East Metropolitan Health Service v Ellis (by his next friend Christopher Graham Ellis)

[2020] WASCA 147

JURISDICTION     :   SUPREME COURT OF WESTERN AUSTRALIA

TITLE OF COURT  :   THE COURT OF APPEAL (WA)

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

CORAM:   QUINLAN CJ

MITCHELL JA

BEECH JA

HEARD:   14, 15 & 16 OCTOBER 2019

DELIVERED          :   10 SEPTEMBER 2020

FILE NO/S:   CACV 37 of 2018

BETWEEN:   EAST METROPOLITAN HEALTH SERVICE

Appellant

AND

COOPER ELLIS (by his next friend CHRISTOPHER GRAHAM ELLIS)

Respondent

FILE NO/S:   CACV 54 of 2018

BETWEEN:   EAST METROPOLITAN HEALTH SERVICE

Appellant

AND

COOPER ELLIS (by his next friend CHRISTOPHER GRAHAM ELLIS)

Respondent

FILE NO/S:   CACV 93 of 2018

BETWEEN:   EAST METROPOLITAN HEALTH SERVICE

Appellant

AND

COOPER ELLIS (by his next friend CHRISTOPHER GRAHAM  ELLIS)

Respondent

ON APPEAL FROM:

Jurisdiction              :   DISTRICT COURT OF WESTERN AUSTRALIA

Coram:   GETHING DCJ

Citation: ELLIS -v- EAST METROPOLITAN HEALTH SERVICE [2018] WADC 91

File Number            :   CIV 2206 of 2012

Catchwords:

Tort - Negligence - Medical negligence - Causation - Factual causation - Finding that negligence in the management of a child's birth caused the developmental and cognitive impairments - Satisfaction of factual causation on the balance of probabilities - Relevance of evidence of possibilities - Circumstantial case - Inference of factual causation

Tort - Negligence - Causation - Factual causation - Material contribution - Whether an appropriate case within Civil Liability Act 2002 (WA), s 5C(2)

Costs - Offer of settlement

Legislation:

Civil Liability Act 2002 (WA), s 5C, s 5D
District Court Rules 2005 (WA), Rule 42A

Result:

Appeals dismissed

Category:    A

Representation:

CACV 37 of 2018

Counsel:

Appellant	:	GR Donaldson SC
Respondent	:	DR Campbell SC & RD McCabe

Solicitors:

Appellant	:	HWL Ebsworth Lawyers (Perth)
Respondent	:	Slater & Gordon - Perth

CACV 54 of 2018

Counsel:

Appellant	:	GR Donaldson SC
Respondent	:	DR Campbell SC & RD McCabe

Solicitors:

Appellant	:	HWL Ebsworth Lawyers (Perth)
Respondent	:	Slater & Gordon - Perth

CACV 93 of 2018

Counsel:

Appellant	:	GR Donaldson SC
Respondent	:	DR Campbell SC & RD McCabe

Solicitors:

Appellant	:	HWL Ebsworth Lawyers (Perth)
Respondent	:	Slater & Gordon - Perth

Case(s) referred to in decision(s):

Adelaide Stevedoring Co Ltd v Forst (1940) 64 CLR 538

Alsco Pty Ltd v Mircevic [2013] VSCA 229

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

Amaca Pty Ltd v Ellis (2010) 240 CLR 111

Apostolic Church Australia Ltd v Dixon [2018] WASCA 146

Austic v The State of Western Australia [2010] WASCA 110

BGC Residential Pty Ltd v Fairweather Pty Ltd [2012] WASCA 268

Bonnington Castings Ltd v Wardlaw [1956] AC 613

Cavanett v Chambers [1968] SASR 97

Chief Executive Officer, Department for Child Protection and Family Support v IGR [2019] WASCA 20; (2019) 54 WAR 222

Child and Adolescent Health Service v Mabior [2019] WASCA 151

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

Ellis (by his Next Friend Christopher Graham Ellis) v East Metropolitan Health Service [2018] WADC 36

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

EMI (Australia) Ltd v BES [1970] 2 NSWR 238

Fairchild v Glenhaven Funeral Services Ltd [2002] 1 AC 32

Fazio v Fazio [2012] WASCA 72

Fernandez v Tubemakers of Australia Ltd (1975) 2 NSWLR 190

Fletcher Construction Australia Ltd v Lines Macfarlane & Marshall Pty Ltd (No 2) [2002] VSCA 189; (2002) 6 VR 1

