore all the arrows, got this sort of global asymmetry here which is mild. We don’t have an obvious malformation of the cortex which is overlying it, which is often the associated finding, particularly in seizures, but then we have lots of these dots which I think are more than acceptable for any physiological state, so I think they’re pathologic.
AP COLEMAN: I would agree with [Dr Keenan] on that. I think there is some form of developmental anomaly of the left parietal occipital lobe and I agree that those other areas, I often call them brain ‘freckles’ because we often see quite a few of them in the older children that we scan for a collection of reasons, white matter punctuate foci without underlying disease and we postulate is it dysmyelination, is it demyelination? micro ischaemic changes small vessel disease? Has it even occurred because this child’s had seizures? We are speculating, that’s the problem as to what the cause is.
In my opinion, there is no evidence of parietal volume loss, although I think the corpus callosum looks like a little dysmorphic but that may be a reflection the myelin is not exactly normal in the left temporo occipitoparietal lobe that’s going on in the brain.
But then we come down to well, what has caused this? We could say okay, there is developmental, I’ll use the term dysplastic but process that’s affected the left temporoparietal occipital lobe. Has this child had an insult (I’m not saying perinatal) where you’ve got some ischaemic change that has caused these areas of gliosis? This is an acquired insult, we are speculating but suggesting it’s acquired injury, could it have been acquired post-delivery?
The child has obviously had significant seizures, has there ever been any hypotensive episode? I just can’t say. I think the pattern, in my opinion, is not classic of perinatal ischaemic injury, but what caused it I cannot say. We can argue, we can look at the clinical history and that goes down to the clinicians, in my opinion. [Emphasis added]
DR KEENAN: I think we’ve agreed pretty much on the findings. I think the black dots are pathologic, they shouldn’t be there. I think those white dots on top of everything else also shouldn’t be there. When I talk about tip of the iceberg, what we sometimes do is go to a very sophisticated imaging like this where we can actually look at the microscopic white matter tracts and you can analyse this. So we do that, for example, in concussion and we can pick up abnormalities which you can’t visualise.
Very often the brain can look normal but this thing here, which is a diffusion tensor (DTI) or HARDI image, can be totally abnormal. We can only see what we can see, and my feeling is that we have two things going on here. I agree with [Professor Coleman], there’s a background process where there is something that is not, there’s an asymmetry of the white matter on the left side, whether it’s very delayed and will finally get there as a fully myelinate or whether it’s an abnormal substrate, I don’t think we can tell.
On top of that I think there’s actually evidence of an acquired brain injury, so the black dots and the white dots are signs of something that is at this baby’s brain and caused at least some of his problems. You can’t look at these in isolation. When they talk about microbleeds they have very significant associations, particularly in the cerebellum, and usually they are first mothers, older mothers, both of which were present here. The baby had foetal distress which I don’t think is in too much debate, and then baby came out was said to be flat and centrally depressed.
I’m pretty sure there was a neonatal encephalopathy as well. More than just your average baby getting delivered and having a rough time. I think some of these, certainly these acquired findings can be ascribed to either the hypoperfusion insult as a perinatal asphyxia or to some of the things that had to be done to deal with that perinatal asphyxia like the instrumental delivery. Sometimes you can’t always separate the cure from the disease.
I agree with AP Coleman and I think there’s definitely asymmetry of the white matter. You could probably debate about exactly what’s causing it but it seems to probably be a developmental thing, either developmental delay or developmentally different tissue.
I think on top of that we have an acquired brain injury which is almost certainly a perinatal injury. We shouldn’t have these white dots and black dots on the side of the brain. I attribute maybe more significance probably than [Professor Coleman] does to them, that’s probably where we are divergent in our opinions.
AP COLEMAN: I think we’re absolutely speculating because this child may have had, and did have from the history, needed some resuscitation but the child was not clinically ever diagnosed as being encephalopathic. The child never seized and was in fact discharged, to my understanding, home on day 4 so we are speculating. [Emphasis added]
Some of those things might have happened antenatally. The child has obviously had significant seizures postnatally, I’m not saying the seizures caused the areas of what we are speculating as gliotic change, but needed significant anti-convulsants to control the seizures. I have no concept of what is happening clinically with the child, or has happened clinically with the child, but [Dr Keenan] and I agree to disagree, shall we say, on the cause of the white dots.
DR KEENAN: That’s right, it’s a complex case.”

These experts were then asked to offer their opinions upon the critical question of whether the imaging was consistent with a perinatal hypoxic ischaemic insult. Their responses were as follows:

“DR KEENAN: All the patterns of hypoxic ischaemic injury in a term baby, this does fit into sort of the number 4 version, from my point of view. But as [Professor Coleman] is probably going to say and I agree, there are changes on the scan which also can’t be ascribed to hypoxic ischaemic, like an acute perinatal insult. So we have two things going on. One of them I feel can be ascribed to hypoxic ischaemic injury, that is the black dots and white dots, but the other thing which we’ve been talking about, which is the left sided asymmetric white matter, that’s a different kettle of fish and I’m not sure totally, even now, what’s actually causing that. I think it’s not an acute perinatal insult.
AP COLEMAN: The left temporo-parietal occipital lobe abnormality is not a perinatal insult, in my opinion. As far as the gliotic small white matter changes that you’re saying is potentially a perinatal ischaemic injury you could debate, it could have happened pre-delivery, antenatally, or it could have happened postnatally. For me, it could have happened at any stage postnatally, including during when the child has had seizures.
To me it is not the classic categoric pattern of hypoxic ischaemic encephalopathic injury. Especially given that the child also was not encephalopathic after delivery. I accept that the child required some resuscitation, a lot of babies require some short-term resuscitation, and I do not believe this is the classic pattern of hypoxic ischaemic encephalopathy. This is where [Dr Keenan] and I digress but I agree there is some acquired white matter injury, superimposed on a brain that’s got a developmental abnormality in the left temporo-parietal occipital region and it’s as simple as that.”

