EAST METROPOLITAN HEALTH SERVICE -v- ELLIS (by his next friend CHRISTOPHER GRAHAM ELLIS) [2020] WASCA 147 (10 September 2020)

(b) by 'attempting an instrumental delivery in circumstances where there had been no descent of the foetal head between the vaginal examination at 4.30 pm and that performed at 8.40 pm';[3]

(c) by 'not undertaking the instrumental delivery in an operating theatre that was already set up for an emergency caesarean section';[4] and

(d) by 'not abandoning the instrumental vaginal delivery following the third pull on the Kiwi cup'.[5]

1. There is no challenge to the findings of negligence.
2. His Honour also found that, in the absence of these breaches, the respondent would either have been safely delivered by the use of instruments or, if that did not occur after three pulls of a correctly placed instrument, safely delivered by caesarean section. In either case, the respondent would not have suffered the periods of perinatal asphyxia that he did.[6]
3. It was also not in dispute, at trial or on appeal, that as a consequence of the respondent's difficult birth, he suffered a number of injuries. The learned trial judge described the undisputed injuries as: perinatal asphyxia, global hypotonia, right sided Erb's palsy and renal impairment.[7] It may be open to debate whether perinatal asphyxia, as such, should be characterised as an injury (i.e. 'impairment' of a person's physical condition).[8] A lack of oxygen is perhaps better described as a physiological event, which may, or may not, result in an injury or impairment.
4. The other undisputed 'injuries' described by his Honour (global hypotonia, right sided Erb's palsy and renal impairment), however, clearly meet the description of damage, necessary to complete the cause of action in negligence. Accordingly, while those injuries were transient in nature, they nevertheless amounted to damage, which is the gist of an action in negligence.[9]
5. Nor, subject to some refinement of the issue we will set out later, is there any question that, as a consequence of the respondent's difficult and prolonged birth, he suffered an injury to his brain. The respondent pleaded that he had suffered hypoxic ischaemic encephalopathy and a traumatic brain injury as a result of the birth process.[10]
6. Hypoxic ischaemic encephalopathy (HIE) refers to an abnormal condition of the brain tissue (encephalopathy) caused by a lack of oxygen (hypoxia) in the blood supplying the tissue (ischaemia). A related term, an hypoxic ischaemic insult (HII), refers to the circumstance of insufficiently oxygenated blood getting to a particular part of the body, which, in turn, leads to damage to the tissue.[11]
7. That the respondent suffered injury to his brain, or indeed that he had suffered hypoxic ischaemic encephalopathy as a consequence of his birth process, was not in dispute at trial. As will be seen, it was the degree (or stage) of HIE that was in dispute.
8. None of the above matters are in issue in the appeal.
9. What is in issue in the appeal are what the learned trial judge described as the respondent's Developmental and Cognitive Impairments. The Developmental and Cognitive Impairments were:[12]

(a) hypotonic or reduced muscle tone in the respondent's lower limbs;

(b) poor coordination of the respondent's upper and lower limbs;

(d) cognitive issues with processing speed, working memory, attention, executive functioning, social cognition and adaptive functioning.

1. The respondent contended, at trial, that his Developmental and Cognitive Impairments were caused by injuries to his brain suffered in or as a consequence of the birth process. The appellant contended that they were not.
2. Whether the respondent's Developmental and Cognitive Impairments were caused by injuries to his brain resulting from the appellant's negligence was a question of fact to be established, on the balance of probabilities.[13] That ultimate fact could only be proven by way of inference from all the facts and circumstances as found by the learned trial judge and required the analysis and synthesis of a large body of expert opinion evidence.
3. The learned trial judge was satisfied that the fact was established. His Honour found that the respondent's Developmental and Cognitive Impairments are more likely than not sequelae of his birth injuries which, in turn, were caused by the defendant's fault.[14]
4. His Honour gave, in summary, eight reasons for reaching that finding, culminating in the following conclusion:[15]

These reasons are ample to support a reasonable and definite inference that Cooper's Developmental and Cognitive Impairments are sequelae of Cooper's Birth Injuries and that the defendant's fault was a necessary condition of the occurrence of both Cooper's Birth Injuries and Cooper's Developmental and Cognitive Impairments. To the extent that some of the primary facts are in the realm of the possible, for example the full extent of the damage to Cooper's brain in the area of the right cerebellar tonsil, I am entitled to give 'weight to the united force of all the evidence together'.

1. While (as will be seen) there are a number of subsidiary issues, ultimately, it is this finding that the appellant must overcome in order to succeed in its appeal (CACV 37 of 2018).[16]
2. For the reasons set out below, while we would uphold one of the subsidiary grounds (ground 17), the grounds of appeal challenging that finding and challenging the learned trial judge's ultimate finding that the respondent's Developmental and Cognitive Impairments were caused by the appellant's fault, must be rejected. As a consequence the appeal must be dismissed.
3. The appeal was also heard with two related appeals: CACV 54 of 2018, which concerns the costs order made by the learned trial judge (the Costs appeal) and CACV 93 of 2018, which concerned an application by the appellant to amend its Defence after trial (the Pleading appeal). The Pleading appeal fell away at the hearing of the appeal. We would also dismiss the Costs appeal.

1. While the question as to the cause of the respondent's Developmental and Cognitive Impairments was a question of some factual complexity, it nevertheless concerned a relatively discrete and narrow issue.
2. It is surprising, then, that the appeal raises no less than 22 grounds of appeal. It is, recalling McHugh J's observation in Tame v New South Wales,[17] inherently unlikely that a question of causation such as this would give rise to 22 issues, or that a judge of the District Court would make so many errors. There is, in this regard, a considerable degree of overlap between the various grounds of appeal. In that context, it is worthwhile identifying a number of broad themes that emerge from the grounds and the appellant's submissions.
3. First, the appellant challenges a number of the primary facts found by the learned trial judge and his Honour's preference for the evidence and opinions of some of the witnesses over others.
4. For example, the learned trial judge found that the respondent had suffered moderate, or 'stage 2', hypoxic ischaemic encephalopathy.[18] His Honour also made the related finding that the respondent had suffered seizures during his admission at Princess Margaret Hospital.[19] In so finding, his Honour accepted the judgment of Dr Shripada Rao, the respondent's treating Neonatal Physician, who gave evidence at trial. His Honour gave detailed reasons for accepting Dr Rao's judgment. [20]
5. In conducting a 'real review' of the evidence given at trial in relation to these (and other) findings, the necessity for the appellant to identify error and the principles of appellant restraint must be steadily borne in mind. Those principles are grounded in the advantages possessed by the learned trial judge, not only in having seen and heard the witnesses but in the 'feeling of a case' that usually emerges from running a trial and an appreciation of the way the trial was run.[21]
6. Secondly, the appellant places much emphasis on the fact that the learned trial judge, particularly when addressing a number of the primary facts in isolation, made findings expressed in terms of what was 'possible'. Many of the grounds of appeal rely upon passages of the Primary reasons that refer to certain 'possibilities'.[22]
7. A good example of this is his Honour's finding that 'it is quite possible' that Magnetic Resonance Imaging (MRI) scans performed on the respondent in 2014 and 2015 showed damage to the respondent's brain that extended beyond the right cerebellar tonsil.[23] The appellant contends that the learned trial judge erred in law in finding that 'this possibility of damage was sufficient to prove a causal link between breach and the [respondent's] 'Developmental and Cognitive Impairments''.[24]
8. Whether his Honour in fact found that 'the possibility of [such] damage was sufficient to prove [such] a causal link' is very much open to question. Certainly there is no express finding by the learned trial judge to that effect. It will be important, therefore, in addressing the grounds of appeal to determine what, on a proper construction of the Primary reasons (including what can be legitimately inferred from the reasons),[25] his Honour, in fact, found.
9. Given the significance of both the factual issues and the proper construction of the Primary reasons for the resolution of the appeal, it is appropriate to commence with a summary of:

(b) the expert evidence that bore upon the cause of the respondent's Developmental and Cognitive Impairments; and

(c) the learned trial judge's reasons for finding that Developmental and Cognitive Impairments are more likely than not sequelae of his birth injuries.

Background The course of the respondent's condition

1. The following summary of the course of the respondent's condition is, largely, drawn from the Primary reasons. Unless otherwise stated, it is uncontroversial in this appeal.
2. As noted above, when the respondent was born, at 9.42pm on 24 August 2009, he was 'flat', meaning he was not breathing, not moving and showed poor muscle tone.[26]
3. The respondent was assessed using 'Apgar' ratings at 1, 5 and 10 minutes, as follows:[27]

1. The respondent was immediately placed on a resuscitation cot where CPAP (continuous positive airway pressure) was employed, following which Dr Amira carried out CPR (cardiopulmonary resuscitation). The respondent did not take his first breath until five minutes after birth and underwent resuscitation for 20 minutes. He was administered adrenalin through his umbilical vein.[28]
2. At 10.01pm Dr Jack Vercoe, Consultant Paediatrician, arrived at the labour ward.[29] The respondent was still in a very poor condition, so much so that Dr Vercoe could not say whether he would survive. He was making gasping movements. He was trying to breathe, but clearly not doing it effectively. The respondent was making some respiratory effort but it was feeble.[30]
3. Dr Vercoe intubated the respondent (placing a tube through the trachea into the lungs). He also administered intravenous saline, to increase the respondent's circulating blood volume, and adrenalin to improve his heart beat.[31]
4. When the respondent was about 60 minutes of age, Dr Vercoe observed that the respondent started moving his legs.[32]
5. At 10.42 pm, the Western Australian Neonatal Transport Service team arrived from Princess Margaret Hospital (PMH) and took the respondent to PMH.[33]
6. The respondent was admitted to PMH and managed in the neonatal intensive care unit. He was given ventilation, inotropic support and therapeutic hypothermia. Therapeutic hypothermia, or cooling, involves keeping the baby's temperature down to between 33.5 and 34 degrees Celsius for approximately 72 hours. The learned trial judge observed that it was common ground that therapeutic hypothermia was beneficial for babies with moderate to severe HIE, both in terms of reducing mortality and in improving neurodevelopmental outcomes.[34]
7. At 7.30 am on 25 August 2009, the progress notes recorded:

Baby moving spontaneously, 'jittery' at times, no overt seizures seen.

The respondent was administered phenobarbitone, an anticonvulsant medication used for the treatment of seizures.[35]

1. At 9.25 am the progress notes record an assessment by Dr Rao and a Dr Gardiner. Under the heading 'problems' there was a note:

Other notes around the same time recorded the respondent as being 'intermittently irritable' and, around 9.30 am, having 'suspected seizures'.[36]

1. On 25 August 2009, an electroencephalography (EEG) was conducted on the respondent. No clinical seizures occurred during the recording.
2. The EEG report concluded:[37]

CONCLUSION: There is spontaneous variability on this EEG. There is responsiveness. The background is abnormal because of the predominantly very low amplitude interrupted by brief periods of normal looking activity. There is a suggestion of significant dysfunction, however it has to be interpreted with caution because the temperature of the baby was 33.8 at the time of the recording. Suggest repeat.

1. On 25 August 2009, the respondent also underwent a cranial ultrasound (Day 1 Ultrasound). The Day 1 Ultrasound showed evidence of cerebral oedema, namely excessive fluid in the brain substance.[38]
2. The progress notes for 26 August 2009 record the respondent as being 'very irritable most of the night' and also records 'no seizures overnight'. A later note records the respondent as 'jittery' and, at around 4.00 pm, nursing staff observed 'increasing jittery/seizure ? movements', in response to which phenobarbitone was administered 'to good effect'.[39]
3. On 26 August 2009, a registrar made a request to a consultant neonatologist for an opinion, which identified the presenting problems as including 'HIE' and seizures.[40]
4. Later that day a second EEG study was conducted on the respondent. He was 'irritable' throughout the study but no electrographic seizures were recorded. His temperature was 33.6 degrees.[41]
5. The progress notes for 27 August 2009 record the respondent as being jittery most of the night and occasionally irritable. He was given a further dose of phenobarbitone later in the day, with another note of 'no overt seizures'. The therapeutic hypothermia continued until midnight on 27 August 2009 when warming was commenced to bring the respondent up to a normal temperature.[42]
6. The progress notes for 28 August 2009 recorded that the respondent continued to be jittery and that there were no physical signs of seizures.[43] Similar entries appear for 29 August 2009, during which time the respondent was still being administered phenobarbitone.[44]
7. There were occasional references in the progress notes to the respondent being jittery in subsequent days but no obvious seizure activity was noted. By 31 August 2009, the respondent had developed good suck reflexes and was off intensive care support.[45]
8. On 31 August 2009, Dr Rao sent a consultation request to a neurology consultant. The reason for consultation was stated to be 'HIE' and the consultation request included the following:

Hypertonic + jittery since birth.

Jitteryness was suspected to be seizures and loaded with Phenobarb 20 + 10 mg/kg. No frank seizures. Also has R brachial plexus injury. Renal impairment x 48 hours ...[46]

1. On 31 August 2009, an MRI scan was conducted on the respondent's brain (Day 7 MRI). The Day 7 MRI was the subject of much expert evidence at trial and will be addressed further in that context. The report of the Day 7 MRI, prepared by Dr Thai Nguyen, dated 31 August 2009 reads:[47]

Findings:

There is an area of haemorrhagic contusion involving the inferior margin of the right cerebellar hemisphere extending into the right flocculus. There is also minor haemorrhage within the inferior cerebellar tonsil which herniates below the foramen magnum to the C1/2 level.

A further area of haemorrhage is seen lying superior to the superior cerebellar vermis. There are multiple small petechial haemorrhages within the right cerebellar hemisphere.

There is subdural blood lining the tentorium cerebelli and evidence of subdural collections over both parieto-occipital convexities. This is slightly larger on the left measuring approximately 5mm in maximal depth.

Minor intraventricular blood is also seen within the dependent portions of both occipital horns and the third ventricle.

There also appears to be a tiny focus of petechial haemorrhage within the left superior temporal lobe. There is a further small focus of haemorrhage within the left side of the suprasellar cistern which I suspect subarachnoid in nature.

The DWI sequence demonstrates diffusion restriction at the site of the right inferior cerebellar haemorrhagic contusion. No other restricted focus is identified.

The cortical ribbon is preserved throughout.

The cerebral white matter volume and myelination is appropriate for a term baby. A small focus of increased T2 signal is seen within the left lentiform nucleus likely representing a VR space. The basal ganglia and thalami are otherwise normal. No abnormality is seen within the brain stem.

There is no evidence of hydrocephalus.

Note is made of a small right parietal cephalhaematoma.

COMMENT:

There is evidence of traumatic brain injury with an area of haemorrhagic contusion involving the right inferior cerebellar hemisphere extending into the flocculus and further haemorrhage within the cerebellar tonsil. There are foci of petechial haemorrhages within the right cerebellar hermisphere, a focus of parenchymal haemorrhage within the left superior temporal lobe and evidence of likely subarachnoid haemorrhage just superior to the superior cerebellar vermis and also within the left side of the suprasella cistern.

Shallow subdural haematomata are seen over both parieto-occipital convexities and minor haemorrhage is seen within the lateral and third ventricles.

No cortical or basal ganglia infarct is identified.

1. On 2 September 2009, the neonates registrar (Dr Gardiner) sent a consultation request to neurology. The request included the following:

Had seizures initially, 30 mg/kg PB given → none since D3.

The EEG consultant's report included 'abnormal EEG with (variability) in background but no seizure activity'.[48] The respondent was discharged on 11 September 2009 with arrangements put in place for follow-up care.

1. In addition to the Day 7 MRI, the respondent underwent two further MRI scans. The first took place on 26 September 2014 (2014 MRI) and the second took place on 18 September 2015 (2015 MRI).[49]

1. The parties called a number of expert witnesses at trial, from a variety of expert disciplines. Not all of the expert witnesses gave evidence in relation to the causation of the respondent's Cognitive and Developmental Impairments (and some only marginally so).[50]
2. The respondent called the following expert witnesses relevant to that issue:

(b) Dr Mark Tracy, a Senior Newborn Intensive Care Specialist; and

(c) Dr Carmela Pestell, a Clinical Psychologist, Clinical Neuropsychologist and Associate Professor.

1. The respondent also called Dr Rao, the respondent's treating Neonatal Physician and Dr Nguyen, the Paediatric Radiologist who reported on the 7 Day MRI Scan. To the extent that Dr Rao and Dr Nguyen gave opinion evidence, no issue was taken with their expertise.
2. The appellant called the following expert witnesses in relation to the causation of the respondent's Cognitive and Developmental Impairments:

(a) Professor Michael Ditchfield, a Specialist Paediatric Radiologist;

(b) Professor Rodney Hunt, a Consultant Neonatologist; and

1. As is apparent, while there were areas of overlap in relation to their evidence, the expert witnesses fell within three broad areas of speciality. The different areas of speciality are important to understanding their contribution to the question of causation at issue in the appeal.
2. The first speciality related to the radiological investigations, and in particular the MRI scans (the Day 7 MRI, the 2014 MRI and the 2015 MRI) and the Day 1 Ultrasound. The radiologists, Dr Keenan and Professor Ditchfield, had particular expertise in that field, as did Dr Nguyen.
3. The second broad speciality was that of the neonatal physicians, Dr Tracy, Professor Hunt and Dr Rao. While each of these witnesses also gave evidence in relation to the radiological investigations, their evidence also dealt more broadly with the clinical evidence.
4. The final broad speciality was that of the neuropsychologists, Dr Pestell and Dr Do. Their evidence was concerned with the nature and pattern of the respondent's neurological impairments, and whether they are consistent with the respondent having sustained serious damage to his brain at birth, such as hypoxic ischaemic encephalopathy.
5. We now turn to summarise the effect of the experts' evidence. We will commence with the treating practitioners, Dr Rao and Dr Nguyen.

1. Dr Rao is a Neotatal Physician. As noted above, he treated the respondent during his admission to PMH after his birth. He continued to treat the respondent in the neonatal follow up clinic in the years following his birth.
2. The evidence before the learned trial judge included four reports from Dr Rao to the respondent's general practitioner, Dr Paul Tan. Those reports are dated 2 November 2009,[51] 21 April 2010,[52] 21 June 2010,[53] and 3 December 2010.[54]
3. All of those reports refer to the respondent's past diagnoses as including:

(b) 'Stage II hypoxic ischaemic encephalopathy: therapeutic cooling in the neonatal period'.

1. In his evidence, Dr Rao explained his diagnosis of stage 2 HIE as follows:[55]

The reason is that this baby had suffered definitely perinatal asphyxia because he had required a resuscitation in the form of IPPV, that is intermittent positive pressure ventilation, chest compression, even giving adrenaline. All this suggested that this baby had required - had suffered from perinatal asphyxia. That's why he required all this help. Inhalation, he required intubation by about 20 minutes of age by the paediatrician at that hospital because the baby was not having enough respiratory effort and when our team went there, our team - were - have what's called a NETS Team, Neonatal Emergency Transport Service Team. When we went - when they went there, they noticed that the child was quite hypotonic. Hypotonia is degrees of tone and when you see a baby who has perinatal asphyxia who has got hypotonia then you would think most likely this baby has stage 2 Hypoxic Ischemic Encephalopathy, hence we did commence cooling and subsequently this baby had seizures I think about 10 hours of age and a repeat seizure around - after 24 hours of age. Again when babies have seizures, that means it is stage 2 rather than stage 1.

1. Dr Rao was asked about the difference between jitteriness and seizures, which (as is evident from the transcript) he explained by a physical movement (i.e. 'jitteriness will be sort of jittery like this') and which he distinguished from seizures. He said that jitteriness was part of stage 1 HIE but that the clinical markers for HIE were cumulative: 'once [the baby] has a seizure then it is no more stage 1. Even if it has ongoing jitteriness, now it becomes stage 2'.[56]
2. Dr Rao was extensively cross-examined in relation to his evidence that the respondent had experienced seizures early on in his admission. He agreed that he did not personally observe the respondent having a seizure, saying 'because seizures are usually brief and they don't wait for the consultant to arrive'.[57]
3. In this regard, Dr Rao gave evidence that the diagnosis of seizures was a matter of clinical judgment. He said that there is no way one can prove or disprove a seizure unless 'you have a 24-hour video EEG'.[58] In describing his clinical judgment, Dr Rao explained that '[p]rophylactic phenobarbitone is not used in our unit - or for that matter any units in the world. And it is used when the suspicion of seizures goes up.'[59]
4. Dr Rao also confirmed that the presence of seizures was not the only criteria for reaching a diagnosis of moderate HIE, and referred to the following other matters informing his judgment:[60]

If the baby's so much lethargic that the period to which he - the baby was not having enough breathing efforts, the doctor had to put a tube into the trachea to help breathe. That means the baby was quite hypotonic, not enough strength in his body. And second thing our doctor who reached the Bentley Hospital she has documented that this child had hypotonia, means decreased tone. So in the presence of perinatal asphyxia a child who has hypotonia and lethargy so much so that one has to put in tracheal tube at 20 minutes after birth suggests to me that this child at that stage had moderate encephalopathy, your Honour.

1. Dr Rao confirmed that the diagnosis of stage 2 HIE was his diagnosis and not someone else's.[61]
2. Dr Rao was also cross-examined in relation to Professor Ditchfield's interpretation of the Day 7 MRI, and Professor Ditchfield's observation that the scan showed very minor parenchymal involvement (i.e. in the functional tissues of the brain). In that context Dr Rao gave evidence that if the MRI did not show ischaemic injury, that did not rule out moderate HIE 'because we cooled the baby'.[62]
3. Dr Rao also gave evidence that having a normal MRI did not give assurance that the 'child is going to be fine' He said that:[63]

You look at the clinical picture, EEG, MRI, family, the whole thing because development alone comes from the child ... not only the MRI.

1. Dr Nguyen is a Consultant Radiologist, specialising in paediatric radiology and neuroradiology. Her report of the Day 7 MRI is set out at [52] above.
2. Prior to giving evidence, Dr Nguyen reviewed the Day 7 MRI and, in addition to injury to the right cerebellar hemisphere and tonsillar region identified in her report dated 31 August 2009, she identified a further 'tiny' abnormality to the left side.[64]
3. In cross-examination, Dr Nguyen was asked about the 2014 MRI and the 2015 MRI. She confirmed that the subsequent scans showed cystic encephalomalacia (a cystic area filled with fluid) in the region of the initial cerebellar haemorrhage, being an 'evolution of damaged tissue'.[65]
4. Dr Nguyen was asked about Professor Ditchfield's expert reports. In that regard, she agreed that the subdural haemorrhage evident in the Day 7 MRI was unlikely to have any developmental sequelae.[66] She also agreed with Professor Ditchfield's opinion that the pattern of injury to shown on the Day 7 MRI was not typical of that found in cases of hypoxic ischaemic injury (see [[136 No, only that I know in clinical practice that MRIs sometimes can be normal in patients with hypoxic ischaemic encephalopathy and they have to be taken into the clinical context as well.

1. Dr Keenan is a Consultant Radiologist, specialising in neuroradiology, including neuro-paediatrics.[69] Dr Keenan provided two reports prior to trial (dated 30 October 2016[70] and 26 January 2017[71]) and produced a signed substance of evidence dated 13 August 2017.[72] The substance of evidence effectively reproduced the salient parts of the reports.
2. Dr Keenan's substance of evidence sets out his interpretation of the Day 1 Ultrasound, the 7 Day MRI and the 2014 MRI. The substance also included extensive commentary on the reports and opinions of Professor Hunt.
3. Dr Keenan stated that the Day 1 Ultrasound showed cerebral oedema and increased intracranial pressure.[73] He gave evidence that cerebral oedema was a condition, not a cause and that the cause of the oedema was likely secondary to a hypoxic ischaemic insult from perinatal asphyxia, rather than from a traumatic brain injury.[74]
4. In relation to the 7 Day MRI, Dr Keenan's substance of evidence described a number of features including resolution of the previous cerebral oedema, in keeping with a hypoxic ischaemic insult and multicompartmental post instrumental delivery intracranial haemorrhage.[75]
5. Dr Keenan identified bilateral haemorrhagic contusions to the cerebellum, with the damage to the right being greater than the left, especially in an area known as the cerebellar tonsils.[76] He said, for example:[77]

So the images together confirm bilateral and midline injury to cerebella structures. More - more so on the right, but also significantly involving the left. And I guess there there's fairly extreme damage occurring. I guess better demonstrated on the right, because it's almost like - the tissue's become almost watery. It's sort of necrosing.

1. In addition to the injury to the cerebellar tonsils, Dr Keenan also identified injury to the anterior cerebellar hemisphere,[78] the flocculus (a small egg shaped lobe which is on the under surface of the cerebellum, adjacent to the cerebellar tonsils)[79] and to the vermis (a middle section of the cerebellum).[80]
2. Dr Keenan also identified the following areas of intracranial injury beyond the cerebellum on the Day 7 MRI:

(a) microbleeds in the left temporal lobe, which is part of the cerebrum. This finding was also described as a 'supratentorial injury' (the tentorium being a structure between the cerebrum and the cerebellum). Dr Keenan described this finding as ominous and can be a signature for a much more diffuse or widespread injury;[81]

(b) intraventricular haemorrhage in the lateral ventricles (the cavities in the cerebral hemispheres);[82]

(c) subarachnoid haemorrhage (i.e. haemorrhage into the subarachnoid space, between the arachnoid membrane and the pia mater membrane surrounding the brain). This is an area outside the brain;[83]

(d) subdural haemorrhage (i.e. haemorrhage between the arachnoid membrane and the dura mater membrane surrounding the brain). This is also an area outside the brain;[84] and

(e) subgaleal haematoma, being bruising on the scalp.[85]

1. Dr Keenan summarised the injuries evident in the Day 1 Ultrasound and the MRI scans as follows:[86]

I believe the cerebellar injury is a direct result of TBI [traumatic brain injury] either by direct parenchymal contusion or less likely venous congestion due to compression.

There is a very strong likelihood of superimposed HII resulting in a more global microscopic injury. More advanced imaging would be required to define the extent and severity. The best imaging technique being hybrid advanced MR techniques and molecular imaging implementing FDG PET MR which we have experience with

1. In relation to whether there was a causal relationship between the respondent's disabilities and his injuries identified in his report, Dr Keenan reported:[87]

Based on my own imaging experience with TBI insults causing cerebellar injury and attached literature it is highly likely the degree of neurologic insult resulting from the MRI visualized cerebellar insult is underestimated.

Various literature:

1. indicates very significant neurodevelopmental, cognitive, motor, behavioural and social impairments resulting from cerebellar injury or haemorrhage.
2. also points to the common association between cerebellar injury and more global insults especially HII.

Superadded HII insult is highly likely to have augmented the degree of microscopic brain injury.

On the balance of probabilities I believe Cooper's clinical syndrome results from combined cerebellar TBI and global HII.

1. In response to reports provided by Professor Hunt, Dr Keenan said, inter alia:[88]

Associate Professor Hunt despite agreeing there has been an HII, and admitting there may be very significant brain injury causing neurologic impairment including cerebral palsy amongst other less well defined syndromes, does not believe Cooper has sustained a significant supratentorial insult due to the 'normal neuroimaging'.

In fact as discussed both the head US 1 and MRI 1 are not 'normal' in the supratentorial compartment either within (intra-axial) or outside (extra-axial).

Despite this Associate Professor Hunt bases his argument on a purely clinical basis which can be highly non-specific or at least difficult to demonstrate 'hard symptoms or signs'.

He then chooses to 'normalize' the very abnormal EEG findings.

On the contrary I believe the HII insult we 'all agree occurred', but which is clinically tricky to grade, has shown multiple neuroimaging abnormalities and although there is not a 'classical' positive HII pattern, there is nevertheless a very likely global microscopic injury which cannot be defined on conventional MRI.

In fact as defined by Bax et al (JAMA 2008) 'normal MRI' is one of the expected post HII patterns associated with neurodevelopmental sequelae. Using the simple example of cerebral palsy as a marker of neurologic injury Bax et al found so-called 'normal MRls' in 11.7%, whilst Associate Professor Hunt quotes 13% at his Melbourne based center. 'Normal MRI was seen in all clinical syndromes including spastic diplegia, spastic hemiplegia and the much more severe spastic quadriplegic and dystonic group. Of interest so-called CP, a motor disorder was commonly associated other deficits in higher function such as intellectual deficits... despite 'normal conventional MRI'.

This is why we use advanced neuroimaging in our clinical and research studies, to detect the signatures of brain microscopic injuries which cause syndromes such as global developmental delay, intellectual disability and behavioural/learning disorders..

1. The ''classical' positive HII pattern' referred to by Dr Keenan is a reference to the typical pattern of injury for a hypoxic ischaemic injury (see [136] below).
2. In his evidence-in-chief, Dr Keenan was also taken to a paper identified by Dr Pestell entitled 'Consensus Paper: The Cerebellum's Role in Movement and Cognition',[89] in relation to which he gave the following evidence:[90]

And do you agree with the proposition that the cerebellum is involved in cognitive and language function as well as coordination and gross motor movement?---Totally agree.

1. In cross-examination, Dr Keenan confirmed that the MRI scans did not show the typical pattern of injury of hypoxic ischaemic injury to the brain (agreeing that '[t]here is no imaging evidence').[91] He agreed elsewhere in the cross-examination that the MRI scans did not show a 'classical' pattern for HIE.[92]
2. Dr Keenan disagreed, however, with the proposition that the changes from the Day 7 MRI to the 2014 MRI meant that there was no injury:[93]

And then on the second MRI, many of those are not seen as damaged anymore, on the MRI?---The evolution is as I'd often expect because your year - you know, you've gone from day 7 to year 5. It's five years later. The brain does all sorts of stuff so unless you make a hole, a lot of the damage is probably microscopic. You know, we don't necessarily see it. It's at - it's at a - - -

Well, when you say, 'Probably microscopic', you can't see it?---Well, whether you do a scan late, some of the biomarkers which you've been observed - because all these things are biomarkers whereas a diffusion restriction, high T2 signal, high T1 signal, all these are biomarkers. Five years later, a lot of those will disappear but it doesn't mean the tissue is not injured because we - we know that it was injured on - on day 7.

Well, it doesn't mean that it's not injured, but it doesn't mean that it is injured, does it, if - if you can't see it on an MRI, on the second MRI?---Well, I - I wouldn't be looking at the second MRI in isolation.

No?---So knowing what I know from the first scan, and seeing what I saw on the second scan, I'd say that's interesting. If I really wanted to know what was going on I would do a different test.

All right?---Which I'm not sure Michael Ditchfield would probably do because he doesn't do PET imaging. But for us PET imaging would give us an answer.

So you would - and I know that you recommend or recommended at one stage a PET scan being done?---In my experience and more recently we've found that to be the most eloquent way of demonstrating the exact extent of neural injury in the setting of an MRI which is unhelpful.

1. Dr Keenan also agreed with the reporting radiologist for the 2014 MRI, Dr Michael Mason, that the cystic area extended from the right tonsil into the immediately adjacent inferior vermis and right foramen of Luschka, a cerebrospinal fluid space in the cerebellum. Dr Keenan gave evidence that, to involve the foramen of Luschka, there must be more involvement than just the tonsil.[94]
2. Dr Keenan maintained his view in cross-examination that there was a strong likelihood of hypoxic ischaemic injury in the respondent's case.[95] In expressing that view, Dr Keenan referred to both the MRI scans and what he described as the 'grossly abnormal ultrasound' (i.e. the Day 1 Ultrasound).
3. In relation to the Day 1 Ultrasound, Dr Keenan disagreed with Professor Ditchfield's interpretation that the timing of the hypoxic ischaemic insult was at least 24 hours prior to delivery. He said it was his 'experience and experience in our institution' of seeing the signs of cerebral oedema and swelling 12 hours after the insult.[96]
4. Dr Keenan was cross-examined in relation to the relationship between the imaging and his conclusions as to the respondent's clinical syndrome both in relation to the presence of HIE and a global microscopic injury. In relation to the latter he was asked:[97]

[W]hen you refer to a global microscopic injury that is something that cannot be observed on any of the scans that you have?---Not on - not on the type of MR scans that have been performed or MRI.

That's right. So you are drawing an inference that there may be what you describe as global microscopic injury?---Yes. Well, in the - I mean, we don't deal with imaging in isolation. So in the setting of the clinical syndrome and with a grossly abnormal ultrasound, you know, we have to explain that. That doesn't just happen for no good reason.

What doesn't happen for no good reason?---Your whole brain swelling up and the whole brain oozing fluid into it.

I see. That's evidence of a Hypoxic Ischaemic Injury. But you're simply inferring that that may have given rise to what you call microscopic injury, which can't be observed?---Well, I think it is an inference in that - it is an inference. However, we do know of course that we can have a totally normal scan and still have, you know, cerebral palsy or an acquired brain injury, or whatever you like to call it -

1. In re-examination, Dr Keenan was taken back to his evidence in cross-examination that the MRI scans did not show the 'classical' pattern for HIE:[98]

What did you mean by not classical?---So simplistically - Barkovich also simplistically and most authors simplistically talk about, you know, four or five different patterns of brain injury. Those of us who are actually doing this day in and day out know that we get all forms of combinations of, you know, prolonged partial basal ganglia, total cortical, all sorts of patterns, including normal patterns where we just know there has been only one definable catastrophic event and the brain is completely functionally abnormal but we've still got a normal scan and if we try hard enough - and we don't do it very often because usually there's no clinical need because there's not much you can do, but when we have done some of these other tests such as PET, we find in fact there's global abnormality or sometimes patchy abnormality. We can never quite predict what we're going to see until we go to a different form of imaging. So because it looks normal on an MRI - and I'm well beyond the phase of thinking a normal MRI is a normal brain because that just is not the case.