G v H [1994] HCA 48; (1994) 181 CLR 387

Gordon M Jenkins & Associates Pty Ltd v Coleman (1989) 23 FCR 38

Harriton v Stephens [2004] NSWCA 93; (2004) 59 NSWLR 694

Harriton v Stephens [2006] HCA 15; (2006) 226 CLR 52

House v The King [1936] HCA 40; (1936) 55 CLR 499

Hunt & Hunt Lawyers v Mitchell Morgan Nominees Pty Ltd [2013] HCA 10; (2013) 247 CLR 613

Jones v Dunkel (1959) 101 CLR 298

Joyce v Anderson [2020] WASCA 151

Luxton v Vines (1952) 85 CLR 352

March v E & MH Stramare Pty Ltd [1991] HCA 12; (1991) 171 CLR 506

Martin v Osborne [1936] HCA 23; (1936) 55 CLR 367

McDonald v Moore [2003] WASCA 21

McGhee v National Coal Board [1973] 1 WLR 1

NRMA Insurance Ltd v Tatt (1989) 92 ALR 299

Sarian v Elton [2011] NSWCA 123

Seeley International Pty Ltd v Jeffrey [2013] VSCA 288

Seltsam Pty Ltd v McGuiness [2000] NSWCA 29; (2000) 49 NSWLR 262

Shepherd v The Queen [1990] HCA 56; (1990) 170 CLR 573

South Western Sydney Local Health District v Sorbello [2017] NSWCA 201

Strong v Woolworths Ltd [2012] HCA 5; (2012) 246 CLR 182

Sydney South West Area Health Service v Stamoulis [2009] NSWCA 153

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

Tame v New South Wales [2002] HCA 35; (2002) 211 CLR 317

TCN Channel Nine Pty Ltd v Anning [2002] NSWCA 82; (2002) NSWLR 333

The State of Western Australia v Cunningham [No 3] [2018] WASCA 207

Tubemakers of Australia Ltd v Fernandez (1976) 50 ALJR 720

Wallace v Kam [2013] HCA 19; (2013) 250 CLR 375

Western Australia v Watson [1990] WAR 248

Wiki v Atlantis Relocations (NSW) Pty Ltd [2004] NSWCA 174; (2004) 60 NSWLR 127

Table of Contents

Introduction

The Appeal in Overview

Background

The course of the respondent's condition

Expert Evidence

Dr Shripada Rao

Dr Thai Nguyen

Dr Ross Keenan

Dr Mark Tracy

Dr Carmela Pestell

Professor Michael Ditchfield

Professor Rodney Hunt

Dr Tien Do

The learned trial judge's reasons as to causation

Section 13 of the Primary reasons – Birth Injuries

Section 16 of the Primary reasons – Developmental and Cognitive Impairments

2014 and 2015 MRI scans

Significance of the diagnosis of hypoxic ischaemic encephalopathy

The profile of the respondent's developmental issues

Other potential causes of the Developmental and Cognitive Impairments

Determination as to factual causation

Scope of liability

Grounds of Appeal

Factual causation, inferences and possibilities

General principles

Application of these principles in the Primary Reasons

Conclusion as to the extent of brain injury

References as to 'possibilities'

Disposition of the grounds of appeal

Ground 1 – The possibility of personal injury as 'harm'

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

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

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

The respondent's case at trial

Professor Ditchfield's evidence as to HIE

Finding as to extent of haemorrhagic contusion was not indispensable

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

The learned trial judge's approach in this case

Significance of any error

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

Ground 6 - The possibility of a global microscopic brain injury

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

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

Ground 9 – The finding of Erb's palsy

Ground 10 – The finding of renal impairment

Ground 11 – Dr Nguyen's opinion

Ground 12 – The finding of subdural and intraventricular haemorrhage

Factual findings made by the learned trial judge

Use made of the factual findings

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

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

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

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

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

Ground 20 – The absence of an alternative cause

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

Ground 18 – Scope of Liability

Ground 19 - Scope of Liability revisited

Ground 22 – The ultimate finding of causation

Outcome of the appeal against the primary orders

The Pleading Appeal

The Costs Appeal

Conclusion

JUDGMENT OF THE COURT:

Introduction

1. Cooper Ellis (the respondent) was born at 9.42 pm on 24 August 2009 at Bentley Hospital (the Hospital).  The East Metropolitan Health Service (the appellant) is the legal entity responsible for the medical and nursing care provided by the Hospital, including that of Dr Hamza Amira, the obstetrician responsible for the management of the respondent's birth.