Finally, the experts were asked whether the imaging was consistent with a dysplastic brain parenchyma. Professor Coleman considered that Benny’s brain was developmentally abnormal. Dr Keenan disagreed.

Consideration: Separate Question 2

This question has been the subject of obstetric, neurological and neuroradiological opinions. It distils to the issue of whether the evidence supports the cause for Benny’s foetal/neonatal condition was consistent with an hypoxic ischaemic encephalopathy or other neonatal injury sustained during birth.
Dr Keogh was emphatic that there is no possibility that Benny suffered any kind of perinatal hypoxic ischaemic insult. I have already indicated that I found the emphatic and strident terms in which he expressed his opinion on this issue, quoted earlier to be reliable and persuasive. As Dr Keogh said, Benny “never ever, ever, ever, showed any sign of newborn encephalopathy.” To like effect, Professor Chapman was also of the opinion that what happened to Benny was not consistent with hypoxic ischaemic encephalopathy: Benny was depressed at birth but recovered quickly and subsequently went to his mother. Professor O’Connor did not think Benny had hypoxic ischaemic encephalopathy. Only Dr Schmidt thought that he did.
Of the neurologists, Dr Ryan accepted that there was evidence of intrapartum hypoxia, as demonstrated by the changes in Benny’s heart rate and low pH present at birth on the cord blood, plus the need for resuscitation, but she considered that the hypoxia was transient and did not lead to hypoxic ischaemic brain injury: Benny’s pH normalised quickly, the resuscitation time was relatively minimal and his presentation returned to normal thereafter.
Dr Harbord was of the opinion that Benny suffered from intrapartum hypoxia and ischaemia. He placed significant emphasis upon Benny’s feeding difficulties and attachment problems, among other things. These included severe acidosis and pH anomalies. Regular spontaneous respiration did not occur for 5 minutes following delivery. Other experts, particularly Dr Keogh, were critical of Dr Harbord’s reliance upon Benny’s feeding difficulties as they had maternal anatomical causes and resolved shortly after birth.
Dr Keenan and Professor Coleman were largely in agreement about nearly all matters apart from the issue of the existence of hypoxic ischaemic encephalopathy. The radiographic evidence was not unambiguously determinative. Dr Keenan accepted that there are changes on the scan which also cannot be ascribed to hypoxic ischaemia like an acute perinatal insult. He conceded that whatever happened was not an acute perinatal insult. Professor Coleman considered that Benny’s left temporo-parietal occipital lobe abnormality was not a perinatal insult. Significantly in my opinion, given what amounted to the inconclusive nature of the radiological evidence, was the comment by Professor Coleman to the effect that the clinical history is likely to be the most fertile source of evidence for the answer. That would in my opinion inevitably bring the focus back to the obstetricians and to the emphatic views of Dr Keogh.
Before continuing, it is important to observe that the opinions expressed by the experts were ultimately and necessarily based on an understanding of what occurred on 2 April 2016, which was in turn drawn from the recollections of the specialists in charge of Benny’s care immediately following his birth and what they observed about him. The question of whether Benny exhibited or presented with signs that were conclusive of, or even consistent with, the existence of hypoxic ischaemic encephalopathy, finds its answer in the examination of whether the extreme clinical presentation of the type described by Dr Keogh in infants so affected were seen and recorded by the doctors in this case.

Dr Emily Innes

Dr Innes is a specialist paediatric neurologist. As at April 2016, she had been accepted into the paediatrics training programme with the Royal Australasian College of Physicians and was employed as a senior resident medical officer through the neonatology department at the Royal Hospital for Women. Dr Innes was present at 11:38 hours on 2 April 2016 when Benny was born. She gave oral evidence in the proceedings. Her statement is dated 24 April 2024. It included the following observations:

“10. I observe that my clinical note does not contain a comment on the antenatal ultrasound, which appears to be an oversight on my behalf. It was my usual practice to review the available antenatal ultrasound reports and record whether they were normal or document any concerns. For the purpose of this statement, I have reviewed the antenatal ultrasound reports and they are essentially normal as concerns foetal wellbeing. It is likely that I have inadvertently overlooked documenting this in my note.
11. Given the history of a suspicious trace prior to delivery, I was prepared for prompt intervention if required after Bendeguz’ birth. When Bendeguz was born, I observed meconium-stained liquor with poor respiration. I was able to promptly transfer Bendeguz to the resuscitaire within 20 seconds of life. As Bendeguz did not immediately release a cry, I attempted suctioning the trachea to ensure clear airways. Whilst attempting suction, Bendeguz’ heart rate dropped. I promptly commenced him on Invasive Positive Pressure Ventilation (IPPV) for thirty seconds to ensure adequate oxygenation was maintained. His heart rate normalised by 90 seconds of age and remained normal. I successfully completed oropharynx and nasopharynx suctioning by three minutes of age and maintained CPAP until six minutes of age. Whilst there was initially increased work of breathing and bronchial breath sounds, with time the bronchial breath sounds resolved. When I removed his ventilation mask at 6 minutes of life Bendeguz let go a strong cry. That was a reassuring sign. As he continued to have moderate work of breathing I kept Bendeguz on ventilation until Dr Sinclair, neonatal fellow, arrived to further assess the need for a potential transfer to the nursery. I can say that this was a relatively standard and uncomplicated resuscitation.
12. Prior to the arrival of Dr Sinclair, I conducted an initial neonate examination and documented my findings in the clinical notes. In accordance with my usual practice in 2016, this involved a top-to-toe review of Bendeguz. Had I identified anything of concern or significance during my examination, it was (and remains) my practice to document that in the clinical notes.
13. On cranial examination, I observed and documented that Bendeguz had a right caput posteriorly. This is not unexpected following pelvic pressure or a forceps delivery. I carefully examined his face, ears, eyes and nose and apart from a left pre-auricular skin tag, this examination was unremarkable. Likewise, oropharyngeal examination was normal with no abnormalities detected. Whilst it was usual practice to test a neonate’s suck reflex during the oropharyngeal examination, I cannot recall whether I assessed his suck reflex at this time. This involves placing a gloved finger in the neonate’s mouth to check the palate and strength of suck function. I would not have normally checked this whilst an infant requires CPAP.
14. I conducted and documented my assessment of Bendeguz’ lungs and cardiovascular system. Bendeguz had initial increased work of breathing, assessed by looking for signs of respiratory distress including sternal recession, sub-costal and intercostal recessions and abdominal breathing. I also looked for grunting or tachycardia. As I have said earlier in this statement, he had a “strong cry” at 6 minutes of age with moderate work of breathing. In accordance with my usual practice in 2016, I requested senior assistance to determine the infant’s ongoing need for CPAP which would require a transfer to the nursery. I auscultated his heart and lungs and Bendeguz had dual heart sounds with no murmur. I have documented that his heart rate was 170 beats per minute (normal) at three minutes of age, with bilateral and equal femoral pulses. My assessment of his cardiovascular system was unremarkable.
15. I conducted and documented an abdominal examination. Bendeguz had a three-vessel umbilical cord (normal) and his abdomen was soft (normal). In accordance with my usual practice of 2016, my abdominal examination would have included inspection of the anus. I conducted and documented an examination of Bendeguz genitalia which was unremarkable, with descended testes. I conducted and document musculoskeletal examination. There were no abnormalities on palpation and examination of his spine and his hips were symmetrical. He had all his digits.
16. In accordance with my usual practice in 2016, I also assessed tone and reflexes during my neonatal assessment. In accordance with that practice, I assessed truncal tone by handling and peripheral muscle tone by observing their posture, whether the arms and or legs are flexed or extended and move the elbow and knee joints through their range of movement. I look for spontaneous kicking or stretching of arms. As part of my usual neonate assessment in 2016, I tested reflexes, specifically the Moro reflex and spinal reflexes such as the Galant and Landau reflex and peripheral reflexes. Had there been any abnormality in Bendeguz’ tone or reflexes following my examination, I would have documented them in my clinical note. Bendeguz did not have abnormal tone or reflexes on assessment.
17. I can see from my clinical note that Dr Sinclair arrived when Bendeguz was 13 minutes of age. My usual practice in 2016 was to remain with the neonate while the fellow was examining him or her and I believe I followed that practice on this occasion. By the time Dr Sinclair arrived, Bendeguz had had an Apgar at 10 minutes of age which was normal (9). Bendeguz had a good heart rate and oxygen levels. My physical assessment of Bendeguz was essentially normal. Following Dr Sinclair’s arrival at 13 minutes of age, a second trial off CPAP was attempted. The infant no longer had signs of respiratory distress requiring ongoing CPAP. Dr Sinclair ceased ventilation and gave Bendeguz to his mother for skin-to-skin contact.

18. After approximately ten minutes of skin-to-skin contact, I reviewed Bendeguz again. Whilst I do not now recall, it is very likely that I remained in the room observing Bendeguz whilst he was with his mother. When I examined him again at 25 minutes of life, his respiratory rate was normal (48 breaths per minute). Apart from a ‘very occasional nasal flare’, there was no increased working of breath. His oxygen saturations were 98% and his heart rate was 182 beats per minute. He was doing well. I documented that his tone was good. Bendeguz weighed 3540g, was 51cm in length and had a head circumference of 35cm.
19. I have documented that the plan at that stage was for three hourly observations and to page me with the cord gases. In accordance with usual practice, this plan would have been discussed with and approved by Dr Sinclair. The plan did not involve transfer to the NICU as he was essentially a well baby.
20. I am aware from my review of the notes that following receipt of the cord blood gasses, Bendeguz was transferred for observations to NICU. I was not involved in his care in NICU. However, I can see from my review of his clinical notes the gas obtained from Bendeguz at 3 hours of age was essentially normal and the plan was for him to be returned to the ward.”