1. Dr Tracy is a Senior Newborn Intensive Care Specialist at the Westmead Hospital and a Clinical Senior Lecturer in the Division of Paediatrics and Child Health at the University of Sydney.[99] Dr Tracy provided two reports prior to trial dated 11 June 2016,[100] and 3 March 2017.[101]
2. In his first report, Dr Tracy was asked whether the respondent suffered from HIE and answered:[102]

Do you consider that Cooper suffered from a hypoxic-ischaemic injury?

Yes. Cooper had well defined criteria for perinatal asphyxia leading to HIE stage two. To expand the intrapartum CTG abnormalities strongly suggested fetal hyperoxia/ischaemia during this difficult delivery. His very low Apgar scores and requirement for protracted resuscitation is consistent with perinatal asphyxia. His clinical course at Bentley hospital and KEM NICU was typical of generalised hypoxic-ischaemia with HIE, hyperlactinaemia, acute renal impairment with recovery and probable seizures.

1. In relation the MRI images, Dr Tracy reported as follows:[103]
   1. If the MRI images are abnormal, how are they abnormal and what is the most likely cause of the abnormalities?

The paediatric radiologist reporting the MRI study listed characteristic findings that I have detailed above. Approximately 27% of the term newborn infants with clinical HIE will have no abnormalities detected on MRI studies obtained at 5 to 7 days of life. Well conducted large population studies have shown that instrumental vaginal birth carries increased risks of cerebral haemorrhage including cerebellar with an odds ratio between 2.7 and 3.4. Estimates suggest cerebellar haemorrhage is a definite but uncommon association of traumatic deliveries, GBS perinatal infection, primiparous births and HIE.

Historically, the association has been well described. Increased surveillance of ill term newborns with MRI has shown higher frequencies of this disease. Definite associations have been shown with traumatic delivery, instrumentation assisted delivery (vacuum, Kiwi cup, forceps), primiparous women and GBS infection. In Cooper's case specifically perinatal asphyxia followed by shoulder dystocia and two forms of suction device instrumental delivery which failed on several pulls are the principal causes.

...

1. Whether the infant's disabilities (as claimed and as evidence in the reports) are consistent with his MRI images.

Yes Cooper's neurophysical examination and findings from Dr Peter Chauvell at age 5 1/2 years are entirely consistent with the MRI images as reported.

1. Dr Tracy's second report responded to reports provided by Professor Hunt. He disagreed with Professor Hunt's opinion that the respondent experienced only mild (stage 1) HIE.
2. In relation to Professor Hunt's opinion that the respondent did not have the features consistent with the sort of HIE that would result in his development impairment, Dr Tracy said:[104]

I disagree with Dr Hunts interpretation of the clinical picture. The clinical team treating Cooper diagnosed HIE grade 2, · applied therapeutic cooling reserved for stage 2/3 HIE and treated likely or suspected seizures. The EEGs were reported as abnormal although no seizures were noted during the recordings. Cerebellar haemorrhage in term infants is rare whereas HIE is not. The case series of 20 term infants with cerebellar haemorrhage by Drs Catherine Limperopoulos and Andre du Plessis 'Cerebellar Injury in Term Infants: Clinical Characteristics, Magnetic Resonance Imaging Findings, and Outcome' 15% were found to be ischemic. They found 'Intrapartum factors included significant fetal heart rate abnormalities (i.e., sustained fetal bradycardia with

Given the rarity of cerebellar haemorrhage and the combination with stage 2 HIE it is difficult to be clear if there are additive negative effects on surviving infants neurological outcomes but it would seem logical.

I summarise my response:

Having the opportunity to read Associate Professors Hunts comments on my report I do not wish to alter in any way my comments or my findings. I disagree on his interpretation that the treating Neonatal team were incorrect in diagnosing and treating Cooper for Stage 2 HIE, His likely neurological outcome is in keeping with stage 2 HIE with a concurrent cerebellar haemorrhage.

1. In evidence-in-chief, Dr Tracy expanded on his view as to the severity of the respondent's HIE:[105]

[W]hat are the factors to be taken into account in the grading of an infant stage 1 or stage 2?---The - the features that were listed in the medical reports from the hospital, the treating neonatal team, were entirely consistent with the prehistory which is started from resuscitation of the infant from the - the level of illness, the level of resuscitation required, the noted low tone of the child, the probable nature of fits or seizures, the - the - they are the same thing. The lack of EEG evidence confirming an electrical seizure of the brain during the brief period of EEG recording does not exclude seizure activity. Seizures in the newborn period, particularly with Hypoxic Ischemic Encephalopathy, can range from very mild and subtle and often seen with heartrate changes, blood rate - blood pressure changes where there's arterial line insertion and is often suspected rather than proven on EEG. The biochemistry indicating a severe metabolic acidosis and the renal impairment or kidney impairment, I think the creatinine elevated up to an - not in sort of terrible terms but the - the - the creatinine, which is a marker of renal function, increased to over 113 or 14 from memory and the treating team, in my view correctly, applied the only option we have currently of therapeutic mild hypothermia to 33 to 34 degrees Celsius up to 72 hours and the - the - the response of the baby in terms of being fluid restricted during that period and the management were all very consistent with a stage 2 Hypoxic Ischemic Encephalopathy.

1. Dr Tracy gave evidence that the absence of the 'classic signs' of HIE injury on the Day 7 MRI would not make any difference to his conclusion. In relation to the relative importance of the various inputs into a diagnosis, Dr Tracy said:[106]

History is about 80, 85 per cent; the physical examination is about 10 per cent; scans, about five per cent; MRI is about five per cent in terms of weighting.

1. In cross-examination, Dr Tracy accepted that he was reliant on the expert paediatric neuroradiologists for the interpretation of the MRI scans.[107] He also agreed that there was no definitive evidence for respondent's seizures based on EEG. He said, rather, that it was based on strong clinical suspicion, which in the context of clinical practice was very typical.[108]
2. Dr Tracy said that his opinion was based on the current state of knowledge around the respondent's condition. He said that 'MRIs assist but a normal MRI at this age or indeed three weeks of age did not preclude major neurosensory impairment of a permanent nature'.[109]
3. In evidence consistent with that of Dr Rao described at [70] above, Dr Tracy agreed that his inference was that there had been seizures (which he described as 'high[110]likely'):110

Yes. The treating team, which I know them - I know of them pretty well. They're the largest neonatal team in Australasia - are very experienced in dealing with these sorts of cases. We - the therapeutic is not instituted for stage 1 HIE. Phenobarbitone which carries a number of side effects and is not instigated prophylactically.

1. It was in this context that Dr Tracy said that he would accept the judgment of the treating team at PMH, together with the other evidence (the ultrasound, the use of adrenaline and prolonged resuscitation).[111]
2. Dr Tracy also agreed that the findings evident on the MRI scans were not a typical pattern reported as a consequence of HIE, although he said it was 'a typical finding ... quite consistent with traumatic birth injury ... and traumatic birth injury is quite consistent with HIE'.[112]
3. Dr Tracy was taken to the reports of Professor Ditchfield in cross-examination, and accepted that he was not qualified to comment on the MRI. He accepted that Professor Ditchfield was better qualified to make an observation based on the MRI but did not accept his observation that the respondent's injuries were very unlikely to have any developmental sequelae. To that suggestion, Dr Tracy said:[113]

[N]o. The paediatric radiologists don't counsel parents in terms of the likely future of their children. They - nor do they do long term paediatric neurodevelopmental follow up. They rely on the images in certain specific studies to - to do linkages with - with specified outcomes. The totality of the picture is what the prudent clinician would gauge the likely output in - in a view to counsel parents which is what they need to know in the first weeks of life.

1. Dr Tracy returned to the role of MRI scans in the diagnosis, observing that 'there are published works indicating the presence of a normal MRI does not exclude, in the presence of stage 2 HIE, the development of significant long-term neurological handicaps'.[114]
2. Dr Tracy was also taken in cross-examination to the predictive use of HIE staging. He agreed, for example, that stage 1 HIE was associated with a normal neurodevelopmental outcome in 90 % of cases. To which he added:[115]

It still means that up to 10 per cent are not normal ... and have evidence of neurodisability.

1. Dr Pestell is a Registered Psychologist, practising in both clinical psychology and neuropsychology. Prior to trial, Dr Pestell provided three reports dated 13 October 2013,[116] 1 February 2015[117] and 16 May 2017.[118]
2. Dr Pestell's reports were principally directed to describing the results of her neuropsychological assessment, including the battery of tests used to assess the respondent's intellectual and cognitive functioning. The reports, therefore, are primarily concerned with describing the respondent's Developmental and Cognitive Impairments - including their nature and level of severity (rather than being primarily concerned with their cause). In this regard, the reports were particularly relevant to the assessment of the respondent's future care and treatment needs (and the learned trial judge's assessment of damages in that regard).
3. Dr Pestell did, however, give evidence in relation to the cause of the respondent's Developmental and Cognitive Impairments. In her first report, for example, she said:[119]

In my opinion and based on the available evidence, it appears that the pattern and nature of Cooper's current presenting problems and neuropsychological deficits are in keeping with a history provided of brain damage evident soon after birth. It is not unusual for children with a history of hypoxic ischaemic encephalopathy to experience significant cognitive deficits, particularly profound disruption to attention, learning and memory function.

1. In her second[120] and third[121] reports, Dr Pestell repeated her opinion that the respondent had sustained a severe acquired brain injury at birth which has resulted in developmental delay, particularly with regard to his motor, speech and cognitive abilities.
2. In her evidence-in-chief, Dr Pestell confirmed her opinion in the following terms:[122]

So this description that you apply, of severe acquired brain injury, is that the description you apply as a neuropsychologist or is it picking up someone else's works?---It's my opinion. Traditionally acquired brain injury is classified as mide - mild, moderate or severe.

GETHING DCJ: Yes?---And we look at the neuropsychological test results as well as the history to determine the severity. And that's why it was my opinion that the nature of his deficits on the testing in conjunction with the MRI evidence would suggest to me that his deficits were severe.

Okay. So there's a - so - so do I understand your evidence to be that looking at Cooper on all the - as you found him at - at that particular date, your clinical assessment was that his brain injury was severe?---That's right.

1. Dr Pestell clarified, in answer to questions from the learned trial judge, the extent to which her opinion relied upon the input from other professionals:[123]

So - so you're - so the - so really the - the essence of your evidence is, 'I have Cooper. I've assessed him on using all these scales. I can assess that his brain injury at the current stage is severe'?---Yes.

'And this is how I unpack that'?---Yes. But in terms of what was the cause of that brain injury, that's really a - a field for others?---That's right. It's out of my area - - -

Okay?--- - - - of expertise to look at [aetiology].

1. Dr Pestell was asked about the contrary opinion expressed by Dr Do as to the relationship between the respondent's brain injury and his deficits:

And I think you'll recall from Dr Do's report that the relationship between his cognitive deficits and the original brain injury are disputed by Dr Do?---Yes, she changes her opinion.

So what do you say is the significance of the initial brain injury to Cooper's presentation as you found him in 2013, 2015 and 2017?---I - I find his neuropsychological profile entirely consistent with the - the early history of brain damage that was identified in his first MRI scan. For example, he had problems learning to walk, he had an ataxic gait and so on which is very typical of cerebella injuries so in my opinion, his problems are due to that rather than be - been caused by an ADHD like profile mediated by the prefrontal striatal circuit which is what Dr Do is suggesting. To be honest, I was somewhat surprised that she discounted that the earlier evidence - because we know with subsequent MRI scans that just because an MRI scan might be normal doesn't mean there isn't underlying brain damage still. It's just that the test is not particularly sensitive and so we look to how the child is actually performing on neuropsychological testing in their everyday life to determine how they're actually functioning.

1. Finally, in evidence-in-chief, Dr Pestell was taken to the role that the cerebellum plays in cognition, referring to the Consensus Paper (referred to at [91] above)[124]She said:124

Well, it's my understanding based on reading this paper and my other readings of literature that the - the basic theory is that there's connections between the cerebellum to other areas of the brain that the cerebellum is no longer just involved in - in movement and the synchronisation of movement and the - the learning or complex motor behaviour; that it actually plays into other aspects, for example executive functions that it - because of those circuits that - that go through to the - the frontal lobes.

1. Dr Pestell said she supported the conclusions of the Consensus Paper based on her clinical experience.[125]
2. Dr Pestell was cross-examined on a separate occasion in the following week of the trial.
3. In cross-examination Dr Pestell was taken to Professor Ditchfield's reports, which she had not previously seen. She said those reports would be potentially relevant to the existence and extent of any brain injury, but that she put the majority of her weight on the neuropsychological assessment results and the history.[126]
4. Dr Pestell was cross-examined in relation to the reasoning process for her opinion that the respondent has a severe brain injury. In that context she said that the respondent's profile was in keeping with his history:[127]

And you say that symptomology is consistent with brain injury?---Yes, and the encephalopathy that he sustained and the ischemia.

Right, the HIE?---It's the type of - - -

The HIE?---Yes, it's the type of brain injury as well that he sustained.

But what type of brain injury do you think that Cooper has now?---Well, he has a - given the history that's been provided to me, he - his brain was deprived of oxygen at birth.

So that's hypoxia?---Yes.

That's the HE - HIE?---Yes. And - so that's affected his brain development. It means that he sustained brain damage. That is a permanent condition in my opinion.

Are you aware of what other characteristic features of an hypoxic ischemic insult to brain tissue?---That's starting to get out of my area of expertise.

1. When taken to the specific opinions in Professor Ditchfield's report it was put to Dr Pestell that other than the damage to the right cerebellar tonsil the respondent's brain is normal:[128]

So what he has seen is that but for or other than the damage to the right cerebella tonsil, the brain is normal?---Well, as we discussed last week, MRIs don't always show up underlying brain pathology so - - -

They don't always not?---That's correct.

So to think that there might be damage that is not picked up on an MRI is, on your part, pure speculation?---No, because it's based on the neuropsychological findings as well. So we also integrate all the information that we have based on the history, how the child presents, their results and determine whether it's still in keeping with a particular condition. So we don't rely solely on MRI evidence. And that's why neuropsychologists are so important because we - we are able to assess the functional impact of - of a child's - you know, what their underlying pathology is or their condition is and how it's actually impacting their everyday life.

So - so you're making an assumption that there is brain tissue that can't be picked up on an MRI?---That's - that's quite a - a typical occurrence, yes.

But it's, again, pure speculation?---I - I wouldn't agree that it's speculation because there's a lot of literature that would support that. For example, we might see as - an adult with early dementia and their MRI scans are normal but they're showing quite significant changes in their everyday life and it's not until there's a repeat scan two or four years later that the changes start to appear on an MRI scan. But the neuropsychological tests are far more sensitive to those changes.

1. Dr Pestell accepted that the absence of any brain damage as a result of an hypoxic ischaemic event would impact upon her opinion. However, she maintained that the lesion to the respondent's cerebellum would account for the deficits identified in her assessment.[129]
2. Dr Pestell responded to a number of questions arising from Professor Ditchfield's report that she was 'starting to move out of my area of expertise' and 'can only just take his word' for what appeared in the reports.[130] She said, when pressed to accept that Professor Ditchfield would be in a better position to express a link between injury to the brain and developmental consequences:[131]

Yes, although he's not a neuropsychologist and so I don't believe it's in his area of expertise to be commenting on the neuropsychological consequences of particular conditions.

1. At the conclusion of her cross-examination, Dr Pestell accepted, on the basis of material that had been put to her, that she would qualify her opinion. The exchange was as follows:[132]

And would you now wish to change that opinion?---I would argue that he still has - he had a developmental delay at that - - -

Yes?--- - - - point in time.

Yes?---And it's really not within my area of expertise to say what's caused that delay. I can only base my opinion on the information that's provided to me at that point in time. So I wouldn't want to change my opinion as to the fact that he had a developmental delay - - -

No?--- - - - that resulted in a number of deficits.

No. I'm not asking you to withdraw that opinion?---No.

It's linking those to brain injury?---Yes.

You withdraw that opinion?---I would qualify that opinion, yes.

1. In re-examination, Dr Pestell stated that when giving her answers in cross-examination she was accepting the assumptions that were being put to her, for example, as to the grading of the respondent's HIE. She was then taken to the information in relation to Dr Rao's clinical diagnosis and asked:[133]

If you include the information that you have, for example, from this report from Dr Rao, what do you say about the concession you made that if there was no hypoxic injury shown in the MRI scan, then it would be unlikely that there'd be - that there was a hypoxic ischemic injury?---I would revert to my former opinion.

1. Dr Pestell was also asked about the assumptions she was asked to make in relation to the MRI scans:[134]

If it's the case that the evidence as to radiological findings was accepted to show also involvement of the left tonsil?---Yes.

Both in the original scan and subsequently, and if it involved abnormalities in the vermis?---Yes.

And if the damage on the right side extended into the hemisphere of the cerebellum - well, in - sorry, into the cerebral hemisphere, what would you say of the concessions you made in relation to the propositions that if it's only the right tonsil then it's difficult to draw a conclusion in terms of Cooper's developmental problems and cognitive deficits?---I would revise my opinion and I would also go on to say that - that Cooper's neuropsychological profile is in keeping that particular pattern of deficit as shown on imaging.

1. Professor Ditchfield is a Specialist Paediatric Radiologist. He is the head of paediatric imaging at Monash Children's Hospital and professor of paediatric imaging at Monash University.[135]
2. Professor Ditchfield provided a total of five expert reports to the appellant's solicitors, dated 26 February 2017,[136] 27 February 2017,[137] 28 February 2017[138] and two reports dated 1 March 2017.[139]
3. In his first report Professor Ditchfield described a number of the features that he observed on the 7 Day MRI and the 2014 MRI. In particular he identified, on the 7 Day MRI, minor subdural haemorrhage, intraventricular haemorrhage in both ventricles, oedema of the right cerebellar tonsil containing focal areas of haemorrhage and extra axial haemorrhage adjacent to the right tonsil. Professor Ditchfield reported that the appearance favoured a haemorrhagic contusion. On the 2014 MRI, Professor Ditchfield identified cystic encephalomalacia representing evolution of the haemorrhagic contusion.
4. Professor Ditchfield described subdural haemorrhage as very common post delivery in neonates, and very unlikely to have developmental sequelae.
5. Significantly, in relation to the other features that he described, Professor Ditchfield said:[140]

The lesion in the right cerebellar tonsil has the appearance of haemorrhagic contusion. The presence of extra axial blood makes it most likely traumatic in origin. The distribution is not typical of an embolic infarct.

Hypoxic ischaemic injury to the brain has 2 major patterns, in prolonged partial hypoxia, damage occurs in the cerebral cortex and the intervascular boundary zones (both the cortex and subcortical white matter) resulting in a watershed infarct. In an acute severe hypoxia ischaemic episode the pattern of damage is to the deep grey matter (thalami and basal ganglia), posterior brain stem and the motor cortex (References 2, 3 and 4). In this case, these structures are normal and there is therefore no MRI evidence of a hypoxic ischaemic injury.

1. The '2 major patterns' of hypoxic ischaemic injury to the brain referred to in this passage are the patterns referred to by the other expert witnesses as the 'typical' or 'classical' pattern for such injury (see [78], [89], [92], [98] and [110] above)
2. Professor Ditchfield stated that:[141]

The right cerebellar tonsillar injury is the only finding with potential to have neurological developmental sequele. Abnormality of the cerebellar tonsil can be associated with movement disorders of the eyes (Reference 5). I am not aware of the cerebellar tonsils having other motor functions. The specialist opinion of a neuropsychologist would be useful in confirming this.

1. Consequently, in relation to each of the symptoms forming part of the respondent's Developmental and Cognitive Impairments, Professor Ditchfield said that the abnormalities demonstrated on the MRIs were 'minor and unlikely to be associated' which each of those claimed symptoms.
2. Professor Ditchfield's report of 27 February 2017 responded to Professor Hunt's reports. While he agreed with Professor Hunt's description of the MRI findings, Professor Ditchfield disagreed that the damage to the right cerebellar tonsil was most likely an infarct associated with a vertebral artery dissection. Professor Ditchfield continued to favour a traumatic cause (haemorrhagic contusion).[142]
3. Professor Ditchfield's report of 28 February 2017 responded to aspects of Dr Tracy's report of 11 June 2016 (including the portion reproduced at [101] above). Professor Ditchfield's report includes th[143]ollowing:143

[Dr Tracy] then discusses that newborn infants with HIE may have a normal brain MRI which is true. However, in these cases the brain injury will be minimal or non existent.

He also discusses how instrumental vaginal deliveries have an increased risk of cerebellar haemorrhage, which is true.

1. In his report of 28 February 2017 Professor Ditchfield also adhered to his opinion that there is no MRI evidence of hypoxic ischaemic injury to the brain and that, in the respondent's case 'there is an isolated right tonsular injury'.[144]
2. Professor Ditchfield's first report dated 1 March 2017 responded to the reports of Dr Keenan, including Dr Keenan's findings in relation to the Day 1 Ultrasound, the 7 Day MRI and the 2014 MRI.
3. Concerning the Day 1 Ultrasound, Professor Ditchfield stated that he had not been provided with the imaging to review but reported that the changes described by Dr Keenan were uncommon prior to 2 days after the insult and it was uncommon to have such gross findings and no changes on an MRI performed on day 7.
4. In relation to the 7 Day MRI and the 2014 MRI, Professor Ditchfield simply reported:

I agree with his description of the MRI performed on 31/8/2009 (2016 report pp 25-26) except I believe the left cerebellar tonsil is normal.

I agree with his description of the MRI performed on 26/9/2014 (2016 report p 26) except I believe the vermis is normal in appearance.

1. It is clear from this that Professor Ditchfield disagreed with Dr Keenan in relation to there being injury to the left cerebellar tonsil and the vermis. It is, however, not clear whether Professor Ditchfield agreed with Dr Keenan's finding that there was a supratentorial injury (see [860] above), an injury that was not referred to in Professor Ditchfield's first report. Professor Ditchfield, however, did say in his first re[145]t dated 1 March 2017:145

In his report of 2017 (p 34 of 129) Dr Keenan discusses the potential significance of the solitary supratentorial microbleed. These foci are common findings in a neonatal MRI scan, and in isolation, my experience is that the finding is very unlikely to have clinical significance, especially when it has disappeared in an MRI performed at a later time, as in this case.

1. Professor Ditchfield also said in that report that Dr Keenan had no evidence for his conclusion that the HII resulted in a microscopic pattern of brain injury occult on conventional MRI, a statement that Professor Ditchfield considered 'completely speculative'.
2. Professor Ditchfield's second report dated 1 March 2017 related to the Day 1 Ultrasound, the images of which had since been provided to him. He described the Day 1 Ultrasound as having the 'pattern of a prolonged partial hypoxic-ischaemic episode'. In relation to the timing of the hypoxic ischaemic insult, Professor Ditchfield proffered the opinion that it occurred at least 24 hours prior to delivery.
3. As to the prognostic use of the ultrasound, Professor Ditchfield said:[146]

Ultrasound on the first day of life is not an accurate predictor of the clinical prognosis of a neonate. The MRI performed on 31/8/2009 at the age of 7 days, which demonstrates no evidence of hypoxic ischaemic damage, is the most accurate imaging available for prognostication

1. In his evidence-in-chief Professor Ditchfield confirmed that it was his opinion that the two MRIs are not consistent with the respondent having suffered a hypoxic injury.[147]
2. In relation to the possibility, referred to by the other witnesses, of the existence of hypoxic injury in the presence of a normal scan Professor Ditchfield said:[148]

[T]he literature of cerebral palsy and - and MRI imaging is that approximately 85 per cent of MRIs will be abnormal and 15 per cent will be normal. And in those 15 per cent, it's difficult, often, to determine the underlying cause. The causes of cerebral palsy are greater than just hypoxic-ischaemic injury. They can also be from congenital malformations of the brain, which can be visualised on MRI and not visualised on MR. So in those - in those 15 per cent we - we have - which have a normal MRI, some of those will be caused by hypoxic-ischaemic injury, or will have a - at least have a past history of a hypoxic-ischaemic injury. In - in those patients, there is quite a good correlation of the severity of the abnormality on MR with those with hypoxic-ischaemic injury and the clinical outcome of the child, and so it would be unlikely that a child that has minimal to no changes on an MRI, who had a hypoxic-ischaemic injury, will have significant deficit.

...

Could you perhaps explain - and I know it's written there but if you might explain to his Honour why it is that you disagree with Dr Tracy that the MRI images and reports are consistent with an Hypoxic Injury?---Well, there - the MRIs demonstrate no evidence of a Hypoxic Injury. So in that regard, they are - they're not normal because there is evidence of a traumatic injury but there is no abnormality corresponding to a Hypoxic Injury. So from that point of view, it's normal. And so I guess what he's saying could be true in that it's possible to have a normal scan in the setting of a hypoxic-ischaemic injury, but there is no evidence for that - - ... because - because they're normal.

1. Similarly, in relation to Dr Keenan's opinion that there might be injury that cannot be seen on a conventional MRI, Professor Ditchfield said:[149]

[T]hat is completely speculative in that if the scan is normal on imaging I can't - whether it's normal at biopsy is another matter but the likelihood, knowing the literature of prognosticating of disability from MRI in the setting of a normal scan it's very unlikely to have a clinical scenario of Hypoxic-Ischemic injury later on.

1. In cross-examination, Professor Ditchfield returned to this issue: [150]

[I]s it fair to say that the absence of MRI damage in the context of known Hypoxic Insult doesn't exclude deficits that follow?---Correct. There is no absolutes.

Now, were you aware that the clinical assessment of Cooper Ellis was that he was a stage 2 Hypoxic-Ischemic Encephalopathy?---Yes.

And ultrasound does not exclude that diagnosis, does it?---The ultrasound is compatible with that Hypoxic Insult. The assessment of the grading of Hypoxic-Ischemic Encephalopathy is independent of the imaging.

1. Professor Ditchfield agreed that the fact that there was not a 'typical' pattern for HII on the MRI scans did not exclude there having been a hypoxic insult. In that regard he said: 'I believe there has been a Hypoxic Insult, both clinically and on the ultrasound.'[151]
2. In relation to Professor Ditchfield's opinion that the left cerebellar tonsil was not damaged, he gave the following evidence:[152]

If Dr Nguyen, on reviewing the imaging, saw an area of damage in the left tonsil, does that just mean some of these things are a matter of interpretation?---I think the difference between Dr Keenan and myself really illustrates that.

1. Professor Ditchfield was cross-examined in relation to the role that the radiological results played in the attribution of the cause of a disability. That evidence included the following:[153]

[T]he longer things are studied and the better imaging techniques become available and the more sophisticated the modelling is to try to understand all of these things, the more those connections are found to be important?---Yes.

And so sometimes one aspect of an investigation into a brain injury may produce the evidence to explain a consequence and in other - so, for example, an MRI scan might show damage which would explain a subsequent disability?---Yes.

Okay. In other cases, different type of modelling or investigation might give you the answer as to whether or not there's a connection between any initial injury and the (inaudible)?---Yes.

And so the radiological picture is an important - sorry, the radiological results are an important part of the picture but they're not the only part of the picture in assessing the connection between injury and deficit?---That's correct.

...

But the answer to the question of cause isn't confined just to the imaging, is it, so the imaging doesn't give us the full answer on cause, does it?---No, it's not the full answer but it's a major part of the - it's one of our few ways of pathologically determining an abnormality is present.

And - and it - - -?---And so it's a major part of the jigsaw ...puzzle.

...

But it has to be seen in the context of, for example, the early metabolic changes in - in the child after birth?---Correct.

1. In re-examination Professor Ditchfield confirmed that the Day 7 MRI was the 'gold standard for prognostication in evidence based medicine'.[154]

1. Professor Hunt is a Consultant Neonatologist and Director of the Department of Neonatal Medicine at the Royal Children's Hospital in Melbourne. He is also an Associate Professor at the University of Melbourne, and a Senior Research Fellow at the Murdoch Children's Research Institute.
2. Professor Hunt provided three reports to the appellant's solicitors, dated 18 August 2015,[155] 18 April 2016,[156] and 3 December 2016.[157]
3. Professor Hunt's first report described what he identified as the abnormal features of the MRI images (the Day 7 MRI and the 2014 MRI). Those features identified by Professor Hunt were the injury to the right cerebellar tonsil, extending to the adjacent flocculus, which, by the time of the 2014 MRI revealed encephalomalacia.
4. In relation to the cause of the injury and subsequent encephalomalacia, Professor Hunt gave the opinion that it was most likely due to dissection of the vertebral artery, with a small embolus occluding the right posterior cerebellar artery.[158] This is the opinion referred to by Professor Ditchfield (see [140] above), with which Professor Ditchfield disagreed.
5. When asked what symptoms or disabilities he would expect to find in a child with the MRI images, Professor Hunt responded:[159]

Injury to the right cerebellar tonsil, like the injury demonstrated on Cooper's MRI, is not primarily associated with any deficit in development or cognitive function. In fact, in isolation it should not cause any symptoms or deficit.

With associated blood around this injury, it is possible that there may be associated arachnoiditis, and if this were to occur, a syrinx in the adjacent cord may eventually develop. In this unlikely scenario, the symptoms would relate to gradual deterioration in motor function of the limbs, related to impaired function of the motor pathways that travel along the spinal cord. There would not be any associated cognitive or intellectual deficit. Global developmental delay would not present in this way.

1. Professor Hunt's report dated 18 April 2016 responded to a number of further questions posed by the appellant's solicitors. In answer to the first question 'Is there any other evidence supporting the possibility of a hypoxic-ischaemic event?', Professor Hunt said:[160]

In answer to question 1, there is definite evidence supporting a hypoxic-ischaemic event, however insufficient criteria are fulfilled for the severity of this event to be held responsible for Cooper's current clinical condition. The criteria above were drafted and published as a guide to determine whether an asphyxial event was (a) present and (b) severe enough to cause cerebral palsy. Used in the current context, the early acidosis, need for resuscitation, low Apgar scores and multisystem involvement all point to a hypoxic-ischaemic event having occurred.

However, Cooper only had mild encephalopathy at worst, and his cerebral imaging findings did not show convincing evidence of hypoxic-ischaemic encephalopathy. For this reason, I think the chances of the hypoxic-ischaemic event being responsible for Cooper's global developmental delay are significantly less than 50%. (emphasis in original)

1. In expressing this conclusion, Professor Hunt considered the various criteria identified in the international consensus statement template for defining a causal relationship between acute intrapartum events and cerebral palsy. In that context, Professor Hunt stated that the respondent suffered no seizures.[161]
2. Professor Hunt's report of 18 April 2016 concludes as follows:[162]

3. In view of the above, are these observations more likely than not consistent with an HIE injury, or are they explained by other factors. If the latter, what are those factors likely to be?

The early acidosis, low Apgar scores, need for resuscitation and mild multi-organ dysfunction all point to a mild hypoxic-ischaemic insult. There is no evidence of significant hypoxic-ischaemic encephalopathy, by which I mean that there is no evidence, either clinically or from the cerebral imaging, that there is a cerebral injury from hypoxia-ischaemia. The EEG abnormalities described above, may be a function of the therapeutic hypothermia, the administration of phenobarbitone, or both. The pattern of some early recovery to the background pattern on the EEG suggests that the chances of a normal neurodevelopmental outcome for Cooper are great than 50%.

As described above, the jitteriness may be accounted for by cerebral irritation secondary to the subdural blood. Where seizures occur as a consequence of subdural blood (and Cooper's encephalopathy was too mild to manifest as seizures, presenting as jitteriness at worst) the chances of a normal neurodevelopmental outcome (in the absence of other significant supratentorial cerebral injury) are greater than 90%.

4. Can other factors be identified that more likely explain the subsequent global developmental delay identified in this child?

As outlined in my initial report, I think that Cooper's global developmental delay may be accounted for by subtle underlying genetic abnormality, and this would best be further explored through the laboratory of Emeritus Professor Alastair MacLennan in Adelaide.

1. Professor Hunt's final report responds the first reports provided by Dr Keenan and Dr Tracy respectively.
2. In relation to Dr Keenan's reports, while he agreed that there was evidence of birth trauma, Professor Hunt disagreed with Dr Keenan's opinion that there was a traumatic brain injury with superimposed HII resulting in more global microscopic injury. In this context Professor Hunt again stated that the 'clinical picture is one of mild hypoxic ischaemic encephalopathy', referring to the absence of neonatal seizures, either clinically or electrographically.[163]
3. Similarly, in relation to Dr Tracy's report, Professor Hunt disagreed with Dr Tracy's opinion as to the severity of the respondent's HIE. He said:[164]

I disagree. Cooper did have evidence of hypoxic ischaemic encephalopathy but his symptoms of irritability and jitteriness are in keeping with stage 1 (mild) HIE. Sarnat's 3 stages of encephalopathy (mild, moderate and severe) are defined by a number of criteria. Level of consciousness in Stage 1 (mild) is irritable and hyperalert, which is how Cooper's behaviour was described. Level 2 (moderate) is associated with a depressed level of consciousness. There is no definite evidence of seizures in Cooper - seizures being a feature associated with Stage 2 (moderate) encephalopathy.