2. The respondent's birth was prolonged and difficult, in the course of which Dr Amira made a number of unsuccessful attempts to deliver the respondent by a Kiwi cup vacuum extraction, a form of instrumental delivery.  When the respondent was ultimately delivered, via a combination of techniques, he was 'flat', meaning he was not breathing, not moving and showed poor muscle tone.  It was not in dispute that the respondent suffered periods of perinatal asphyxia, meaning that, around the time of his birth, he suffered from a lack of oxygen or a lack of blood supply.[1] 

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

3. The respondent claimed that he suffered significant injuries in the course of his birth process, and that those injuries were caused by the negligence of Dr Amira.  There was no issue that the appellant was vicariously responsible for the actions of Dr Amira.

4. Gething DCJ found the respondent's case proven and, on 16 March 2018, ordered that judgment be entered for the respondent against the appellant in the sum of $5,231,149.  There is no challenge to the assessment of damages.

5. The learned trial found that Dr Amira was negligent in the following respects:

   (a)by 'attempting an instrumental delivery when the foetus was mid-cavity';[2]

   (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]

   [2] Primary reasons [386]-[394].

   [3] Primary reasons [440].

   [4] Primary reasons [441]-[497].

   [5] Primary reasons [498]-[543].

6. There is no challenge to the findings of negligence.

7. 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]

   [6] Primary reasons [735].

8. 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.

   [7] Primary reasons [578].

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

9. 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]

   [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. 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] 

    [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).

11. 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]

    [11] Primary reasons [549].

12. 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.

13. None of the above matters are in issue in the appeal.

14. 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;

    (c)delayed gross motor and fine motor skills; and

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

    [12] Primary reasons [790].

15. 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. 

16. 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.

    [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). 

17. 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] 

    [14] Primary reasons [932].

18. 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'.

    [15] Primary reasons [941].

19. 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] 

    [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).

20. 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.

21. 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.

The Appeal in Overview

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.

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

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] 

   [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.

   [20] Primary reasons [676]-[707].

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]

   [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).

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]

   [22] See grounds 1, 2, 5, 6, 16.

1. 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]

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

   [24] Ground 5.

2. 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.

   [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).

3. 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:

   (a)the course of the respondent's condition;

   (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] 

   [26] Primary reasons [173].

3. The respondent was assessed using 'Apgar' ratings at 1, 5 and 10 minutes, as follows:[27]

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

1 minute	5 minutes	10 minutes
Colour	0	1	1
Respiration	0	1	1
Reflex irritability	0	0	0
Muscle tone	0	0	0
Heart rate	1	2	2
1	4	4

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]

   [28] Primary reasons [176].

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]

   [29] Primary reasons [178].

   [30] Primary reasons [319].

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]

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

4. When the respondent was about 60 minutes of age, Dr Vercoe observed that the respondent started moving his legs.[32]

   [32] Primary reasons [182].

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]

   [33] Primary reasons [184].

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]

   [34] Primary reasons [553]-[554].

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]

   [35] Primary reasons [555].

8. 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:

   HIEII w/ likely seizures

   cooled.

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

   [36] Primary reasons [556].

9. On 25 August 2009, an electroencephalography (EEG) was conducted on the respondent.  No clinical seizures occurred during the recording. 

10. 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.

    [37] GAB 3; Primary reasons [557].

11. 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]

    [38] Primary reasons [596]-[597].

12. 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]

    [39] Primary reasons [559].

13. 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]

    [40] Primary reasons [560].

14. 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]

    [41] Primary reasons [561].

15. 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]

    [42] Primary reasons [562]-[563].

16. 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]

    [43] Primary reasons [564].

    [44] Primary reasons [566].

17. 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]

    [45] Primary reasons [567]-[568].

18. 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]

    [46] Primary reasons [569]; GAB 17.

19. 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]

    [47] GAB 7-8.

    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.

20. 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.

    [48] Primary reasons [573]; GAB 18.

21. 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]

Expert Evidence

[49] Primary reasons [835].

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]

   [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.

2. The respondent called the following expert witnesses relevant to that issue:

   (a)Dr Ross Keenan, a Consultant Radiologist;

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

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

3. 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.

4. 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

   (c)Dr Tien Do, a Paediatric Neuropsychologist.

5. 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.

6. 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.

7. 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.

8. 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.

9. We now turn to summarise the effect of the experts' evidence.  We will commence with the treating practitioners, Dr Rao and Dr Nguyen.