Dr Ruth Sinclair

Dr Sinclair is a specialist neonatologist. As at April 2016, she was employed by the South Eastern Sydney Local Health District as a paediatrics fellow at the Royal Hospital for Women. Dr Sinclair gave oral evidence in the proceedings. Her statement is dated 24 April 2024. It included the following observations:

“9. … My interpretation of the contemporaneous documentation was that Bendeguz had evidence of perinatal hypoxia given the low Apgar scores but that he responded well to the resuscitation provided in line with the NLS guideline in 2016. On my review, he did not require ongoing respiratory support and that neurologically he had normal tone and vigorous cry. It would have been my standard of practice to consider hypoxic ischaemic encephalopathy with the Apgars provided. My decision to place him skin to skin with his mother would have only been made if I was very happy with his overall appearance at that time. If there was any concern, I would have continued to observe him on the resuscitaire and admitted him to NICU if further concerns.
…
18. I can say that in accordance with my usual practice then and now, when a baby has an initial cord blood pH below 7.1 but especially below pH 7.0, I am specifically concerned with the risk of Hypoxic Ischaemic Encephalopathy (HIE). HIE is assessed in stages pursuant to what is known as the Sarnat Classification of HIE, specifically HIE Stage 1 (mild), Stage 2 (moderate) or Stage 3 (severe). Sarnat scoring has been the standard for assessing HIE throughout my career and was certainly applied by me in 2016. Staging HIE requires assessment of a patient’s level of consciousness, spontaneous activity, posture, tone, primitive reflexes such as the Moro and suck reflexes and respiration status. Seizures are commonly seen in moderate encephalopathy. Whilst Stages 2 and 3 HIE are associated with long term neurological injury, this is not the expected outcome for most patients with a Stage 1 HIE.
19. Patients with Stage 2 or 3 typically require some form of respiratory support ongoing from the time of birth. They often have multiorgan impairment and critically unwell requiring extensive intensive care. Bendeguz did not present with either a Stage 2 or 3 HIE. What had to be excluded by observation and assessment were the mild symptoms associated with HIE Stage 1. Stage 1 HIE infants typically present with irritability and difficulty settling, high pitched cry, increased tone, decreased suck reflex and an increased Moro. I have specifically documented completing a neurological examination describing that he settles, had a normal cry, no evidence of increased tone and had normal reflexes. He also has a normal respiratory rate and work of breathing. I am confident from this documentation that I have considered an HIE diagnosis and that he did not have evidence of encephalopathy. If I formed the impression that Bendeguz had or likely had HIE, it was and remains my practice to clearly document that in the clinical notes. As I have not documented an impression of HIE, I can say with confidence that I did not identify signs and symptoms consistent with a HIE on my careful and detailed examination of him on 2 April 2016.
…
21. In accordance with my usual practice, I can say that I reviewed Bendeguz’ available clinical notes when I reviewed him in the NICU on 2 April 2016. Having reviewed those notes again in preparation for this statement, I can say that I was aware at the time of my review that Bendeguz was observed by NICU nursing staff to be pink and active, his capillary blood gasses were reassuringly normalising quickly and he had no observations out of the normal range. Bendeguz did not require any respiratory or other intervention while in NICU.
22. My usual practice when assessing babies in the NICU was (and remains) to perform a head to toe newborn examination. I observed and documented that Bendeguz was afebrile, had a normal heart rate, normal respiratory rate and normal oxygen saturation on room air. Cardiovascular assessment was normal (dual heart sounds no murmur) and Bendeguz had good bilateral femoral pulses. Abdominal examination was unremarkable. I have documented a settled baby. I can say that whilst Bendeguz was in a poor condition at birth he responded quickly with IPPV and a brief period of CPAP. At the time of my assessment in the NICU there were no signs of increase working of breath and his breath sounds were clear. Bendeguz did not have any clinical signs to suggest further investigations for infection was warranted.
…
26. As I was satisfied on assessment that Bendeguz did not have HIE (that is, he had not sustained any brain injury around the time of birth) or ongoing need for feeding or intensive care and was in summary a well baby, I was content for him to be discharge from NICU to the ward to have ongoing monitoring there. If I had any suspicion of even a mild HIE, I can say I would not have discharged Bendeguz to the ward and would have kept him in the NICU for further observation.”