There is no question that Cooper did have evidence of an asphyxial insult, but it is my opinion that this was mild. Stage 1 encephalopathy is associated with a normal neurodevelopmental outcome in more than 90% of cases.

1. Professor Hunt's final report concluded:[165]

In summary, Cooper had a traumatic delivery that resulted in the MR findings as I described in my original report. His clinical course was consistent with mild hypoxic ischaemic encephalopathy, which in itself confers a normal neurodevelopmental prognosis. I do not believe the injury localised to the right cerebellar hemisphere accounts for his neurodevelopmental impairment.

1. In his evidence-in-chief Professor Hunt confirmed his opinions set out in his reports. He also gave evidence in relation to the three-stage staging of hypoxic ischaemic encephalopathy, including its development over time since it was first described in 1976 by Sarnat and Sarnat.[166]
2. In that context, Professor Hunt referred to the staging of HIE as providing clinicians with a mechanism to counsel parents about possible future outcomes for their babies. In that regard, he referred to the body of work which showed that:[167]

for infants based on this classification system who had mild HIE or encephalopathy, more than 90 per cent of those children would have a normal neurodevelopmental outcome. For those with severe encephalopathy or stage 3, 100 per cent of those babies either died or were left with some severe neurodevelopmental impairment. But for the moderate group, the prediction was much less certain and roughly 50 per cent of those with a moderate or stage 2 HIE had a normal outcome and 50 per cent had neurodevelopmental deficits when they were assessed in childhood.

1. Professor Hunt went on to give evidence that the prognostic value of the staging of HIE has not been examined closely following the introduction of therapies such as therapeutic hypothermia (i.e. 'cooling').[168]
2. Professor Hunt was also asked to identify what was the best tool for determining what the consequence for the respondent is of the hypoxic ischaemic event. He answered:[169]

The best predictive tool available to us currently is magnetic resonance imaging of the brain at a time that we would suggest in the current clinical guidelines around day 7 to 10 which is what Cooper had. I should add though that no one tool is used in isolation to predict outcome and that all these tools like EEG, MRI, the clinical picture, are used collectively to make an assessment of outcome.

1. Professor Hunt went on to say, in relation to the respondent specifically, that 'his clinical picture, a picture of mild or stage 1 HIE, according to the Sarnat staging, in combination would lead me to predict that this insult was not significant in terms of causing a poor neurodevelopmental outcome'.[170]
2. In cross-examination, Professor Hunt agreed that in preparing his reports he did not address or refer to assessment of the respondent made by Dr Rao.[171] He also confirmed that it was important to his opinion, as to the cause of the respondent's clinical condition, that the classification of his HIE was stage 1 rather than stage 2.[172] In that context Professor Hunt was cross-examined extensively in relation to whether the respondent had stage 1 or stage 2 HIE, including in relation to the use of phenobarbitone and therapeutic hypothermia to treat the respondent and the difference between seizures and jitteriness.
3. In relation to the injury evident on the MRI scans, Professor Hunt agreed with Dr Keenan that the damage to the cerebellum extended beyond the right tonsil into the flocculus, but did not agree it extended into the vermis or the left tonsil.[173] He agreed that, to some extent that might be a matter of interpretation of the imaging.[174]

1. Dr Do is a registered Clinical Neuropsychologist. Dr Do provided three reports prior to trial dated 17 June 2016,[175] 24 August 2017[176] and 6 September 2017.[177]
2. As in the case of Dr Pestell, Dr Do's reports were principally directed to describing the results of her neuropsychological assessment, including the battery of tests used to assess the respondent's intellectual and cognitive functioning. While there were differences between Dr Pestell and Dr Do as to the extent of the respondent's developmental delays and cognitive difficulties, Dr Do did assess that the respondent suffered from impairments, which she described as mild overall, but with moderate to severe impairment with aspects of his sustained attention and auditory working memory.[178]
3. Dr Do, however, also commented on the likely cause of the respondent's symptoms. In her first report she drew a causal connection between those symptoms and the respondent's birth process. She said:[179]

d. What could have caused the particular symptoms?

In my opinion, it is likely that Cooper's stormy neonatal history likely contributes to the pattern of cognitive vulnerabilities observed on testing. Cooper's medical records document that Cooper has been diagnosed with Grade II Hypoxic Ischemic Encephalopathy (HIE) with perinatal asphyxia. A number of studies have found that children with neonatal encephalopathy (NE) of hypoxic-ischemic origin were at increased risk of cognitive deficits. For instance, Robertson and colleagues (1989) found that while children with mild NE were normal, children with moderate NE at 5.5 years and 8 years post-birth had good receptive vocabulary and perceptual motor skills, but were significantly delayed with reading, spelling and arithmetic, and likely to be approximately 1 year below normal controls or those with mild NE. Similarly, Marlow and colleagues (2005) founded that children with who had moderate encephalopathy scored similarly with regards to overall intelligence, but scored significantly lower than comparison children in the language and sensorimotor scales, and with narrative and sentence memory on the NEPSY. Achievement was at a lower level.

Medical records also indicate that Cooper has a traumatic brain injury with findings on brain MRI identifying areas of damage within the cerebellar region. Cerebellar disorders can manifest with a range of cognitive impairments. For instance, Levisohn and colleagues (2000) found that children who had undergone resection of cerebellar tumours exhibited difficulties with initiation of language, verbal fluency and word findings difficulties, decreased story retrieval, deficits in sequencing, planning and maintaining set, and visual spatial deficits. It is noted that these children had intact development of cognitive abilities prior to resection of the cerebellar tumour, which is different than Cooper's history as he has not acquired these abilities, then lost them. Rather, his profile is one of delayed/slower development of skills.

Other contributing factors for Cooper's profile include his significant difficulties with attentional processing and auditory processing difficulties, which can contribute to difficulties with learning capacity, recall and retention of information.

Missed exposure to teaching (due to not being able to see material on the board secondary to possible visual acuity difficulties prior to Cooper prescribed glasses, and absences from therapy/school) can also contribute to gaps in early skills development.

Finally, Cooper's father reports a history of suspected ADHD and possible dyslexia, which may be contributing factors for Cooper's difficulties with academic achievement as the heritability of dyslexia is estimated to be around 40-80% (Schumacher et al, 2008) with some epidemiological studies suggesting a twofold increase in the risk for boys relative to girls (Rutter et al., 2004). Similarly, the heritability of ADHD has been estimated to be around 75% (Farone et al, 2005).

1. Following provision of this report, the appellant's solicitors, by letter dated 31 July 2017, asked Dr Do whether she continued to hold the opinion expressed above (namely that '[the respondent's] stormy neonatal history likely contributes to the pattern of cognitive vulnerabilities observed on testing'), in light of a number of assumptions that Dr Do was asked to make.
2. Given their significance for Dr Do's later evidence, it is worth setting out those assumptions in full:[180]

1. There has been extensive consideration of all relevant MRI scans that have taken of Cooper by an expert neonatal physician and neurologist and by an expert in paediatric radiology.
2. In responding to my questions would you please assume the following?
3. First, that Cooper's MRI scans at birth show very minor parenchymal injury and the scans at 5 years none.
4. Second, Cooper's MRI scans at birth show restricted diffusion in the right cerebellar tonsil and on the T1 and T2 weighted images in all planes, there is injury to the right cerebellar tonsil with some haemorrhage into this structure extending to the flocculus immediately adjacent to the cerebellar tonsil.
5. Third, the lesion in the right cerebellar tonsil is traumatic in origin and not the result of an embolic infarct.
6. Fourth, the MRI scans otherwise show that Cooper's brain is normal, with normal development and normal myelination. There is no impairment of myelination within the posterior limb of the internal capsule. There is no injury to the basal ganglia. There is normal corticomedullary differentiation.
7. Fifth, MRI scans done when Cooper was aged 5 years show encephalomalacia of the right cerebella tonsil with some extension into the right flocculus. Otherwise the brain is normal.
8. Sixth, isolated injury to a cerebella tonsil, is not consistent with known patterns of injury following hypoxic ischaemic encephalopathy.
9. Seventh, injury to the right cerebellar tonsil is not associated with any deficit in development or cognitive function. In fact, in isolation it does not cause any symptoms or deficit.
10. Eight, hypoxic ischaemic injury to the brain has 2 major patterns. First, in prolonged partial hypoxia, damage occurs in the cerebral cortex and the intervascular boundary zones (both the cortex and subcortical white matter) resulting in a watershed infarct. Second in an acute severe hypoxic ischaemic episode the pattern of damage is to the deep grey matter (thalami and basal ganglia), posterior brain stem and the motor cortex. These structures in Cooper's brain are normal.
11. Ninth, accordingly, there is no MRI evidence of an hypoxic ischaemic injury to Cooper.
12. Tenth, at trial, expert evidence will be given to the effect that the disabilities for which Cooper suffers are not consistent with the abnormalities seen on the relevant MRI images.
13. The learned trial judge observed that a number of these assumptions did 'seem to suggest the answer to the very question asked of Dr Do'.[181] This observation, to our mind, rather understates the effect of the solicitor's letter of instructions.
14. Dr Do's subsequent report, dated 24 August 2017, did indeed report a change in her views. She said:[182]

My opinion regarding Cooper's early neonatal history contributes to the pattern of cognitive vulnerabilities has changed in light of review of his 26/09/2014 Brain MRI report which documented 'a 15mm by 10mm by 14mm well-circumscribed cystic area centred in the right cerebellar tonsil region and right foramen of Luschka' which was considered in keeping with the area of haemorrhage demonstrated on the 31/08/2009 Brain MRI. The radiologist, Dr Michael Mason, commented that 'appearances may be relative to changes of cystic encephalomalacia secondary to the previous haemorrhage although a secondary arachnoid cyst could give a similar appearance' and 'the brain otherwise looks normal.' Cooper does not exhibit difficulties in keeping with cerebellar contributions to cognitive functioning. Rather his difficulties appear more associated with tasks mediated by the prefrontal-striatal circuit (prefrontal cortex and along the striatum), areas which appeared to be normal on his last brain MRI.

1. As the learned trial judge pointed out,[183] this passage does not adequately explain the change of opinion, given that Dr Mason's report of the 2014 MRI scan had been provided to Dr Do prior to her having provided her first report. Even more curiously, Dr Do makes no reference in her second report to the letter from the appellant's solicitors dated 31 July 2017 or the assumptions contained in that letter.
2. Dr Do's final report dated 6 September 2017, expands upon her altered opinion:[184]

[I]t was my opinion that Cooper's pattern of performance on the assessment was not in keeping with what would be expected from isolated damage to the tonsil of the cerebellum. The difficulties that I had I outlined in my earlier report would relate to children who had acquired cerebellar lesions secondary to resectioning to broad areas of the cerebellum, including the vermis.

It was also my opinion that the results on the current neuropsychological assessment outlining Cooper's particular weaknesses with aspects of his attention, working memory, and response inhibition within the context of largely age-appropriate development of general cognitive functioning skills within language and visual-spatial processing domains, would be in keeping with disorders that are often associated with frontal-striatal deficits such as ADHD.

1. In her evidence-in-chief, Dr Do confirmed her view that the respondent had difficulties with ADHD symptoms.[185]
2. Dr Do was also taken to the letter of instructions dated 31 July 2017 and confirmed that she had regard to the information and assumptions in that letter in preparing her second report.[186] In particular she confirmed that her view was expressed based on the assumptions that 'there wasn't a hypoxic event and that the area of deficit ... was located specifically to the tonsil'.[187]
3. In cross-examination Dr Do agreed that 'a normal MRI [did] not necessarily equal a normal brain'.[188]
4. In relation to the assumptions that she had made for the purposes of her second report, Dr Do gave the following evidence:[189]

So when you were asked to review your opinion in that regard in 2017 - - -?---Yes.

- - - you were asked to make an assumption to change your starting point, if I can put it that way?---Yes, if the assumption if he hasn't had an HIE. No psychological - our data is based on medical record history, so if he has sustained this injury then would that contribute to the difficulties.

Can we safely assume that if his Honour finds that - - -?---Yes.

- - - Cooper sustained a stage 2 - - -?---Yes.

- - - hypoxic ischemic encephalopathy injury - - -?---Yep.

- - - and the opinion that you expressed in 2016 - - -?---Yep.

- - - unconstrained by assumptions that were put to you in the letter of instruction in 2017 - - -?---Yes.

- - - is in fact your opinion?---That he would - that some of the difficulties would be contributed to the HIE, yes.

And in relation to the traumatic brain injury?---Yes.

To the extent that you now say you don't think that that contributes to his cognitive profile - - -?---Yes.

- - - is that on the basis of the assumption that you were asked to make that the injury is confined to the right cerebellar tonsil?---If it was just to the cerebellar tonsil then it - then I wouldn't say that he would have these - these broad range of difficulties. (Emphasis added)

1. It may be noted that, while counsel's proposition to Dr Do in this exchange specifically referred to stage 2 HIE, Dr Do's answers suggest that her second report was based upon an assumption that the respondent did not suffer HIE at all (even at stage 1). This would be consistent with her earlier evidence that she had assumed (as she was asked to do) that 'there wasn't a hypoxic event' (see [187] above).
2. While Dr Do was taken to the different grades of HIE in re-examination, this particular aspect of her evidence was not, in our assessment, clarified in re-examination.
3. We turn now to the learned trial judge's reasons for finding that Developmental and Cognitive Impairments are more likely than not to be sequelae of his birth.

The learned trial judge's reasons as to causation

1. There are two critical sections of the Primary reasons that are important for understanding the learned trial judge's reasons in relation to causation.
2. The first section, section 13, contains findings in relation to the injuries sustained at the time of the respondent's birth, which his Honour described as 'Cooper's Birth Injuries' (Birth Injuries). In that context, his Honour made certain findings as to what was revealed by the Day 1 Ultrasound, the Day 7 MRI and found that the respondent suffered stage 2 HIE.
3. The second critical section of the Primary reasons relevant to causation is section 16. In section 16 of the Primary reasons, the learned trial judge turned to whether the Developmental and Cognitive Impairments as described at [14] above were relevantly caused by his Birth Injuries, and in particular his traumatic brain injury and hypoxic ischaemic encephalopathy.
4. Dealing with section 13 and section 16 of the Primary reasons in turn.

Section 13 of the Primary reasons - Birth Injuries

1. Under the heading 'Injuries which are not in dispute' (section 13.3) the learned trial judge found that there were three time periods during the respondent's birth in which it is more likely than not that he suffered from perinatal asphyxia. The first was immediately prior to his birth, from when Dr Amira commenced using the vacuum device (9.12pm) and when the respondent's head was delivered (9.38pm).[190] The second period was between when the respondent's head was delivered and the rest of his body (9.42pm). [191] The third period was from when the respondent was delivered until he began to breathe independently.[192]
2. His Honour was not satisfied that the respondent suffered a hypoxic event in the 24 hours preceding his birth (as suggested by Professor Ditchfield), finding it was more likely than not that he did not.[193]
3. After reviewing the expert evidence in relation to the Day 1 Ultrasound, the learned trial judge found:[194]

(a) the Day 1 Ultrasound showed an abnormal resistive index and cerebral oedema;

(b) the Day 1 Ultrasound is consistent with a hypoxic ischaemic insult having occurred; and

(c) the cerebral oedema was caused by the perinatal asphyxia.

1. The learned trial judge then turned to the Day 7 MRI. His Honour summarised the evidence of each of the experts who gave evidence in relation to the Day 7 MRI: Dr Nguyen, Dr Keenan, Professor Ditchfield and Professor Hunt. In this context, his Honour gave particular attention to the areas of dispute between Dr Keenan and Professor Ditchfield. His Honour's conclusion in relation to their opinions was as follows:[195]

So I am left with the position that two very experienced radiologists looked at the same series of images, with one identifying a series of abnormalities (and pointing them out to me) and the other saying the abnormalities were not present. As I remarked at the time, this type of evidence is ideally suited to experts giving their evidence concurrently. I obviously do not have the expertise to decide which of the two is correct. Nor is there any rational basis in the evidence before me to be able to prefer the evidence of one over the other. In the end, I am left with the conclusion that reviewing an MRI scan is a matter of interpretation and opinion on which experts may legitimately differ. Professor Ditchfield accepted this, as did Professor Hunt. This conclusion is reinforced by the fact that Dr Nguyen and Professor Hunt identified more abnormalities than Professor Ditchfield, but not as many as Dr Keenan, so there is a range of interpretations. (emphasis added)

1. His Honour then made three groups of findings in relation to the injuries evidence on the Day 7 MRI. First, his Honour found that the following injuries were present on the Day 7 MRI:[196]

(a) a haemorrhage contusion to the area of the right cerebellar tonsil;

(b) multi-compartment haemorrhage comprising intraventricular haemorrhage, subarachnoid haemorrhage and subdural haemorrhage; and

1. Secondly, his Honour found that it was 'quite possible' that the haemorrhagic contusion to the area of the right cerebellar tonsil extended beyond the right cerebellar tonsil into the adjacent structures, including the flocculus, vermis, left cerebellar tonsil and adjacent cerebellar hemisphere.[197]
2. Thirdly, his Honour found that the Day 7 MRI scan did not show the classic pattern of hypoxic ischaemic injury to the brain but that this finding of itself did not mean that the respondent did not suffer from moderate hypoxic ischaemic encephalopathy to his brain.[198]
3. It is apparent from these findings that the first set of findings relate to those injuries for which there was a consensus among the experts that the injury was evident on the Day 7 MRI.
4. The second set of injuries (which his Honour found to be 'quite possible') were those identified by only some of the experts (principally Dr Nguyen and Dr Keenan). In context, that finding was based upon those injuries being apparent to those experts and the fact that 'reviewing an MRI scan is a matter of interpretation and opinion on which experts may legitimately differ'.[199]
5. Finally, in relation to the injuries evident on the Day 7 MRI, the learned trial judge found that the injuries were traumatic in nature, that is, as a result of an injury. His Honour further found that they were sustained in the process of the respondent's birth.[200]
6. The learned trial judge then turned (in sections 13.6 and 13.7) to the extent of the respondent's hypoxic ischaemic encephalopathy.
7. His Honour made the following findings, based on the medical records and Dr Rao's explanations:[201]

(a) the PMH clinical team, led by Dr Rao, assessed the respondent as having stage 2 HIE on admission, based on the PMH Cooling Guideline, and proceeded to treat him with therapeutic cooling;

(b) the PMH clinical team formed the clinical judgment that, at about 10 hours of age, and then at about 24 hours of age, the respondent had seizures;

(c) the assessment of seizures formed the basis for the respondent to be given phenobarbitone and for him to be referred for neurological review; and

(d) on his discharge from PMH, Dr Rao confirmed the diagnosis of stage 2 HIE, and reiterated this in his subsequent reports.

1. The learned trial judge then turned to determining the level of the HIE, giving detailed consideration to the competing expert opinions. His Honour concluded that Dr Rao was correct to diagnose the respondent as suffering from stage 2 HIE.[202] In that context, his Honour rejected various aspects of the evidence given by Professor Hunt, including Professor Hunt's evidence that the respondent did not suffer seizures and his interpretation of the respondent's 'jitteriness' (see [168] above).
2. Critically, his Honour placed particular weight on the judgment of Dr Rao:[203]

In my view, what is critical to the determination in this case is that Dr Rao had the opportunity to examine Cooper at the time as part of the process of forming the diagnosis. Dr Rao was well aware of the difference between jitteriness and a seizure. Neither Professor Hunt nor Dr Tracy had this opportunity. Dr Tracy emphasised the significance of the clinical examination. He also commented that 'being there and seeing it, typically and sadly, medical records are, as you know, woefully inadequate in actually recording sufficiently rich clinical details when it comes to these sorts of cases'.

1. His Honour summarised his findings as to the injuries suffered by the respondent during the birth process as follows:[204]

(a) During the birth process, Cooper sustained perinatal asphyxia, global hypotonia, right sided Erb's palsy, renal impairment, traumatic brain injury and hypoxic ischaemic encephalopathy (Cooper's Birth Injuries).

(b) The Day 1 Ultrasound showed an abnormal resistive index and cerebral oedema, caused by the perinatal asphyxia.

(c) The Day 1 Ultrasound is consistent with a hypoxic ischemic insult having occurred.

(d) The Day 7 MRI scans shows a series of injuries to Cooper's brain being:

• a haemorrhage contusion to the area of the right cerebellar tonsil;

• multi-compartment haemorrhage comprising intraventricular haemorrhage, subarachnoid haemorrhage and subdural haemorrhage; and

• a subgaleal haematoma.

(e) It is quite possible that the haemorrhagic contusion to the area of the right cerebellar tonsil extended beyond the right cerebellar tonsil into the adjacent structures, including the flocculus, vermis, left cerebellar tonsil and adjacent cerebellar hemisphere.

(f) The Day 7 MRI scan did not show the classic pattern of hypoxic ischemic injury to the brain, being a watershed infarct or damage to the basal ganglia.

(g) The finding in (f) does of itself not mean that Cooper did not suffer moderate (stage 2) HIE (hypoxic ischaemic encephalopathy) to his brain.

(h) The injuries to Cooper's brain set out in (d) were traumatic in nature; specifically they were injuries which he sustained in the process of his birth.

(i) The PMH clinical team, led by Dr Rao, assessed Cooper as having stage 2 HIE on admission, based on the PMH Cooling Criteria, and proceeded to treat him with therapeutic cooling.

(j) The PMH clinical team formed the clinical judgment that, at about 10 hours of age, and then at about 24 hours of age, Cooper had seizures.

(k) Cooper was correctly diagnosed as having sustained stage 2 or moderate HIE.

Section 16 of the Primary reasons - Developmental and Cognitive Impairments

1. The learned trial judge commenced this part of the Primary Reasons (in section 16.1) by identifying what his Honour understood the respondent's case to be. In that regard, he referred to how the appellant construed the respondent's case, namely that: 'that the perinatal asphyxia caused stage 2 HIE, and that the stage 2 HIE in turn caused the cognitive dysfunction, cognitive difficulties and other developmental issues identified'.[205]
2. It may at once be observed that this is how, in the appeal, the appellant described its understanding of the respondent's case at trial. Indeed the appellant's submissions in the appeal closely mirror its closing submissions at trial.[206]
3. The learned trial judge, however, did not construe the respondent's case so narrowly. In that regard his Honour said:[207]

As I understand the [respondent's] pleaded case, and consistently with how the trial proceeded, the [respondent] did not seek to differentiate between the impairments caused by the HIE and impairments caused by the traumatic brain injury. Indeed, it was clear from the evidence led from Dr Keenan and Dr Tracy, which I will go through in detail below, that the [respondent's] case was that the developmental and cognitive impairments experienced by Cooper arose from a combination of the HIE and traumatic brain injury.

1. The learned trial judge recognised that the respondent's case on causation required the use of inferential reasoning and, in section 16.2 of the Primary reasons, his Honour set out sixteen principles derived from the authorities in relation to the use of inferences to determine the question of causation. We will return to a number of those 'principles' later in these reasons. For present purposes it is sufficient to observe that the application of those principles concerns the question of 'factual causation' identified in s 5C(1)(a) of the Civil Liability Act.
2. Section 5C of the Civil Liability Act relevantly provides:

5C. General principles

(1) A determination that the fault of a person (the tortfeasor) caused particular harm comprises the following elements -

(a) that the fault was a necessary condition of the occurrence of the harm (factual causation); and

(b) that it is appropriate for the scope of the tortfeasor's liability to extend to the harm so caused (scope of liability).

(2) In determining in an appropriate case, in accordance with established principles, whether a fault that cannot be established as a necessary condition of the occurrence of harm should be taken to establish factual causation, the court is to consider (amongst other relevant things) -

(a) whether and why responsibility for the harm should, or should not, be imposed on the tortfeasor; and

(b) whether and why the harm should be left to lie where it fell.

...

(4) For the purpose of determining the scope of liability, the court is to consider (amongst other relevant things) whether and why responsibility for the harm should, or should not, be imposed on the tortfeasor.

1. His Honour also, in section 16.3, identified from the case law a number of 'issues' associated with expert medical evidence.
2. The learned trial judge then proceeded to address the issue of causation under the following headings:

(b) the significance of the diagnosis of hypoxic ischaemic encephalopathy (section 16.5);

(c) the profile of the respondent's developmental issues (section 16.6);

(d) other potential causes of the respondent's Developmental and Cognitive Impairment (section 16.7);

(e) determination as to factual causation (section 16.8); and

1. We have adopted these headings in the summary of the Primary reasons that follows.

1. As in the case of the Day 7 MRI, the learned trial judge summarised the opinions of the various experts. His Honour again observed that there were a range of interpretations of the images, and no rational basis to discount the interpretation of any particular expert.
2. His Honour found, on the balance of probabilities, that:[208]

(a) the 2014 MRI and the 2015 MRI show that the respondent has an area of cystic encephalomalacia in the area where the right cerebellar tonsil used to be, corresponding to the injury to the right cerebellar tonsil shown in the Day 7 MRI; and

(b) it is quite possible that the area of injury extended beyond the right cerebellar tonsil to the adjacent structures of the cerebellum, in particular the vermis, left cerebellar tonsil, flocculus and right foramen of Luschka.

1. In relation to these findings, his Honour made two related findings.
2. First, his Honour found that an injury to the right cerebellar tonsil alone was unlikely to have caused the respondent's Developmental and Cognitive Impairments.[209]
3. Secondly, his Honour found that if the injury to the respondent's brain extended beyond the right cerebellar tonsil into the adjacent structures of the cerebellum, in particular the vermis, left cerebellar tonsil, flocculus and right foramen of Luschka, then this did have the potential to give rise to neurological and developmental impairments.[210]
4. The learned trial judge also specifically addressed the limitations of MRI scans and the evidence of the experts to the effect that significant neurological injuries abnormalities may be present in a patient, notwithstanding that they may not appear on an MRI scan. The specific finding made by his Honour in this context was that the fact that the 2014 MRI and 2015 MRI did not show areas of damage to the respondent's brain beyond the area of the right cerebellar tonsil, and possibly adjacent areas, did not of itself mean that there is not wider damage to the respondent's brain.[211]
5. His Honour also addressed the potential for the respondent to have suffered a global microscopic brain injury. He referred to Dr Keenan's evidence that (i) such an injury was likely contributed to by the HII suffered by the respondent, and (ii) such an injury explains how there can be injury to the brain that does not show up on MRI imaging.[212] In finding that it was 'quite possible' that the respondent suffered such an injury, His Honour said:[213]

In summary, Dr Keenan's clinical experience, which seemed to be different to that of Professor Ditchfield, was that he had regularly seen instances in which a child with a clinical syndrome similar to Cooper had shown global microscopic brain injury on more sophisticated imaging than that carried out in this case. From this, I find that it is quite possible that Cooper sustained a global microscopic brain injury. However, aside from Dr Keenan's clinical experience, there is no objective basis from which I can attribute a degree of likelihood to the possibility that Cooper in fact sustained a global microscopic brain injury.

Significance of the diagnosis of hypoxic ischaemic encephalopathy

1. The learned trial judge then turned, as he put it, to 'weave into the analysis' his finding in relation to the diagnosis that the respondent suffered hypoxic ischaemic encephalopathy. In that context, of course, his Honour has earlier found that the respondent suffered stage 2 HIE (see [209] above).
2. His Honour referred to the evidence of Dr Keenan, Dr Tracy and Professor Hunt in relation to the causal connection, if any, between the respondent's HIE and his Developmental and Cognitive Impairments.
3. In that context, his Honour observed that the evidence of Dr Tracy and Dr Keenan provides clear expert evidence that the respondent's Developmental and Cognitive Impairments are sequelae of his Birth Injuries. His Honour said that this was not a case in which the court was being asked to make a finding of causation where no expert is either able to do so, or prepared to do so.[214]
4. His Honour then went on to conclude that, as he had found that the respondent suffered stage 2 HIE, he preferred the evidence of Dr Tracy to that of Professor Hunt, to the extent that Professor Hunt's opinions were based on the respondent having only suffered mild encephalopathy (stage 1 HIE).[215]
5. The learned trial judge concluded that medical science does not deny a connection between stage 2 HIE and the types of impairments comprising the respondent's Developmental and Cognitive Impairment. Rather, his Honour found that the existence of this connection was well established given the research referred to by Dr Tracy and Professor Hunt, this conclusion being even more justified where the HIE is accompanied by a traumatic brain injury.[216]

The profile of the respondent's developmental issues

1. The learned trial judge summarised the differing opinions of Dr Pestell and Dr Do, noting in relation to the evidence of Dr Do that the assumption underpinning her revised opinion fell away, in light of his Honour's finding that the respondent suffered stage 2 HIE.[217]
2. The specific findings made by the learned trial judge from the evidence of Dr Pestell and Dr Do were as follows.
3. First, the pattern and nature of the respondent's Developmental and Cognitive Impairments is consistent with a brain injury of a traumatic nature, as opposed to being of a congenital nature.[218]
4. Secondly, his Honour found that, from a neuropsychological perspective, the pattern and nature of the respondent's Developmental and Cognitive Impairments were consistent with him having suffered serious damage to his brain, of a traumatic nature, soon after birth, in particular damage consistent with him sustaining HIE.[219]

Other potential causes of the Developmental and Cognitive Impairments

1. While the appellant did not, in its pleaded case, identify a specific alternative cause of the respondent's Developmental and Cognitive Impairments, the learned trial judge addressed a number of other potential causes or explanations raised by the evidence.
2. The first was a genetic issue. His Honour noted that Professor Hunt commented, almost in passing, that the respondent's global developmental delay 'may be accounted for by subtle underlying genetic abnormality' (see [165] above). In the absence of any evidence that any testing had occurred in relation to the suggestion, the learned trial judge did not regard this comment by Professor Hunt as comprising a plausible alternate hypothesis for the respondent's Developmental and Cognitive [220]airments.220
3. The second potential cause was ADHD (attention deficit hyperactivity disorder). In light of the evidence of Dr Pestell and Dr Do, his Honour concluded that the evidence did not establish that ADHD was a plausible alternate hypothesis for all of the respondent's Developmental and Cognitive Impairments.[221]
4. The third potential cause was the possibility, raised by Dr Do, that lack of sleep may have caused the respondent's problems with attention and inhibition. That suggestion did not, however, extend to all of the respondent's developmental and cognitive issues and his Honour concluded that lack of sleep was not a plausible alternate hypothesis for all of the respondent's Developmental and Cognitive Impairments.[222]
5. The learned trial judge also addressed the appellant's submission in closing that the respondent may well just be an ordinary child at the lower end of the relevant developmental spectrum. His Honour concluded that there was no basis in the evidence for that contention.[223]
6. Bringing these matters together, his Honour concluded that he did not consider that there was a plausible inference competing with the inference that the respondent's Birth Injuries caused or materially contributed to Cooper's Developmental and Cognitive Impairments.[224]
7. Finally, his Honour observed that, to the extent that ADHD (or any other alternative causes) may have been a cause of the respondent's Developmental and Cognitive Impairments, his Honour found that the appellant had not satisfied the evidential onus on it to disentangle the alternative causes.[225]

1. Based on, and drawing together all of, the matters referred to above, the learned trial judge found that the respondent's Developmental and Cognitive Impairments are more likely than not to be sequelae of his Birth Injuries, which were caused by the defendant's fault.[226]
2. This is the critical finding as to causation in this appeal. His Honour went on to summarise the reasoning behind that finding in eight points. It is appropriate to set out those points in full:
   1. First, there is firm expert evidence that Cooper's Developmental and Cognitive Impairments are sequelae of Cooper's Birth Injuries. This is not a case in which the court is being asked to make a finding of causation where no expert is either able to do so, or prepared to do so. It is not a case in which where there is no expert evidence that rises above the 'possible'.
   2. Second, to the extent that the expert evidence to the contrary is based on the premise that Cooper only sustained stage 1 HIE in the process of his birth, this premise falls away by reason of my finding that he sustained stage 2 HIE.
   3. Third, it is the case that the injury to Cooper's brain most apparent on the MRI scans is to his right cerebellar tonsil, and that an injury of that kind only is unlikely to have caused Cooper's Cognitive and Developmental Impairments. However, it is quite possible that the injury to Cooper's brain is more widespread, in particular extending into some of the structures adjacent to the right cerebellar tonsil. This is a matter of interpretation of the relevant MRI images. Moreover, the fact that the 2014 MRI and 2015 MRI images do not show areas of damage to Cooper's brain beyond the area of the right cerebellar tonsil, and possibly adjacent structures, does not of itself mean that there is not wider damage to Cooper's brain. In particular, it is also quite possible that Cooper sustained a global microscopic brain injury.
   4. Fourth, there is no compelling medical evidence to the effect that Cooper's Developmental and Cognitive Impairments are not sequelae of Cooper's Birth Injuries; only matters of interpretation and opinion. Rather, the medical evidence is to the effect that it is quite possible that Cooper's Developmental and Cognitive Impairments are sequelae of Cooper's Birth Injuries. In particular, if the injury to Cooper's brain extended beyond the right cerebellar tonsil into the adjacent structures of the cerebellum, in particular the vermis, left cerebellar tonsil, flocculus and right foramen of Luschka, then this has the potential to give rise to neurological and developmental impairments.
   5. Fifth, there is well-established research to the effect that 50% or so of children with stage 2 HIE will go on to suffer from neurological and developmental issues. This is obviously not a basis for a finding that Cooper is in this 50%. However, it is a basis for a finding that it is quite possible that the fact that Cooper sustained stage 2 HIE caused or materially contributed to Cooper's Developmental and Cognitive and Impairments. The connection between stage 2 HIE and the types of impairments comprising Cooper's Developmental and Cognitive Impairments is well established, in particular where the HIE is accompanied by a traumatic brain injury.
   6. Sixth, from a neuropsychological perspective, the pattern and nature of Cooper's Developmental and Cognitive Impairments are consistent with him having suffered serious damage to his brain, of a traumatic nature, soon after birth, in particular damage consistent with him sustaining HIE.
   7. Seventh, this is not a case in which there is any other plausible inference competing with the inference that Cooper's Birth Injuries caused or materially contributed to Cooper's Developmental and Cognitive Impairments. It is not a case in which the court is left with two conflicting inferences, each of equal probability.
   8. Eighth, to the extent that ADHD may be considered as a possible alternate cause of Cooper's Developmental and Cognitive Impairments, the defendant has not discharged the evidential onus on it to disentangle those causes, and show that Cooper's Birth Injuries did not materially contribute to Cooper's Developmental and Cognitive Impairments.
   9. These reasons are ample to support a reasonable and definite inference that Cooper's Developmental and Cognitive Impairments are sequelae of Cooper's Birth Injuries and that the defendant's fault was a necessary condition of the occurrence of both Cooper's Birth Injuries and Cooper's Developmental and Cognitive Impairments. To the extent that some of the primary facts are in the realm of the possible, for example the full extent of the damage to Cooper's brain in the area of the right cerebellar tonsil, I am entitled to give 'weight to the united force of all the evidence together'.
3. His Honour added that, even if he was wrong in his conclusion that the defendant's fault was a necessary condition of the occurrence of the respondent's Developmental and Cognitive Impairments, the reasons he had set out were more than ample to support a reasonable and definite inference that the appellant's fault materially contributed to the respondent's Developmental and Cognitive Impairments for the purposes of s 5C(2) of the Civil Liability Act. His Honour stated that a finding of material contribution is a sufficient reason why responsibility for both the respondent's Birth Injuries and Developmental and Cognitive Impairments should be imposed on the appellant for the purposes of s 5C(2)(a) and (b) that Act.[227]

1. Having concluded that the respondent had proven factual causation for the purposes of s 5C(1)(a) of the Civil Liability Act, the learned trial judge turned to s 5C(1)(b): the scope of liability.
2. In that regard, his Honour observed that the appellant did not argue that, should factual causation be established, it was not appropriate for liability to extent to the harm so caused. His Honour concluded that the respondent's case was one in which the scope of liability for the consequences of the harm was coextensive with the content of the duty of the appellant that had been breached.[228]
3. Accordingly, the learned trial judge concluded that it was appropriate for the scope of the appellant's liability to extend to the respondent's Developmental and Cognitive Impairments and that the appellant's fault caused both the respondent's Birth Injuries and Developmental and Cognitive Impairments.[229]
4. We turn now to the grounds of appeal.