Dr Shripada Rao

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] 

   [51] Exhibit 1.35.

   [52] Exhibit 1.36.

   [53] Exhibit 1.37.

   [54] Exhibit 1.38.

3. All of those reports refer to the respondent's past diagnoses as including:

   (a)'Perinatal asphyxia'; and

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

4. 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.

   [55] Ts 223.

5. 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]

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

6. 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]

   [57] Ts 257.

7. 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]

   [58] Ts 233.

   [59] Ts 234.

8. 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.

   [60] Ts 259.

9. Dr Rao confirmed that the diagnosis of stage 2 HIE was his diagnosis and not someone else's.[61]

   [61] Ts 245.

10. 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] 

    [62] Ts 266.

11. 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.

Dr Thai Nguyen

[63] Ts 267.

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]

   [64] Ts 277-278.

1. 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]

   [65] Ts 283.

2. 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] below).[67] 

   [66] Ts 288.

   [67] Ts 289.

3. When asked whether there was anything in the 2015 MRI that would cause her to have a different opinion to Professor Ditchfield, Dr Nguyen said:[68] 

   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.

Dr Ross Keenan

[68] Ts 291.

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.

   [69] Ts 618.

   [70] Exhibit 3.13.

   [71] Exhibit 3.15.

   [72] Exhibit 3.16 (GAB 148-183).

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]

   [73] Exhibit 3.16 (GAB 151), ts 633.

   [74] Ts 634-635.

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] 

   [75] Exhibit 3.16 (GAB 152).

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.

   [76] Exhibit 3.16 (GAB 152).

   [77] Ts 645.

6. 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] 

   [78] Ts 639.

   [79] Ts 639.

   [80] Ts 642.

7. 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]

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

   [82] Exhibit 3.16 (GAB 151-152).

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

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

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

8. 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

   [86] Exhibit 3.16 (GAB 155).

9. 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.

   [87] Exhibit 3.16 (GAB 157-158).

10. 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..

    [88] Exhibit 3.16 (GAB 162-163).

11. 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).

12. 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.

    [89] Exhibit 11; Ts 411.

    [90] Ts 670.

13. 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] 

    [91] Ts 701.

    [92] Ts 1147 (see also ts 1137).

14. 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.

    [93] Ts 702-703.

15. 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]

    [94] Ts 703-706.

16. 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).

    [95] Ts 725.

17. 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] 

    [96] Ts 1124.

18. 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 -

    [97] Ts 1129.  See also ts 1152-1153.

19. 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.

Dr Mark Tracy

[98] Ts 1169-1170.

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] 

   [99] Ts 731.

   [100] Exhibit 3.8 (GAB 109-115).

   [101] Exhibit 3.10 (GAB 117-120).

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.

   [102] Exhibit 3.8 (GAB 112).

3. In relation the MRI images, Dr Tracy reported as follows:[103]

   [103] Exhibit 3.8 (GAB 112-113).

   a.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.

   …

   d.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.

4. 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.

5. 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 <100 beats/minute, decreased variability, and late decelerations), vaginal vs cesarean birth, use of instrumentation (i.e., forceps or vacuum extraction), Apgar score at 5 minutes, and need for resuscitation (defined as assisted bag­mask ventilation or endotracheal intubation).' These features are common also to cases of HIE. The concurrence of labour dystocia and cerebellar haemorrhage seen with Cooper concurs with their report. Abnormal neurological outcome was common in this study 39% Limperopoulos and colleagues found 'Gross motor delays, expressive language deficits,  and externalizing behavioural problems were the most common (44%). Cognitive deficits were present in one third of cases.  Larger cerebellar lesions were associated significantly lower cognitive, gross motor, expressive language, and social-behavioural scores.' A recent review by Dr Limperopoulos on injury to the developing cerebellum: causes and mechanisms details the well described pattern of injury to term infants cerebellum due to hypoxic-ischemic injury.

   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.

   [104] Exhibit 3.10 (GAB 119).

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.

   [105] Ts 734.

2. 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.

   [106] Ts 736.

3. 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]

   [107] Ts 740.

   [108] Ts 741.

4. 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]

   [109] Ts 742.

5. 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 'highly 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.

   [110] Ts 748-749. 

6. 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]

   [111] Ts 748. 

7. 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]

   [112] Ts 759. 

8. 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.

   [113] Ts 766. 

9. 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]

   [114] Ts 772.

10. 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.

Dr Carmela Pestell

[115] Ts 775.

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] 

   [116] Exhibit 3.19 (GAB 186-198).