Having regard to the evidence of Dr Innes and Dr Sinclair, to their particular specialties, and to the evidence in this case which suggests that it is “not a subtle diagnosis”, I am unable to accept that if Benny had been born with hypoxic ischaemic encephalopathy, it would not have been observed, recorded and followed up by these doctors and others at the hospital immediately following his birth and at the very latest prior to his discharge.
I acknowledge that Dr Innes and Dr Sinclair were both cross-examined and that the plaintiffs would wish to assert that, conformably with the questions they were asked, they had an interest in the outcome of the proceedings and that such an interest should at least be taken into account by me in the assessment or their evidence. I acknowledge the force of such a forensic concern. However, I remain of the view that if Benny had been as severely compromised by an intrapartum insult as the plaintiffs are attempting to establish, it is extremely unlikely that this would not have been reflected in the contemporaneous records or the later recollections of any one, if not everyone, concerned with Ms Nemes’ confinement, Benny’s antenatal care and his delivery.
I should also note that I am disinclined to place too great an emphasis upon the recollections of Benny’s parents, lest it be thought I have been unfairly critical having regard to the understandable difficulties that Benny’s condition has created for them. However, each provided an evidentiary statement for use in these proceedings. It is sufficient for present purposes to observe that Ms Nemes only relevant observation about Benny’s condition while at the hospital before discharge is to be found at paragraph 23 of her first evidentiary statement dated 17 July 2020:

“23. After Bendeguz was born he was taken to NICU. When I got to see him he seemed okay but he did not want to take the breast so I ended up giving him formula. He got a K1 injection at the hospital and passed a hearing test.”

Mr Nemes’ evidentiary statement is dated 17 July 2020. The only reference in that statement to Benny’s condition at the hospital is in paragraph 13 as follow:

“13. I do not recall prior to discharge being told that there were any abnormalities during the labour or that there was any particular features of monitoring that concerned the doctors.”

I reiterate that neither of Benny’s parents is medically trained and I do not wish to appear to criticise them for any perceived inadequacies or deficiencies in their statements. What was or was not included in those statements cannot in my experience always or only be attributed to the parties. I merely wish to record that if Benny had been exhibiting the extreme signs described by Dr Keogh that are characteristic of hypoxic encephalopathy, it is unusual that these would not have been referred to by his parents for the purposes of their evidence in these proceedings on such a critical issue. `
Having regard to the evidence, which I take to be partly reflected in the statements of doctors Innes and Sinclair, I am not satisfied that any of Benny’s injuries or disabilities were caused or contributed to by delay in his delivery. He did not sustain an hypoxic ischaemic insult and he does not now suffer from hypoxic ischaemic encephalopathy. I am content to repeat, and to rely upon, Dr Keogh’s evidence in concurrent session, which is set out in greater detail and context earlier in these reasons at [77], where he said:

“I can say with absolute 100 per cent confidence that the long-term neurological injury that this baby demonstrates is unrelated to the birth because it never became encephalopathic. I’m not saying this baby doesn’t have that long term injury; it definitely does, but it’s due to a developmental congenital anomaly in the baby’s brain and it was there before the labour and if I had delivered this baby by Caesarean section electively at 39 weeks we would still be seeing this same baby today with the same neurological injury and there’s no doubt about that.” [Emphasis added]

It follows that this question must be answered “No”.

SEPARATE QUESTION 3: DID THE DEFENDANT BREACH ITS DUTY OF CARE BY NOT PRESCRIBING PROPHYLACTIC ANTIBIOTICS?

SEPARATE QUESTION 4: WAS ANY PURPORTED FAILURE TO PRESCRIBE ANTIBIOTICS IN (3) CAUSATIVE OF THE PLAINTIFF’S SUBSEQUENT DISABILITY?

As will be apparent, these issues have been dealt with earlier in these reasons.

SEPARATE QUESTION 5: DID THE DEFENDANT BREACH ITS DUTY OF CARE IN THE MANNER IN WHICH IT AUGMENTED THE MOTHER'S LABOUR WITH SYNTOCINON?

SEPARATE QUESTION 6: WAS THE PURPORTED MANNER OF ADMINISTRATION OF SYNTOCINON IN (5) CAUSATIVE OF THE PLAINTIFF'S SUBSEQUENT DISABILITY?

Joint Question 2 that the obstetricians were asked dealt with these issues and is as follows:

2. Please comment on the reasonableness of the augmentation of the mother's labour with Syntocinon, including:
(a) whether it was reasonable to continue Syntocinon up and until transfer to the delivery suite [sic, operating theatre] , and if not, when should it have been ceased?

Professor O'Connor considered that the use of Syntocinon has to be curtailed and discontinued if there are repeated foetal heart rate abnormalities. His opinion was that it is not reasonable to use Syntocinon when recurrent decelerations are present.
Dr Schmidt agreed with Professor O'Connor. He said that Syntocinon stimulation, with a foetal heart rate of 160-170 bpm which has increased from 130 bpm in early labour, was contraindicated, even more so with recurrent decelerations superimposed on foetal tachycardia.
Professor Keogh gave a more expansive answer to this question in the following terms:

"DR KEOGH: I can see either argument there to be honest with you. I can see some people would have stopped it and some people would have kept it going. So, let's think what is the consequence of keeping it going. The consequence of keeping it going is you have a risk that the contraction may come one on top of the other. So do they come one on top of the other? They do not. They remain widely spaced despite the increased rate of Syntocinon. I think it was reasonable to keep it going on the same line of reasoning that Professor Chapman said, they were going for a normal delivery.
Second, there is clear evidence that putting up the Syntocinon did not cause the contractions to become rapid or prolonged. In other words, yes, they kept it going, they had a strategy for doing that, trying for a normal delivery. They were monitoring the contractions. Did the increase in Syntocinon cause any complications here? No, it did not, because the contractions remain widely spaced and Ms Nemes did not become hyperstimulated. Therefore there was no adverse consequence to keeping the Syntocinon going.
Whether you think people should have stopped it or whether you think people should have kept it going, the bottom line is no adverse consequence came as a result of either stopping or increasing it because the contractions remained widely spaced and at no time in this second stage became problematic." [Emphasis added]

Joint Question 2(b) is as follows:

(b) Whether on the balance of probabilities the continuation of Syntocinon had any impact on foetal outcome?