1. As noted above, the appellant's grounds of appeal are legion. They are as follows:
   1. The trial judge erred in law by construing the word harm in s.5C(l) of the Civil Liability Act 2002 to include the possibility of personal injury; [648]-[651], [935], [936], [946], [948].
   2. The trial judge erred in law in concluding that expert evidence stating the possibility of a causal link between fault and harm is sufficient to prove a causal link between fault and harm; [815], [817], [818], [895], [935], [936].
   3. The trial judge erred in law by finding that the plaintiff's 'brain injuries' were 'traumatic' based on material that was not in evidence at trial and which the defendant could not consider; [37], [653]-[663].
   4. The trial judge erred in law and fact by not making a finding as to whether the haemorrhagic contusion to the right cerebellar tonsil extended into adjacent structures, including the flocculus, vermis, left cerebellar tonsil and adjacent cerebellar hemisphere; [648]-[651], [933], [936], [938].
   5. The trial judge erred in law in finding that 'it is quite possible' that the 2014 and 2015 MRI scans showed damage to the plaintiff's brain that extended beyond the right cerebellar tonsil to the adjacent structures of the cerebellum, in particular the vermis, left cerebellar tonsil, flocculus and right foramen of Luschka which damage was caused by a breach of duty by the defendant; and that this possibility of damage was sufficient to prove a causal link between breach and the plaintiff's 'Developmental and Cognitive Impairments'; [852(b)], [862], [910], [935], [936], [941], [946], [948].
   6. The trial judge erred in law in finding that it was 'quite possible' that the plaintiff sustained a global microscopic brain injury caused by a breach of duty of the defendant; Judgment [880], [935], [936], [937], [938], [941], [946] and [948].
   7. The trial judge erred in law by not addressing an issue which had to be addressed in order to determine the case; being that classification of the plaintiff as suffering from moderate or stage 2 hypoxic ischemic encephalopathy (HIE) was irrelevant to determining whether any of the plaintiff's 'Developmental and Cognitive Impairments' were caused by any breach of duty by the defendant; [664]-[704], [933], [934], [937], [941], [946], [948].
   8. In the alternative to Ground 7, if relevant to find whether the plaintiff suffered at any time from HIE stage 2, the trial judge erred in fact in so finding; [664]-[709], [933], [934], [937], [938], [941], [966], [968]. The finding is against the weight of the evidence.
   9. The trial judge erred in fact by (in effect) finding that the plaintiff suffering a right sided Erb's palsy was relevant to breach causing 'Cooper's Developmental and Cognitive Impairments'; [590], [709], [790], [932], [933], [935], [936], [941], [946], [948].
   10. The trial judge erred in fact by (in effect) finding that the plaintiff suffering renal impairment was relevant to breach causing 'Cooper's Developmental and Cognitive Impairments'; [709], [790], [932], [933], [941], [946], [948].
   11. The trial judge erred in fact in finding that Dr Nguyen gave evidence to the effect that the first (Day 7) MRI showed injury to the left cerebellar tonsil; [614], [616], [935], [941], [946], [948].
   12. The trial judge erred in fact by finding that minor subdural haemorrhage and intraventricular haemorrhage seen in the Day 7 MRI were caused by any breach of duty by the defendant and caused the plaintiffs 'Developmental and Cognitive Impairments'; [709], [663], [933], [935], [939], [941], [942], [946] and [948].
   13. The trial judge erred in law in finding that there existed 'clear expert evidence' that the plaintiff's Developmental and Cognitive Impairments were, in terms of s.5C(1) of the Civil Liability Act 2002, caused by a breach of duty of the defendant; [891], [894], [933], [939], [941], [946] and [948].
   14. The trial judge erred in fact in preferring the evidence of Dr Tracy to that of Professor Hunt that the plaintiff's Developmental and Cognitive Impairments were caused by the plaintiff's Birth Injuries; [892], [933], [937], [941], [946], [948].
   15. The trial judge erred in fact in finding that there was a consensus between expert witnesses that, of children classified as stage 2 HIE, 50% (or so) suffered from neurodevelopmental deficits and 50% (or so) did not; [893], [934], [937], [941], [946], [948].
   16. The trial judge erred in law in finding that the fact that 50% (or so) of children with HIE stage 2 suffer from neurodevelopmental deficits is a basis for a finding that it is 'quite possible' that the plaintiff suffered from stage 2 HIE which caused or materially contributed to his Developmental and Cognitive Impairments; [894], [934], [937], [941], [946], [948].
   17. The trial judge erred in law in determining that, for s.5C(2) of the Civil Liability Act 2002, it is an established principle that, as a matter of ordinary common sense and experience, negligence 'materially contributed' to and thereby caused harm; [718]-[720], [894], [914], [926], [931], [937], [939], [941], [946] and [948].
   18. The trial judge erred in law by imposing a burden upon the defendant to disprove that, in terms of s.5C(l)(b) and s.5C(4) of the Civil Liability Act 2002, this case was an appropriate case for the scope of the defendant's liability to extend to the harm so caused; [743], [937], [939], [941], [942], [945], [946], [948].
   19. The trial judge erred in law by determining that in terms of s.5C(l)(b) and s.5C(4) of the Civil Liability Act 2002 there existed well-established precedent, with which this matter was consistent, that rendered the scope of liability for the consequences of the harm coextensive with the content of the duty of the defendant which has been breached; [743], [941], [946], [947], [948].
   20. The trial judge erred in law in concluding that there exists a principle of law that a significant circumstance in favour of drawing an inference of causation is that a defendant has not established or suggested an alternative cause; [813], [939], [941], [946], [948].
   21. The trial judge erred in law and in fact in finding that it is not possible that the plaintiff is a child at the lower end of the developmental spectrum; [925].
   22. By reason of Grounds 1-21 the trial judge erred in making the finding at [946] and [948].
2. Before turning to the individual grounds of appeal, we commence with the broad construction of the learned trial judge's reasons, in light of the accepted principles in relation to inferring causation and the relevance of evidence of 'possibilities'.
3. It is to those principles that we first turn.

Factual causation, inferences and possibilities

1. As we stated at the commencement of these reasons, whether the respondent's Developmental and Cognitive Impairments were caused by injuries to his brain resulting from the appellant's negligence was a question of fact to be established, on the balance of probabilities. In the context of the Civil Liability Act, that factual question arises in s 5C(1)(a) (i.e. 'factual causation').[230]

1. In March v E & MH Stramare, Mason CJ explained the distinction between the legal concept of causation and philosophical or scientific notions of causation:[231]

That is because 'questions of cause and consequence are not the same for law as for philosophy and science', as Windeyer J. pointed out in The National Insurance Co of New Zealand Ltd v Espagne [1961] HCA 15; (1961) 105 CLR 569, at p 591. In philosophy and science, the concept of causation has been developed in the context of explaining phenomena by reference to the relationship between conditions and occurrences. In law, on the other hand, problems of causation arise in the context of ascertaining or apportioning legal responsibility for a given occurrence. The law does not accept John Stuart Mill's definition of cause as the sum of the conditions which are jointly sufficient to produce it. Thus, at law, a person may be responsible for damage when his or her wrongful conduct is one of a number of conditions sufficient to produce that damage.

1. As this passage also makes clear, the law's concern, in relation to causation, is with the attribution, in a particular case, of a causal connection between an identified negligent act or omission (or other wrong) and a given occurrence. In the context of the present case, for example, the question was whether, on the balance of probabilities, the identified negligence (for which the appellant was responsible) was the cause of the respondent's given (or known) Developmental and Cognitive Impairments.[232]
2. To be clear: the question in the present was not whether, in general, negligence of the kind that occurred in the present case is more or less likely to give rise to the kind of Developmental and Cognitive Impairments suffered by the respondent. No doubt that general question - the answer to which will be given by medical science - may be of importance (and may indeed be decisive) in a given case. But it would be a mistake, and potentially misleading, to confuse that scientific question with the legal one.
3. An example from the present case may perhaps illustrate this point. As is apparent from the above summary of the expert evidence, much attention was given, in the present case, to the likelihood of a child with stage 1 or stage 2 HIE going on to experience neurological deficits. The learned trial judge, for example, referred to the research to the effect that 90% of infants with stage 1 HIE would be expected to have a normal neurodevelopmental outcome, a percentage which reduced to 50% of infants with stage 2 HIE.[233]
4. One might draw from these general statistics the proposition that, as a matter of prediction (or prognosis), a child who suffers stage 1 HIE will have only a 10% chance of developing neurological deficits. It is necessary to be clear, however, what this general statistic does not mean. It does not mean that, in the case of a child who has suffered stage 1 HIE and has known neurological deficits, there is only a 10% chance that the former caused the latter.
5. That is a matter of basic logic and mathematics. The fact that the probability that a given event will cause an adverse outcome is unlikely (say 10%) does not necessarily mean that the probability that such an outcome was caused by that event is equally unlikely (or indeed that it is unlikely at all).
6. To take a simplified example, it may be that, as a matter of medical science, a particular medical condition (disease X) has only one possible cause (cause Y), such that all cases of disease X would be caused by cause Y. The probability of cause Y given disease X would be 100% (i.e. P(Y|X) = 100%). That causal relationship, however, does not say anything about the probability that a person exposed to cause Y will develop disease X. It may, for example, be that only 10% of persons exposed to cause Y will develop disease X (i.e. P(X|Y) = 10%). It is not possible, therefore to reason simply from the fact that P(X|Y) is unlikely that P(Y|X) is also unlikely.
7. As French CJ explained in Amaca v Booth,[234] an after‑the‑event inference of causal connection may be reached on the balance of probabilities notwithstanding that the statistical correlation between the first event and the second event indicated, prospectively, no more than a 'mere possibility' that the second event would occur given the first.
8. It is in this context (namely, the determination of factual causation) that the relevance of 'possibilities' revealed by the evidence arises for consideration.
9. In this regard, it is clear, and there can be no doubt, that mere proof by a plaintiff of the possibility that a defendant's breach caused the plaintiff to suffer harm is insufficient. The court must be satisfied that it is more probable than not that the defendant's breach caused the relevant harm; it is not sufficient to conclude that the breach may have been a cause of the harm.[235]
10. At the same time, it is also well‑established that causation may be proved by inference. If direct proof is not available, an inference of causation may be drawn if the circumstantial evidence is sufficiently strong and coherent to support a definite inference to that effect.[236] Before such an inference can be drawn, there must be more than two conflicting inferences of equal probability.[237]
11. The drawing of an inference has been described as 'an exercise of the ordinary powers of human reason in the light of human experience'.[238] A court must, of course, avoid conjecture, but the distinction between permissible inference and conjecture occurs on a continuum in which there is no bright line division.[239]
12. Accordingly, even if other disciplines may not be able to give a conclusive answer, questions of causation, as a step in the determination of liability in negligence, call for 'sufficient reduction to certainty to satisfy the relevant burden of proof for the attribution of liability'.[240]
13. There will, no doubt, be cases where expert evidence of a scientific or medical nature (where it is accepted) will preclude a finding of causation. As Dixon J said in Adelaide Stevedoring Co Ltd v Forst,[241] in a paragraph cited with approval by the plurality in Amaca v Booth:[242]

upon question of fact of a medical or scientific description, a court can only say that the burden of proof has not been discharged where, upon the evidence, it appears that the present state of knowledge does not admit of an affirmative answer and that competent and trustworthy expert opinion regards an affirmative answer as lacking justification, either as a probable inference or as an accepted hypothesis.

1. The appellant submits that this passage, or the paragraphs in Amaca v Booth immediately preceding it, require a plaintiff to prove by expert evidence the mechanism by which a breach, or its immediate consequence, caused the damage claimed by the plaintiff, at least if there is expert evidence suggesting a lack of association.[243] The appellant submits that, applied to this case, this requirement meant that the respondent was obliged to prove, and the learned trial judge was obliged to find, (i) an identified injury to a particular part of the brain and (ii) a scientific explanation as to how injury to that part of the brain results in cognitive or other mental deficits.[244]
2. We do not accept that any such requirement exists, or that this passage establishes or suggests such a requirement. In our view, this passage is not concerned with identifying requirements of proof, by expert evidence, upon a plaintiff. As Mason J later observed in Tubemakers v Fernandez, this passage 'emphasizes the restrictions upon a court's power to hold that a plaintiff has not discharged the burden of proof'.[245] Only if expert opinion regards an inference of causation as unjustified as a probable inference or as an accepted hypothesis is a court positively precluded from dismissing that inference by reason of the expert evidence.
3. In the earlier passages in Amaca v Booth upon which the appellant also relies, Gummow, Hayne and Crennan JJ:

(a) observed that cases lying outside the realm of common knowledge and experience fell to be determined by reference to expert evidence; the investigation of difficult and complicated facts is not to be separated from an appreciation of any special branch of knowledge which affects them;[246] and

(b) adopted statements by Sir Owen Dixon that the 'wealth of knowledge put by science at the disposal of the processes of the law meant that, in place of what in simpler times had been "the rough and ready answers of the practical man", an exact and reasoned solution was now required'.[247]

1. These observations make clear that in cases where expert evidence is led bearing upon a question of causation, the court must consider, and reason with reference to, the expert evidence led. However, nothing in these observations requires a plaintiff to prove, or a trial judge to find, by reference to expert evidence, the specific mechanism by which one event caused another event.
2. The approach outlined above is also reflected in Seltsam v McGuiness, a decision upon which the learned trial judge in the present case heavily relied. In that case Spigelman CJ enunciated the following propositions.
3. A court may draw an inference of causation notwithstanding that, in the particular case, expert witnesses do not express an opinion that the damage was caused by the relevant breach.[248] An inference of causation may be drawn without medical evidence to support it, or when the expert evidence does not rise above the opinion that a causal connection is possible if, but only if, the materials as a whole justify an inference of probable connection.[249]
4. In circumstances where the aetiology is uncertain, or subject to significant scientific dispute, the courts are not thereby disabled from making decisions as to causation on the balance of probabilities. In this regard, Spigelman CJ cited with approval the following passage from EMI (Australia) Ltd v BES:[250]

Medical science may say in individual cases that there is no possible connection between the events and the death, in which case, of course, if the facts stand outside an area in which common experience can be a touchstone, then the judge cannot act as if there were a connection. But if medical science is prepared to say that it is a possible view, then, in my opinion, the judge after examining the lay evidence may decide that it is probable. It is only when medical science denies that there is any such connection that the judge is not entitled in such a case to act on his own intuitive reasoning. It may be, and probably is, the case that medical science will find a possibility not good enough on which to base a scientific deduction, but courts are always concerned to reach a decision on probability and it is no answer, it seems to me that no medical witness states with certainty the very issue which the judge himself has to try.

1. This last point is also illustrated by the decision of the High Court in Tubemakers v Fernandez, in which the Court confirmed that the sequence of events can be called in aid of drawing an inference which, according to expert evidence, is open.[251] As Barwick CJ said in that case, other circumstances may 'unite to warrant a conclusion that what the medical evidence established as a possible cause was the probable cause [of the plaintiff's damage]'.[252]
2. Again, none of this is to downplay the significance of expert medical evidence in cases such as the present where the issue lies 'outside the realm of common knowledge and experience'. In these cases, as the plurality observed in Amaca v Booth 'the investigation of difficult and complicated facts cannot be separated from an appreciation of any special branch of knowledge which affects them'.[253]
3. As Pullin JA said in BGC Residential Pty Ltd v Fairwater Pty Ltd,[254] referring to Amaca v Booth:

In many cases in place of the 'rough and ready answers of the practical man' an 'exact and reasoned solution' is now required. This is so in cases where the wealth of knowledge of science may provide such an exact and reasoned solution to a causation issue: Booth [68]. However, the plurality in Booth accepted [69] that there will still be cases (and this is one such case) where 'other disciplines' cannot give any conclusive answer, in which case a commonsense assessment of the evidence is the only method which can be used to reach a conclusion about whether a breach of contract has caused the claimed damage. The question to be asked is whether it is possible to infer, on the balance of probabilities and applying a commonsense approach, that but for the breach the damage would not have occurred.

1. In this context, Spigelman CJ in Seltsam v McGuiness specifically addressed the relevance of evidence as to 'possibilities'. The particular issue in Seltsam v McGuiness was whether the respondent's renal cell carcinoma was caused by his inhalation of asbestos at the appellant's premises. The respondent's case on causation relied heavily on epidemiological evidence directed to establishing what research studies had shown as to the relationship between asbestos and various diseases, including, relevantly, renal carcinoma.
2. Consistent with the observations made at [255] to [259] above, Spigelman CJ observed that epidemiology is not directed to the circumstances of an individual case. In that sense, for the purpose of determining whether exposure to a particular substance was the legal cause of a particular disease in the plaintiff in a particular case, epidemiology only provides [255]dence of possibility.255 In that context, Spigelman CJ accepted that evidence of possibility was admissible in determining whether an inference of causation can be dra[256] He said as follows:256

Evidence of possibility, including expert evidence of possibility expressed in opinion form and evidence of possibility from epidemiological research or other statistical indicators, is admissible and must be weighed in the balance with other factors, when determining whether or not, on the balance of probabilities, an inference of causation in a specific case could or should be drawn. Where, however, the whole of the evidence does not rise above the level of possibility, either alone or cumulatively, such an inference is not open to be drawn.

1. Evidence of possibility, including epidemiological studies, can therefore be regarded as circumstantial evidence which may, alone or in combination with other evidence, establish causation in a specific case.[257] As in any circumstantial case, an inference as to the probabilities may be drawn from a number of pieces of particular evidence, each piece of which does not itself rise above the level of possibilities.[258]
2. Causation, like any other fact to be established by a process of inference, may be established by a process that combines primary facts like strands in a cable rather than links in a chain.[259] In those where the evidence does consist of strands in a cable, rather than essential links in a chain, as long as the ultimate inference is reached to the required standard, it is not necessary for an intermediate fact to be established to the legal standard. This principle of course applies, in a criminal case, to proof beyond reasonable doubt;[260] a fortiori it applies to the proof of causation on the balance of probabilities.[261]
3. As will be seen, in our view, the respondent's case at trial was of the 'strands in a cable' variety.

Application of these principles in the Primary Reasons

1. In our view, it is clear from the Primary reasons, properly construed, that the learned trial judge positively found that it was more likely than not that the respondent's Developmental and Cognitive Impairments were caused by the appellant's negligence. The ultimate factual finding, as it appears in the Primary reasons, is expressed in those terms[262] and in terms that the appellant's fault was a necessary condition of both the respondent's Birth Injuries and his Developmental and Cognitive Impairments.[263]
2. There is no basis for construing the Primary reasons as meaning anything other than what they say in this regard.
3. It follows that the learned trial judge did not find, either expressly or impliedly, that the possibility that the appellant's breach caused the respondent's Developmental and Cognitive Impairments was sufficient to establish factual causation. Indeed, his Honour expressly recognised that the respondent needed to do more than merely show that it was possible that the respondent's Developmental and Cognitive Impairments were caused by the appellant's fault (or that the appellant's fault might have caused that harm).[264]
4. Insofar as the learned trial judge found that certain of the primary facts were in the realm of the possible (which is undoubtedly how his Honour expressed a number of the primary findings of fact), it is clear that his Honour's ultimate finding was one made on the balance of probabilities.

1. It must be recognised in this context that, notwithstanding the comprehensive nature of the Primary reasons, there are certain matters (in terms of the learned trial judge's findings) that must be inferred from the Primary reasons as a whole.
2. For example, given the finding that an injury to the right cerebellar tonsil alone was unlikely to have caused the respondent's Developmental and Cognitive Impairments, and his Honour's ultimate finding that the injury to the respondent's brain did, more likely than not, cause those impairments, it must follow, as a matter of logic, that his Honour was satisfied that the injury to the respondent's brain was not confined to the right cerebellar tonsil and that he had sustained further injury to his brain (either to the cerebellum or more globally).
3. In response to this proposition the appellant observed, not without some justification: 'well, except that he didn't say that'.[265]
4. With respect to the learned trial judge, there is merit in this observation. His Honour did not make an express finding, in terms, that the respondent had sustained injuries to his brain beyond the right cerebellar tonsil. And given the significance of the issue (at least to the appellant), in our view, it would have been preferable if his Honour had done so. Again, and with respect to the learned trial judge, it would ordinarily be expected that a factual issue of this significance would not be left to be inferred from the reasons.
5. Nevertheless, and notwithstanding that criticism of the Primary reasons, the real issue for present purposes, is whether, on a proper construction of the Primary reasons, his Honour implicitly so found. That is: should it legitimately be inferred from the Primary reasons that his Honour was satisfied that the injuries to the respondent's brain consequent upon the appellant's negligence were more extensive than the injury to the right cerebellar tonsil?[266]
6. In our view, this is the proper construction to be given to the Primary reasons. The learned trial judge must be taken to have found that the injuries to the respondent's brain were more extensive than the injury to his right cerebellar tonsil. As explained in [311] below, this may have occurred in (either or both of) at least two different ways - either because the traumatic injury to the cerebellum went beyond the right tonsil, or because there was a global microscopic injury.
7. So much is to be inferred from the matters identified at Primary reasons [935] and [936], in which his Honour refers to the evidence as to the potential for more widespread injury to the respondent's brain, as identified by the expert evidence called by the respondent, in contradistinction to the evidence as to the injury to the right cerebellar tonsil. In the circumstances, the combination of those findings, together with the other circumstances identified by his Honour at Primary reasons [933] to [940], are such that, to paraphrase Barwick CJ's formulation in Tubemakers v Fernandez, the other circumstances united to warrant a conclusion that what the medical evidence established as a possible cause was the probable cause of the respondent's Developmental and Cognitive Impairments.[267]
8. In this regard, it is important to notice that the implicit finding identified in [292] above is not, as some of the appellant's submissions tended to suggest was necessary, a step towards the ultimate conclusion, by inference, that the injury to the respondent's brain caused the respondent's developmental and cognitive impairments. Rather, it is a finding implicitly made in so concluding.
9. In other words, expressed in the language of criminal law jurisprudence, a finding that the injuries to the respondent's brain were more extensive than the injury to his right cerebellar tonsil was not an intermediate fact - it is not an indispensable link in a chain of reasoning towards the ultimate conclusion.[268] The position was explained by McLure P in Austic v The State of Western Australia:[269]

Whether or not an intermediate fact is an indispensable link in a chain of reasoning towards guilt depends upon the issues and evidence in a particular case. As noted by Dawson J in Shepherd v The Queen [1990] HCA 56; (1990) 170 CLR 573, 581, whether or not the presence of the accused when the crime was committed is an indispensable link in the chain of reasoning depends on the circumstances of the case.

A fact will be an indispensable link in a chain of reasoning if it is a discrete step which must be proven before addressing the next step in the reasoning process towards the ultimate inference of guilt: Shepherd (576) (Mason CJ). That is, proof of the fact is a necessary condition for establishing a further (and different) fact.

The trial judge directed the jury that they had to be satisfied beyond reasonable doubt that the appellant killed the deceased, that being an element of the offence of wilful murder. The appellant could not have killed the deceased unless he had the opportunity to and was in the presence of the deceased when she was killed. However, opportunity and/or presence were not discrete steps in the reasoning process in this case. All of the circumstantial evidence in the case comprised strands in a cable rather than links in a chain on the issue of whether the appellant killed the deceased. (emphasis added)

1. In DKA v The State of Western Australia, Mitchell JA explained the concept of an intermediate fact in a similar manner. In rejecting an argument that, on a charge of sexual assault where the defence case was that the accused was incapable of an erection and ejaculation, the State was obliged to prove beyond reasonable doubt that the accused was so capable, his Honour said as follows:[270]

As a matter of fact, acceptance of the complainant's evidence would carry with it a conclusion that the appellant must have been capable of sustaining an erection and ejaculating in the manner the complainant described. However, the jury did not need to be satisfied beyond reasonable doubt that the appellant was impotent before deciding whether it was satisfied beyond reasonable doubt that the accused engaged in the charged conduct. (original emphasis)

1. The position is similar here. The learned trial judge did not need to find that the injury to the respondent's brain extended beyond the injury to his right cerebellar tonsil before deciding whether he was satisfied as to his ultimate conclusion. The first finding was not a discrete step in the reasoning process towards the ultimate conclusion. Nor did the judge make such a finding before reaching his conclusion as to factual causation. Rather, the ultimate conclusion carried with it a finding that the injury to the respondent's brain extended beyond the right cerebellar tonsil.
2. As we explain in resolving ground 4, a contrary assumption appears to be implicit in many of the appellant's submissions. The appellant appears to contend, in effect, that the learned trial judge was required first, to resolve the question of whether the brain injury extended beyond the right tonsil, and to do so primarily or exclusively by reference to the expert evidence as to the MRIs, and then use the finding on that question to inform the determination of the ultimate causation question. For the above reasons, and for the reasons relating to ground 4, the learned trial judge was not required to, and did not, reason in that manner.

1. In construing the Primary reasons, it should be recognised that there were a number and variety of medical 'possibilities' identified and found by his Honour, to which his Honour had regard. Those findings as to the various 'possibilities' reflected different kinds or types of uncertainty or contingency.
2. For example, one kind of 'possibility' was the possibility arising from the epidemiological research in relation to the outcomes of children diagnosed with the various 'stages' of HIE.[271] Findings of this type are expressed in terms of possibility because of the nature of epidemiological research.[272]
3. Another kind of 'possibility' was the possibility arising from the limitations of MRI imaging itself. As his Honour expressly found, the absence of visible injury on an MRI does not necessarily mean that no injury is present. That is, there may be injuries to the brain that are not 'picked up' on MRI but which are clinically present. His Honour so found.[273]
4. The possibility, for example, of a global microscopic brain injury was therefore one found by his Honour, in part, because of the limitations of MRI imaging. It is not dependent upon a difference of opinion or interpretation of the imaging itself.
5. By contrast, a third kind of 'possibility' found by the learned trial judge was the consequence of what his Honour described as 'matter of interpretation and opinion on which experts may legitimately differ'.[274] This was clearly the case in relation to his Honour's findings that it was 'quite possible' that the haemorrhagic contusion to the area of the right cerebellar tonsil extended beyond the right cerebellar tonsil into the adjacent structures, including the flocculus, vermis, left cerebellar tonsil and adjacent cerebellar hemisphere.[275]
6. That finding was clearly based upon the evidence of Dr Keenan (and, in some respects Dr Nguyen[276] and Professor Hunt[277]), who identified those features on his examination of the Day 7 MRI. Expressing a finding such as this in terms that it was 'quite possible' requires some unpacking.
7. In understanding this finding, it should first be observed that it is not an expression of 'mere' possibility arising as a hypothesis in the absence of evidence.[278] It was a specific finding based on evidence from expert witnesses as to the content of the MRI scan. In that sense, in our view, his Honour's characterisation of the extension of the injury beyond the right cerebellar tonsil as 'quite possible', should be understood in the sense of 'distinctly possible', 'rationally plausible' or a 'plausible hypothesis'. It did not, as the appellant suggests, mean 'possible in the sense of ... a spaceship landing on the front lawn'.[279]
8. Secondly, it was a finding based on the evidence of an expert (Dr Keenan) who the learned trial judge found to be a very experienced radiologist[280] and whose evidence his Honour evidently accepted as reliable and credible. The identification of the abnormalities identified by Dr Keenan as 'quite possible' necessarily involved acceptance of his opinion evidence to that extent.
9. Thirdly, it was also necessarily a finding to the effect that Professor Ditchfield's evidence (which was contrary to Dr Keenan's evidence in this regard) did not satisfy the learned trial judge that he could exclude, as an available hypothesis, that the injury to the cerebellum extended beyond the right tonsil to the adjacent structures. The reference to more extensive injury being 'quite possible'[281] must be understood by reference to the finding that reviewing an MRI scan is a matter of interpretation and opinion on which experts may legitimately differ.[282] It is implicit in his Honour's reasons that both Dr Keenan's and Professor Ditchfield's interpretations of the Day 7 MRI were legitimate and reasonable interpretations of the image. The possibility arose from the learned trial judge's conclusion that a legitimate interpretation of the Day 7 MRI was that it showed the haemorrhagic contusion extending into structures including the vermis.
10. Fourthly, and most importantly, the finding that the additional abnormalities identified by Dr Keenan were 'quite possible' was expressed as a 'primary' factual finding, in isolation from all of the other evidence. This is clear from the structure of the Primary reasons as a whole, in which the learned trial judge addressed each of the relevant circumstances separately and individually, before arriving at his ultimate findings. It is reflected in the manner in which, in the introductory summary, his Honour foreshadowed his finding that '[d]rawing all the threads together, a reasonable and definite inference may be drawn' as to the ultimate factual causation question.[283] It was also made clear in the Primary reasons at the point at which his Honour stated his ultimate conclusion (where his Honour referred to some of the 'primary facts' being in the realm of the possible).[284]
11. The fact that there were a number of primary facts which, alone, did not rise above the level of possibility, may serve to explain why the finding that the injuries to the respondent's brain were more extensive than the injury to his right cerebellar tonsil was left to be inferred from the Primary reasons as a whole.
12. That is because, as is likely the case, the learned trial judge did not specifically find in what way the respondent's injury so extended. In that regard, there were a number of 'possibilities' as to how, or in what way, the respondent sustained brain injuries other than to the right cerebellar tonsil in such a way as to cause the respondent's Developmental and Cognitive Impairments.
13. To take the clearest examples, the learned trial judge found, as separate and distinct possible mechanisms of injury:

(a) that the injury in the cerebellum extended beyond the right cerebellar tonsil into the adjacent structures of the cerebellum, in particular the vermis, left cerebellar tonsil, flocculus and right foramen of Luschka;[285] and

(b) that the respondent had a global microscopic injury to his brain as a whole, likely arising from, or contributed to by, the HIE suffered by the respondent.[286]

1. If either (or both) of these mechanisms had occurred the injuries to the respondent's brain could properly be said to have been more extensive than an injury to his right cerebellar tonsil. In addition a finding that either (or both) of them did occur would, together with other matters relied upon by the learned trial judge (stage 2 HIE, the pattern and nature of the impairments, and the absence of any other plausible inference), be a sufficient basis for a finding of factual causation between the appellant's negligence and the respondent's Developmental and Cognitive Impairments.
2. In the context of the issues in the trial, it was not necessary for his Honour to be satisfied which of the two (or more) possible mechanisms of injury was present in the respondent's case. That is, while his Honour was required to be (and was) satisfied, on the balance of probabilities, that the necessary causal link between the appellant's negligence and the respondent's Developmental and Cognitive Impairments was established, his Honour did not have to find the precise physiological mechanism that formed that link.[287]
3. It is significant, in that regard, that on the facts of this case, whichever precise mechanism gave rise to the respondent's Developmental and Cognitive Impairments, the appellant's negligence was responsible for each of them.
4. In some cases, of course, the precise mechanism for the development of a particular injury may be crucial. This will be the case, for example, where one mechanism of injury can be attributed to the negligence of the defendant and the other mechanism (or other mechanisms) cannot be. Amaca v Ellis was such a case, in which the exposure to two carcinogens (tobacco smoke and asbestos) may have caused the respondent's lung cancer, but only one of them (asbestos) was actionable. In those circumstances it was necessary for the court to be satisfied that one of the mechanisms (asbestos) was more probable than the other.[288]
5. In the present case, it was not necessary for the learned trial judge to find precisely how (in the sense of injury to which part of the respondent's brain) the appellant's negligence was the probable cause of the respondent's Developmental and Cognitive Impairments, so long as the primary facts found by his Honour supported a reasonable and definite inference that there was such a causal link and that his Honour drew that inference.
6. Clearly, in our view, the latter is what his Honour did.
7. It will be apparent from these observations that, when the Primary reasons are properly construed, and read as a whole, the learned trial judge did not find that the mere possibility of a causal link between the appellant's negligence and the respondent's injuries (and in particular his Developmental and Cognitive Impairments) was sufficient to prove factual causation under s 5C(1)(a) of the Civil Liability Act. Insofar as the grounds of appeal are premised upon the proposition that his Honour did so, we reject that premise.
8. We turn now to the individual grounds of appeal. For reasons that will become apparent, we have altered the order of them slightly to better reflect the logical order in which they arise for consideration.