   [117] Exhibit 3.21 (GAB 201-209).

   [118] Exhibit 3.23 (GAB 212-226).

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.

   [119] Exhibit 3.19 (GAB 196).

4. 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.

   [120] Exhibit 3.21 (GAB 207).

   [121] Exhibit 3.23 (GAB 222-223).

5. 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.

   [122] Ts 390-391.

6. 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].

   [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.

7. 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.

8. 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). 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.

   [124] Ts 413.

9. Dr Pestell said she supported the conclusions of the Consensus Paper based on her clinical experience.[125]

   [125] Ts 416.

10. Dr Pestell was cross-examined on a separate occasion in the following week of the trial.

11. 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]

    [126] Ts 939.

12. 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.

    [127] Ts 943.

13. 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.

    [128] Ts 946.

14. 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]

    [129] Ts 949-950.

15. 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.

    [130] Ts 951-952.  See also ts 969.

    [131] Ts 953.

16. 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.

    [132] Ts 975.

17. 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.

    [133] Ts 982.

18. 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.

Professor Michael Ditchfield

[134] Ts 983.

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]

   [135] Ts 1318

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]  

   [136] Exhibit 6.9 (GAB 233-240).

   [137] Exhibit 6.11 (GAB 242).

   [138] Exhibit 6.13 (GAB 244-245).

   [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.

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.

   [140] Exhibit 6.9 (GAB 237).

1. 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.

2. 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.

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

3. Ground 20 is not made out.

4. 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.

5. 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).

4. 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.

5. 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.

6. 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'.

7. The learned trial judge's analysis of that issue was as follows:[441]

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

   [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)

8. 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]

   [442] Appellant's submissions [173].

9. 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].

10. 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).

11. 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.

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

12. 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'.

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

13. The majority of the High Court explained this in Hunt & Hunt Lawyers v Mitchell Morgan Nominees Pty Ltd as follows:[445]

    [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).

    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).

14. 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]

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

15. 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.

    [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 Act2002 (NSW), which is identical terms to s 5C(1)(a) of the Civil Liability Act.

16. 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.

17. 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]

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

    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)

18. '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.

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

19. 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]

    [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]).

20. This is where s 5C(2) comes in.

21. 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]

    [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). 

22. 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 Act2002 (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]

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

    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.

23. 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]

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

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

    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.

24. 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. 

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

    [456] McGhee v National Coal Board [1973] 1 WLR 1 (McGhee).

25. 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]

    [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). 

26. 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.

    [460] Amaca vEllis [70].

27. 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).

28. 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).

29. 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. 

Ground 18 – Scope of Liability

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)).

1. 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]

   [461] Primary reasons [947].

2. 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]

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

3. The appellant submits that the learned trial judge thereby imposed a burden of proof on the appellant. 

4. The submission must be rejected.

5. 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.

6. As the High Court stated in Wallace v Kam:[463]

   [463] Wallace v Kam [14] (French CJ, Crennan, Kiefel, Gageler & Keane JJ). References in this passage to provisions in the Civil Liability Act2002 (NSW) have been substituted with the equivalent provisions in the Civil Liability Act.

   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 [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.

7. 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.

8. 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.

9. Ground 18 is not made out.

Ground 19 - Scope of Liability revisited

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]

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

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]

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

   [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. 

6. 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.

7. 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.

8. 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.

   [466] Appeal ts 177-178.

9. Ground 19 is not made out.

Ground 22 – The ultimate finding of causation

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.

The Pleading Appeal

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]

   [467] Appeal ts 32.

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.

   [468] Appeal ts 190-192.

3. In our view the appropriate order in relation to the Pleading appeal (CACV 93 of 2018) is that it be dismissed.

The Costs Appeal

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;

3. 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:

   (3) Subrule (4) applies if —

   (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.

4. 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]

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

   [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.

5. 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.

6. The learned trial judge declined to order otherwise.  His reasons for doing so were as follows:

   49 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.

   50However, 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.

   51 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.

   52 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.

   53 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.

7. 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]

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

8. In our view, the Costs reasons do not disclose error, and nor was order 1(a) unreasonable or plainly unjust.

9. 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. 

10. 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 Cognitive Impairments'.[471]

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

11. 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. 

12. 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.

13. 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.

14. The Costs appeal (CACV 54 of 2018) must be dismissed.

Conclusion

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.

JS
Principal Associate to the Honourable Chief Justice Quinlan

10 SEPTEMBER 2020