Professor O'Connor's answer to this question was "possibly". That was because he was of the view that the Syntocinon was continued in the presence of foetal heart rate abnormalities.
Professor Chapman thought the fact that the deceleration ceased made him believe that the Syntocinon did not contribute anything. He would have continued the Syntocinon "as it was done and doesn't affect the outcome."
Professor Keogh agreed that hyperstimulation was dangerous, but insisted, consistently with the views he had earlier expressed, that it was irrelevant here because "hyperstimulation did not at any stage occur". He explained this as follows:

"The contractions remain the same despite increasing Syntocinon. When she stops pushing, the decelerations disappear completely, despite the Syntocinon continuing. There is no way we can say the Syntocinon is causing the compromise. The point, well made by Professor Chapman, is that it is the pushing that is causing the decelerations. They don't happen before she pushes. They disappear as soon as she stops pushing.
…
Two points. The first is that the Syntocinon can only modify risk by causing either very prolonged or very frequent contractions. It did neither. The second thing, and this is very important, is this baby's outcome is completely unrelated to intrapartum hypoxia. This discussion about the CTGs is effectively a diversion, because this baby did not have hypoxic ischaemic encephalopathy. None of this baby's outcomes are related to birth asphyxia.
The child's problem arose from a brain malformation that occurred in utero, during development, and became more apparent as the baby grew. Neither Syntocinon, nor the labour, caused the outcome here. None of this was relevant to the outcome which is due to developmental anomaly." [Emphasis added]

Professor Keogh's concurrent evidence about this should also be noted as follows:

"But I hasten to point out that Syntocinon is not damaging to babies. There is, it doesn't matter how much Syntocinon you give in the absence of a uterine response. Syntocinon does not damage babies. What damages babies is if the contractions become so frequent, or so long, that they can't compensate in between. So, John is not correct in saying that the Syntocinon will be contraindicated, unless it was causing an abnormal response from the uterus, which it was not."

Dr Keogh’s evidence in joint session should also be noted:

“CRANITCH: That doesn’t seem to be the case, with respect, because we’re getting a different view from--
WITNESS KEOGH: Well, in consensus we all agreed, you know, and so it seems to me we’re, we’re, we, we’re having to imagine things. We’re having to imagine an HIE that we can’t demonstrate. We’re having to imagine, you know, hyperstimulation, which we can’t see. We’re having to think about infection for which there’s no evidence. It, it, it, it seems to me like we’re fishing for things that we have no evidence for trying to explain something that already has a very clear explanation in a congenital abnormality.
CRANITCH: What is the congenital abnormality to which you refer?
WITNESS KEOGH: The congenital abnormality is the cortical dysplasia and the deep, the deep brain abnormality that was seen on the MRI.
CRANITCH: That’s your view, is it?
WITNESS KEOGH: Very strongly.
CRANITCH: Thank you. Would you agree, however, Professor Keogh, that it was ill advised, to say the least, that no matter what the bearing outcome might have been for an ever-increasing dose of SYNTOCINON to be administered at a second stage to the extent that it was here? It just went up automatically to some quite extraordinary amount.
WITNESS KEOGH: First of all, it was not an extraordinary amount. We used to run these at 250 mls an hour. So it’s not an extraordinary amount. SYNTOCINON has a half-life of about a minute and a half in the circulation so it’s very quickly broken down. All about SYNTOCINON is titrating it against the response and here there was no excessive response. They were trying to get the head down to make the baby deliverable when they got her to theatre and I, therefore, have no criticism. If they had had rapid, rapid contractions already and they were pushing it stronger to try and get it and, and taking a risk that they were decreasing the during between contractions I would have criticised it.
CRANITCH: What about the strength of the contractions?
WITNESS KEOGH: Well, I think we’ve already addressed that, that the contractions were not too long, there were not too frequent and, when it comes to strength, the strength of the contraction itself has no adverse impact on the baby.”

Consideration: Separate Questions 5 and 6

In my view, both questions must be answered “No”.
Even if it were to be assumed for the purpose of the inquiry that the Syntocinon administration were flawed in some way, there is absolutely no satisfactory evidence to establish on the balance of probabilities that it caused any enduring loss of the type that is claimed to have been sustained in this case. It is clear that a review of the transcript of the concurrent evidence of the obstetricians will reveal that Mr Cranitch was implicitly, if not explicitly, critical of the way in which Dr Keogh gave his evidence. In making that comment I do not intend to suggest that Mr Cranitch was doing any more or less than legitimately attempting in an adversarial contest to maintain his clients’ best interests in a difficult case. However, as I have already noted elsewhere, Dr Keogh’s evidence and opinions were expressed with a significant degree of confidence that did not to my observation at any stage appear to descend into a partisan analysis. The scientific evidence in this case required expert explanation before it can be understood and applied by me. Dr Keogh’s explanations were well reasoned and persuasive. More particularly, the evidence that Benny was never encephalopathic is in my view overwhelming. Experts hypothesising about Syntocinon infusions did not serve to cast any doubt upon that fact.