Disposition of the grounds of appeal Ground 1 - The possibility of personal injury as 'harm'

1. Ground 1 alleges that the learned trial judge erred in law by construing the word 'harm' in s 5C(l) of the Civil Liability Act to include 'the possibility of personal injury'.
2. As the appellant's submissions correctly observe, 'harm' is defined in the Civil Liability Act to include 'personal injury', which is, in turn, defined to include:

(a) death; and

(b) pre-natal injury; and

(c) impairment of a person's physical or mental condition; and

(d) disease.

1. Consistent with the common law position that 'damage' for the purposes of the causation action in negligence does not include the loss of a chance of a better outcome,[289] it may readily be accepted that the mere 'possibility of impairment or injury' is not 'harm' within the meaning of the Civil Liability Act.
2. Leaving aside damage to property and economic loss, what a plaintiff must prove, to found an action in negligence, is that the defendant's negligence probably caused a personal injury as defined; not that the defendant's negligence caused the possibility of a personal injury. As Hayne and Bell JJ put it in Tabet v Gett, ''damage' refers to some difference to the plaintiff'.[290]
3. It would therefore be an error of law to conclude that the possibility of an injury (that has not 'in fact come home') [291] is a personal injury for the purposes of the definition of 'harm' in the Civil Liability Act.
4. The learned trial judge, however, made no such error. His Honour did not find that the appellant's fault was a necessary condition of 'the possibility of the respondent's injuries and impairment'; his Honour found that the appellant's fault was a necessary condition of the respondent's actual injuries and impairments.[292]
5. In none of the paragraphs of the Primary reasons referred to in this ground,[293] does the learned trial judge expressly (or impliedly) make the error alleged in ground 1. Indeed, none of them refer to the definition of 'harm' or 'personal injury' in the Civil Liability Act at all, let alone include the possibility of injury within those definitions. Insofar as the paragraphs refer to 'possibilities', as already explained, those references were to the primary findings that preceded the ultimate finding of causation.
6. Ground 1 is not made out.

Ground 2 - Expert evidence as to the possibility of a causal link

1. Ground 2 alleges that the learned trial judge erred in law in concluding that expert evidence stating the possibility of a causal link between fault and harm is sufficient to prove a causal link between fault and harm.
2. His Honour did not so find, in the paragraphs of the Primary reasons referred to in ground 2[294] or otherwise. Indeed, in one of those paragraphs (Primary reasons [815]), the learned trial judge expressly adopted Spigelman CJ's statement in Seltsam v McGuiness to precisely the opposite effect, namely:

Where, however, the whole of the evidence does not rise above the level of possibility, either alone or cumulatively, such an inference [of causation] is not open to be drawn.

1. In the context of this ground, the appellant submitted that Amaca v Booth reflects a change in the law (or at least a change in approach) to that summarised by Spigelman CJ in Seltsam v McGuiness, including his Honour's approval of Herron CJ's reasons in EMI (Australia) Ltd v BES.[295] The appellant submitted:[296]

As observed in Amaca Pty Ltd v Booth, even if scientific proof or disproof is not available, 'an exact and reasoned solution' is 'required'. A more exacting and principled approach than that in EMI is now mandated by Amaca Pty Ltd v Booth.

1. The suggestion that Amaca v Booth represents a change in the law (i.e. 'now mandated') is misplaced. The plurality's reference in Amaca v Booth to the need for 'an exact and reasoned solution' in cases of causation was taken directly from extra-curial remarks made by Sir Owen Dixon.[297] Sir Owen made those remarks in 1933, seven years before his Honour's judgment in Adelaide Stevedoring Co Ltd v Forst. We refer to what we have said in [267]-[271] above.
2. The need for an exact and reasoned answer to the question of causation is nothing new. In our assessment, that is what, on a fair reading of the Primary reasons, the learned trial judge in the present case provided.
3. Before leaving ground 2, we would also make the following observations.
4. First, the appellant's submissions as to the learned trial judge's reasoning in relation to this ground present, in our view, an unjustified caricature of that reasoning. The appellant submitted, for example:[298]

What is then left is the reasoning as to the possibility that damage beyond the right cerebellar tonsil (say into the vermis) and (unobservable) microscopic brain injury could have caused the impairments. This process of reasoning is seen at [815], [817], [818], [895], [935] and [936]; injury to the vermis is possible (in the sense that it cannot be absolutely excluded as being present); it is possible (in the sense that it cannot be absolutely excluded), that injury to the vermis could cause the plaintiff's impairment; therefore, as a matter of law, injury to the vermis has caused the impairments. This is a process of reasoning unknown to the common law; is illogical and thereby erroneous.

1. His Honour did not, in our respectful view, so reason, either as to the premises or the conclusion suggested by the appellant.
2. As regards the premise of 'injury to the vermis is possible', as we have set out above, his Honour's finding that injury to the vermis (amongst other injuries) was 'quite possible', was not used 'in the sense that it cannot be absolutely excluded as being present'. On the contrary, it was a finding as to a plausible hypothesis presented by an experienced radiologist and whose evidence his Honour evidently accepted as reliable and credible.[299]
3. Furthermore, in our view, this submission reveals a flaw in the appellant's analysis generally; namely an unduly piecemeal analysis of the evidence, in contradistinction to the approach (taken by the learned trial judge) of arriving at an inference based on 'the united force of all the evidence together'.[300]
4. To take the example provided in the appellant's submissions, his Honour did not reason, as the appellant submits, according to the following syllogism:

Premise 2: Injury to the vermis could cause the respondent's impairments.

Conclusion: Injury to the vermis has caused the impairments.

1. Reducing the learned trial judge's reasoning process (see [244] above) to something akin to a syllogism would more accurately represented as follows:

Premise 1: The respondent suffered, during his birth process, both a traumatic brain injury and hypoxic ischaemic encephalopathy (HIE).

Premise 2: There is credible expert evidence that the respondent's impairments were caused by the appellant's birth injuries.

Premise 3: The respondent suffered stage 2 HIE, which is associated with neurological impairments in approximately 50% of cases.

Premise 4: There are a variety of possible physiological mechanisms, supported by credible expert evidence, that can explain the respondent's impairments, including:

(a) that the injury in the cerebellum extended beyond the right cerebellar tonsil into the adjacent structures of the cerebellum, in particular the vermis, left cerebellar tonsil, flocculus and right foramen of Luschka; and

(b) that the respondent suffered a global microscopic injury to the brain.

Premise 5: The respondent's impairments are, from a neuropsychological perspective, consistent with him having suffered serious injury to his brain, in particular damage consistent with HIE.

Premise 6: There is no compelling medical evidence that the respondent's impairments are not the consequence of his birth injuries.

Premise 7: There is no other plausible explanation for the respondent's impairments other than his birth injuries.

Conclusion: The combined effect of premises 1, 2, 3, 4, 5, 6, and 7 is that it is more likely than not that the respondent's impairments were in fact caused by his birth injuries.

1. Unlike that proffered by the appellant (see [334] above), this is a process of reasoning known to the common law. It is logical and it is not erroneous.
2. It is Premise 4 in the above example that is concerned with the 'possibilities' of which the appellant complains. As is clear from the reasoning as a whole, those 'possibilities' were but individual strands in a cable of circumstances.
3. A final point to make in this context relates to Premise 2 set out in [339] above: namely that there was firm expert evidence to the effect that there was a causal relationship between the appellant's fault and the respondent's Developmental and Cognitive [301]airments.301 That is a reference to the evidence of Dr Tracy and Dr&[302]Keenan.302 Not only does the learned trial judge's ultimate conclusion necessarily reflect the acceptance of their opinions in that regard (see ground 13 below), in the case of Dr Tracy, his Honour had previously expressed a preference for his evidence over that of Pro[303]sor Hunt.303
4. Ground 2 is not made out.

Ground 3 - Mosby's Medical Dictionary and the meaning of trauma

1. Ground 3 contends that the learned trial judge erred in law by finding that the respondent's 'brain injuries' were 'traumatic' based on material that was not in evidence at trial and which the appellant could not consider.
2. The 'material that was not in evidence' referred to in this ground was a definition from Mosby's Dictionary of Medicine, Nursing & Health Professions (Mosby's Medical Dictionary).[304] The relevant passage in the Primary reasons that refers to that dictionary (at [654]) is:

In medical terms, the word 'traumatic' means pertaining to an injury, usually a serious and unexpected injury.

1. The specific finding to which this passage in the Primary reasons related, and which the appellant submits should be set aside, is the finding at Primary reasons [663]:[305]

I find that the brain injuries suffered by Cooper as identified in the Day 7 MRI were traumatic in nature, that is as a result of an injury. I further find that they were sustained in the process of his birth.

1. The nature of the error alleged in ground 3 is a denial of natural justice, in relation to which the appellant relies upon the decisions in Cavanett v Chambers[306] and Gordon M Jenkins & Associates Pty Ltd v Coleman.[307]
2. In Cavanett v Chambers a magistrate had made use of two textbooks as to the effect that a certain blood alcohol percentage would have had on a driver (the appellant), in circumstances where the sample was taken some two hours after the relevant driving. There had been no evidence proffered as to the significance of the percentage, either absolutely, or at the time of the driving. Bray CJ allowed the appeal, concluding that the Magistrate should not have made use of the textbooks without the consent of the parties.
3. Similarly, in Gordon M Jenkins & Associates Pty Ltd v Coleman the Court held that the trial judge had erred by having resort to a Practice Note issued by the Royal Australian Institute of Architects in relation to a claim that the appellants (a firm of architects and their employee) had provided negligent advice. The Practice Note was not in evidence and no mention of it was made before the trial judge. The Court, referring to Cavanett v Chambers, said:[308]

In our opinion, this reasoning applies here. The professional standard of care required to be observed by the second appellant was a central question in the proceedings. The Practice Notes suggest that an estimate which was inaccurate by a margin in excess of 10 per cent was prima facie negligent. Given that it appears that no expert evidence was called on the point, the suggestion made by the Practice Notes assumed considerable significance. The rules of natural justice require that the material should have been disclosed to the parties if it were to be taken into account by the judge, albeit that the extent and result of such usage may be called into question. It appears that some use of the material was made by the judge. It must follow that the rules of natural justice were not observed.

1. Thus it is clear that the failure of a trial judge to disclose material to the parties, where that material is used to make a finding of fact in relation to a matter in issue, may amount to a denial of natural justice. In such a case, the relevant finding of fact is liable to be set aside on appeal.
2. The use of Mosby's Medical Dictionary by the learned trial judge to provide a definition of 'traumatic' as pertaining to an injury is, however, not such a case. His Honour did not use a medical text to reach a conclusion as to a disputed question of fact or to resolve conflicts in the evidence. Rather, the learned trial judge merely referred to a dictionary definition of a term used in the evidence and his reasons. Although his Honour referred to a medical dictionary, the definition of an ordinary English term was not materially different to that available from reference to a standard dictionary such as the Macquarie Dictionary.
3. The dictionary definition of 'traumatic', with respect, added nothing to the evidence adduced by the parties as to the use of 'traumatic'. In particular, the appellant's submission on this ground, that '[t]here is no basis for the finding that [the respondent] suffered traumatic brain injuries and no basis for the findings at [663] or [938]',[309] must be rejected.
4. Contrary to this submission, every expert witness who gave evidence relevant to the issue was of the view that the injuries to the respondent's brain shown in the Day 7 MRI were traumatic injuries sustained in the process of his birth. While there were, no doubt, differing views expressed as to the extent of those injuries (and whether they were evident on the MRI scans), all of the experts were agreed that those injuries were traumatic.
5. In this context it should be recognised that the term 'traumatic' was specifically used to describe injuries shown on the Day 7 MRI that occurred as a result of the physical processes of the respondent's instrumental birth (i.e. the traction on the tissues and blood vessels leading to haemorrhage and other visible damage).[310] In this regard, the term 'traumatic' was used in contradistinction to the injury caused to the respondent's brain by a lack of oxygen (perinatal asphyxia), namely hypoxic ischaemic encephalopathy.
6. Without attempting to be exhaustive, for example, in relation to the witnesses called by the respondent:

(a)` Dr Nguyen described the injuries in the Day 7 MRI, in her initial report as a 'traumatic brain injury' (see [52] above). Indeed, the appellant's counsel put to Dr Nguyen that the presence of extra-axial blood in the cerebellum 'makes it most likely traumatic[311] origin';311

(b) Dr Keenan was of the opinion that the respondent had suffered both a hypoxic ischaemic insult (i.e. from perinatal asphyxia) and a traumatic brain injury (see [82] and [87] above). In that context, Dr Keenan referred to the latter (traumatic brain injury) in the sense of the direct physical effects of the instrumental birth (i.e. apart from the asphyxia). He gave as an example of traumatic brain injury 'say in a car[312]cident or something'.312 The 'giveaway for trau[313] was the haemorrhage.313 Again, in answer to the appellant's counsel, Dr Keenan described the traumatic brain injury as [314]shing it, basically';314

(c) Dr Tracy, whose evidence was principally focussed upon the respondent's HIE, also identified the respondent as having suffered a concurrent traumatic injury.[315] Indeed, it was the appellant's counsel that specifically put to Dr Tracy (which he accepted) that the presence of blood in the MRI scans was 'traumatic in origin';[316] and

(d) the appellant's counsel also put to Dr Pestell (which she accepted) that the presence of blood in the MRI scans was 'traumatic in origin'.[317]

1. As these references reveal, far from suggesting (as it now submits) that 'there is no basis for the finding that [the respondent] suffered traumatic brain injuries', it was the appellant's case at trial that the injuries revealed on the MRI scans were traumatic brain injuries; that is physical injuries caused by the traumatic birth (producing haemorrhage) as opposed to HIE (i.e. a condition caused by asphyxia or lack of oxygen).
2. That this was the appellant's case at trial is clear from the evidence of the appellant's own witnesses:

(a) the tenor of Professor Ditchfield's evidence generally was that the injuries revealed by the MRI scans were 'most likely traumatic in origin' (see [136], [140] and [151] above). The purport of his evidence was that the injuries were traumatic and not ischaemic (i.e. from lack of oxygen). Indeed, in his initial reports Professor Ditchfield did not accept that there was any evidence of hypoxic injury. It was not until Professor Ditchfield's final report that he accepted, based on the Day 1 Ultrasound that there was 'a pattern of a prolonged partial hypoxic-ischaemic episode' (see [148] above);

(b) Professor Hunt had a different view as to the process of injury causing the injuries shown on the Day 7 MRI, which he thought was most likely related to dissection of the vertebral artery (see [161] above). That process was nevertheless described by Professor Hunt as resulting from his 'traumatic delivery' (see [169] above); and

(c) Dr Do was specifically asked to assume that the lesion to the right cerebellar tonsil apparent on the MRI scans (which she was asked to assume was the only injury), was 'traumatic in origin' (see [181] above).

1. In our view it is clear that, not only was the learned trial judge correct to find that the respondent had suffered a traumatic brain injury, the fact that he had suffered such an injury was not a matter seriously in contest at trial. Indeed, inasmuch as the appellant ran its case on the basis that the respondent had suffered only mild hypoxic ischaemic encephalopathy, identification of the respondent's injuries as 'traumatic' in nature was central to the appellant's case that they were not hypoxic.
2. That finding was open to the learned trial judge on all of the evidence and indeed, was clearly correct. Moreover, there was no practical injustice to the appellant in the learned trial judge's finding - to the contrary, the finding reflected an element of the appellant's case. The learned trial judge's reference to the definition of 'traumatic' in Mosby's Medical Dictionary was of no moment in the circumstances - it was not material. There was no denial of natural justice as a result of his Honour having referred to it.
3. As it was, the learned trial judge expressly found that the respondent suffered both a traumatic brain injury and stage 2 hypoxic ischaemic encephalopathy, a finding addressed in the context of later grounds of appeal.[318]
4. Ground 3 is not made out.

Ground 4 - The findings as to the extent of the haemorrhagic contusion to the cerebellum

1. Ground 4 contends that the learned trial judge erred in law and fact by not making a finding as to whether the haemorrhagic contusion to the right cerebellar tonsil extended into adjacent structures, including the flocculus, vermis, left cerebellar tonsil and adjacent cerebellar hemisphere.
2. In this context, the appellant is, of course, referring to the areas of disagreement between the radiological experts as to the extent of the changes to the respondent's cerebellum visible on the MRI scans. More specifically, it is a reference to the learned trial judge's finding that it was 'quite possible' that the haemorrhagic contusion to the area of the right cerebellar tonsil extended beyond the right cerebellar tonsil into those adjacent structures.[319]
3. The appellant contends, in effect, that his Honour erred by not making a definitive finding (i.e. beyond 'possibility') as to whether the damage apparent on the MRI extended to those adjacent structures.[320]
4. In our view, it was open to the learned trial judge to make a finding as to whether the MRI scans revealed damage extending to the adjacent structures. Moreover, in our view, it would have been better for his Honour to have found which competing legitimate interpretation of the MRI scans was to be preferred. Nevertheless, for the reasons below, the failure to make such a finding does not give rise to an appellable error of fact or law in the present case.

1. As discussed above (see [311]), there were at least two different possible mechanisms supported by the expert evidence, as to how, or in what way, the injuries to the respondent's brain went beyond the right cerebellar tonsil in such a way as to cause the respondent's Developmental and Cognitive Impairments. So long as the learned trial judge was satisfied, on the balance of probabilities, that one or more of those mechanisms had in fact come to pass, it was not necessary (on the facts of the present case) for his Honour to make a definite finding as to which one of them had done so.
2. This is particularly so, given that the respondent's case was that his Developmental and Cognitive Impairments arose from a combination of traumatic brain injury and hypoxic ischaemic encephalopathy.
3. It is in this way that, in our view, ground 4 misses the mark. The ground of appeal proceeds upon the assumption that the only way in which the respondent's Developmental and Cognitive Impairments could have been caused by his birth process was if they extended into the adjacent structures in the cerebellum.
4. That is, the appellant's case, in this regard, focusses entirely on the disagreement between the radiological experts as to the extent of the changes to the respondent's cerebellum visible on the MRI scans. Put another way, it proceeds upon the basis that if the learned trial judge accepted Professor Ditchfield's evidence that the MRI scans did not show any injury beyond the right cerebellar tonsil, the respondent's case was therefore bound to fail.
5. This assumption, with respect, takes too narrow a view of the respondent's case at trial and too narrow a view of the Primary reasons. The respondent's case was not confined to an allegation that the injuries that were visible on the MRI scans, and those injuries alone, were what caused the respondent's Developmental and Cognitive Impairments. Neither the respondent's pleading[321] nor the manner in which he put his case at trial so confined the respondent's case.
6. On the contrary, the witnesses called by the respondent emphasised the combined effect of all of the investigations (including MRI and ultrasound) and the entirety of the clinical picture, including the respondent's clinically diagnosed hypoxic ischaemic encephalopathy. Indeed, insofar as the expert evidence called by the respondent accepted that the damage evident on the MRI was 'traumatic' (in the sense discussed at [354] above) their opinions in relation to the effect of the respondent's HIE were unaffected by the disagreement as to what was visible on the MRI scans.
7. Indeed, every expert witness (including the witnesses called by the appellant), confirmed, in essence, that a 'normal MRI does not necessarily equal a normal brain'.[322]
8. Accordingly, it might have been open to find, on the balance of probabilities, that the respondent's Developmental and Cognitive Impairments were caused by his traumatic birth based on the clinical symptoms and diagnosis of HIE alone (i.e. even if he had a completely normal MRI). That was certainly the view of Dr Tracy, who based his conclusions on the clinical presentation of stage 2 HIE rather than the MRI scans.[323]
9. Of course, the prospect of such a finding did not arise in the present case because, on any view, the respondent did not have a 'normal MRI'. The presence of abnormalities evident on the MRI (whether expressed as probabilities or possibilities) were therefore simply further strands in the overall circumstantial case, to be assessed together with all of the other circumstances.
10. The fact, emphasised by the appellant on appeal, that in opening and closing submissions to the learned trial judge the respondent invited his Honour to make a positive finding - based on Dr Keenan's evidence - that the contusion to the cerebellum extended beyond the right cerebellar tonsil, did not mean that the respondent's case depended on such a finding being made. It was open to the learned trial judge to consider the cumulative force of the evidence as a whole in the manner that he did and, in doing so, to draw the conclusion that he did as to the competing expert opinions.

1. At the hearing of the appeal, while the appellant placed a great deal of emphasis on Professor Ditchfield's evidence as to what he could, or could not, see on the MRI, it ultimately accepted that Professor Ditchfield was not saying 'because it's not there, it could never be there'.[324] That acceptance was consistent with Professor Ditchfield's evidence at trial.[325]
2. Professor Ditchfield's evidence, therefore, did not preclude a finding of causation on the balance of probabilities. Indeed, the manner in which Professor Ditchfield's reports and his evidence developed over time were revealing as to what conclusions could be drawn from the MRI evidence alone.
3. Professor Ditchfield's first report was quite categorical: 'In this case, these structures are normal and there is therefore no MRI evidence of a hypoxic ischaemic injury'.[326] While the opinion quite properly refers to 'no MRI evidence' there is no suggestion in the report that there could be any other basis for diagnosing a hypoxic ischaemic injury.
4. The same is true of Professor Ditchfield's second and third reports, which confine themselves to reference to the MRI scans.[327]
5. Professor Ditchfield's fourth report, having received Dr Keenan's report, also in no way accepted that the respondent had suffered a hypoxic ischaemic injury, referring to Dr Keenan's view as 'speculative'. Perhaps surprisingly in this context, Professor Ditchfield noted that he had not seen the Day 1 Ultrasound but offered comment as to how it might be interpreted in any event.[328]
6. It was not until he received the Day 1 Ultrasound that, in his final report, Professor Ditchfield recognised that the respondent had experienced a 'prolonged partial hypoxic episode'.[329]
7. Even then, Professor Ditchfield proffered the opinion that the hypoxic insult occurred at least 24 hours prior to delivery. In this way, while he ultimately accepted that there had been a hypoxic ischaemic insult, Professor Ditchfield suggested that it was unrelated to the respondent's birth.[330] No other expert suggested the possibility of a hypoxic event (asphyxia) 24 hours prior to delivery.[331]
8. Contrary to Professor Ditchfield's opinion in this regard, the learned trial judge expressly rejected the proposition that the respondent had suffered a hypoxic event in the 24 hours proceeding his birth. His Honour found on balance that he had not.[332] The appellant does not challenge that finding.
9. Accordingly, in assessing the combined effect of all of the circumstances, including the clinical and ultrasound evidence of hypoxic ischaemic encephalopathy, it is significant that the learned trial judge had rejected Professor Ditchfield's evidence as to the cause of the respondent's HIE.

Finding as to extent of haemorrhagic contusion was not indispensable

1. Given that conclusion, the only circumstance in which the learned trial judge would have been required to make a definitive finding, as between Professor Ditchfield and Dr Keenan, in relation to the interpretation of the MRI scans, would have been if a finding that Professor Ditchfield was correct would have prevented the learned trial judge from drawing an inference of causation based on all of the circumstances. Conversely, that could only have been the case if acceptance of the evidence of Dr Keenan that the damage to the right cerebellar tonsil extended into adjacent structures of the cerebellum was indispensable to a finding of causation.
2. For the reasons set out above, a finding of such damage was not an essential or indispensable link in the chain of reasoning towards an inference of causation. Rather, it was sufficient that the possible involvement of the adjacent structures (in addition to the other possible mechanisms to explain a broader brain injury) was one of the many strands in the cable. Another was that the respondent had suffered a global microscopic brain injury as a result of his HIE.
3. All of the authorities relied upon by the appellant in relation to this ground were authorities dealing with the duty of a trial judge to give adequate reasons for his or her decision, including in relation to the resolution of disputes between expert witnesses.[333] As those authorities make clear, where a trial judge prefers the evidence of one expert over another, he or she should give adequate reasons for that preference, even if it is simply that the judge, having seen and heard the witnesses, considered one more authoritative than the other.
4. The appellant's complaint on this ground, of course, was somewhat different. The appellant does not complain that the learned trial judge did not give adequate reasons for preferring one expert (Dr Keenan) over the other (Professor Ditchfield). Rather, it complains that his Honour did not make a finding as to which evidence he preferred, when his Honour was required to do so.
5. In that regard, as the Victorian Court of Appeal said in Fletcher Construction v Lines Macfarlane & Marshall:[334]

The duty to deal with facts or evidence is not absolute. The evidence must be significant in the sense that, unless disposed of, it stands in the way of the Court's conclusions. The Court need not deal in terms with evidence when its importance falls away because of the manner in which the Court disposes of the case. Nevertheless, if evidence is significant, it is not to be peremptorily shunted aside or ignored.

1. It could hardly be suggested, in our respectful view, that the learned trial judge in the present case 'peremptorily shunted aside or ignored' any evidence. His Honour comprehensively considered all of the relevant evidence, including the expert evidence. Moreover, the Primary reasons, as a whole, adequately discharged the learned trial judge's obligation to disclose the intellectual process that led to his conclusion that the respondent's Developmental and Cognitive Impairments are more likely than not to be sequelae of his birth, which in turn were caused by the appellant's fault.
2. Further, the extent of the haemorrhagic contusion in the right cerebellum shown on the MRI scans was not an issue that, unless disposed of, stood in the way of the learned trial judge's ultimate finding that factual causation was established. For the reasons explained above, given the manner in which his Honour determined the case at trial, he was not required to reach a final conclusion, on the balance of probabilities, as to whether the structures adjacent to the right cerebellar tonsil were damaged. It was sufficient that the possible involvement of the adjacent structures was one of the many strands in the cable of the circumstantial case. The manner in which his Honour reached his conclusion as to causation did not require that he make a finding, on the balance of probabilities, as to whether the structures adjacent to the right cerebellar tonsil were actually damaged.

Whether there was a rational basis for preferring one view over the other

1. Nevertheless, in a contest between witnesses, such as that between Dr Keenan and Professor Ditchfield as to the interpretation of the MRI scans, it might reasonably have been expected that the learned trial judge would reach a finding in relation to whose evidence he preferred. It would have been preferable for his Honour to have done so. In a case such as the present, such a finding would have the potential, at least, to be relevant to an appeal (depending upon the conclusions that might be reached by an appeal court in relation to other findings of fact).
2. In this context, in our respectful view, his Honour discounted (or at least undervalued) his own advantage as the trial judge by his conclusion that there was no 'rational basis in the evidence before me to be able to prefer the evidence of one over the other'.[335]
3. The learned trial judge had the advantage of seeing and hearing the witnesses give their evidence. His Honour's own impression of the way in which they gave their evidence, together with the consistency of that evidence with other evidence, were all rational bases by which his Honour could arrive at a preference for one expert over another. Other bases existed, including those advanced by the appellant.[336]
4. It is also notable that there were other aspects in which his Honour preferred Dr Keenan's (and other experts') opinions over that of Professor Ditchfield. We have, for example, referred to the learned trial judge's rejection of Professor Ditchfield's opinion, once he had accepted that the respondent suffered a hypoxic ischaemic insult, that the insult occurred at least 24 hours prior to the respondent's birth (see [377] to [384] above). The rejection of Professor Ditchfield's opinion in this regard would itself have provided a rational basis for preferring Dr Keenan's evidence more generally.
5. Sometimes, of course, resolving differences in expert evidence will pose particular difficulties. In the present case, as the learned trial judge remarked, it may have been preferable, when particular disputed features of the MRI were being identified, for both experts to be present. Nevertheless, a trial judge's task is 'to endeavour to reconcile and grapple with the competing views as best' as he or she can in the circumstances.[337] In so doing a trial judge should not be timorous in using his or her full advantage in seeing and hearing the expert witnesses to resolve their competing views where there is no other way of doing so. Not only must an appeal court give respect to the advantage of the trial judge; the effective discharge of the appeal court's function will often depend upon it.

The learned trial judge's approach in this case

1. Thus, in the abstract, there were rational bases upon which the learned trial judge could have arrived at a preference for the opinion of one of these witnesses over the opinion of the other. However, the learned trial judge was not speaking in the abstract. His Honour was speaking by reference to the evidence and, understood in context, by reference to his evaluation of the competing evidence in the case as a whole. His Honour should be taken to have meant that, having seen and heard the witnesses giving their evidence, he did not find a basis, satisfactory to his mind, to resolve the conflict as to the interpretations of the MRI. That is, his Honour was not persuaded that one interpretation could be said to be wrong and the other right; both interpretations were reasonable and legitimate.
2. In finding that it was quite possible that the contusion to the right cerebellar tonsil extended beyond that tonsil into the adjacent structures,[338] the learned trial judge found, in effect, that Dr Keenan's interpretation of the MRIs to that effect was reasonable and legitimate. It was also implicit in this finding that Professor Ditchfield's interpretation of the Day 7 MRI, while also reasonable and legitimate, did not exclude the presence of those abnormalities as an available hypothesis.
3. Moreover, in the final analysis the learned trial judge essentially followed the same path of reasoning, and drew the same inference, as that drawn by Dr Keenan and Dr Tracy. In that regard, like those witnesses, his Honour considered all of the known facts and circumstances and was persuaded that their combined force sustained an inference of factual causation of the respondent's Cognitive and Developmental Impairments.
4. Therefore, in the permissible manner in which the learned trial judge resolved the case, it was not necessary for his Honour to reach a final conclusion as to which of the competing reasonable and legitimate interpretations of the Day 7 MRI (that it did and did not show damage to the structures adjacent to the right cerebellar tonsil) were to be preferred. While the learned trial judge did not expressly say that it was not necessary to reach a conclusion on that question, his Honour evidently considered it unnecessary, as he proceeded to determine the case without coming to a view on the balance of probabilities as to that question. While it would have been conducive to clarity, and distinctly preferable, for the learned trial judge to have expressly said that it was unnecessary (and to explain why), it was not an appellable error for his Honour not to have done so.