Failure to administer a foetal scalp test

The plaintiffs contended that a foetal scalp test ought to have been conducted. The question is whether in the clinical circumstances it was reasonable not to perform that intervention and whether, even if performed, it would have altered the mode and timing of delivery or outcome.

Defendant’s submissions

There was no clinical indication to perform a foetal scalp blood sample before the second stage. During the second stage, it would have been reasonable to consider checking foetal welfare by way of a foetal blood scalp sample in light of decreased variability and decelerations. However, the decision to proceed to instrumental delivery without delay was also appropriate and reasonable. Nor was a foetal blood scalp sample required during the first stage.
Professor O’Connor contended each time the trace was either non-reassuring or pathological by reason of reduced variability or a deceleration, a foetal scalp blood sample was indicated. Dr Schmidt contended a foetal blood scalp sample was “actually very easy to do”. The defendant maintained that neither opinion should be accepted.
The Guidelines to which Professor O’Connor refers in his report do not recommend a foetal scalp blood sample on each occasion that a trace is non-reassuring. Section 4 of the Guidelines notes the poor predictive value of FHR pattern interpretation and recommends that foetal scalp blood sampling and/or expedited birth be considered in the presence of a pathological FHR pattern. At no time was the trace pathological during the first stage of labour.
Consistently with the Guidelines, Dr Keogh deposed that at no time in the first stage of labour was there a situation where the team would have been significantly worried about the baby and as such, there was no need for a scalp sample. Scalp samples are not common practice.
Likewise, Dr Chapman estimated that at St George Hospital, they would perform a foetal scalp sample approximately twice a week in a 2000 delivery-a-year unit. It is not done commonly and is an invasion. The defendant submitted that I would accept that foetal scalp blood samples are not common and certainly not performed every time a trace is “non-reassuring” as suggested by Professor O’Connor.
As to the suggestion that the scalp sampling procedure was “easy”, Dr Keogh indicated in the concurrent evidence of the obstetricians that they are hard to do: “they’re tricky, they’re super uncomfortable for women, and, and they’re very invasive and, you know, you have a woman in a very compromising position when you’re doing one. So no-one likes them and so you don’t rush to do them just when you get a minor abnormality, especially if its self-correcting”.
The defendant contended that I would accept that foetal scalp blood sampling is not common, not easily performed and is invasive. Guidelines suggest it should be considered with a pathological trace. At no time in the first stage of labour was this trace pathological and there was no indication to proceed to foetal blood scalp sampling.
Nor was such sampling indicated in the first stage of labour.
Dr McCormack documented in her operation report that following her review of Ms Nemes from 10:15 hours, she formed the view that intervention was indicated due to “prolonged second stage, suspicious CTG in [Delivery Suite] and head persistently at spines”. Dr McCormack gave evidence that it is “most likely” that she considered a lactate (foetal scalp blood sampling) but decided against it in favour of avoiding delay and making the necessary arrangements to facilitate transfer to theatre to expedite the birth of the baby.
The decision to proceed promptly to deliver Benny, avoiding the delay of scalp sampling, was appropriate. Dr Keogh agreed that foetal blood scalp sampling was an option “but what they have done instead is take her to the theatre for delivery” which was a reasonable alternative step. Dr Chapman says the only indication for a scalp sample in that scenario would be if the baby were undeliverable or the skill of the registrar involved was such that she was not comfortable getting on forceps or a vacuum extraction. Dr McCormack was credentialled and competent to perform forceps delivery. Her competence was demonstrated by her successful and prompt mid-cavity instrumental delivery.
Dr Keogh observed further that Dr McCormack’s decision making was entirely consistent with recommendations in the Guidelines:

“WITNESS KEOGH: It very much represents what happened here in, when, in the second stage with pushing, the contract- the decelerations became a little more complicated and increased the concern so you would only have done a scalp sample there if you were going to keep on going pushing, and, and you were looking for a reason not to intervene. But they made an alternative and equally valid decision that they would move to theatre and deliver this baby instead.
And it turned out to be very wise, didn’t it, because actually when they topped up the epidural and the baby decompensated, it meant they were in theatre and able to quickly respond with all the staff that they needed available to look after that mother and child, so that was a very wise, clever and sensible clinical decision made by the staff.”

The defendant submitted that I would accept that whilst a foetal scalp blood sample in the second stage was an option, the decision to proceed to expedited delivery by trial of forceps or Caesarean was in accordance with peer professional opinion as to competent professional practice.