1. Moreover, given the way the learned trial judge resolved the causation question - and as explained below, on our view of that question - even if his Honour had, as the appellant insists was necessary, made a finding as to the conflict of interpretation of the MRIs, and found in favour of Professor Ditchfield, the conclusion on the ultimate causation question would have been the same.
2. First, a preference for Professor Ditchfield's interpretation of the MRIs would not detract from the learned trial judge's finding that Dr Keenan's interpretation was reasonable and legitimate and that, consequently, it was quite possible that the contusions extended beyond the right cerebellar tonsil into the adjacent structures. It was that finding of primary fact which fed into his Honour's final evaluation of whether, on the balance of probabilities, the respondent's Developmental and Cognitive Impairments were caused by the appellant's breaches of duty.
3. Secondly, in our view, even if it were found, as a matter of certainty, that Dr Keenan's interpretation of the MRIs was correct and that the contusion did not extend beyond the right cerebellar tonsil, given our rejection of the other grounds of appeal, in all the circumstances the proper inference would be that causation was established.
4. The learned trial judge's findings with which, as explained elsewhere in these reasons, we would not interfere, include the following:

(a) in the course of the birth process, the respondent's brain suffered prenatal asphyxia, HIE and injuries in the form of a contusion in the right cerebellar tonsil, a multi‑compartment haemorrhage comprising intraventricular haemorrhage, subarachnoid haemorrhage and subdural haemorrhage, and a subgaleal haematoma [709];

(c) medical science does not deny a connection between stage 2 HIE and impairments of the kind suffered by the respondent. Studies suggest that 50% of those with stage 2 HIE will later suffer from neurological and developmental issues [894];

(d) Professor Ditchfield expressed the view that cognitive and linguistic difficulties of the kind suffered by the respondent were consistent with his having suffered a hypoxic insult and a clinical assessment of stage 2 HIE [868];

(e) all experts agreed that the fact that MRIs show no abnormalities does not mean that no abnormality exists [640]‑[642]; [863]‑[870];

(f) Dr Keenan had substantial experience of children with cognitive and developmental issues of the nature and extent broadly similar to the respondent who showed no damage on MRI, but who showed global microscopic injury to the brain on more sophisticated imaging [871]-[880];

(g) it was quite possible - in the sense of a plausible hypothesis - that the respondent suffered a global microscopic injury to his brain, caused or contributed to by the HIE [880];

(h) from a neuropsychological perspective, the pattern and nature of the respondent's developmental and cognitive impairments are consistent with brain injury of a traumatic nature, as opposed to being of a congenital nature, and are consistent with his having suffered serious damage to his brain soon after birth [911], [913];

(i) there is no evidence to support the appellant's contention that the respondent's developmental and cognitive impairments may simply reflect that he is an ordinary child at the lower end of the developmental spectrum [924]-[925];

(j) there is no other plausible alternative inference as to the cause of the respondent's Developmental and Cognitive Impairments [926].

1. In our view, the combined force of these findings sustains satisfaction, on the balance of probabilities, that but for the problems in the birth process arising from the appellant's negligence, the respondent would not have his Developmental and Cognitive Impairments. We would draw that inference on the facts found by the learned trial judge that have not been successfully appealed (even making the assumption in [403] above).
2. Ground 4 is not made out.

Ground 5 - The possibility arising from the 2014 and 2015 MRI scans

1. Ground 5 contends that the learned trial judge erred in law in finding that 'it is quite possible' that the 2014 and 2015 MRI scans showed damage to the plaintiff's brain that extended beyond the right cerebellar tonsil to the adjacent structures of the cerebellum, which damage was caused by a breach of duty by the appellant and that this possibility of damage was sufficient to prove a causal link between breach and the respondent's Developmental and Cognitive Impairments.
2. Ground 5 alleges an error of law. It is, in essence, the same error alleged in grounds 1 and 2 but more specifically directed to the extent of the injury as revealed on the 2014 MRI and the 2015 MRI. The relevant finding of his Honour as to that 'possibility' is set out at [220] and [221] above.
3. The appellant's submissions as to the error include the following:[339]
   1. The reasoning in respect of the 2014 and 2015 MRI scans appears to be as follows. First, 'it is quite possible' that the 2014 and 2015 MRI scans show damage beyond the right cerebellar tonsil; [857]. Second, such damage is capable of causing neurological and developmental impairments, including the plaintiff's Developmental and Cognitive Impairments; [857], [862], [936]. Third, this possibility of this capability is relevant to inferring that the plaintiff's Birth Injuries caused his Developmental and Cognitive Impairments; [936].
   2. The logic is; it is possible that X exists. X is capable of causing Y. Y exists. Therefore, X caused Y.
4. We reject ground 5, essentially for the reasons we have given in the relation to grounds of appeal 2 and 4.
5. As for the logic attributed to the learned trial judge by the appellant, again, in our view the appellant's submissions do not fairly represent the learned trial judge's reasoning. His Honour did not reason from the possibility of injury to the cerebellum beyond the right tonsil (as revealed by the 2014 MRI and the 2015 MRI) that those possible injuries therefore caused the respondent's Developmental and Cognitive Impairments.
6. As in the case of ground 2, the appellant's submission suffers from a piecemeal analysis of the evidence, which is to be contrasted with the approach (taken by the learned trial judge) of arriving at an inference based on 'the united force of all of the evidence together'.[340]
7. Indeed, we would also note that there is a significant difference between the reasoning and logic posited at [88] of the appellant's submissions and the short-form logic posited at [89] of those submissions (reproduced at [409] above). Unlike the conclusion at [89] ('Therefore X caused Y'), [88] of the appellant's submissions suggests a more modest conclusion (namely that the possibility of further damage 'is relevant to inferring that the [respondent's] Birth Injuries caused his Developmental and Cognitive Impairments').
8. This last proposition (namely that the possibility of more extensive damage capable of causing neurological and developmental impairments is 'relevant to inferring' causation) is, as a step in the reasoning process, entirely consistent with the authorities discussed above (see especially at [279] above).
9. Of course, such a possibility, on its own, would not be a sufficient basis to draw an inference of causation. Nevertheless it is admissible [i.e. relevant] and 'must be weighed in the balance with other factors, when determining whether or not, on the balance of probabilities, an inference of causation in a specific case could or should be drawn'.[341]
10. Ground 5 is not made out.

Ground 6 - The possibility of a global microscopic brain injury

1. Ground 6 contends that the learned trial judge erred in law in finding that it was 'quite possible' that the plaintiff sustained a global microscopic brain injury caused by a breach of duty of the appellant.
2. The ground, again, alleges an error of law. Insofar as it alleges an error of law, the error is said to be the same erroneous reasoning the appellant described in its submissions in support of ground 5. Indeed paragraphs [96] and [97] of the appellant's submissions are essentially identical to paragraphs [88] and [89] (reproduced at [409] above) save that the reference to 'damage beyond the right cerebellar' is replaced with reference to 'global microscopic brain injury'.
3. Our conclusions in relation to those submissions are the same as set out in relation to ground 5. Indeed, there is a certain irony in the appellant's submission that the learned trial judge made precisely the same error in relation to two separate potential mechanisms of injury - namely in reasoning 'it is possible that X exists. X is capable of causing Y. Y exists. Therefore, X caused Y.'
4. The repetition of that submission in relation to both 'damage beyond the right cerebellar tonsil' and 'a global microscopic brain injury' (i.e. each of them is X), rather demonstrates that his Honour did not follow that logic in relation to either of them. It points up the piecemeal reading of the Primary reasons, which is not justified by those reasons as a whole.
5. While ground 6, strictly, only alleges an error of law, the appellant also developed submissions to the effect that the finding of fact (as to the possibility that the respondent suffered a global microscopic injury) was not open on the evidence as a matter of fact.[342]
6. In this regard, the appellant submitted that the finding was based solely on the evidence of Dr Keenan. Assuming, for present purposes, that to be the case, that does not necessarily reveal error on the part of the learned trial judge. His Honour was entitled to accept Dr Keenan's evidence in preference to Professor Ditchfield in that regard. And that is indeed, what his Honour did in the finding set out at [226] above.
7. His Honour did not, as the appellant submitted, ignore Professor Ditchfield's evidence. Indeed, his Honour referred to Professor Ditchfield's evidence, and concluded that Dr Keenan's clinical experience was different to Professor Ditchfield's in this regard and that Dr Keenan 'had regularly seen instances in which a child with a clinical syndrome similar to [the respondent] had shown global microscopic brain injury on more sophisticated imaging than that carried out in this case'.
8. Significantly, in this context, Dr Keenan's evidence was not that he could visualise a global microscopic injury on the MRI scans. His evidence was that it could not be observed on any of the scans.[343] The issue was, therefore, not one of radiological interpretation, as implied by the appellant's submission that 'the opinion of all of Ditchfield, Hunt, Nguyen, Shipman and Mason was the MRI scans did not show it'.[344]
9. On the contrary, Dr Keenan's evidence on this issue was based on the 'the setting of the clinical syndrome and with a grossly abnormal ultrasound' and 'many years of experience where we have very good evidence that in fact there has been neurologic deficits which we can't see'.[345]
10. This points to another aspect of the evidence as to the possibility of a global microscopic injury. It was not, as the appellant submits, solely based on the evidence of Dr Keenan. In that regard, as the learned trial judge expressly said, it served as an explanation for the evidence given by all of the expert witnesses (see [372] above) that not all injury to the brain will show up on [346] imaging.346 His Honour also referred to other explanations, such as damage to pathways in the brain that do not show up as struct[347]l damage.347
11. This is the context in which the finding as to the potential for a global microscopic injury is to be understood: the context of the entirety of the evidence and circumstances that are relevant to an inference as to the issue as to causation.
12. The learned trial judge was not in error in making that finding.
13. Ground 6 is not made out.

Ground 7 - The relevance of the severity of the respondent's HIE

1. Ground 7 alleges that the learned trial judge erred in law by not addressing an issue which had to be addressed in order to determine the case; namely that classification of the respondent as suffering from moderate or stage 2 hypoxic ischaemic encephalopathy was irrelevant to determining whether any of the respondent's Developmental and Cognitive Impairments were caused by any breach of duty by the appellant.
2. The 'staging' or degree of the respondent's hypoxic ischaemic encephalopathy was a matter that received much attention at trial. As the expression suggests, the 'staging' of HIE is a clinical determination of the severity of HIE. It is based on clinical criteria to designate HIE as mild (stage 1), moderate (stage 2) or severe (stage 3).
3. The learned trial judge reproduced the following extract from the criteria applicable at PMH:[348]

The PMH Cooling Guideline states that the 'presence of moderate/ severe HIE according to the modified Sarnat Classification is defined as seizures OR presence of signs in at least three of the six categories given below', being a reference to this table:

1. Apart from any relevance it may have for the legal question of causation (the issue raised by this ground), the staging of HIE has direct relevance in the treatment of patients - indeed, the purpose of the staging is for treatment and prognostication. The staging of HIE determines, for example, whether a child is enrolled in therapeutic cooling (see [39] above). Only a child with the presence of moderate or severe (stage 2 or 3) is 'cooled'.
2. The respondent specifically pleaded that one of the injuries he sustained was 'stage 2 hypoxic ischaemic encephalopathy'.[349] The appellant did not admit that plea. [350]
3. Prior to trial the parties exchanged expert reports as to whether the respondent had suffered only mild (stage 1) or moderate (stage 2) hypoxic ischaemic encephalopathy. Being a clinically determined condition, the focus of the evidence in this regard was contained in the reports of the neonatal physicians, Dr Tracy,[351] Professor Hunt[352] and Dr Rao.[353] The degree (or severity) of the respondent's HIE was a matter of apparent significance to Professor Hunt's overall opinion (he being of the opinion that the respondent suffered only mild (or stage 1) HIE):[354]

His clinical course was consistent with mild hypoxic ischaemic encephalopathy, which it itself confers a normal neurodevelopmental prognosis.

1. Notwithstanding the appellant's complaint that the respondent's written opening submission was 'hopelessly incomplete',[355] the submissions filed by the parties prior to trial both identified the presence, or otherwise, of stage 2 hypoxic ischaemic encephalopathy as a relevant issue.[356]
2. As the above summary of the evidence at trial reveals, the 'staging' of the respondent's HIE was also the subject of a good deal of evidence at trial.[357]
3. Notwithstanding all of this, the appellant submits, as it did in closing at trial,[358] that the clinical ascription of stage 2 HIE was 'irrelevant and meaningless'.[359] We should emphasise, in this regard, that ground 7 alleges an error of law: that is, it does not simply submit that the learned trial judge gave undue weight to the evidence as to the severity of the respondent's HIE. Rather, it submits that it was 'irrelevant' and ought to have been disregarded entirely.
4. The ground is based on the evidence of Professor Hunt. The appellant submitted that: 'Hunt gave evidence explaining why the staging system for HIE is irrelevant; ts 1398-1400'.[360] The appellant also relied on ts 1402.[361]
5. Professor Hunt did not give evidence that the staging system for HIE was irrelevant, either in the transcript pages identified in this submission, or otherwise. The evidence identified in the submissions is referred to in [170] to [171] above. That evidence does not suggest that the staging is irrelevant. Indeed, the evidence referred to in [171] above specifically recognises that it is used by clinicians to counsel parents as to the possible future outcomes for their babies.
6. Of course, as noted at [256] to [260] above, those prognostic uses of the staging of HIE cannot, and do not, determine the answer to the cause of a plaintiff's condition in a particular case. But they are not thereby irrelevant. This was expressly recognised by [362] learned trial judge:362

The research to the effect that 50% or so of children with stage 2 HIE will go on to suffer from neurological and developmental issues is obviously not a sufficient basis for a finding that Cooper is in this 50%, and not in the other 50% or so of children who have a normal outcome. However, it is a basis for a finding that it is quite possible that the fact that Cooper sustained stage 2 HIE caused or materially contributed to Cooper's Developmental and Cognitive Impairments.

1. At the hearing of the appeal, when asked to identify any other evidence relied upon for the purposes of ground 7, the appellant referred to the following evidence from Professor Hunt:[363]

Well, to start with, the only therapy that's been shown to have any consistent significant benefit in the context of clinical hypoxic ischemic encephalopathy has been therapeutic hypothermia. ... People have moved away from - whilst the Sarnat staging system or a modification thereof has been useful in the enrolment of patients, it hasn't really been examined closely as an outcome so much as an enrolment mechanism. And so what the studies of cooling show us is that cooling is beneficial for children with moderate to severe HIE both in terms of reducing mortality and improving neurodevelopmental outcome. I can't give you the figures immediately for - for changes to the staging system. It hasn't really been employed as an outcome measure so much as an enrolment criteria.

1. This evidence formed part of an answer concerning the effect of the practice of 'cooling' on the prognostic value of staging. It was not, with respect, evidence that the staging of the respondent's HIE was irrelevant to whether an inference of causation should be drawn in the present case. It simply identified that the principal use of the staging of HIE, clinically, is as an enrolment criteria and that, as an outcome measure, it hasn't been examined as closely. It certainly does not discount the relevance of the staging as a prognostic indicator.
2. In our view, Professor Hunt did not give evidence that the staging of the respondent's HIE was irrelevant to the issues in the trial. Certainly no proposition to that effect was put to any of the witnesses called by the respondent. Indeed, the tenor of Professor Hunt's evidence as a whole revealed that he regarded the staging as relevant to the question of causation in the present case, as he accepted in cross-examination:[364]

There is no question that Cooper did have evidence of an asphyxial insult but in my opinion this was mild. Stage 1 encephalopathy is associated with a normal neurodevelopmental outcome in more than 90 per cent of cases.

?---That's right.

... Just - just to complete that, whatever else you took into account in expressing your conclusion on the consequences of whatever injury he sustained, it was your expert evidence set out in your reports that the classification of his HIE as stage 1 or stage 2 was central to the opinions you expressed, is that - would you agree with that?---That was important, yes.

Ground 8 - The finding as to the severity of the respondent's HIE

1. Ground 8 alleges, in the alternative to ground 7, that if it was relevant to find whether the respondent suffered at any time from stage 2 HIE, the learned trial judge erred in fact in so finding.
2. While the appellant's submissions were that the finding of fact was against the weight of the evidence, those submissions also made passing reference to the adequacy of the learned trial judge's reasons.
3. The appellant submitted, for example, that 'The totality of his Honour's reasoning is at [707]'.[365] That paragraph reads:

The defendant did not challenge Dr Rao's experience. Dr Tracy described the treating team at PMH as being very experienced, noting that they were the largest neonatal team in Australia, and said that he would accept their judgment. For the reasons set out above, so do I.

1. The submission that this paragraph represented 'the totality of his Honour's reasoning' is, with respect, remarkably unfair to the learned trial judge.
2. On the contrary, those parts of the Primary reasons dealing with the determination of the level of the respondent's HIE included:

(a) a discussion and findings in relation to the assessment by the PMH clinical team;[366] and

(b) a detailed response to the matters raised by the appellant in support of its position that 'that Dr Rao over-diagnosed [the respondent] and that he is correctly diagnosed as only having stage 1 HIE'.[367]

1. As to the latter, the learned trial judge identified seven bases for the appellant's position. His Honour then dealt with each of them in detail. In doing so, his Honour dealt with all of the evidence now identified by the appellant in support of the proposition that his Honour's finding was against the weight of the evidence. The seven matters relied upon by the appellant were as follows.
2. First, the appellant relied upon Professor Hunt's evidence that the Sarnat stage 2 criteria required that the respondent suffer from seizures. His Honour referred to the conflicting evidence in this regard, including the various entries in the PMH records. His Honour continued:[368]

Dr Rao also observed that Cooper's EEG studies took place after he had been administered phenobarbitone. He explained that once you have given phenobarbitone, the seizures would have disappeared as the baby had been treated for them. Professor Hunt also commented that the fact that Cooper was on phenobarbitone at the time of the EEG 'may have supressed the EEG background'. He also comments that this EEG 'suggests mild to moderate encephalopathy within 24 hours of delivery'. Dr Keenan was of a similar opinion.

Dr Tracy opined that it is highly likely that seizures occurred given the clinical suspicion and treatment of cooling and phenobarbitone.

As I have found, there was sufficient confidence in the clinical judgment of seizures for Cooper to be treated for them with phenobarbitone and referred for a neurological review.

1. In this context, the appellant placed a great deal of emphasis on the fact that some of the medical notes refer to 'suspected seizures',[369] although there are other references to 'likely seizures'[370] and 'had seizures initially'.[371] The appellant sought to characterise the use of 'suspected' to suggest insufficiency or absence of evidence. It went so far as to characterise the treating doctors' identification of likely seizures as a 'guess'.[372]
2. That is not how the learned trial judge understood the evidence in this regard. Nor is it how we would understand that evidence. 'Suspicion' was not used in this context to mean (as a lawyer might), 'a preliminary hypothesis which must await further evidence'. Rather, 'suspicion' in this context referred to the clinical determination of the presence of a symptom, without direct observation, the existence of which was necessary for the implementation of a particular treatment. In other words, 'suspected seizures' meant 'inferred seizures'. In the present case, for example, the presence of seizures was the condition for the administration of phenobarbitone (which carries a number of side effects and is not given prophylactically).[373] Phenobarbitone, was of course, administered to the respondent in the present case, causing the neonatal registrar to report 'none [i.e. seizures] since D[ay] 3'.[374]
3. Secondly, the learned trial judge addressed Professor Hunt's evidence that 'jitteriness' was not consistent with a diagnosis of stage 2 HIE. His Honour, having referred to the evidence in this regard, concluded (in a passage not the subject of challenge):[375]

Dr Rao gave evidence as to how the difference between jitteriness and seizures is clinically determined. Jitteriness will relax if the baby is held, even firmly, whereas seizures continue. Dr Tracy gave evidence in the same terms. Professor Hunt accepted that Dr Rao would know how to distinguish between seizures and jitteriness. I infer that the clinicians at PMH, supervised by Dr Rao, were likewise competent. So I do not consider that this reason undermines Dr Rao's diagnosis.

1. Thirdly, the learned trial judge referred to Professor Hunt's evidence that phenobarbitone may have been administered prophylactically. In this context, Professor Hunt referred to 'trial evidence in the literature' and that 'phenobarbitone may actually have some neuroprotective role' and that 'there's a lot of clinical practice that goes on in this space'.[376] The learned trial judge rejected this as undermining Dr Rao's diagnosis. His Honour did so based on facts applicable to PMH in 2009. Whatever the practice may have been elsewhere, his Honour accepted the evidence of Dr Rao that 'at PMH in 2009 it was not the practice to administer phenobarbitone prophylactically'.[377]
2. The fourth matter dealt with by the learned trial judge was Professor Hunt's evidence that there was a tendency to 'over-cool' and referred to studies in that regard. Dr Rao displayed familiarity with those studies when cross-examined and, indeed, had published himself in relation to the issue of cooling babies who did not meet the criteria for stage 2 HIE.[378] Nevertheless, his evidence, which the learned trial judge accepted, was that in the present case the guidelines were applied to reach a diagnosis of stage 2 HIE.[379]
3. The fifth matter dealt with by the learned trial judge was Professor Hunt's evidence that there was no sentinel hypoxic event occurring immediately before or during labour.[380] In this regard, his Honour referred to his previous findings (that are not in dispute) that the respondent suffered serious perinatal asphyxia.[381]
4. Next, the learned trial judge dealt with the early imaging. It is sufficient to set out his Honour's conclusions in that regard (which are not the subject of challenge):[382]

The sixth reason advanced by Professor Hunt is that there is no early imaging evidence of acute cerebral abnormality. However, he did accept that the fact that Cooper had been placed on ventilator support for more than 10 minutes constituted a serious risk for HIE. In addition, as I have noted above, Professor Hunt's initial opinion was based on a normal resistive index. I found that the resistive index was abnormal, and that the Day 1 Ultrasound showed evidence of cerebral oedema. Dr Keenan described the ultrasound results as being 'clearly abnormal'. He opines that 'it is highly likely that Cooper ... suffered multiple synchronous cerebral insults with significant TBI on a background of significant HII'. So this sixth reason does not undermine Dr Rao's opinion.

1. The final reason dealt with by the learned trial judge returns to the central theme of the appellant's appeal: that the Day 7 MRI did not show the classic patterns of hypoxic injury to the brain. While his Honour dealt with this at length, it is sufficient to repeat the finding, ultimately not challenged on the appeal, that the absence of classic patterns of hypoxic injury to the brain on MRI does not exclude the conclusion that the respondent suffered moderate (stage 2) HIE.[383] Indeed, insofar as the clinical diagnosis of stage 2 HIE is concerned, as the learned trial judge said:[384]

Moreover, Professor Ditchfield accepted that the grading of the severity of HIE is independent of the imaging, and that the MRI scans did not exclude the possibility of a diagnosis of stage 2 HIE. He accepted that on the ultrasound and clinically a hypoxic insult had occurred.

1. To all of his conclusions in relation to these matters, the learned trial judge added that, critical to the determination of the severity of the respondent's HIE in the present case was that Dr Rao (and he alone) had the opportunity to examine the respondent at the time to make his clinical judgment that the respondent had suffered from stage 2 HIE. The learned trial judge saw and heard Dr Rao give evidence explaining his own thought processes and the basis upon which he made that determination.
2. The learned trial judge was entitled to take into account his own assessment as to the quality of Dr Rao's clinical judgment.
3. His Honour has not been shown to be in error in accepting that Dr Rao's diagnosis was correct. The finding was open to him on the evidence and, indeed, was in our view correct - on our review of the record, we would make the same finding.
4. Ground 8 is not made out.

1. Ground 9 alleges that the learned trial judge erred in fact by (in effect) finding that the respondent suffering a right sided Erb's palsy was relevant to breach causing his Developmental and Cognitive Impairments.
2. Erb's palsy is a paralysis of the nerves of the brachial plexus caused by stretching of the nerves, leading to weakness in the upper limb.[385] It was uncontroversial that the respondent suffered Erb's palsy in his right arm as a consequence of having shoulder dystocia during his birth (i.e. his shoulder was stuck at the front of the pelvis). It is the mechanism of trying to 'pop' the shoulder out which causes the palsy.
3. Erb's palsy is a usually a temporary condition and indeed it resolved in the respondent's case. It, nevertheless, formed part of the Birth Injuries caused by the appellant's negligence.[386]
4. As might be expected, Erb's palsy, while illustrative of the prolonged and difficult nature of the respondent's birth, had nothing to do with injury to his brain. Needless to say, none of the expert witnesses suggested that it was in any way implicated in the respondent's Developmental and Cognitive Impairments.
5. The phrase 'in effect' contained in this ground of appeal is telling. That is because the learned trial judge did not find that the respondent suffering a right sided Erb's palsy was relevant to breach causing his Developmental and Cognitive Impairments.
6. The basis for the respondent's submission that his Honour 'in effect' made such a finding is that the defined term 'Cooper's Birth Injuries' in the Primary reasons referred to a number of separate injuries, listed in a summary of certain primary findings, namely:[387]

During the birth process, Cooper sustained perinatal asphyxia, global hypotonia, right sided Erb's palsy, renal impairment, traumatic brain injury and hypoxic ischaemic encephalopathy (Cooper's Birth Injuries).

1. From this, the appellant submitted, the fact that the learned trial judge's findings in relation to the cause of the respondent's Developmental and Cognitive Impairments were expressed in terms that they were the 'sequelae of Cooper's Birth Injuries' means that his Honour found, inter alia, that the respondent's Developmental and Cognitive Impairments were caused by his Erb's palsy.
2. Put another way, in a proposition that the appellant embraced at the hearing of the appeal, 'the mention of the Erb's palsy as one of the birth injuries and the statement that the impairments were caused by the birth injuries carries with it the implication that each and every one of those birth injuries played a role in the impairments'.[388]
3. This is not a construction of the Primary reasons that would commend itself to the reasonable reader.
4. If this were not obvious from a fair reading of the Primary reasons as a whole, it is clear from the passage reproduced at [214] above. In that passage, which introduces all of the learned trial judge's analysis as to the cause of the respondent's Developmental and Cognitive Impairments, his Honour expressly identified which of the Birth Injuries are the subject of that analysis: namely traumatic brain injury and hypoxic ischaemic encephalopathy (or more accurately a combination of the two).
5. Ground 9 is without merit.

1. Ground 10 alleges that the learned trial judge erred in fact by (in effect) finding that the respondent suffering renal impairment was relevant to breach causing his Developmental and Cognitive Impairments.
2. Everything said in relation to ground 9 concerning Erb's palsy applies equally to the finding that the respondent suffered renal impairment, save to note that that injury provided corroboration (if any were needed) that the respondent suffered perinatal asphyxia.[389]
3. Ground 10 is also without merit.

1. Ground 11 alleges that the learned trial judge erred in fact in finding that Dr Nguyen gave evidence to the effect that the Day 7 MRI showed injury to the left cerebellar tonsil.
2. The relevant portion in the Primary reasons is not a finding, as such, but part of his Honour's summary of the evidence:[390]

Dr Nguyen reviewed the images again for the purpose of preparing to give evidence. With one caveat, she confirmed that the report accurately records what she identified. The caveat is that she identified a further, smaller, injury to the left cerebellar tonsil.

1. When Dr Nguyen gave the evidence referred to by his Honour, it is apparent that she was actually referring to a display of the images themselves. The relevant evidence-in-chief was:[391]

[O]n my report, what I commented was a - an area of injury to the right inferior cerebellum - cerebellar hemisphere and tonsillar region, but on review, there's just a tiny area of signal change on the left, to the left of midline as well.

...

[T]he big white area here is the abnormality that I reported on. But on review, there's a tiny little area of abnormal signal and this is the midline - just to the left of midline, so the - involving the - the - the inferior aspect of the left side. It's very tiny.

...

Yes, so on the left-hand side there's a darker grey area - - -?---It's the bright signal area. This is the abnormality, this tiny little dot. I don't know whether - I will try and zoom in if I can.

1. Dr Nguyen does not appear to refer to the abnormality again in her evidence.[392]
2. The appellant, in its submissions, referred to the fact that Dr Nguyen agreed with a number of propositions taken from the report of Professor Ditchfield.[393] Nowhere in that evidence, however, was it put to Dr Nguyen, or does she accept, that her evidence in relation to abnormality left of the midline was wrong. Nor indeed was she asked to comment on the significance, if anything, of its small size.[394]
3. His Honour was therefore presented with evidence from Dr Nguyen that she observed a 'tiny' area of 'abnormality'. To describe such an appearance, visible on an MRI to a radiologist, as an 'injury' does not, in our view, amount to an error of fact.
4. In any event, even accepting that it would have been more accurate for his Honour to describe Dr Nguyen's evidence as identifying a 'tiny abnormality' rather than a 'smaller injury', it could have no consequence for the correctness of his Honour's ultimate findings.
5. Ground 11 is not made out.

Ground 12 - The finding of subdural and intraventricular haemorrhage

1. Ground 12 alleges that the learned trial judge erred in fact by finding that minor subdural haemorrhage and intraventricular haemorrhage seen in the Day 7 MRI were caused by any breach of duty by the defendant and caused the respondent's Developmental and Cognitive Impairments.
2. The appellant preferred not to make oral submissions in relation to ground 12, confining itself to the written submissions.[395] Those submissions are, with respect, a little difficult to follow. They involve a rather elaborate process of construction of the Primary reasons.
3. It is clear that they relate, however, to the findings, at Primary reasons [650(b) and (c)], that the Day 7 MRI showed the following injuries to the respondent's brain:

(a) multi-compartment haemorrhage comprising intraventricular haemorrhage, subarachnoid haemorrhage and subdural haemorrhage ([650(b)]; and

1. The appellant's submissions appear to challenge both the factual findings as to the existence of those injuries (which findings the learned trial judge undoubtedly made) and an alleged finding that those injuries caused the respondent's Developmental and Cognitive Impairments (a finding that does not appear in the Primary reasons).

Factual findings made by the learned trial judge

1. We turn first to the factual findings.
2. The first, in [650(b)] identifies three specific injuries:

1. The learned trial judge described those injuries as 'multi-compartment haemorrhage'. The appellant's submissions appear to consider this to be a finding of an additional or separate injury (i.e. in addition to the three haemorrhages described in the previous paragraph), based entirely on the evidence of Dr Keenan.[396] It is not. It is simply a recognition that haemorrhage occurred in multiple compartments (i.e. spaces) of the brain: the intraventricular space, subarachnoid and the subdural space.
2. As to these haemorrhages, all of the radiological experts identified that there was haemorrhage into the intraventricular space (the ventricles being the compartments in each hemisphere of the cerebrum). Dr Keenan identified intraventricular haemorrhage (IVH) in his report.[397] So did Dr Nguyen ('minor haemorrhage is seen within the lateral and third ventricles').[398] As did Professor Ditchfield ('intraventricular haemorrhage in both lateral ventricles').
3. The learned trial judge was not in error in finding that there had been an intraventricular haemorrhage.
4. A subarachnoid haemorrhage is haemorrhage into the subarachnoid space, between the arachnoid membrane and the pia mater membrane surrounding the brain. This is an area outside the brain.[399] It was identified in Dr Nguyen's original report ('evidence of likely subarachnoid haemorrhage').[400] Dr Keenan also referred to subarachnoid haemorrhage (SAH) in his report[401] and in his evidence.[402]
5. It is true that Professor Ditchfield did not comment on the existence of subarachnoid haemorrhage one way or the other. Its existence does not appear, however, to have been contentious at trial. In cross-examination of Dr Keenan, for example, far from suggesting that a subarachnoid haemorrhage was not present, the appellant's counsel sought to emphasise that it demonstrated an injury outside the brain. For example:[403]

There is a further small focus of haemorrhage within the left side of the suprasellar system, which I suspect is subarachnoid.

So that again is actually not in the brain at all?---No, it's in the fluid around the brain. So subarachnoid, yes.

1. The evidence that the Day 7 MRI showed a subarachnoid haemorrhage was not challenged. His Honour was not in error in accepting it.
2. The third injury referred to in Primary reasons [650(b)] was subdural haemorrhage. This is a haemorrhage between the arachnoid membrane and the dura mater membrane surrounding the brain. This is also a compartment outside the brain.
3. The existence of a subdural haemorrhage was identified by all of the radiological experts and the appellant, in its submissions, did not suggest otherwise.[404] His Honour was not in error in accepting that evidence. It was, in any event, a finding of little consequence. The learned trial judge accepted that such a finding was common post-delivery in neonates.[405]
4. The final injury the subject of this ground (in Primary reasons [650(c)]) was a subgaleal haematoma. As the appellant submits, the only expert who expressly referred to a subgaleal haematoma was Dr Keenan, although, as his Honour noted, none of the other radiological experts expressly suggested otherwise.[406]
5. His Honour evidently accepted Dr Keenan's evidence.
6. It is not surprising that his Honour did so.
7. The evidence at trial revealed that the subgaleal haematoma in the respondent's case was 'just bruising on the scalp'.[407] The appellant specifically led evidence to that effect from Professor Hunt, who also identified it:[408]

So the subgaleal haematoma is a soft tissue injury, and it's really to do with the tissue outside of the skull, rather than within the skull. ... I think I make reference to it in this report, because it's evident on Cooper's imaging that there was a subgaleal haematoma present, almost certainly as a consequence of the instrumental delivery. But because it sits outside of the skull, like a bruise, it will resorb with time, and it has no developmental consequence.

1. In addition to the medical evidence that the respondent had bruising on his scalp, of course, the learned trial judge also heard unchallenged evidence from the respondent's father (which he accepted) describing the respondent's appearance when he was born. That description included that the respondent's 'head ... looked bruised in part, and - almost black on his head in parts where - and red and purple ... like it'd been hit by a baseball bat a few times'.[409]
2. As we have said, it is therefore not surprising that the learned trial judge accepted that the respondent had suffered a subgaleal haematoma. His Honour was not in error in doing so.

1. We turn now to the submission that the learned trial judge erred by finding that these particular injuries, some of which are self-evidently minor and would not give rise to developmental consequence, caused the respondent's Developmental and Cognitive Impairments.
2. The submission is misconceived - the learned trial judge did not so find.
3. In one sense, it is simply another variant of the argument underpinning grounds 9 and 10, namely that the learned trial judge found that each and every injury sustained by the respondent in the course of his birth, no matter how minor, played a role in his ongoing impairments.[410]
4. We have already rejected such a reading of the learned trial judge's reasoning.
5. The submission also reveals a flaw that pervades much of the appellant's appeal: namely that only those specific injuries visible in the MRI scans are relevant to the assessment of causation in the present case and that unless those specific injuries visible on the MRI scan can be shown, on the balance of probabilities, to have caused the respondent's Developmental and Cognitive Impairments, the respondent's case must fail.
6. We have already explained why that proposition cannot be sustained.[411]
7. Ground 12 is not made out.