Plaintiffs’ submissions

It is the plaintiffs’ case that due to oversight, inaction and a failure to take appropriate measures such as a foetal scalp analysis, the pregnancy went longer than it should have, thereby exposing Benny to an hypoxic insult. The plaintiffs maintained that the CTG indications, together with other features of the pregnancy, required better monitoring during first stage by way of a foetal blood sample and more decisive management once Benny was deliverable at 8.20.
Professor O'Connor believed foetal blood sampling was required as early as 21.00 on 1 April 2016. Dr Schmidt considered that foetal blood sampling was necessary shortly after deceleration at 01:40. He was attacked on the basis that his initial opinion was that there was no need to deliver the baby before 9.34 on 2 April 2016. Whilst Dr Schmidt changed his opinion after closer analysis of the CTG, he was not saying that Benny should have been delivered the night before but rather that, on his interpretation of the trace which showed a prolonged period of tachycardia without any variability, a lactate should have been performed to determine the direction of labour.
Dr Keogh thought that it would have been reasonable to do a foetal blood sample in the second stage but both he and Dr Chapman thought it reasonable not to do so when the team had decided to take the mother to theatre. The plaintiffs submitted that this ignores the suspicious nature of the trace from 03.14. On the evidence of Dr Stamatopoulos, a suspicious trace for this length of time would be pathological and required foetal lactate analysis. Drs Keogh and Chapman were silent on whether foetal blood sampling was required during the first stage of labour.
On balance, Dr Schmidt appears to be of the view that a scalp sampling at the second stage would not have made a difference.
The plaintiffs submitted that Dr Schmidt’s opinion that the second stage was complicated by indecision is justified. The evidence discloses that Ms Nemes was first assessed by a doctor at 10:15 approximately 2 hours after she entered the second stage of labour. From the commencement of the shift at about 8 am, Ms Nemes was under the care of Midwife Ellis, who did not here give evidence as to what happened during that period or why it took until 10:15 for her to arrange for a medical examination. Midwife Ellis was not called to give evidence despite being the midwife who took care of Ms Nemes when she presented to hospital on 1 April 2016 when her suggestion that she go home was overruled. She was also the midwife in charge of Ms Nemes’ care during the second stage of labour. An inference should be drawn that evidence Midwife Ellis would have given would have been adverse to the defendant's case, particularly in circumstances where she still works with the defendant.

Consideration

The allegation that the defendant failed to take a foetal scalp sample has no force or effect in these proceedings unless that failure can be tied to the cause of some loss or damage. It is necessarily the plaintiffs’ position that Benny’s antenatal condition would have been better understood if scalp monitoring had occurred in a way and at a time when what Dr Schmidt has characterised as indecision was stalling the appropriate response to the clinical indications. The plaintiffs contend that a foetal scalp sample would have clarified the position and dispelled the indecision.
The difficulty with that proposition, for the purposes of the proceedings, is that I have concluded that Benny did not sustain any injury as the result of a failure to deliver him earlier, or as the result of what in the present context the plaintiffs would characterise as indecision. Even accepting, once again for the sake of argument, that a foetal scalp sample was indicated, the failure to proceed to administer such a test was without identifiable consequences.

Conclusion

The answers I have provided to the separate questions are sufficient to dispose of the proceedings. Those answers mean that the plaintiffs have not established that any alleged breach of duty of care during labour was causative of Benny’s seizures or Global Developmental Delay. I am satisfied that Benny was never encephalopathic. He was well until five months after birth. In the absence of encephalopathy, it is not possible to establish that Benny’s brain condition can be attributed to a perinatal cause. I am satisfied that Benny has a brain malformation that occurred or developed in utero but which is unrelated to the birthing process.

Orders

In the circumstances, I make the following orders:

Judgment for the defendant.

Order the plaintiffs to pay the defendant’s costs.

**********

Decision last updated: 05 May 2025

Medium Neutral Citation:	Nemes v South Eastern Sydney Local Health District [2025] NSWSC 418
Hearing dates:	29 April to 2 May, 9 July, 3 and 4 September, 25 October 2024
Date of orders:	05 May 2025
Decision date:	05 May 2025
Jurisdiction:	Common Law
Before:	Harrison CJ at CL
Decision:	(1) Judgment for the defendant. (2) Order the plaintiffs to pay the defendant’s costs.
Catchwords:	NEGLIGENCE – professional negligence – medical negligence – where child has disabilities including infantile seizures and Global Developmental Delay – whether disabilities are a result of a failure to deliver the baby earlier – obstetric evidence – conclave of experts – Civil Liability Act 2002 (NSW) s 5O – where the defendant is a Local Health District – whether the defendant acted in accordance with widely accepted peer professional practice – whether the defendant breached its duty of care – where there are multiple experts with competing opinions – whether any alleged breach of duty of care during labour was causative of the child’s disabilities
Legislation Cited:	Civil Liability Act 2002 (NSW) ss 5B, 5C, 5O
Cases Cited:	Dean v Pope (2022) 110 NSWLR 398; [2022] NSWCA 260 Makaroff v Nepean Blue Mountains Local Health District [2021] NSWCA 107
Category:	Principal judgment
Parties:	Bendeguz Nemes (Plaintiff - 2019/269249) Erika Nemes (Plaintiff - 2019/250366) Zsolt Nemes (Plaintiff - 2019/250377) South Eastern Sydney Local Health District (Defendant)
Representation:	Counsel: M Cranitch SC with A Campbell and M Summerhayes (Plaintiffs) R Cheney SC with B Bradley (Defendant) Solicitors: Gerard Malouf & Partners (Plaintiffs) Makinson d’Apice Lawyers (Defendant)
File Number(s):	2019/269249; 2019/250366; 2019/250377
Publication restriction:	Nil