Ground 13 - Was there 'clear expert evidence' supporting causation?

1. Ground 13 alleges that the learned trial judge erred in law in finding that there existed 'clear expert evidence' that the respondent's Developmental and Cognitive Impairments were caused by a breach of duty of the appellant.
2. This ground challenges the following passage from the Primary reasons:[412]

The evidence of Dr Tracy and Dr Keenan provides clear expert evidence that Cooper's Developmental and Cognitive Impairments are sequelae of Cooper's Birth Injuries. This is not a case in which the court is being asked to make a finding of causation where no expert is either able to do so, or prepared to do so.

1. The observation is repeated later in the reasons in terms that there was 'firm expert evidence' to that effect.[413]
2. The appellant does not, by this ground, challenge the observation that both Dr Keenan and Dr Tracy were of the opinion that the respondent's Developmental and Cognitive Impairments were caused by the injuries sustained during his birth. They were both clearly of that view. Both Dr Keenan and Dr Tracy expressed that view on the basis of the combined effect of the respondent's hypoxic ischaemic encephalopathy and traumatic brain injury:

(a) 'on the balance of probabilities I believe that [the respondent's] clinical syndrome results from combined cerebellar [traumatic brain injury] and global [hypoxic ischaemic encephalopathy]' (per Dr Keenan);[414] and

(b) 'his likely neurological outcome is in keeping with stage 2 HIE with a concurrent cerebellar haemorrhage' (per Dr Tracy).[415]

1. Rather, the appellant submits that the learned trial judge erred in law by having regard to their opinions without first expressly rejecting, or otherwise satisfactorily dealing with, expert evidence to the contrary.[416]
2. We have already remarked, in relation to the specific issue of the abnormalities revealed by the MRI scans, that it would have been preferable, in reaching his ultimate conclusions, for the learned trial judge to express his preference for the evidence of one expert over another in relation to all significant matters in contention.[417] We need not repeat those remarks.
3. Nevertheless, as we have also said, the Primary reasons, as a whole, in our view, reveal an available and permissible path of reasoning, and adequately discharged his Honour's obligation to disclose the intellectual process that led to his conclusion on causation.
4. Insofar as Dr Tracy's evidence is concerned, the learned trial judge did expressly record his preference for the evidence of Dr Tracy to the extent that Professor Hunt's evidence was based on the respondent suffering only mild HIE (a preference challenged in ground 14).
5. As for the evidence of Dr Keenan and Dr Tracy generally, it is significant that both of them reached their conclusions as to causation as an inference from all of the clinical data and the investigations; and not based on, for example, the MRI alone. For example, in addition to the passage at [97] above, Dr Keenan described the process of inference[418] follows:418

And so for the process of inference here, what you have done is you have taken the fact that this child has certain symptoms and you have inferred back from that, that they may be caused by damage to the brain which you cannot observe?---Probably in reverse of that. I look at the scan and the imaging first because I'm a radiologist.

Yes?---I say that I've got an extremely abnormal ultrasound which is not explained by the subsequent MRI. And in the clinical setting of what appears to be a pretty clear-cut perinatal Hypoxic Ischaemic Injury or encephalopathy, putting those two things together we then, I guess, rate what else could be going on, because that's what the - that's what the clinicians need. The clinicians need to know are they going to cool the baby or not. If you've got a traumatic brain injury you're not going to cool the baby. If you've got a Hypoxic Ischaemic Injury you're going to cool the baby. So that's why we - and - and that's why we would draw that conclusion.

All right. So again just so that I understand the process of inference that you've gone through. You saw the ultrasound. You concluded that the ultrasound showed what you've identified it as showing, which is some evidence of an Hypoxic Ischaemic Injury. You know - - -?---It's severe - it's - it's severe evidence. I mean, it's a very abnormal ultrasound.

...

As I understand it, Dr Keenan, one of the pieces that led you to reach your inference was the fact that there was a perinatal hypoxic event. So basically a period of time at or around the time Cooper was born when his brain was deprived of oxygen?---Correct.

1. Dr Tracy, similarly, referred to the totality of the evidence (history, examination and radiological investigations) in reaching his conclusions.[419]
2. The competing evidence from the expert witnesses called by the appellant did not give evidence that the inference of causation was not open. Rather their evidence was simply that they would not draw such an inference.
3. Take, for example, Professor Ditchfield, upon whose evidence the appellant relied for the proposition that the MRI scans could not explain the respondent's Developmental and Cognitive Impairments. While Professor Ditchfield recognised that imaging did not give the full answer on causation, he was cautious as to the inferences he would otherwise draw.
4. The following exchange in his cross examination, for example, is in our view instructive:[420]

Your evidence was in fact that the ultrasound would be consistent with there having been a Hypoxic Insult?---Correct.

Right. And so if we put that together with the clinical assessment of stage 2 HIE, and what I'm putting to you, to assume that this child has ongoing cognitive and language deficits, that could - that would all fit, wouldn't it?---It could all fit, but that is not evidence of it fitting.

All right?---It's an association, and it's very important in medicine to distinguish a causative relationship, rather than an association, because the causation may be very different.

1. This exchange points up, in our view, the important difference, recognised in the authorities, between the evidence required to reach a scientific deduction and the task of a court in determining causation:[421]

It may be, and probably is, the case that medical science will find a possibility not good enough on which to base a scientific deduction, but courts are always concerned to reach a decision on probability and it is no answer, it seems to me that no medical witness states with certainty the very issue which the judge himself has to try.

1. Of course, as the learned trial judge recognised, in the present case there were reputable medical witnesses who were prepared to reach the scientific deduction. His Honour's point, challenged by this ground of appeal, was that the evidence in favour of an inference of causation was stronger in the present case than that in a case where there was no medical witness prepared to draw that inference.
2. In all of the circumstances, his Honour was also prepared to draw that inference. In that regard, in the end, his Honour's final conclusion, in drawing the very inference that had been drawn by Dr Keenan and Dr Tracy, in substance followed the same path of reasoning as they did, in taking all the known facts and circumstances into account.
3. No error is revealed by the impugned passage of the learned trial judge's reasoning.
4. Ground 13 is not made out.

Ground 14 - The learned trial judge's preference for the evidence of Dr Tracy

1. Ground 14 alleges that the learned trial judge erred in fact in preferring the evidence of Dr Tracy to that of Professor Hunt that the respondent's Developmental and Cognitive Impairments were caused by the respondent's Birth Injuries.
2. The appellant was content not to make oral submissions in relation to ground 14, confining itself to the written submissions.[422] Those submissions invite a comparison of Dr Tracy's curriculum vitae with Professor Hunt's curriculum vitae. The appellant submits:[423]

Tracy is not a paediatric neurologist; Hunt is. Tracy's area of particular expertise is perinatal epidemiology; irrelevant to the matters here. Tracy has no expertise in interpreting MRI scans or expressing conclusions based on MRI scans.

1. The submission that Dr Tracy's area of particular expertise is perinatal epidemiology appears based upon a question in cross-examination to the effect that epidemiology was 'another interest' of his.[424] The submission does not accurately reflect the expertise of Dr Tracy, who is a Senior Newborn Intensive Care Specialist at the Westmead Hospital and a Clinical Senior Lecturer in the Division of Paediatrics and Child Health at the University of Sydney. An examination of Dr Tracy's curriculum vitae reveals a broad range of expertise in relation to the issues relevant to the respondent's case, including publications on intrapartum asphyxia, intraventricular haemorrhage, resuscitation of newborns and neonatal cranial ultrasound.
2. The appellant submits that Dr Tracy has no expertise in interpreting MRI scans. He did not profess such expertise. Indeed, as is apparent from the summary of his evidence set out above, of all of the expert witnesses called on the question of causation, Dr Tracy was the one who gave most attention to the respondent's overall clinical condition, drawing upon his expertise as a clinician. That the appellant submits that Dr Tracy's expertise was deficient as he does not interpret MRI scans is telling - it is a further indication of the appellant's near-exclusive focus on the MRI scans to the exclusion of the other evidence.
3. In any event, the learned trial judge's preference for Dr Tracy's evidence over that of Professor Hunt was not based upon their respective expertise, but on the extent to which Professor Hunt's opinions were based on the respondent having only suffered mild encephalopathy (as to which see [444] above).
4. Ground 14 is not made out.

Ground 15 - Statistics as to the prognosis for Stage 2 HIE

1. Ground 15 alleges that the learned trial judge erred in fact in finding that there was a consensus between expert witnesses that, of children classified as stage 2 HIE, 50% (or so) suffered from neurodevelopmental deficits and 50% (or so) did not.
2. The ground is a challenge to Primary reasons [893] in which the learned trial judge said:

There was a consensus among the relevant experts as to the research in relation to the outcomes of infants with HIE based on the three stage classification. Of the infants who had mild or stage 1 HIE, more than 90% or so would be expected to have a normal neurodevelopmental outcome. For those with severe or stage 3 HIE, 100% of those babies either died or were left with some severe neurodevelopmental impairment. For those with moderate or stage 2 HIE, 50% or so had a normal outcome and 50% had neurodevelopmental deficits when they were assessed in childhood.

1. It is apparent that there is a subtle difference between this passage and how it is paraphrased in ground 15 itself. The consensus referred to by the learned trial judge was 'as to the research in relation to outcomes of infants with HIE based on the three stage classification'. Ground 15 omits any reference to 'the research'.
2. The difference is significant.
3. That is because all of the experts did agree that the effect of the research was as described by his Honour.
4. The appellant's written submissions on ground 15 referred to part of Dr Pestell's cross examination (with the appellant submitting that 'she could not be part of a consensus')[425]. In that part of the cross-examination Dr Pestell's said that she took into account the research literature as to the long term effects of HIE and that 'they consistently demonstrate permanent cognitive defects'. The cross-examination continued:[426]

At any stage of HIE?---It depends on whether it's mild, moderate or severe.

Yes?---But the research literature shows that children who have had moderate to severe HIE are likely to have ongoing deficits in certain areas.

Well, I think the literature in relation to HIE suggests that if there is a moderate - so that's a stage 2 - - - ?---Yes.

- - - there's something like a 50 per cent chance of it having a developmental sequelae?---Yes, although there's been limited studies in the area so there's - - -

Yes?--- - - - still a lot we don't know about the area.

Quite so. And a stage 1, and the research would suggest that if it's a stage 1 it is - it is very rare for there to be a developmental sequelae?---That's correct but it can happen.

Can happen?---Yes.

And a stage 3 is a much higher degree of likelihood that there will be a developmental sequelae?---That's right and cerebral palsy and so on, yes.

Yes, that's right. And again, with respect, the position is that research is really quite uncertain as to these matters?---That's correct.

1. In our view, these answers support the opposite of the proposition sought to be established by ground 15. Dr Pestell does not deny that the research is to the effect described by the learned trial judge. Indeed, it was the appellant's counsel who put the proposition to Dr Pestell that the literature suggested that in the case of stage 2 HIE 'there's something like a 50 per cent chance of it having a developmental sequelae'. Dr Pestell agreed with that proposition, although she noted that there had been limited studies. That is not to deny the effect of the research; it is simply to observe that the research is limited.
2. The same may be said of Professor Hunt, who gave the most extensive description of the effect of the research, in the terms described by his Honour (see [171], [442]-[444] above).
3. The significance of the research, for the issues in the case at trial, was that the greater the severity of a patient's HIE the more likely it was that that patient will go on to suffer developmental sequelae. No expert gainsaid that proposition.
4. Indeed, the appellant's case at trial (at least in part) embraced it. That is because the appellant's case at trial was that the respondent had suffered only stage 1 HIE. Seen in that context, the cross-examination reproduced at [543] above, was directed towards establishing the proposition that the 'research would suggest that if it's a stage 1 ... it is very rare for there to be a developmental sequelae'. Precisely the same point was made in the cross-examination of Dr Tracy (see [113] above).
5. Of course, as the learned trial judge rejected the appellant's case that the respondent had suffered only mild (stage 1) HIE, that part of the appellant's case at trial fell away.
6. The learned trial judge did not err in his description of the effect of the research literature as described by the expert witnesses.
7. Ground 15 is not made out.

Ground 16 - The relevance of statistics as to the prognosis for Stage 2 HIE

1. Ground 16 alleges that the learned trial judge erred in law in finding that the fact that 50% (or so) of children with HIE stage 2 suffer from neurodevelopmental deficits is a basis for a finding that it is 'quite possible' that the respondent suffered from stage 2 HIE which caused or materially contributed to his Developmental and Cognitive Impairments.
2. The ground misstates the relevant finding. The learned trial judge did not find that 'it is 'quite possible that the [respondent] suffered stage 2 HIE'. His Honour specifically found that the respondent did sustain stage 2 or moderate HIE. That was not a finding as to 'possibility'.
3. The reference to 'possibility' in the context of the research literature, was to the relationship between the epidemiological studies and the particular circumstances of the respondent's case. That is, his Honour, quite properly, said that:[427]

The research to the effect that 50% or so of children with stage 2 HIE will go on to suffer from neurological and developmental issues is obviously not a sufficient basis for a finding that Cooper is in this 50%, and not in the other 50% or so of children who have a normal outcome.

1. To express the relationship between the epidemiological research and the issues before the court in this way, was doing nothing more or less than applying the approach identified by Spigelman CJ set out at [279] above.
2. Ground 16 is not made out.

Ground 21 - Is the respondent just an ordinary child at the lower end of the developmental spectrum?

1. Ground 21 alleges that the learned trial judge erred in law and in fact in finding that it was not possible that the respondent is (just) a child at the lower end of the developmental spectrum.
2. The relevant portion of the Primary reasons is as follows:[428]

As to the alternate explanation, the defendant submitted in closing submissions that Cooper may well just be an ordinary child at the lower end of the relevant developmental spectrums. There is, however, no expert evidence to support the contention that all of Cooper's Developmental and Cognitive Impairments may be explained on this basis. Specifically, Dr Do, who was called by the defendant, was not asked to opine on this issue. Dr Pestell disagreed with the proposition put to her by counsel for the defendant that: 'plainly, there are many children who have certain of the symptoms that Cooper has who don't have any brain injury at all', instead stating:

I wouldn't necessarily agree with that because Cooper was having quite significant gross motor problems at that time, for example, he couldn't even sit on the seat without - his chair without falling off, and so it would be unusual from a neuropsychological perspective for a child to have that degree of impairment without there being some underlying brain pathology.

There is no basis in the evidence for the contention that Cooper is just an ordinary child at the lower end of the developmental spectrum.

1. The appellant accepted that there was no expert witness who gave evidence the respondent was just an ordinary child at the lower end of the spectrum, without an underlying brain pathology. Indeed, as the reference to Dr Pestell's evidence in the passage quoted above reveals, her opinion was that the degree of impairment was from an underlying brain pathology.[429]
2. The appellant's submissions in support of ground 21 however, were not based on the expert evidence. Rather, ground 21 was put as a 'matter of logic, nothing else'.[430] That is, the appellant submitted that the Court could conclude, as a matter of logic, that when each of the respondent's developmental symptoms were analysed, in terms of where he fell in the relevant percentile for children of his age, the fact that he was in a particular percentile could be explained, in essence, as part of the normal distribution of the abilities of children generally. As the appellant put it at the hearing of the appeal:[431]

So in relation to a large number of these matters, an equally plausible explanation, as a matter of logic, is, well, he's just not very good at it, because if he's on the 20th percentile for something, for instance, that means that he's better than 60,000 children in Australia.

1. There a number of difficulties with this approach, as a suggested plausible alternative hypothesis for the respondent's Developmental and Cognitive Impairments (indeed, as the hypothesis suggests, they were not 'impairments' at all).
2. First, the approach could only be applied to each and every developmental symptom in a piecemeal fashion. That is because there were a very large number of functions or abilities that were assessed: including general intellectual functioning, language skills, literacy, numeracy, processing speed, visuo-motor integration and visual search, visual tracking, perceptual reasoning, working memory, attention, executive functioning and social cognition. In each of these different areas, the assessment of the respondent's percentile was different (e.g. 2nd percentile, 4th percentile, 3rd to 8th percentile etc).
3. It might be possible for the Court to calculate what each percentile means, in terms of the number of children in Australia above or below the respondent in relation to each respective ability. It might even be possible (with some hesitation) for a lay person to draw an inference that a particular result, in isolation, is more or less likely to be the result of a brain pathology. For example, a result in the 75th percentile (i.e. the top 25%) on one particular score alone might provide a very poor basis for inferring the existence of a brain pathology.
4. It is, however, altogether a different matter to be able, as a matter of logic, to attempt to analyse the combined effect of all of the respondent's limitations and draw the inference that the respondent may just be an ordinary 'below average' child, without the aid of expert evidence. That is not an exercise that can be undertaken by the Court without expert evidence.
5. This points up the second difficulty with concluding, as a matter of logic, that the respondent is 'just not very good at' some things.
6. In the present case, the inference which the learned trial judge ultimately drew as to factual causation - which inference the appellant challenges - was an inference based on facts (including possibilities) supported by the expert evidence. While some of the experts (such as Professor Ditchfield and Professor Hunt) were not prepared to draw that inference, others (such as Dr Keenan and Dr Tracy) were prepared to do so. No expert, however, ultimately denied the possibility of a causal connection, as a matter of medical science.
7. In such a case, as the authorities make clear, other circumstances may unite to warrant a conclusion that what the medical evidence established as a possible cause was the probable cause.
8. The appellant's position in relation to ground 21, however, is not that common sense permits the drawing of an inference from all of the circumstances that is open on the expert evidence. On this ground the appellant invites the Court to apply what the appellant submits is a common sense (or logical) view despite, and indeed contrary to, the expert evidence.
9. The learned trial judge relied upon the expert evidence before him to conclude that the respondent is not just an ordinary child at the lower end of the developmental spectrum. His Honour did not err in doing so.
10. Ground 21 is not made out.

1. Ground 20 alleges that the learned trial judge erred in law in concluding that there exists a principle of law that a significant circumstance in favour of drawing an inference of causation is that a defendant has not established or suggested an alternative cause.
2. This ground challenges the learned trial judge's statement, in the course of discussing the principles concerning the drawing of inferences, that:[432]

the fact that no alternative cause or hypothesis was established or suggested in the evidence is a significant circumstance in favour of drawing an inference of causation.

1. As is apparent from the Primary reasons, the learned trial judge took into account the fact that there was no plausible inference competing with the inference that the respondent's Birth Injuries caused or materially contributed to Cooper's Developmental and Cognitive Impairments.[433]
2. We would make the following points in relation to this ground and the submissions in support of it.
3. First, there is no suggestion, either in the passage set out in [571] above, or in the Primary reasons as a whole, that his Honour was suggesting any onus 'on a defendant' to establish or suggest an alternative clause. His Honour correctly recognised, pursuant to s 5D of the Civil Liability Act, that the onus was on the respondent to prove, on the balance of probabilities, any fact relevant to the issue o[434]ausation.434 The appellant's submission that the passage set out in [571] above is 'inconsistent with s&#1[435]5D' must be rejected.435
4. Secondly, it perhaps goes a little far, to describe the passage set out in [571] above as articulating 'a principle of law'.
5. Rather, the relevance of the absence of a plausible inference competing with an inference of causation to the question whether such an inference should be drawn, is simply a description of the 'ordinary powers of human reason in the light of human experience'.[436]
6. As Evatt J observed more than 80 years ago, it is in the nature of an ordered process of logical thought that, in determining whether an inference should be drawn from all of the relevant facts and circumstances, regard must be had to every hypothesis which can compete with that inference.[437] The existence of competing hypotheses or inferences (and the strength of them) will affect whether, applying logic and common sense, the proposed inference should be drawn.
7. If there is a paucity, in number or quality, of possible explanations for a certain event, it is, as a matter of common sense, easier to draw the inference that a particular explanation is the only rational explanation (or the most likely explanation).[438] In the absence of any plausible alternative explanation, the particular explanation may be inferred with even greater confidence.
8. Leaving aside the matter dealt with in ground 21 above, the only possible alternative cause explored in the evidence at trial in the present case was that the respondent had attention deficit hyperactivity disorder (ADHD). The learned trial judge rejected ADHD as a 'plausible alternative hypothesis',[439] a finding not challenged in the appeal.
9. There was therefore nothing erroneous in the learned trial judge taking into account the fact that there was no other plausible explanation revealed by the evidence that competed with the inference that the respondent's Developmental and Cognitive Impairments were caused by the appellant's fault. To the contrary, in our view the absence of any other identified cause for those impairments was a circumstance of some significance in determining whether the ultimate inference of causation should be drawn.
10. His Honour, having thoroughly reviewed all of the evidence, was left with only one plausible inference as to the cause of the respondent's Developmental and Cognitive Impairments, namely an injury sustained in the course of his difficult and prolonged birth.
11. Of course, as the onus was on the respondent, his Honour was not obliged to conclude that that inference should be drawn.[440] Nevertheless, his Honour did draw the inference, and it was open for him to do so in light of all of the facts and circumstances. The absence of any other plausible explanation for the respondent's Developmental and Cognitive Impairments was simply one of the many circumstances.
12. Ground 20 is not made out.
13. The grounds dealt with above (grounds 1 to 16 and grounds 20 and 21) comprise all of the grounds of appeal relevant to the learned trial judge's finding of factual causation pursuant to s 5C(1)(a) of the Civil Liability Act; namely that the appellant's fault was a necessary condition of the occurrence of the respondent's Birth Injuries and his Developmental and Cognitive Impairments.
14. None of those grounds having been established, the appellant's challenge to the finding of factual causation must fail.

Ground 17 - Section 5C(2) of the Civil Liability Act

1. Ground 17 alleges that the learned trial judge erred in law in determining that, for the purposes of s 5C(2) of the Civil Liability Act, it is an established principle that, as a matter of ordinary common sense and experience, negligence 'materially contributed' to and thereby caused harm.
2. In light of our conclusions in relation to grounds 1 to 16 and grounds 20 and 21, ground 17 does not strictly need to be determined.
3. Ground 17 is concerned with the learned trial judge's alternative conclusion in the event that he was wrong in finding that the appellant's fault was a necessary condition of the occurrence of the respondent's Developmental and Cognitive Impairments. That conclusion appears in Primary reasons [942]:

Even if I am wrong in the conclusion that the defendant's fault was a necessary condition of the occurrence of Cooper's Developmental and Cognitive Impairments, these reasons are more than ample to support a reasonable and definite inference that the defendant's fault materially contributed to Cooper's Developmental and Cognitive Impairments for the purposes of CLA s 5C(2). A finding of material contribution is a sufficient reason why responsibility for both Cooper's Birth Injuries and Cooper's Developmental and Cognitive Impairments should be imposed on the defendant for the purposes of CLA s 5C(2)(a) and (b).

1. Section 5C(2) of the Civil Liability Act (see [216] above) is an alternative means of establishing factual causation in 'an appropriate case' where 'a fault that cannot be established as a necessary condition of the occurrence of harm'. Where fault can (and is) established as a necessary condition of the occurrence of the harm, s 5C(2) is irrelevant. For that reason, as the appellant quite properly accepted at the hearing of the appeal, if the learned trial judge's reasoning in relation to s 5C(1)(a) is not disturbed, the correctness of his Honour's approach to s 5C(2) does not arise.
2. Nevertheless, as ground 17 was fully argued and concerns the proper construction of s 5C as a whole, it is appropriate to deal with it.
3. The application of s 5C(2) (where it is said to apply) calls attention whether the instant case is 'an appropriate case, in accordance with established principles'.
4. The learned trial judge's analysis of that issue was as follows:[441]

[718] The plaintiff relies on CLA s 5C(2). That sub-section provides that, even if a fault that cannot be established as a necessary condition of the occurrence of harm, in an 'appropriate case' the fault may nonetheless be sufficient to establish factual causation. This is to be determined on 'established principles'. The 'established principle' relied on by the plaintiff is that, at common law, whether or not a causal connection exists between a breach of duty and any harm suffered by the person to whom the duty is owed is a question of fact to be resolved as a matter of common sense. In relation to this, in BGC Residential Pty Ltd v Fairwater Pty Ltd Pullin JA observed:

The reference to 'commonsense' is to exclude the application of a philosophical or scientific theory of causation. This accepts that in commonsense terms some conditions will have to be disregarded even though 'but for' that condition the injury would not have happened.

[719] Specifically, at common law, it is sufficient that, as a matter of ordinary common sense and experience, the negligence should be regarded as having 'materially contributed' to the harm, in the sense that the contribution was not negligible. It may be that material contribution can be established using the 'but for' test. In any event, negligent conduct that materially contributes to the plaintiff's harm, but which cannot be shown to have been a necessary condition of its occurrence, may, in accordance with established principles, be accepted as establishing factual causation, subject to the normative considerations to which CLA s 5C(2) requires that attention be directed to.

[720] The plaintiff does not rely on any other 'established principles', for example a finding of causation as a result of the cumulative operation of factors in the occurrence of the total harm in circumstances in which the contribution of each factor to that harm is unascertainable or where there is negligent conduct that materially increases the risk of harm in circumstances in which the state of scientific or medical knowledge makes it impossible to prove the cause of the plaintiff's harm. Unlike these two principles, relying solely on material contribution, the plaintiff was not required to specifically particularise or lead evidence in relation to this aspect of causation over and above the evidence going generally to factual causation. (citations omitted)

1. The appellant contends that the learned trial judge erred in law in applying the notion of 'material contribution' to harm as an established principle giving rise to an 'appropriate case' within the meaning of s 5C(2). As part of that contention, the appellant submits that his Honour gave no reason for his conclusion that the present case was an appropriate one for the application of s 5C(2).[442]
2. We accept the appellant's submissions in this regard. In our respectful view, the learned trial judge's analysis of s 5C(2), and in particular his Honour's approach of the notion of 'material contribution' in that context, confused the important difference between s 5C(1)(a) and s 5C(2). Whether, and in what way, 'material contribution' might have a role to play in the application of s 5C has yet to be finally determined. Nevertheless, it does not operate in the manner that the learned trial judge appears to have applied it in Primary reasons [942].
3. To explain why this is so it is necessary both to address the different ways in which 'material contribution' has been used in the past and to address the statutory purpose of s 5C(2).
4. First, dealing with 'material contribution', as the High Court recognised in Strong v Woolworths Ltd,[443] the expression 'material contribution' has come to be used in a number of different ways in the context of causation in tort.
5. The way in which 'material contribution' is more commonly understood in this State following the decision in Western Australia v Watson,[444] is as a synonym for the principle that a plaintiff need only prove that the defendant's negligence is 'a' cause (and not 'the' cause) of his or her damage. It is often said, for example, that the plaintiff must establish that the defendant's negligence 'caused or materially contributed to' his or her loss. In this sense, the phrase is simply a recognition that the defendant's fault need only be one cause (or 'a cause') of the plaintiff's harm. The contribution of other causes does not negate the causal connection if the defendant's negligent act is 'a cause'.
6. The majority of the High Court explained this in Hunt & Hunt Lawyers v Mitchell Morgan Nominees Pty Ltd as follows:[445]

The law's recognition that concurrent and successive tortious acts may each be a cause of a plaintiff's loss or damage is reflected in the proposition that a plaintiff must establish that his or her loss or damage is 'caused or materially contributed to' by a defendant's wrongful conduct. It is enough for liability that a wrongdoer's conduct be one cause. The relevant enquiry is whether the particular contravention was a cause, in the sense that it materially contributed to the loss. Material contribution has been said to require only that the act or omission of a wrongdoer play some part in contributing to the loss. (Citations omitted).

1. In this sense, the notion of 'material contribution' means little more than that the defendant's negligent act or omission was 'a necessary condition' of the plaintiff's harm as opposed to 'the sum of the conditions which are jointly sufficient to produce it', as John Stuart Mill might have required.[446]
2. As will be apparent, 'material contribution' in this sense is therefore picked up in s 5C(1)(a), in the requirement that the plaintiff establish 'that the fault was a necessary condition of the occurrence of the harm' (as opposed, for example, to 'the necessary conditions'). As the High Court recognised in Strong v Woolworths Ltd[447] the determination of factual causation under s 5C(1)(a) is a statutory statement of the 'but for' test of causation.
3. Properly understood, therefore, for a plaintiff to prove that the defendant's fault 'materially contributed' to the plaintiff's harm (in this sense) is not an alternative to what is required by s 5C(1)(a); it is what is required by s 5C(1)(a). That is, 'material contribution' to the harm is what the plaintiff must prove, not how the plaintiff might go about proving it.
4. The other (and, frankly, more difficult) sense in which 'material contribution' has been used in the context of causation was explained by the High Court in in Strong v Woolworths Ltd:[448]

In Bonnington Castings Ltd v Wardlaw, the expression 'material contribution' was employed in determining the causation of the pursuer's pneumoconiosis, a disease caused by the gradual accumulation of particles of silica in the lungs. There were several sources of exposure: the pneumatic hammers, the floor grinders and the swing grinders. The employer's breach of statutory duty lay only in exposing the pursuer to the dust generated by the swing grinders. The greater proportion of the pursuer's exposure to silica dust had come from the use of the pneumatic hammers. Lord Reid characterised the 'real question' as whether the dust from the swing grinders 'materially contributed' to the disease. The swing grinders had contributed a quota of silica dust that was not negligible to the pursuer's lungs and had thus helped to produce the disease. (citations omitted)

1. 'Material contribution' in this sense is applied in a context where the 'but for' test cannot be applied. In Bonnington Castings Ltd v Wardlaw,[449] this was because it could not be said that without ('but for') the 'quota of silica dust' contributed to by the negligence of the appellant, Mr Wardlow would not have developed the disease. And that was, in turn, because it was the accumulated gradual exposure to silica dust that had caused the disease, and no single part of that accumulated exposure could meet a 'but for' test.
2. The difference in the use of the word 'material contribution' in that case might be illustrated by reference to the notion of 'a necessary condition' in s 5C(1)(a) of the Civil Liability Act. In Bonnington Castings Ltd v Wardlaw, the relevant 'necessary condition' for the respondent's pneumoconiosis was the undifferentiated accumulation of exposure to silica, not any particular portion of it (in particular, because it was impossible to 'separate out' the role of any one quota of the silica dust from another). In that case, therefore, while the 'quota of silica dust' contributed to by the negligence of the appellant could not itself be said to be a necessary condition of Mr Wardlaw's disease, it could be said to have 'materially contributed' to a necessary condition (the accumulated exposure). In such a case, notwithstanding that there was an 'evidential gap', the particular circumstances in Bonnington v Wardlaw were such that the 'evidential gap' could be jumped.[450]
3. This is where s 5C(2) comes in.
4. As is apparent from the text of s 5C(2), it is concerned with an 'appropriate case' in which by reason of the particular circumstances fault 'cannot be established as a necessary condition'. The word 'cannot' is, in our view, significant in this context. Section 5C(2) is not concerned, in our view, with a case in which evidence 'does not' establish factual causation (in the sense that there could be evidence to support a finding of a necessary condition, but no such evidence is adduced). It is concerned, rather, with a case in which there 'cannot' be such evidence because of the nature of the case.[451]
5. This, in our view, provides assistance in giving content to what is intended by s 5C(2) to be 'an appropriate case'. While the equivalent provision in New South Wales (s 5D(2) of the Civil Liability Act 2002 (NSW)) refers to 'an exceptional case', the nature for that inquiry is reflected in the High Court's decision in Adeels Palace Pty Ltd v Moubarak:[452]

Whether, or when s 5D(2) is engaged must depend, then, upon whether and to what extent 'established principles' countenance departure from the 'but for' test of causation.

1. In Adeels Palace the Court concluded that the fact that a precaution might have prevented the harm did not give rise to an 'exceptional case'.[453] The Court continued:[454]

It may be that s 5D(2) was enacted to deal with cases exemplified by the House of Lords decision in Fairchild v Glenhaven Funeral Services Ltd where plaintiffs suffering from mesothelioma had been exposed to asbestos in successive employments. Whether or how s 5D(2) would be engaged in such a case need not be decided now. The present cases are very different. No analogy can be drawn with cases like Fairchild. Rather, it would be contrary to established principles to hold Adeels Palace responsible in negligence if not providing security was not a necessary condition of the occurrence of the harm but providing security might have deterred or prevented its occurrence, or might have resulted in harm being suffered by someone other than, or in addition to, the plaintiffs.

1. Fairchild v Glenhaven Funeral Services Ltd[455] (and other cases such as Bonnington v Wardlaw and McGhee v National Coal Board)[456] concern circumstances where an 'evidential gap' existed because it was impossible to determine which of a number of multiple sufficient causes gave rise to an indivisible disease. In such a case, the 'evidential gap' exists not because the evidence called by the plaintiff does establish a causal link but, rather, because no such evidence exists.
2. That s 5C(2) was intended to deal with unusual cases such as this is confirmed by the recommendations of the report to the federal Minister for Revenue and Assistant Treasurer prepared by a Panel chaired by the Hon David Ipp entitled Review of the Law of Negligence Final Report dated September 2002 (the Ipp Report).[457] The word 'appropriate' appears to have been taken from the Ipp Report,[458] and arose in the context of the Committee's discussion of the difficulties created by cases such as Bonnington v Wardlaw and Fairchild.[459]
3. The metes and bounds of what is an 'appropriate case' for the purposes of s 5C(2) of the Civil Liability Act remain to be determined. It is clear, however, that s 5C(2) does not apply merely because a plaintiff is only able to prove that the defendant's fault may have been a cause of the harm.[460] A case is not an 'appropriate case' merely because the plaintiff has failed to discharge his or her onus under s 5C(1)(a). Something more is required.
4. In truth, in our view, s 5C(2) had no role to play in the present case. The respondent either established factual causation under s 5C(1)(a) or he did not. If he failed to do so, there was nothing about the circumstances of the case, based on established principles, to invoke s 5C(2).
5. In particular, no analogy could be drawn between the present case and cases such as Bonnington v Wardlaw, Fairchild and McGhee. The learned trial judge recognised as much in Primary reasons [720] (see [592] above). In those circumstances the notion of 'material contribution' in its more nuanced sense discussed in [602] to [604] above had no role to play. To be fair the learned trial judge, it is not entirely clear in what sense his Honour was invoking the concept of 'material contribution' at Primary reasons [942]. Despite the opening words of that paragraph, his Honour may have been doing no more than using 'material contribution' in its more commonly used sense discussed at [597] to [599] above. If that be the case, however, the finding adds nothing to the finding already made in relation to s 5C(1)(a).
6. For these reasons we would uphold ground 17. Nevertheless for the reasons we have explained, success on ground 17 does not have the consequence that the appeal should be allowed.

1. Ground 18 alleges that the learned trial judge erred in law by imposing a burden upon the appellant to disprove that, in terms of s 5C(l)(b) and s 5C(4) of the Civil Liability Act 2002, this case was an appropriate case for the scope of the appellant's liability to extend to the harm so caused.
2. As appears from its terms, ground 18 is concerned with the second element of s 5C(1), namely that 'it is appropriate for the scope of the tortfeasor's liability to extend to the harm so caused' (s 5C(1)(b)).
3. The relevant conclusion of the learned trial judge, having been satisfied that the respondent had established factual causation between the appellant's fault and the respondent's Developmental and Cognitive Impairments, was that it was appropriate for the scope of the appellant's liability to extend to those Developmental and Cognitive Impairments.[461]
4. In that context his Honour observed that the appellant had not sought to argue that, should factual causation be established, the harm in the present case was of a kind to which it was not appropriate for liability to extend.[462]
5. The appellant submits that the learned trial judge thereby imposed a burden of proof on the appellant.
6. The submission must be rejected.
7. Section 5C(1)(b) is not concerned with a factual inquiry. It is concerned with a normative legal question as to where responsibility for harm should lie.
8. As the High Court stated in Wallace v Kam:[463]

The distinction now drawn by [s 5C(1)] between factual causation and scope of liability should not be obscured by judicial glosses. A determination in accordance with [s 5C(1)(a)] that negligence was a necessary condition of the occurrence of harm is entirely factual, turning on proof by the plaintiff of relevant facts on the balance of probabilities in accordance with [s 5D]. A determination in accordance with s 5C(1)(b)] that it is appropriate for the scope of the negligent person's liability to extend to the harm so caused is entirely normative, turning in accordance with [s 5C(4)] on consideration by a court of (amongst other relevant things) whether or not, and if so why, responsibility for the harm should be imposed on the negligent party.

1. No issue of onus of proof arises in the application of s 5C(1)(b) of the Civil Liability Act. It is a qualitative, normative assessment to be made based on the facts as found.
2. The learned trial judge did not impose a burden upon the appellant to disprove that this case was an appropriate case for the scope of the appellant's liability to extend to the harm so caused. His Honour merely made the observation - correctly - that the appellant had advanced no argument as to scope of liability in a context where his Honour considered (correctly - see ground 19 below) that the case fell within an established class of case.
3. Ground 18 is not made out.

1. Ground 19 alleges that the learned trial judge erred in law by determining that in terms of s 5C(l)(b) and s 5C(4) of the Civil Liability Act 2002 there existed well-established precedent, with which this matter was consistent, that rendered the scope of liability for the consequences of the harm coextensive with the content of the duty of the defendant which has been breached.
2. This ground is closely related to ground 18. It challenges the learned trial judge's conclusion that the present case was one in which, factual causation having been established, it was appropriate in the present case for the scope of the appellant's liability to extend to the respondent's Developmental and Cognitive Impairments.
3. That challenge must also be rejected.
4. Section 5C(1)(b), as noted above, is concerned with a normative question, as to whether (applied to the present case) it was appropriate for the appellant's liability to extend to the harm in fact caused to the respondent.[464]
5. As the learned trial judge recognised, in cases falling with an established class, the normative question posed by s 5C(1)(b) is properly answered through the application of precedent. In that context, as the Court observed in Wallace v Kam:[465]

[T]he scope of liability for the consequences of negligence is often coextensive with the content of the duty of the negligent party that has been breached. That is because the policy of the law in imposing the duty on the negligent party will ordinarily be furthered by holding the negligent party liable for all harm that occurs in fact if that harm would not have occurred but for breach of that duty and if the harm was of a kind the risk of which it was the duty of the negligent party to use reasonable care and skill to avoid.

1. The learned trial judge concluded that the present case was indeed one in which liability for the consequences of negligence was often coextensive with the content of the duty of the negligent party that had been breached. In that respect his Honour was correct. The harm suffered by the respondent as a consequence of the appellant's fault was the very kind of harm that it was the duty of the appellant to avoid. The harm in the present case followed naturally, directly and foreseeably from the appellant's fault.
2. There were no novel circumstances, such as were present in Wallace v Kam to suggest that there was some additional limiting principle, such that the appellant should not have been held liable for the harm that, as a matter of fact, was caused by its negligence.
3. In the end, even at the appeal, the appellant advanced no argument to the effect that, factual causation having been established, there was some policy reason why the appellant's liability should not extend to that harm.[466] Insofar as legal causation within the meaning of s 5C(1)(b) was concerned, the respondent's case was a run of the mill medical negligence case within an established class.
4. Ground 19 is not made out.

1. Ground 22 alleges that by reason of grounds 1 to 21 the learned trial judge erred in making the ultimate finding that the appellant's fault caused the respondent's Birth Injuries and his Developmental and Cognitive Impairments.
2. While we would uphold ground 17, the grounds of appeal challenging that finding and challenging the learned trial judge's ultimate finding that the respondent's Developmental and Cognitive Impairments were caused by the appellant's fault have not been made out.
3. As a consequence, ground 22 must also fail

Outcome of the appeal against the primary orders

1. For the above reasons, the appeal in CACV 37 of 2018 must be dismissed.

1. The Pleading appeal (CACV 93 of 2018) concerned an application to amend the Defence after trial. The application concerned the extent of the appellant's admissions in relation to the quantum of damage. The appellant accepted, at the hearing of the appeal, that the Pleading appeal would only arise for consideration if the appellant was successful in the appeal and the finding as to the causation of the respondent's Developmental and Cognitive Impairments was disturbed.[467]
2. In any event, at the hearing of the appeal, the respondent did not advance the submission that, in the event that finding as to the causation of the Developmental and Cognitive Impairments was set aside, the effect of the appellant's admissions as to quantum would be engaged by the minor injuries that were undisputed (i.e. global hypotonia, right sided Erb's palsy and renal impairment).[468] For this reason, too, the Pleading appeal would have fallen away.
3. In our view the appropriate order in relation to the Pleading appeal (CACV 93 of 2018) is that it be dismissed.

1. The Costs appeal (CACV 54 of 2018) concerns one aspect of the costs order made by the learned trial judge following trial.
2. The particular order was order 1(a), namely that:

(a) subject to order (d), the defendant pay the plaintiff's costs of the action, including reserved costs:

(1) up to 5 April 2017 on a party and party basis, to be taxed if not agreed; and

(2) from 6 April 2017 as between a law practice and its client, to be taxed if not agreed;

1. The basis from the order that the costs from 6 April 2017 be taxed as between a law practice and its client was that the respondent had made an offer of settlement within the meaning of Rule 42A of the District Court Rules 2005 (WA) Rule 42A provides:

(a) an offer is made by a plaintiff; and

(b) the offer is not accepted by the defendant; and

(c) the plaintiff obtains judgment on the claim to which the offer relates; and

(d) the judgment is no less favourable to the plaintiff than the terms of the offer.

(4) Unless the Court otherwise orders, the plaintiff is entitled to an order against the defendant for -

(a) the plaintiff's costs in respect of the claim from the date on which the offer was made, taxed as between a law practice and its client; and

(b) the plaintiff's costs incurred before that date, taxed on a party and party basis.

1. There is no doubt that Rule 42A(4) applied in the present case. As the learned trial judge recorded in his Honour's reasons for decision on costs:[469]

[O]n 6 April 2017 the plaintiff's lawyers served on the defendant's lawyers an offer pursuant to District Court Rules 2005 (WA) (DCR) r 42A) (Rule 42A Offer). The offer to settle was in the amount of $3,946,950, inclusive of trustee's fees, together with costs orders largely mirroring the orders sought set out at [3]. The Rule 42A Offer was not accepted. The Judgment was in terms no less favourable than the Rule 42A Offer.

1. The only issue to be determined by the learned trial judge, in the context of Rule 42A(4) was whether the Court should 'otherwise order', within the meaning of the opening words of the sub-rule. Self-evidently that concerned the exercise of a discretion to depart from the prima facie 'entitlement' of the plaintiff under the sub-rule.
2. The learned trial judge declined to order otherwise. His reasons for doing so were as follows:
   1. For the purposes of determining this application, I accept that:

(a) the case was a difficult one;

(b) it was difficult to predict the result of the trial;

(c) the defendant believed that it had reasonable prospects of success; and

(d) it was reasonable for the defendant to take the view that it did at the time to reject the Rule 42A Offer.

1. However, applying the principles set out above ([44]) none of these findings are sufficient to warrant the exercise of the discretion to displace the default position.
2. The findings in [49] are reflective of an ordinary case in the District Court proceeding to trial. If the defendant did not have evidence, including expert evidence, which it believed, on advice, would be preferred at trial, common sense suggests that it would have settled the action before that point in the life of the action. In this modern age of court sanctioned mediation and case management, a personal injuries case should not proceed to trial unless there is a significant conflict in the evidence or the applicable legal principles. If the mere fact that a defendant had evidence, including expert evidence, which it believed, on advice, would be preferred at trial is a sufficient basis for the court to 'otherwise order' pursuant to DCR r 42A(4), then the rule would cease to have any meaningful effect. Hence the principles set out above [44] have the practical effect that the defendant must point to more than a mere conflict in the evidence in order to move the court to order otherwise.
3. The defendant did not submit that there was any factor in the circumstances in which the Rule 42A Offer was made that would justify the exercise of the discretion to order otherwise. For example, it was not submitted that, at the time of delivery of the Rule 42A Offer, the nature of the plaintiff's case was not clear. Nor was it submitted that the plaintiff only succeeded upon a case which emerged from subsequent amendments to the pleadings or that the extent of the loss and damage only emerged from material subsequently disclosed. There is no suggestion in the materials before the court that the defendant did not have an informed opportunity to assess the chances of doing better than the offer.
4. The defendant has not demonstrated any reason sufficient to justify the exercise of the discretion to 'otherwise order' in DCR r 42A(4). I decline to exercise the discretion with the effect that the plaintiff's costs in respect of the claim from the date on which the offer was made, 6 April 2017, are to be taxed as between a law practice and its client. This includes any reserved costs.

1. In the circumstances, as the learned trial judge's decision in this regard was a discretionary one, the standard of review described in House v The King applies.[470]
2. In our view, the Costs reasons do not disclose error, and nor was order 1(a) unreasonable or plainly unjust.
3. The central proposition in the appellant's submissions in the Costs appeal is that the 'reasoning' in the Primary reasons was not the subject of submissions by the respondent at trial. If by that submission, the appellant suggests that it was, in some way, taken by surprise at trial, we would reject the submission.
4. Clearly, the appellant wished to characterise the issues at trial in the manner it considered most favourable to its case. In that regard, as it did on the substantive appeal, it sought to reduce the respondent's case to particular paths of reasoning (see, for example [212] to [214]). For example, it sought to maintain that MRI is the only rational and scientifically based predictor of linkage between damage to brain tissue and 'Developmental or[471]gnitive Impairments'.471
5. A defendant is, of course, entitled to run its case on the basis that the paths of reasoning it proposes are the only rational ones available to be followed. That does not, however, bind the plaintiff to those paths of reasoning. Less so could it bind the trial judge.
6. In our assessment the reasoning followed by the learned trial judge was consistent with the way in which the respondent ran his case at trial. We are far from satisfied that his Honour made an express error in the exercise of his discretion under Rule 42A.
7. Even if we were of that view, given the terms of the Rule 42A offer in the present case, if we were exercising the discretion afresh we would have reached the same conclusion.
8. The Costs appeal (CACV 54 of 2018) must be dismissed.

1. We would dismiss each of the appeal, the Pleading appeal and the Costs appeal.
2. The parties should be heard as to the appropriate orders, including as to costs.

I certify that the preceding paragraph(s) comprise the reasons for decision of the Supreme Court of Western Australia.

Principal Associate to the Honourable Chief Justice Quinlan

[1] Ellis (by his Next Friend Christopher Graham Ellis) v East Metropolitan Health Service [2018] WADC 36 (Primary reasons) [579].

[8] Civil Liability Act 2002 (WA) (Civil Liability Act), s3 (definitions of harm and personal injury).

[9] Harriton v Stephens [2006] HCA 15; (2006) 226 CLR 52 [251] (Crennan J); Harriton v Stephens [2004] NSWCA 93; (2004) 59 NSWLR 694 [6] (Spigelman CJ). At the hearing of the appeal Senior Counsel accepted that, notwithstanding the orders sought in the appeal that the respondent's action be dismissed, there was a concluded cause of action in relation to the palsy (Appeal ts 28). Whether, and to what extent, that injury alone would have sounded in damages is a different issue.

[10] The specific difference between hypoxic ischaemic encephalopathy and a 'traumatic brain injury', as the latter expression was used in the evidence is explained in the context of ground 3 (see [354]-[358] below).

[13] This being the first element of causation identified in s 5C(1)(a) of the Civil Liability Act (factual causation). It was also, of course, necessary for the respondent to satisfy the second element of causation identified in s 5C(1)(b) of the Civil Liability Act (scope of liability).

[16] As set out in [21] below, the substantive appeal in this matter was heard together with two related appeals. References in these reasons to 'the appeal' are references to the substantive appeal (CACV 37 of 2018).

[17] Tame v New South Wales [2002] HCA 35; (2002) 211 CLR 317 [70] (McHugh J).

[18] Primary reasons [708]. The appellant, by ground 7 contends that whether the respondent had suffered from stage 2 HIE was irrelevant to whether the respondent's Developmental and Cognitive Impairments were caused by the appellant's breach of duty. Ground 8, in the alternative, challenges the finding as against the weight of the evidence.

[19] Primary reasons [685], [706], [709(j)]. The challenge to this finding formed part of ground 8.

[21] Child and Adolescent Health Service v Mabior [2019] WASCA 151 (Mabior) [93]-[95] (Quinlan CJ, Murphy & Pritchard JJA); Joyce v Anderson [2020] WASCA 151 [105]-[108], [128]-[130] Mitchell JA, [206]-[211] (Beech & Vaughan JJA).

[23] Primary reasons [935]. This finding is the subject of ground 5.

[25] Chief Executive Officer, Department for Child Protection and Family Support v IGR [2019] WASCA 20; (2019) 54 WAR 222 [112] (Quinlan CJ, Murphy & Beech JJA).

[27] Primary reasons [174]. An Apgar rating comprises a rating of 0-2 for each component, giving a total potential rating of 10.

[31] Primary reasons [180]-[181], [183].

[50] The parties called expert evidence, in relation to the issues of liability, from Dr Robert Lyneham and Dr Graeme Thompson. The respondent also called a number of allied health professions from the Lighthouse Health Group (Ms Jane Burns, Ms Lindy Williams and Ms Elizabeth Shannon) and a speech pathologist, Ms Michelle Quail. Their evidence related principally to the assessment of the respondent's future care needs, rather than the cause of his impairments. Similarly, the appellant called Ms Ceri Pass, an occupational therapist, whose evidence related to the respondent's future care needs.

[56] Ts 224-225. See also re-examination in relation to jitteriness and seizures at ts 272.

[81] Exhibit 3.16 (GAB 161), ts 674, 692-693.

[83] Exhibit 3.16 (GAB 154), Ts 696.

[84] Exhibit 3.16 (GAB 154), Ts 697.

[85] Exhibit 3.16 (GAB 154), Ts 654.

[89] Exhibit 11; Ts 411.

[123] Ts 393. The transcript incorrectly transcribes the word 'aetiology' (the study of causes of disease or abnormal conditions) as 'ethology' (the study of animal behaviour). The context makes clear that Dr Pestell used the former word in her evidence.

[139] Exhibit 6.15 (GAB 248-249) and Exhibit 6.17 (GAB 254-256). The existence of two reports dated 1 March 2017 is clearly the result of a typographical error. The second report dated 1 March 2017 was in response to a letter dated 9 March 2017.

[149] Ts 1331-1332. See also Ts 1358-1359.

[196] Primary reasons [650]‑[651].

[202] Primary reasons [707]-[708].

[206] Compare e.g. Defendant's Closing Submissions [161]-[167] (BAB 554) and Appellant's Submissions [1]-[7] (WAB 27-28).

[211] Primary reasons [870]; see also [640]‑[642].

[220] Primary reasons [917]-[918].

[222] Primary reasons [922]-[923].

[228] Primary reasons [945]-[946].

[229] Primary reasons [947]-[948].

[230] See Strong v Woolworths Ltd [2012] HCA 5; (2012) 246 CLR 182 (Strong v Woolworths) [18] (French CJ, Gummow, Crennan and Bell JJ). The other element of causation in s 5C(1) of the Civil Liability Act ('scope of liability') raises separate and distinct issues (Wallace v Kam [2013] HCA 19; (2013) 250 CLR 375 (Wallace v Kam) [12] (French CJ, Crennan, Kiefel, Gageler & Keane JJ); Apostolic Church Australia Ltd v Dixon [2018] WASCA 146 [67]).

[231] March v E & MH Stramare Pty Ltd [1991] HCA 12; (1991) 171 CLR 506 (March v E & MH Stramare), 509 (Mason CJ); see also 522 (Deane J).

[232] Subject, of course, to the appellant's argument (in ground 21) that the respondent does not, in fact, suffer from Developmental and Cognitive Impairments but 'just wasn't particularly good at certain things' (Appeal ts 184).

[234] Amaca Pty Ltd v Booth [2011] HCA 53; (2011) 246 CLR 36 (Amaca v Booth) [43].

[235] Amaca Pty Ltd v Ellis [2010] HCA 5; (2010) 240 CLR 111(Amaca v Ellis) [70] (The Court).

[236] Adelaide Stevedoring Co Ltd v Forst [1940] HCA 45; (1940) 64 CLR 538; Luxton v Vines [1952] HCA 19; (1952) 85 CLR 352, 358; Jones v Dunkel [1959] HCA 8; (1959) 101 CLR 298, 304-305 (Dixon CJ), 309-310 (Menzies J); Fazio v Fazio [2012] WASCA 72 (Fazio v Fazio) [48] (Murphy JA).

[238] G v H [1994] HCA 48; (1994) 181 CLR 387, 390 (Brennan & McHugh JJ); Fazio v Fazio [46] (Murphy JA).

[239] Seltsam Pty Ltd v McGuiness [2000] NSWCA 29; (2000) 49 NSWLR 262 (Seltsam v McGuiness) [84] (Spigelman CJ); Fazio v Fazio [50] (Murphy JA).

[240] Amaca v Booth [69] (Gummow, Hayne & Crennan JJ); Amaca v Ellis [6].

[241]Adelaide Stevedoring Co Ltd v Forst, 569 (Dixon J).

[242] Amaca v Booth [69] (Gummow, Hayne & Crennan JJ).

[243] Appeal ts 57‑58, 60‑61, 96-98, 131-133.

[245] Tubemakers of Australia Ltd v Fernandez (1976) 50 ALJR 720 (Tubemakers v Fernandez), 724 (Mason J).

[248] Seltsam v McGuiness [142]-[144]; see also Sydney South West Area Health Service v Stamoulis [2009] NSWCA 153 [138].

[249] Seltsam v McGuiness [83], approving Fernandez v Tubemakers of Australia Ltd (1975) 2 NSWLR 190, 197 (Glass JA).

[250] EMI (Australia) Ltd v BES [1970] 2 NSWR 238, 242 (Herron CJ); Seltsam v McGuiness [94].

[251] Tubemakers v Fernandez, 725 (Mason J).

[252] Tubemakers v Fernandez, 721 (Barwick CJ).

[253] Amaca v Booth [67] (Gummow, Hayne & Crennan JJ).

[254] BGC Residential Pty Ltd v Fairwater Pty Ltd [2012] WASCA 268 [51].

[255] Seltsam v McGuiness [78] (Spigelman CJ).

[256] Seltsam v McGuiness [79] (Spigelman CJ).

[260] Shepherd v The Queen [1990] HCA 56; (1990) 170 CLR 573, 579.

[261] See also Seeley International Pty Ltd v Jeffrey [2013] VSCA 288 [45]-[47].

[266] Chief Executive Officer, Department for Child Protection and Family Support v IGR [112] (Quinlan CJ, Murphy & Beech JJA).

[267] Tubemakers v Fernandez, 721 (Barwick CJ).

[268] See Shepherd v The Queen [1990] HCA 56; (1990) 170 CLR 573, 576, 581.

[269] Austic v The State of Western Australia [2010] WASCA 110 [2]-[4].

[270] DKA v The State of Western Australia [2019] WASCA 123 [173].

[271] Primary reasons [894], [937].

[272] See [279] above.

[273] See Primary reasons [652], [869], [870], [871].

[275] Primary reasons [651]. See [202] above.

[276] See Primary reasons [613], [614], [616], [623], [628].

[278] As in the motivational speaker's 'If you believe in yourself, anything is possible!'

[284] Primary reasons [941], referring back to [820].

[285] Primary reasons [852], [857], [862], [936].

[286] Primary reasons [871], [880], [935].

[287] See, by way of a similar example: Mabior [188]-[190], [197] (Quinlan CJ, Murphy & Pritchard JJA).

[288] Amaca v Ellis [70]. In this context see the distinction drawn with Amaca v Ellis in Amaca v Booth [71].

[289] Tabet v Gett [2010] HCA 12; (2010) 240 CLR 537 (Tabet v Gett).

[290] Tabet v Gett [66] (Hayne & Bell JJ).

[291] Tabet v Gett [69] (Hayne & Bell JJ).

[292] Primary reasons [932], [941].

[293] Primary reasons [648]-[651], [935], [936], [946], [948].

[294] Primary reasons [815], [817], [818], [895], [935], [936].

[295] See [274] above.

[297] Amaca v Booth [68] (Gummow, Hayne & Crennan JJ).

[299] See [306] above.

[304] Harris P, Nagy S, Vardaxis N (eds), Mosby's Dictionary of Medicine, Nursing & Health Professions (2013, 3rd ANZ Edition, Elsevier)

[305] Which finding is incorporated in Primary reasons [938]; See [244] above.

[306] Cavanett v Chambers [1968] SASR 97.

[307] Gordon M Jenkins & Associates Pty Ltd v Coleman [1989] FCA 245; (1989) 23 FCR 38.

[308] Gordon M Jenkins & Associates Pty Ltd v Coleman, 48 (Sheppard, Beaumont & Hill JJ).

[318] Consistent with the manner in which his Honour understood the respondent to put his case (see [214] above).

[319] Primary reasons [651]. See [202] above.

[320] Appellant's submissions [68], [72].

[321] See Amended Statement of Claim dated 18 August 2017 [28] BAB 363.

[322] See above at [89], [98] (Keenan); [101], [105], [107] (Tracy); [126] (Pestell); [152]-[154] (Ditchfield); [173] (Hunt); [188] (Do).

[323] See [104]-[107] above.

[325] See [153]-[156] above.

[326] See [136] above.

[327] See [140]-[142] above.

[328] See [143]-[147] above.

[329] See [148] above.

[330] His evidence at trial was more circumspect in this regard (saying only that 'swelling is often delayed and the appearance on ultrasound is therefore often delayed'). See ts 1334.

[331] See Primary reasons [580], [587]. See also ts 1124 (Keenan).

[332] Primary reasons [586]. See [198] above.

[333] See for example: NRMA Insurance Ltd v Tatt (1989) 92 ALR 299, 311-312 (Samuels JA); English v Emery Reimbold & Strick Ltd [2002] EWCA Civ 605 [20], [73]; Fletcher Construction Australia Ltd v Lines Macfarlane & Marshall Pty Ltd (No 2) [2002] VSCA 189; (2002) 6 VR 1 (Fletcher Construction v Lines Macfarlane & Marshall) [157] (Charles, Buchanan & Chernov JJA); TCN Channel Nine Pty Ltd v Anning [2002] NSWCA 82; (2002) NSWLR 333 [149]-[151] (Spigelman CJ); Wiki v Atlantis Relocations (NSW) Pty Ltd [2004] NSWCA 174; (2004) 60 NSWLR 127 [56]-[68] (Ipp JA; Bryson JA and Stein AJA agreeing); Alsco Pty Ltd v Mircevic [2013] VSCA 229 [80]-[83] (Robson AJA); South Western Sydney Local Health District v Sorbello [2017] NSWCA 201 [65]-[66] (Simpson JA); Sarian v Elton [2011] NSWCA 123 [25]-[26], [62]-[67] (Whealy JA; Beazley JA agreeing); McDonald v Moore [2003] WASCA 21 [37]-[41] (Templeman J; Murray & Anderson JJ agreeing).

[334] Fletcher Construction v Lines Macfarlane & Marshall [157].

[336] Appellant's submissions [79]-[84]; Appeal ts 146-147.

[337] Sarian v Elton [2011] NSWCA 123 [25] (Whealy JA; Beazley JA agreeing).

[338] Primary reasons [651]; see [306] to [307] above.

[339] Appellant's submissions [88]-[89].

[342] See Appellant's submissions [99]; Appeal ts 147-150.

[345] Ts 1129, 1152-1153. See [97] above.

[349] Amended Statement of Claim dated 18 August 2017 [28(b)] (BAB 363).

[350] Amended Defence dated 24 August 2017 [18] (BAB 373).

[351] See [100], [103] above.

[352] See [168]-[169] above.

[353] See [67] above.

[354] Exhibit 6.24 (GAB 300); [169] above.

[355] Defendant's Submissions dated 28 August 2017 [58] (BAB 413).

[356] Plaintiff's Submissions dated 18 August 2017 [145] (BAB 400); Defendant's Submissions dated 28 August 2017 [62]: 'There is an issue as to whether the plaintiff suffered Stage 2 hypoxic ischaemic encephalopathy' (BAB 414).

[357] See above at [67]-[72] (Rao); [104], [108], [113] (Tracy); [170]-[172], [174]-[175] (Hunt).

[358] Defendant's Closing Submissions dated 27 October 2017 [237] (BAB 565).

[359] Appellant's submissions [107].

[360] Appellant's submissions [104].

[365] Appellant's submissions [112].

[366] Primary reasons [664]-[672]; See [208] above.

[368] Primary reasons [680]-[682].

[369] See [41] above.

[370] See [41] above.

[371] See [53] above.

[372] Appellant's submissions [120]; see also [115]-[117].

[373] See [108] above.

[374] See [53] above.

[383] See [203], [300], [372]-[376] above.

[385] Ts 226-227, 237; Primary reasons [588].

[386] Primary reasons [588]-[590].

[390] Primary reasons [614]. The reference is, apparently, referred to in Primary reasons [616].

[392] Her reference, at ts 288, to 'a tiny focus of haemorrhage in the left temporal lobe' must, in context, be a reference to the cerebrum rather than the cerebellum.

[394] When the issue of the size of bleeds was taken up with Dr Keenan, he gave evidence that 'Sometimes size doesn't matter. So small can be just as damaging as large' (ts 691).

[396] Appellant's submissions [141].

[398] See paragraph [52] above; Exhibit 1.34 (GAB 7).

[399] Exhibit 3.16 (GAB 154); Ts 696.

[400] See paragraph [52] above; Exhibit 1.34 (GAB 7).

[403] Ts 693. See also to the same effect at Ts 696 ('she's talking about an area outside the brain?).

[410] See [472] above.

[411] See for example [368]-[375] above.

[413] Primary reasons [933]. The word 'firm' appear to derive from Dr Tracy who expressed as his 'firm expert opinion' that the mechanism of the respondent's birth caused him to suffer his injuries and residual disabilities: Exhibit 3.8 (GAB 113).

[414] See [88] above.

[415] See [103] above.

[416] Appellant's submissions [151]-[152]; Appeal ts 172.

[417] See [392]-[396] above.

[419] See [105] above. See also ts 766.

[421] EMI (Australia) Ltd v BES [1970] 2 NSWR 238, 242 (Herron CJ); Seltsam v McGuiness [94].

[423] Appellant's submissions [154].

[425] Appellant's submissions [158].

[428] Primary reasons [924]-[925].

[434] Primary reasons [715], [803].

[435] Appellant's submissions [182].

[436] G v H [1994] HCA 48; (1994) 181 CLR 387, 390 (Brennan & McHugh JJ); Fazio v Fazio [46] (Murphy JA).

[437] Martin v Osborne [1936] HCA 23; (1936) 55 CLR 367 (Martin v Osborne), 385 (Evatt J); Fazio v Fazio [46].

[438] Martin v Osborne, 385-386 (Evatt J); Fazio v Fazio [46].

[440] Guest v The Nominal Defendant [2006] NSWCA 77 [109] (Ipp JA).

[441] Primary reasons [718]-[720].

[442] Appellant's submissions [173].

[443] Strong v Woolworths Ltd [22] (French CJ, Gummow, Crennan and Bell JJ).

[444] Western Australia v Watson [1990] WAR 248, 286 (Malcolm CJ, Brinsden & Seaman JJ).

[445] Hunt & Hunt Lawyers v Mitchell Morgan Nominees Pty Ltd [2013] HCA 10; (2013) 247 CLR 613 [45] (French CJ, Hayne & Kiefel JJ); The State of Western Australia v Cunningham [No 3] [2018] WASCA 207 [117] (Buss P, Murphy JA).

[446] March v E & MH Stramare, 509; see [254] above.

[447] Strong v Woolworths Ltd [18] (French CJ, Gummow, Crennan and Bell JJ). The Court there was referring to s 5D(1)(a) of the Civil Liability Act 2002 (NSW), which is identical terms to s 5C(1)(a) of the Civil Liability Act.

[448] Strong v Woolworths Ltd [23] (French CJ, Gummow, Crennan and Bell JJ).

[449] Bonnington Castings Ltd v Wardlaw [1956] UKHL 1; [1956] AC 613 (Bonnington v Wardlaw).

[450] It may be observed in passing that the application of this approach did not arise in Amaca v Ellis because it could not even be established that the 'accumulation of asbestos', as opposed to tobacco smoking, was a probable cause of the respondent's lung cancer (see Amaca v Ellis [66]-[68]).

[451] Although as the majority in Strong v Woolworths Ltd point out, that question itself might be affected by developments in medical science (Strong v Woolworths Ltd [27] (French CJ, Gummow, Crennan and Bell JJ).

[452] Adeels Palace Pty Ltd v Moubarak [2009] HCA 48; (2009) 239 CLR 420 (Adeels Palace) [54] (French CJ, Gummow, Hayne, Heydon & Crennan JJ).

[453] Adeels Palace [56] (French CJ, Gummow, Hayne, Heydon & Crennan JJ).

[454] Adeels Palace [57] (French CJ, Gummow, Hayne, Heydon & Crennan JJ).

[455] Fairchild v Glenhaven Funeral Services Ltd [2002] 1 AC 32 (Fairchild).

[456] McGhee v National Coal Board [1972] UKHL 7; [1973] 1 WLR 1 (McGhee).

[457] As to which see Mabior [299] (Quinlan CJ, Murphy & Pritchard JJA).

[458] Ipp Report, Recommendation 29, page 118.

[459] See also Strong v Woolworths Ltd [24]-[26] (French CJ, Gummow, Crennan and Bell JJ).

[462] Primary reasons [945]; see also Primary reasons [743].

[463] Wallace v Kam [14] (French CJ, Crennan, Kiefel, Gageler & Keane JJ). References in this passage to provisions in the Civil Liability Act 2002 (NSW) have been substituted with the equivalent provisions in the Civil Liability Act.

[464] Wallace v Kam [21] (French CJ, Crennan, Kiefel, Gageler & Keane JJ).

[465] Wallace v Kam [26] (French CJ, Crennan, Kiefel, Gageler & Keane JJ).

[469] Ellis (by his Next Friend Christopher Graham Ellis) v East Metropolitan Health Service [2018] WADC 36 (S) (Costs reasons) [6].

[470] House v The King [1936] HCA 40; (1936) 55 CLR 499, 504-505 (Dixon, Evatt and McTiernan JJ).

[471] Appellant's submissions in CACV 37 of 2018 [106].